advanced cardiac life support acls . dr tarek belashher
TRANSCRIPT
ADVANCED CARDIAC LIFE
SUPPORT(ACLS) - 2010
Speaker ndash Dr TAREK BELASHHER
Abusetta hospital
ACLS Course
Arrest scenarios
VF
Pulse less VT
A systole
PEA
Pre-arrest scenarios
Tachyarrhythmias
Bradyarrythmias
Ischemia
Stable Angina
Unstable Angina
MI
Stroke
Key Issues in ACLS
Airway
CPR
Defibrillation
Drug therapy
Post-resuscitation management
Special Situations
BLS Key Concepts
Avoid Hyperventilation (Do not ventilate too fast or too
much volume)
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Resume CPR immediately after shock Interruption in
CPR for rhythm check should not exceed 10 seconds
BLS Key Concepts
Chest compression should not be interrupted except for
Shock delivery
Rhythm check
Ventilation (until an advanced airway is inserted)
Do not interrupt CPR
To insert cannula or to give drugs
To listen to the heart or to take BP
Waiting for charging the Defibrillator
To rotate personnel
Chances of survival with time
ADVANCED CARDIAC LIFE SUPPORT
ACLS impacts multiple key links in the chain of
survival that include interventions to prevent cardiac
arrest treat cardiac arrest and improve outcomes
of patients who achieve return of spontaneous
circulation (ROSC) after cardiac arrest
Interventions aimed at preventing cardiac arrest
include airway management ventilation support
and treatment of bradyarrhythmias and
tachyarrhythmias
AHA ADULT CHAIN OF SURVIVAL
1 Immediate recognition of cardiac arrest and
activation of the emergency response system
2 Early CPR with an emphasis on chest
compressions
3 Rapid defibrillation
4 Effective advanced life support
5 Integrated postndashcardiac arrest care
CARDIOPULMONARY RESUSCITATION (CPR)
Cardiopulmonary resuscitation (CPR) is a series of
life saving actions that improve the chance of
survival following cardiac arrest
KEY CHANGES FROM THE
2005 BLS GUIDELINES
Immediate recognition of SCA based on assessing
unresponsiveness and absence of normal breathing
ldquoLook Listen and Feelrdquo removed from the BLS
algorithm
Encouraging Hands-Only (chest compression only)
CPR
Sequence change CAB rather than ABC
Health care providers continue effective chest
compressions CPR until return of spontaneous
circulation or termination of resuscitative efforts
A CHANGE FROM A-B-C TO C-A-B
o 2010 (New) ldquoLook listen and feelrdquo was removed from the CPR sequence After delivery of 30 compressions the lone rescuer opens the victimrsquos airway and delivers 2 breaths
2005 (Old) ldquoLook listen and feelrdquo was used to assess breathing after the airway was opened
2010 (New) Initiate chest compressions before ventilations
2005 (Old) The sequence of adult CPR began with opening of the airway checking for normal breathing and then delivery of 2 rescue breaths followed by cycles of 30 chest compressions and 2 breaths
2010 (New) It is reasonable for lay rescuers and
healthcare providers to perform chest
compressions at a rate of at least100min
2005 (Old) Compress at a rate of about 100mi
2010 (New) The adult sternum should be
depressed at least 2 inches (5 cm)
2005 (Old) The adult sternum should be depressed
approximately 1 to 2 inches (approximately 4 to 5
cm)n
2005 (Old) Cricoid pressure should be used only if
the victim is deeply unconscious and it usually
requires a third rescuer not involved in rescue
breaths or compressions
2010(new)routine use of cricoid pressure in
cardiac arrest is not recommended
17
CRICOID PRESSURE
ThyroidCartilage
Cricoid
2005 TO 2010 CHANGES
Component of CPR 2005 ECC recommendations
2010 ECC Recommendations
DEPTH OF COMPRESSION
1 frac12 - 2 inches Greater than 2 inches
RATE 100 MINUTE At least 100 MIN
VENTILATION 8-10 MINUTE 8-10 MINUTE
CHEST RECOIL 100 100
INTURUPTIONS Minimized Less than 10 seconds goal
PULSE CHECK HCP Only HCP only Checking for ldquoDEFNITE pulserdquo
2010 (New) The precordial thump should not be
used for un witnessed out-of-hospital cardiac arrest
The precordial thump may be considered for
patients with witnessed monitored unstable VT
(including pulse less VT) if a defibrillator is not
immediately ready for use but it should not delay
CPR and shock delivery
SUMMARY OF KEY ISSUES AND MAJOR CHANGES
The major changes in advanced cardiovascular life support
(ACLS) for 2010 include the following
bull Quantitative waveform capnography is recommended for
confirmation and monitoring of endotracheal tube placement
and CPR quality
bull The traditional cardiac arrest algorithm was simplified and an
alternative conceptual design was created to emphasize the
importance of high-quality CPR
bull There is an increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
bull Atropine is no longer recommended for routine use in the
management of pulse less electrical activity (PEA)asystole
CAPNOGRAPHY RECOMMENDATION
2010 (New) Continuous quantitative waveform
capnography is now recommended for intubated
patients throughout the per arrest period When
quantitative waveform capnography is used for
adults applications now include recommendations
for confirming tracheal tube placement and for
monitoring CPR quality and detecting ROSC based
on end-tidal carbon dioxide (PETCO2) values
PROGNOSTIC INDICATORS IN THE ADULT POSTARREST
PATIENT TREATED WITH THERAPEUTIC HYPOTHERMIA
2010 (New) In adult postndashcardiac arrest patients
treated with therapeutic hypothermia it is
recommended that clinical neurologic signs
electrophysiologic studies biomarkers and imaging
be performed where available at 3 days after
cardiac arrest
Hypothermia
ILCOR Advisory statement (2003)
Unconscious adult patients with spontaneous
circulation after out-of-hospital cardiac arrest
should be cooled to 32-34degC for 12-24 hrs when the
initial rhythm was ventricular fibrillation (VF)
Such cooling may also be beneficial for other
rhythms or in-hospital cardiac arrests
Hypothermia
Cooling
Retard enzymatic suppress production of free
radicals
Reduction of O2 demand in low-flow regions
Protection of membrane fluidity
Reduction of intracellular acidosis
Decrease in cerebral edema and ICP
2010 (New) Advanced life support training
should include training in teamwork
Why Resuscitation skills are often performed
simultaneously and healthcare providers must be
able to work collaboratively to minimize
interruptions in chest compressions Teamwork and
leadership skills continue to be important
particularly for advanced courses that include ACLS
and PALS providers
MONITORING DURING CPR
Physiologic parameters
Monitoring of PETCO2 (35 to 40 mmHg)
Coronary perfusion pressure (CPP) (15mmHg)
Central venous oxygen saturation (ScvO2)
Abrupt increase in any of these parameters is a
sensitive indicator of ROSC that can be monitored
without interrupting chest compressions
Quantitative waveform capnography
If Petco2 lt10 mm Hg attempt to improve CPR
quality
Intra-arterial pressure
If diastolic pressure lt20 mm Hg attempt to improve
CPR quality
If ScvO2 is lt 30 consider trying to improve the
quality of CPR
HIGH QUALITY CPR
Chest compressions of adequate rate 100min
A compression depth of at least 2 inches (5 cm) in
adults and in children a compression depth of at
least 15 inches [4 cm] in infants
Complete chest recoil after each compression
Minimizing interruptions in chest compressions
Avoiding excessive ventilation
If multiple rescuers are available rotate the task of
compressions every 2 minutes
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
ACLS Course
Arrest scenarios
VF
Pulse less VT
A systole
PEA
Pre-arrest scenarios
Tachyarrhythmias
Bradyarrythmias
Ischemia
Stable Angina
Unstable Angina
MI
Stroke
Key Issues in ACLS
Airway
CPR
Defibrillation
Drug therapy
Post-resuscitation management
Special Situations
BLS Key Concepts
Avoid Hyperventilation (Do not ventilate too fast or too
much volume)
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Resume CPR immediately after shock Interruption in
CPR for rhythm check should not exceed 10 seconds
BLS Key Concepts
Chest compression should not be interrupted except for
Shock delivery
Rhythm check
Ventilation (until an advanced airway is inserted)
Do not interrupt CPR
To insert cannula or to give drugs
To listen to the heart or to take BP
Waiting for charging the Defibrillator
To rotate personnel
Chances of survival with time
ADVANCED CARDIAC LIFE SUPPORT
ACLS impacts multiple key links in the chain of
survival that include interventions to prevent cardiac
arrest treat cardiac arrest and improve outcomes
of patients who achieve return of spontaneous
circulation (ROSC) after cardiac arrest
Interventions aimed at preventing cardiac arrest
include airway management ventilation support
and treatment of bradyarrhythmias and
tachyarrhythmias
AHA ADULT CHAIN OF SURVIVAL
1 Immediate recognition of cardiac arrest and
activation of the emergency response system
2 Early CPR with an emphasis on chest
compressions
3 Rapid defibrillation
4 Effective advanced life support
5 Integrated postndashcardiac arrest care
CARDIOPULMONARY RESUSCITATION (CPR)
Cardiopulmonary resuscitation (CPR) is a series of
life saving actions that improve the chance of
survival following cardiac arrest
KEY CHANGES FROM THE
2005 BLS GUIDELINES
Immediate recognition of SCA based on assessing
unresponsiveness and absence of normal breathing
ldquoLook Listen and Feelrdquo removed from the BLS
algorithm
Encouraging Hands-Only (chest compression only)
CPR
Sequence change CAB rather than ABC
Health care providers continue effective chest
compressions CPR until return of spontaneous
circulation or termination of resuscitative efforts
A CHANGE FROM A-B-C TO C-A-B
o 2010 (New) ldquoLook listen and feelrdquo was removed from the CPR sequence After delivery of 30 compressions the lone rescuer opens the victimrsquos airway and delivers 2 breaths
2005 (Old) ldquoLook listen and feelrdquo was used to assess breathing after the airway was opened
2010 (New) Initiate chest compressions before ventilations
2005 (Old) The sequence of adult CPR began with opening of the airway checking for normal breathing and then delivery of 2 rescue breaths followed by cycles of 30 chest compressions and 2 breaths
2010 (New) It is reasonable for lay rescuers and
healthcare providers to perform chest
compressions at a rate of at least100min
2005 (Old) Compress at a rate of about 100mi
2010 (New) The adult sternum should be
depressed at least 2 inches (5 cm)
2005 (Old) The adult sternum should be depressed
approximately 1 to 2 inches (approximately 4 to 5
cm)n
2005 (Old) Cricoid pressure should be used only if
the victim is deeply unconscious and it usually
requires a third rescuer not involved in rescue
breaths or compressions
2010(new)routine use of cricoid pressure in
cardiac arrest is not recommended
17
CRICOID PRESSURE
ThyroidCartilage
Cricoid
2005 TO 2010 CHANGES
Component of CPR 2005 ECC recommendations
2010 ECC Recommendations
DEPTH OF COMPRESSION
1 frac12 - 2 inches Greater than 2 inches
RATE 100 MINUTE At least 100 MIN
VENTILATION 8-10 MINUTE 8-10 MINUTE
CHEST RECOIL 100 100
INTURUPTIONS Minimized Less than 10 seconds goal
PULSE CHECK HCP Only HCP only Checking for ldquoDEFNITE pulserdquo
2010 (New) The precordial thump should not be
used for un witnessed out-of-hospital cardiac arrest
The precordial thump may be considered for
patients with witnessed monitored unstable VT
(including pulse less VT) if a defibrillator is not
immediately ready for use but it should not delay
CPR and shock delivery
SUMMARY OF KEY ISSUES AND MAJOR CHANGES
The major changes in advanced cardiovascular life support
(ACLS) for 2010 include the following
bull Quantitative waveform capnography is recommended for
confirmation and monitoring of endotracheal tube placement
and CPR quality
bull The traditional cardiac arrest algorithm was simplified and an
alternative conceptual design was created to emphasize the
importance of high-quality CPR
bull There is an increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
bull Atropine is no longer recommended for routine use in the
management of pulse less electrical activity (PEA)asystole
CAPNOGRAPHY RECOMMENDATION
2010 (New) Continuous quantitative waveform
capnography is now recommended for intubated
patients throughout the per arrest period When
quantitative waveform capnography is used for
adults applications now include recommendations
for confirming tracheal tube placement and for
monitoring CPR quality and detecting ROSC based
on end-tidal carbon dioxide (PETCO2) values
PROGNOSTIC INDICATORS IN THE ADULT POSTARREST
PATIENT TREATED WITH THERAPEUTIC HYPOTHERMIA
2010 (New) In adult postndashcardiac arrest patients
treated with therapeutic hypothermia it is
recommended that clinical neurologic signs
electrophysiologic studies biomarkers and imaging
be performed where available at 3 days after
cardiac arrest
Hypothermia
ILCOR Advisory statement (2003)
Unconscious adult patients with spontaneous
circulation after out-of-hospital cardiac arrest
should be cooled to 32-34degC for 12-24 hrs when the
initial rhythm was ventricular fibrillation (VF)
Such cooling may also be beneficial for other
rhythms or in-hospital cardiac arrests
Hypothermia
Cooling
Retard enzymatic suppress production of free
radicals
Reduction of O2 demand in low-flow regions
Protection of membrane fluidity
Reduction of intracellular acidosis
Decrease in cerebral edema and ICP
2010 (New) Advanced life support training
should include training in teamwork
Why Resuscitation skills are often performed
simultaneously and healthcare providers must be
able to work collaboratively to minimize
interruptions in chest compressions Teamwork and
leadership skills continue to be important
particularly for advanced courses that include ACLS
and PALS providers
MONITORING DURING CPR
Physiologic parameters
Monitoring of PETCO2 (35 to 40 mmHg)
Coronary perfusion pressure (CPP) (15mmHg)
Central venous oxygen saturation (ScvO2)
Abrupt increase in any of these parameters is a
sensitive indicator of ROSC that can be monitored
without interrupting chest compressions
Quantitative waveform capnography
If Petco2 lt10 mm Hg attempt to improve CPR
quality
Intra-arterial pressure
If diastolic pressure lt20 mm Hg attempt to improve
CPR quality
If ScvO2 is lt 30 consider trying to improve the
quality of CPR
HIGH QUALITY CPR
Chest compressions of adequate rate 100min
A compression depth of at least 2 inches (5 cm) in
adults and in children a compression depth of at
least 15 inches [4 cm] in infants
Complete chest recoil after each compression
Minimizing interruptions in chest compressions
Avoiding excessive ventilation
If multiple rescuers are available rotate the task of
compressions every 2 minutes
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
Key Issues in ACLS
Airway
CPR
Defibrillation
Drug therapy
Post-resuscitation management
Special Situations
BLS Key Concepts
Avoid Hyperventilation (Do not ventilate too fast or too
much volume)
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Resume CPR immediately after shock Interruption in
CPR for rhythm check should not exceed 10 seconds
BLS Key Concepts
Chest compression should not be interrupted except for
Shock delivery
Rhythm check
Ventilation (until an advanced airway is inserted)
Do not interrupt CPR
To insert cannula or to give drugs
To listen to the heart or to take BP
Waiting for charging the Defibrillator
To rotate personnel
Chances of survival with time
ADVANCED CARDIAC LIFE SUPPORT
ACLS impacts multiple key links in the chain of
survival that include interventions to prevent cardiac
arrest treat cardiac arrest and improve outcomes
of patients who achieve return of spontaneous
circulation (ROSC) after cardiac arrest
Interventions aimed at preventing cardiac arrest
include airway management ventilation support
and treatment of bradyarrhythmias and
tachyarrhythmias
AHA ADULT CHAIN OF SURVIVAL
1 Immediate recognition of cardiac arrest and
activation of the emergency response system
2 Early CPR with an emphasis on chest
compressions
3 Rapid defibrillation
4 Effective advanced life support
5 Integrated postndashcardiac arrest care
CARDIOPULMONARY RESUSCITATION (CPR)
Cardiopulmonary resuscitation (CPR) is a series of
life saving actions that improve the chance of
survival following cardiac arrest
KEY CHANGES FROM THE
2005 BLS GUIDELINES
Immediate recognition of SCA based on assessing
unresponsiveness and absence of normal breathing
ldquoLook Listen and Feelrdquo removed from the BLS
algorithm
Encouraging Hands-Only (chest compression only)
CPR
Sequence change CAB rather than ABC
Health care providers continue effective chest
compressions CPR until return of spontaneous
circulation or termination of resuscitative efforts
A CHANGE FROM A-B-C TO C-A-B
o 2010 (New) ldquoLook listen and feelrdquo was removed from the CPR sequence After delivery of 30 compressions the lone rescuer opens the victimrsquos airway and delivers 2 breaths
2005 (Old) ldquoLook listen and feelrdquo was used to assess breathing after the airway was opened
2010 (New) Initiate chest compressions before ventilations
2005 (Old) The sequence of adult CPR began with opening of the airway checking for normal breathing and then delivery of 2 rescue breaths followed by cycles of 30 chest compressions and 2 breaths
2010 (New) It is reasonable for lay rescuers and
healthcare providers to perform chest
compressions at a rate of at least100min
2005 (Old) Compress at a rate of about 100mi
2010 (New) The adult sternum should be
depressed at least 2 inches (5 cm)
2005 (Old) The adult sternum should be depressed
approximately 1 to 2 inches (approximately 4 to 5
cm)n
2005 (Old) Cricoid pressure should be used only if
the victim is deeply unconscious and it usually
requires a third rescuer not involved in rescue
breaths or compressions
2010(new)routine use of cricoid pressure in
cardiac arrest is not recommended
17
CRICOID PRESSURE
ThyroidCartilage
Cricoid
2005 TO 2010 CHANGES
Component of CPR 2005 ECC recommendations
2010 ECC Recommendations
DEPTH OF COMPRESSION
1 frac12 - 2 inches Greater than 2 inches
RATE 100 MINUTE At least 100 MIN
VENTILATION 8-10 MINUTE 8-10 MINUTE
CHEST RECOIL 100 100
INTURUPTIONS Minimized Less than 10 seconds goal
PULSE CHECK HCP Only HCP only Checking for ldquoDEFNITE pulserdquo
2010 (New) The precordial thump should not be
used for un witnessed out-of-hospital cardiac arrest
The precordial thump may be considered for
patients with witnessed monitored unstable VT
(including pulse less VT) if a defibrillator is not
immediately ready for use but it should not delay
CPR and shock delivery
SUMMARY OF KEY ISSUES AND MAJOR CHANGES
The major changes in advanced cardiovascular life support
(ACLS) for 2010 include the following
bull Quantitative waveform capnography is recommended for
confirmation and monitoring of endotracheal tube placement
and CPR quality
bull The traditional cardiac arrest algorithm was simplified and an
alternative conceptual design was created to emphasize the
importance of high-quality CPR
bull There is an increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
bull Atropine is no longer recommended for routine use in the
management of pulse less electrical activity (PEA)asystole
CAPNOGRAPHY RECOMMENDATION
2010 (New) Continuous quantitative waveform
capnography is now recommended for intubated
patients throughout the per arrest period When
quantitative waveform capnography is used for
adults applications now include recommendations
for confirming tracheal tube placement and for
monitoring CPR quality and detecting ROSC based
on end-tidal carbon dioxide (PETCO2) values
PROGNOSTIC INDICATORS IN THE ADULT POSTARREST
PATIENT TREATED WITH THERAPEUTIC HYPOTHERMIA
2010 (New) In adult postndashcardiac arrest patients
treated with therapeutic hypothermia it is
recommended that clinical neurologic signs
electrophysiologic studies biomarkers and imaging
be performed where available at 3 days after
cardiac arrest
Hypothermia
ILCOR Advisory statement (2003)
Unconscious adult patients with spontaneous
circulation after out-of-hospital cardiac arrest
should be cooled to 32-34degC for 12-24 hrs when the
initial rhythm was ventricular fibrillation (VF)
Such cooling may also be beneficial for other
rhythms or in-hospital cardiac arrests
Hypothermia
Cooling
Retard enzymatic suppress production of free
radicals
Reduction of O2 demand in low-flow regions
Protection of membrane fluidity
Reduction of intracellular acidosis
Decrease in cerebral edema and ICP
2010 (New) Advanced life support training
should include training in teamwork
Why Resuscitation skills are often performed
simultaneously and healthcare providers must be
able to work collaboratively to minimize
interruptions in chest compressions Teamwork and
leadership skills continue to be important
particularly for advanced courses that include ACLS
and PALS providers
MONITORING DURING CPR
Physiologic parameters
Monitoring of PETCO2 (35 to 40 mmHg)
Coronary perfusion pressure (CPP) (15mmHg)
Central venous oxygen saturation (ScvO2)
Abrupt increase in any of these parameters is a
sensitive indicator of ROSC that can be monitored
without interrupting chest compressions
Quantitative waveform capnography
If Petco2 lt10 mm Hg attempt to improve CPR
quality
Intra-arterial pressure
If diastolic pressure lt20 mm Hg attempt to improve
CPR quality
If ScvO2 is lt 30 consider trying to improve the
quality of CPR
HIGH QUALITY CPR
Chest compressions of adequate rate 100min
A compression depth of at least 2 inches (5 cm) in
adults and in children a compression depth of at
least 15 inches [4 cm] in infants
Complete chest recoil after each compression
Minimizing interruptions in chest compressions
Avoiding excessive ventilation
If multiple rescuers are available rotate the task of
compressions every 2 minutes
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
BLS Key Concepts
Avoid Hyperventilation (Do not ventilate too fast or too
much volume)
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Resume CPR immediately after shock Interruption in
CPR for rhythm check should not exceed 10 seconds
BLS Key Concepts
Chest compression should not be interrupted except for
Shock delivery
Rhythm check
Ventilation (until an advanced airway is inserted)
Do not interrupt CPR
To insert cannula or to give drugs
To listen to the heart or to take BP
Waiting for charging the Defibrillator
To rotate personnel
Chances of survival with time
ADVANCED CARDIAC LIFE SUPPORT
ACLS impacts multiple key links in the chain of
survival that include interventions to prevent cardiac
arrest treat cardiac arrest and improve outcomes
of patients who achieve return of spontaneous
circulation (ROSC) after cardiac arrest
Interventions aimed at preventing cardiac arrest
include airway management ventilation support
and treatment of bradyarrhythmias and
tachyarrhythmias
AHA ADULT CHAIN OF SURVIVAL
1 Immediate recognition of cardiac arrest and
activation of the emergency response system
2 Early CPR with an emphasis on chest
compressions
3 Rapid defibrillation
4 Effective advanced life support
5 Integrated postndashcardiac arrest care
CARDIOPULMONARY RESUSCITATION (CPR)
Cardiopulmonary resuscitation (CPR) is a series of
life saving actions that improve the chance of
survival following cardiac arrest
KEY CHANGES FROM THE
2005 BLS GUIDELINES
Immediate recognition of SCA based on assessing
unresponsiveness and absence of normal breathing
ldquoLook Listen and Feelrdquo removed from the BLS
algorithm
Encouraging Hands-Only (chest compression only)
CPR
Sequence change CAB rather than ABC
Health care providers continue effective chest
compressions CPR until return of spontaneous
circulation or termination of resuscitative efforts
A CHANGE FROM A-B-C TO C-A-B
o 2010 (New) ldquoLook listen and feelrdquo was removed from the CPR sequence After delivery of 30 compressions the lone rescuer opens the victimrsquos airway and delivers 2 breaths
2005 (Old) ldquoLook listen and feelrdquo was used to assess breathing after the airway was opened
2010 (New) Initiate chest compressions before ventilations
2005 (Old) The sequence of adult CPR began with opening of the airway checking for normal breathing and then delivery of 2 rescue breaths followed by cycles of 30 chest compressions and 2 breaths
2010 (New) It is reasonable for lay rescuers and
healthcare providers to perform chest
compressions at a rate of at least100min
2005 (Old) Compress at a rate of about 100mi
2010 (New) The adult sternum should be
depressed at least 2 inches (5 cm)
2005 (Old) The adult sternum should be depressed
approximately 1 to 2 inches (approximately 4 to 5
cm)n
2005 (Old) Cricoid pressure should be used only if
the victim is deeply unconscious and it usually
requires a third rescuer not involved in rescue
breaths or compressions
2010(new)routine use of cricoid pressure in
cardiac arrest is not recommended
17
CRICOID PRESSURE
ThyroidCartilage
Cricoid
2005 TO 2010 CHANGES
Component of CPR 2005 ECC recommendations
2010 ECC Recommendations
DEPTH OF COMPRESSION
1 frac12 - 2 inches Greater than 2 inches
RATE 100 MINUTE At least 100 MIN
VENTILATION 8-10 MINUTE 8-10 MINUTE
CHEST RECOIL 100 100
INTURUPTIONS Minimized Less than 10 seconds goal
PULSE CHECK HCP Only HCP only Checking for ldquoDEFNITE pulserdquo
2010 (New) The precordial thump should not be
used for un witnessed out-of-hospital cardiac arrest
The precordial thump may be considered for
patients with witnessed monitored unstable VT
(including pulse less VT) if a defibrillator is not
immediately ready for use but it should not delay
CPR and shock delivery
SUMMARY OF KEY ISSUES AND MAJOR CHANGES
The major changes in advanced cardiovascular life support
(ACLS) for 2010 include the following
bull Quantitative waveform capnography is recommended for
confirmation and monitoring of endotracheal tube placement
and CPR quality
bull The traditional cardiac arrest algorithm was simplified and an
alternative conceptual design was created to emphasize the
importance of high-quality CPR
bull There is an increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
bull Atropine is no longer recommended for routine use in the
management of pulse less electrical activity (PEA)asystole
CAPNOGRAPHY RECOMMENDATION
2010 (New) Continuous quantitative waveform
capnography is now recommended for intubated
patients throughout the per arrest period When
quantitative waveform capnography is used for
adults applications now include recommendations
for confirming tracheal tube placement and for
monitoring CPR quality and detecting ROSC based
on end-tidal carbon dioxide (PETCO2) values
PROGNOSTIC INDICATORS IN THE ADULT POSTARREST
PATIENT TREATED WITH THERAPEUTIC HYPOTHERMIA
2010 (New) In adult postndashcardiac arrest patients
treated with therapeutic hypothermia it is
recommended that clinical neurologic signs
electrophysiologic studies biomarkers and imaging
be performed where available at 3 days after
cardiac arrest
Hypothermia
ILCOR Advisory statement (2003)
Unconscious adult patients with spontaneous
circulation after out-of-hospital cardiac arrest
should be cooled to 32-34degC for 12-24 hrs when the
initial rhythm was ventricular fibrillation (VF)
Such cooling may also be beneficial for other
rhythms or in-hospital cardiac arrests
Hypothermia
Cooling
Retard enzymatic suppress production of free
radicals
Reduction of O2 demand in low-flow regions
Protection of membrane fluidity
Reduction of intracellular acidosis
Decrease in cerebral edema and ICP
2010 (New) Advanced life support training
should include training in teamwork
Why Resuscitation skills are often performed
simultaneously and healthcare providers must be
able to work collaboratively to minimize
interruptions in chest compressions Teamwork and
leadership skills continue to be important
particularly for advanced courses that include ACLS
and PALS providers
MONITORING DURING CPR
Physiologic parameters
Monitoring of PETCO2 (35 to 40 mmHg)
Coronary perfusion pressure (CPP) (15mmHg)
Central venous oxygen saturation (ScvO2)
Abrupt increase in any of these parameters is a
sensitive indicator of ROSC that can be monitored
without interrupting chest compressions
Quantitative waveform capnography
If Petco2 lt10 mm Hg attempt to improve CPR
quality
Intra-arterial pressure
If diastolic pressure lt20 mm Hg attempt to improve
CPR quality
If ScvO2 is lt 30 consider trying to improve the
quality of CPR
HIGH QUALITY CPR
Chest compressions of adequate rate 100min
A compression depth of at least 2 inches (5 cm) in
adults and in children a compression depth of at
least 15 inches [4 cm] in infants
Complete chest recoil after each compression
Minimizing interruptions in chest compressions
Avoiding excessive ventilation
If multiple rescuers are available rotate the task of
compressions every 2 minutes
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
BLS Key Concepts
Chest compression should not be interrupted except for
Shock delivery
Rhythm check
Ventilation (until an advanced airway is inserted)
Do not interrupt CPR
To insert cannula or to give drugs
To listen to the heart or to take BP
Waiting for charging the Defibrillator
To rotate personnel
Chances of survival with time
ADVANCED CARDIAC LIFE SUPPORT
ACLS impacts multiple key links in the chain of
survival that include interventions to prevent cardiac
arrest treat cardiac arrest and improve outcomes
of patients who achieve return of spontaneous
circulation (ROSC) after cardiac arrest
Interventions aimed at preventing cardiac arrest
include airway management ventilation support
and treatment of bradyarrhythmias and
tachyarrhythmias
AHA ADULT CHAIN OF SURVIVAL
1 Immediate recognition of cardiac arrest and
activation of the emergency response system
2 Early CPR with an emphasis on chest
compressions
3 Rapid defibrillation
4 Effective advanced life support
5 Integrated postndashcardiac arrest care
CARDIOPULMONARY RESUSCITATION (CPR)
Cardiopulmonary resuscitation (CPR) is a series of
life saving actions that improve the chance of
survival following cardiac arrest
KEY CHANGES FROM THE
2005 BLS GUIDELINES
Immediate recognition of SCA based on assessing
unresponsiveness and absence of normal breathing
ldquoLook Listen and Feelrdquo removed from the BLS
algorithm
Encouraging Hands-Only (chest compression only)
CPR
Sequence change CAB rather than ABC
Health care providers continue effective chest
compressions CPR until return of spontaneous
circulation or termination of resuscitative efforts
A CHANGE FROM A-B-C TO C-A-B
o 2010 (New) ldquoLook listen and feelrdquo was removed from the CPR sequence After delivery of 30 compressions the lone rescuer opens the victimrsquos airway and delivers 2 breaths
2005 (Old) ldquoLook listen and feelrdquo was used to assess breathing after the airway was opened
2010 (New) Initiate chest compressions before ventilations
2005 (Old) The sequence of adult CPR began with opening of the airway checking for normal breathing and then delivery of 2 rescue breaths followed by cycles of 30 chest compressions and 2 breaths
2010 (New) It is reasonable for lay rescuers and
healthcare providers to perform chest
compressions at a rate of at least100min
2005 (Old) Compress at a rate of about 100mi
2010 (New) The adult sternum should be
depressed at least 2 inches (5 cm)
2005 (Old) The adult sternum should be depressed
approximately 1 to 2 inches (approximately 4 to 5
cm)n
2005 (Old) Cricoid pressure should be used only if
the victim is deeply unconscious and it usually
requires a third rescuer not involved in rescue
breaths or compressions
2010(new)routine use of cricoid pressure in
cardiac arrest is not recommended
17
CRICOID PRESSURE
ThyroidCartilage
Cricoid
2005 TO 2010 CHANGES
Component of CPR 2005 ECC recommendations
2010 ECC Recommendations
DEPTH OF COMPRESSION
1 frac12 - 2 inches Greater than 2 inches
RATE 100 MINUTE At least 100 MIN
VENTILATION 8-10 MINUTE 8-10 MINUTE
CHEST RECOIL 100 100
INTURUPTIONS Minimized Less than 10 seconds goal
PULSE CHECK HCP Only HCP only Checking for ldquoDEFNITE pulserdquo
2010 (New) The precordial thump should not be
used for un witnessed out-of-hospital cardiac arrest
The precordial thump may be considered for
patients with witnessed monitored unstable VT
(including pulse less VT) if a defibrillator is not
immediately ready for use but it should not delay
CPR and shock delivery
SUMMARY OF KEY ISSUES AND MAJOR CHANGES
The major changes in advanced cardiovascular life support
(ACLS) for 2010 include the following
bull Quantitative waveform capnography is recommended for
confirmation and monitoring of endotracheal tube placement
and CPR quality
bull The traditional cardiac arrest algorithm was simplified and an
alternative conceptual design was created to emphasize the
importance of high-quality CPR
bull There is an increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
bull Atropine is no longer recommended for routine use in the
management of pulse less electrical activity (PEA)asystole
CAPNOGRAPHY RECOMMENDATION
2010 (New) Continuous quantitative waveform
capnography is now recommended for intubated
patients throughout the per arrest period When
quantitative waveform capnography is used for
adults applications now include recommendations
for confirming tracheal tube placement and for
monitoring CPR quality and detecting ROSC based
on end-tidal carbon dioxide (PETCO2) values
PROGNOSTIC INDICATORS IN THE ADULT POSTARREST
PATIENT TREATED WITH THERAPEUTIC HYPOTHERMIA
2010 (New) In adult postndashcardiac arrest patients
treated with therapeutic hypothermia it is
recommended that clinical neurologic signs
electrophysiologic studies biomarkers and imaging
be performed where available at 3 days after
cardiac arrest
Hypothermia
ILCOR Advisory statement (2003)
Unconscious adult patients with spontaneous
circulation after out-of-hospital cardiac arrest
should be cooled to 32-34degC for 12-24 hrs when the
initial rhythm was ventricular fibrillation (VF)
Such cooling may also be beneficial for other
rhythms or in-hospital cardiac arrests
Hypothermia
Cooling
Retard enzymatic suppress production of free
radicals
Reduction of O2 demand in low-flow regions
Protection of membrane fluidity
Reduction of intracellular acidosis
Decrease in cerebral edema and ICP
2010 (New) Advanced life support training
should include training in teamwork
Why Resuscitation skills are often performed
simultaneously and healthcare providers must be
able to work collaboratively to minimize
interruptions in chest compressions Teamwork and
leadership skills continue to be important
particularly for advanced courses that include ACLS
and PALS providers
MONITORING DURING CPR
Physiologic parameters
Monitoring of PETCO2 (35 to 40 mmHg)
Coronary perfusion pressure (CPP) (15mmHg)
Central venous oxygen saturation (ScvO2)
Abrupt increase in any of these parameters is a
sensitive indicator of ROSC that can be monitored
without interrupting chest compressions
Quantitative waveform capnography
If Petco2 lt10 mm Hg attempt to improve CPR
quality
Intra-arterial pressure
If diastolic pressure lt20 mm Hg attempt to improve
CPR quality
If ScvO2 is lt 30 consider trying to improve the
quality of CPR
HIGH QUALITY CPR
Chest compressions of adequate rate 100min
A compression depth of at least 2 inches (5 cm) in
adults and in children a compression depth of at
least 15 inches [4 cm] in infants
Complete chest recoil after each compression
Minimizing interruptions in chest compressions
Avoiding excessive ventilation
If multiple rescuers are available rotate the task of
compressions every 2 minutes
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
Chances of survival with time
ADVANCED CARDIAC LIFE SUPPORT
ACLS impacts multiple key links in the chain of
survival that include interventions to prevent cardiac
arrest treat cardiac arrest and improve outcomes
of patients who achieve return of spontaneous
circulation (ROSC) after cardiac arrest
Interventions aimed at preventing cardiac arrest
include airway management ventilation support
and treatment of bradyarrhythmias and
tachyarrhythmias
AHA ADULT CHAIN OF SURVIVAL
1 Immediate recognition of cardiac arrest and
activation of the emergency response system
2 Early CPR with an emphasis on chest
compressions
3 Rapid defibrillation
4 Effective advanced life support
5 Integrated postndashcardiac arrest care
CARDIOPULMONARY RESUSCITATION (CPR)
Cardiopulmonary resuscitation (CPR) is a series of
life saving actions that improve the chance of
survival following cardiac arrest
KEY CHANGES FROM THE
2005 BLS GUIDELINES
Immediate recognition of SCA based on assessing
unresponsiveness and absence of normal breathing
ldquoLook Listen and Feelrdquo removed from the BLS
algorithm
Encouraging Hands-Only (chest compression only)
CPR
Sequence change CAB rather than ABC
Health care providers continue effective chest
compressions CPR until return of spontaneous
circulation or termination of resuscitative efforts
A CHANGE FROM A-B-C TO C-A-B
o 2010 (New) ldquoLook listen and feelrdquo was removed from the CPR sequence After delivery of 30 compressions the lone rescuer opens the victimrsquos airway and delivers 2 breaths
2005 (Old) ldquoLook listen and feelrdquo was used to assess breathing after the airway was opened
2010 (New) Initiate chest compressions before ventilations
2005 (Old) The sequence of adult CPR began with opening of the airway checking for normal breathing and then delivery of 2 rescue breaths followed by cycles of 30 chest compressions and 2 breaths
2010 (New) It is reasonable for lay rescuers and
healthcare providers to perform chest
compressions at a rate of at least100min
2005 (Old) Compress at a rate of about 100mi
2010 (New) The adult sternum should be
depressed at least 2 inches (5 cm)
2005 (Old) The adult sternum should be depressed
approximately 1 to 2 inches (approximately 4 to 5
cm)n
2005 (Old) Cricoid pressure should be used only if
the victim is deeply unconscious and it usually
requires a third rescuer not involved in rescue
breaths or compressions
2010(new)routine use of cricoid pressure in
cardiac arrest is not recommended
17
CRICOID PRESSURE
ThyroidCartilage
Cricoid
2005 TO 2010 CHANGES
Component of CPR 2005 ECC recommendations
2010 ECC Recommendations
DEPTH OF COMPRESSION
1 frac12 - 2 inches Greater than 2 inches
RATE 100 MINUTE At least 100 MIN
VENTILATION 8-10 MINUTE 8-10 MINUTE
CHEST RECOIL 100 100
INTURUPTIONS Minimized Less than 10 seconds goal
PULSE CHECK HCP Only HCP only Checking for ldquoDEFNITE pulserdquo
2010 (New) The precordial thump should not be
used for un witnessed out-of-hospital cardiac arrest
The precordial thump may be considered for
patients with witnessed monitored unstable VT
(including pulse less VT) if a defibrillator is not
immediately ready for use but it should not delay
CPR and shock delivery
SUMMARY OF KEY ISSUES AND MAJOR CHANGES
The major changes in advanced cardiovascular life support
(ACLS) for 2010 include the following
bull Quantitative waveform capnography is recommended for
confirmation and monitoring of endotracheal tube placement
and CPR quality
bull The traditional cardiac arrest algorithm was simplified and an
alternative conceptual design was created to emphasize the
importance of high-quality CPR
bull There is an increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
bull Atropine is no longer recommended for routine use in the
management of pulse less electrical activity (PEA)asystole
CAPNOGRAPHY RECOMMENDATION
2010 (New) Continuous quantitative waveform
capnography is now recommended for intubated
patients throughout the per arrest period When
quantitative waveform capnography is used for
adults applications now include recommendations
for confirming tracheal tube placement and for
monitoring CPR quality and detecting ROSC based
on end-tidal carbon dioxide (PETCO2) values
PROGNOSTIC INDICATORS IN THE ADULT POSTARREST
PATIENT TREATED WITH THERAPEUTIC HYPOTHERMIA
2010 (New) In adult postndashcardiac arrest patients
treated with therapeutic hypothermia it is
recommended that clinical neurologic signs
electrophysiologic studies biomarkers and imaging
be performed where available at 3 days after
cardiac arrest
Hypothermia
ILCOR Advisory statement (2003)
Unconscious adult patients with spontaneous
circulation after out-of-hospital cardiac arrest
should be cooled to 32-34degC for 12-24 hrs when the
initial rhythm was ventricular fibrillation (VF)
Such cooling may also be beneficial for other
rhythms or in-hospital cardiac arrests
Hypothermia
Cooling
Retard enzymatic suppress production of free
radicals
Reduction of O2 demand in low-flow regions
Protection of membrane fluidity
Reduction of intracellular acidosis
Decrease in cerebral edema and ICP
2010 (New) Advanced life support training
should include training in teamwork
Why Resuscitation skills are often performed
simultaneously and healthcare providers must be
able to work collaboratively to minimize
interruptions in chest compressions Teamwork and
leadership skills continue to be important
particularly for advanced courses that include ACLS
and PALS providers
MONITORING DURING CPR
Physiologic parameters
Monitoring of PETCO2 (35 to 40 mmHg)
Coronary perfusion pressure (CPP) (15mmHg)
Central venous oxygen saturation (ScvO2)
Abrupt increase in any of these parameters is a
sensitive indicator of ROSC that can be monitored
without interrupting chest compressions
Quantitative waveform capnography
If Petco2 lt10 mm Hg attempt to improve CPR
quality
Intra-arterial pressure
If diastolic pressure lt20 mm Hg attempt to improve
CPR quality
If ScvO2 is lt 30 consider trying to improve the
quality of CPR
HIGH QUALITY CPR
Chest compressions of adequate rate 100min
A compression depth of at least 2 inches (5 cm) in
adults and in children a compression depth of at
least 15 inches [4 cm] in infants
Complete chest recoil after each compression
Minimizing interruptions in chest compressions
Avoiding excessive ventilation
If multiple rescuers are available rotate the task of
compressions every 2 minutes
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
ADVANCED CARDIAC LIFE SUPPORT
ACLS impacts multiple key links in the chain of
survival that include interventions to prevent cardiac
arrest treat cardiac arrest and improve outcomes
of patients who achieve return of spontaneous
circulation (ROSC) after cardiac arrest
Interventions aimed at preventing cardiac arrest
include airway management ventilation support
and treatment of bradyarrhythmias and
tachyarrhythmias
AHA ADULT CHAIN OF SURVIVAL
1 Immediate recognition of cardiac arrest and
activation of the emergency response system
2 Early CPR with an emphasis on chest
compressions
3 Rapid defibrillation
4 Effective advanced life support
5 Integrated postndashcardiac arrest care
CARDIOPULMONARY RESUSCITATION (CPR)
Cardiopulmonary resuscitation (CPR) is a series of
life saving actions that improve the chance of
survival following cardiac arrest
KEY CHANGES FROM THE
2005 BLS GUIDELINES
Immediate recognition of SCA based on assessing
unresponsiveness and absence of normal breathing
ldquoLook Listen and Feelrdquo removed from the BLS
algorithm
Encouraging Hands-Only (chest compression only)
CPR
Sequence change CAB rather than ABC
Health care providers continue effective chest
compressions CPR until return of spontaneous
circulation or termination of resuscitative efforts
A CHANGE FROM A-B-C TO C-A-B
o 2010 (New) ldquoLook listen and feelrdquo was removed from the CPR sequence After delivery of 30 compressions the lone rescuer opens the victimrsquos airway and delivers 2 breaths
2005 (Old) ldquoLook listen and feelrdquo was used to assess breathing after the airway was opened
2010 (New) Initiate chest compressions before ventilations
2005 (Old) The sequence of adult CPR began with opening of the airway checking for normal breathing and then delivery of 2 rescue breaths followed by cycles of 30 chest compressions and 2 breaths
2010 (New) It is reasonable for lay rescuers and
healthcare providers to perform chest
compressions at a rate of at least100min
2005 (Old) Compress at a rate of about 100mi
2010 (New) The adult sternum should be
depressed at least 2 inches (5 cm)
2005 (Old) The adult sternum should be depressed
approximately 1 to 2 inches (approximately 4 to 5
cm)n
2005 (Old) Cricoid pressure should be used only if
the victim is deeply unconscious and it usually
requires a third rescuer not involved in rescue
breaths or compressions
2010(new)routine use of cricoid pressure in
cardiac arrest is not recommended
17
CRICOID PRESSURE
ThyroidCartilage
Cricoid
2005 TO 2010 CHANGES
Component of CPR 2005 ECC recommendations
2010 ECC Recommendations
DEPTH OF COMPRESSION
1 frac12 - 2 inches Greater than 2 inches
RATE 100 MINUTE At least 100 MIN
VENTILATION 8-10 MINUTE 8-10 MINUTE
CHEST RECOIL 100 100
INTURUPTIONS Minimized Less than 10 seconds goal
PULSE CHECK HCP Only HCP only Checking for ldquoDEFNITE pulserdquo
2010 (New) The precordial thump should not be
used for un witnessed out-of-hospital cardiac arrest
The precordial thump may be considered for
patients with witnessed monitored unstable VT
(including pulse less VT) if a defibrillator is not
immediately ready for use but it should not delay
CPR and shock delivery
SUMMARY OF KEY ISSUES AND MAJOR CHANGES
The major changes in advanced cardiovascular life support
(ACLS) for 2010 include the following
bull Quantitative waveform capnography is recommended for
confirmation and monitoring of endotracheal tube placement
and CPR quality
bull The traditional cardiac arrest algorithm was simplified and an
alternative conceptual design was created to emphasize the
importance of high-quality CPR
bull There is an increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
bull Atropine is no longer recommended for routine use in the
management of pulse less electrical activity (PEA)asystole
CAPNOGRAPHY RECOMMENDATION
2010 (New) Continuous quantitative waveform
capnography is now recommended for intubated
patients throughout the per arrest period When
quantitative waveform capnography is used for
adults applications now include recommendations
for confirming tracheal tube placement and for
monitoring CPR quality and detecting ROSC based
on end-tidal carbon dioxide (PETCO2) values
PROGNOSTIC INDICATORS IN THE ADULT POSTARREST
PATIENT TREATED WITH THERAPEUTIC HYPOTHERMIA
2010 (New) In adult postndashcardiac arrest patients
treated with therapeutic hypothermia it is
recommended that clinical neurologic signs
electrophysiologic studies biomarkers and imaging
be performed where available at 3 days after
cardiac arrest
Hypothermia
ILCOR Advisory statement (2003)
Unconscious adult patients with spontaneous
circulation after out-of-hospital cardiac arrest
should be cooled to 32-34degC for 12-24 hrs when the
initial rhythm was ventricular fibrillation (VF)
Such cooling may also be beneficial for other
rhythms or in-hospital cardiac arrests
Hypothermia
Cooling
Retard enzymatic suppress production of free
radicals
Reduction of O2 demand in low-flow regions
Protection of membrane fluidity
Reduction of intracellular acidosis
Decrease in cerebral edema and ICP
2010 (New) Advanced life support training
should include training in teamwork
Why Resuscitation skills are often performed
simultaneously and healthcare providers must be
able to work collaboratively to minimize
interruptions in chest compressions Teamwork and
leadership skills continue to be important
particularly for advanced courses that include ACLS
and PALS providers
MONITORING DURING CPR
Physiologic parameters
Monitoring of PETCO2 (35 to 40 mmHg)
Coronary perfusion pressure (CPP) (15mmHg)
Central venous oxygen saturation (ScvO2)
Abrupt increase in any of these parameters is a
sensitive indicator of ROSC that can be monitored
without interrupting chest compressions
Quantitative waveform capnography
If Petco2 lt10 mm Hg attempt to improve CPR
quality
Intra-arterial pressure
If diastolic pressure lt20 mm Hg attempt to improve
CPR quality
If ScvO2 is lt 30 consider trying to improve the
quality of CPR
HIGH QUALITY CPR
Chest compressions of adequate rate 100min
A compression depth of at least 2 inches (5 cm) in
adults and in children a compression depth of at
least 15 inches [4 cm] in infants
Complete chest recoil after each compression
Minimizing interruptions in chest compressions
Avoiding excessive ventilation
If multiple rescuers are available rotate the task of
compressions every 2 minutes
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
AHA ADULT CHAIN OF SURVIVAL
1 Immediate recognition of cardiac arrest and
activation of the emergency response system
2 Early CPR with an emphasis on chest
compressions
3 Rapid defibrillation
4 Effective advanced life support
5 Integrated postndashcardiac arrest care
CARDIOPULMONARY RESUSCITATION (CPR)
Cardiopulmonary resuscitation (CPR) is a series of
life saving actions that improve the chance of
survival following cardiac arrest
KEY CHANGES FROM THE
2005 BLS GUIDELINES
Immediate recognition of SCA based on assessing
unresponsiveness and absence of normal breathing
ldquoLook Listen and Feelrdquo removed from the BLS
algorithm
Encouraging Hands-Only (chest compression only)
CPR
Sequence change CAB rather than ABC
Health care providers continue effective chest
compressions CPR until return of spontaneous
circulation or termination of resuscitative efforts
A CHANGE FROM A-B-C TO C-A-B
o 2010 (New) ldquoLook listen and feelrdquo was removed from the CPR sequence After delivery of 30 compressions the lone rescuer opens the victimrsquos airway and delivers 2 breaths
2005 (Old) ldquoLook listen and feelrdquo was used to assess breathing after the airway was opened
2010 (New) Initiate chest compressions before ventilations
2005 (Old) The sequence of adult CPR began with opening of the airway checking for normal breathing and then delivery of 2 rescue breaths followed by cycles of 30 chest compressions and 2 breaths
2010 (New) It is reasonable for lay rescuers and
healthcare providers to perform chest
compressions at a rate of at least100min
2005 (Old) Compress at a rate of about 100mi
2010 (New) The adult sternum should be
depressed at least 2 inches (5 cm)
2005 (Old) The adult sternum should be depressed
approximately 1 to 2 inches (approximately 4 to 5
cm)n
2005 (Old) Cricoid pressure should be used only if
the victim is deeply unconscious and it usually
requires a third rescuer not involved in rescue
breaths or compressions
2010(new)routine use of cricoid pressure in
cardiac arrest is not recommended
17
CRICOID PRESSURE
ThyroidCartilage
Cricoid
2005 TO 2010 CHANGES
Component of CPR 2005 ECC recommendations
2010 ECC Recommendations
DEPTH OF COMPRESSION
1 frac12 - 2 inches Greater than 2 inches
RATE 100 MINUTE At least 100 MIN
VENTILATION 8-10 MINUTE 8-10 MINUTE
CHEST RECOIL 100 100
INTURUPTIONS Minimized Less than 10 seconds goal
PULSE CHECK HCP Only HCP only Checking for ldquoDEFNITE pulserdquo
2010 (New) The precordial thump should not be
used for un witnessed out-of-hospital cardiac arrest
The precordial thump may be considered for
patients with witnessed monitored unstable VT
(including pulse less VT) if a defibrillator is not
immediately ready for use but it should not delay
CPR and shock delivery
SUMMARY OF KEY ISSUES AND MAJOR CHANGES
The major changes in advanced cardiovascular life support
(ACLS) for 2010 include the following
bull Quantitative waveform capnography is recommended for
confirmation and monitoring of endotracheal tube placement
and CPR quality
bull The traditional cardiac arrest algorithm was simplified and an
alternative conceptual design was created to emphasize the
importance of high-quality CPR
bull There is an increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
bull Atropine is no longer recommended for routine use in the
management of pulse less electrical activity (PEA)asystole
CAPNOGRAPHY RECOMMENDATION
2010 (New) Continuous quantitative waveform
capnography is now recommended for intubated
patients throughout the per arrest period When
quantitative waveform capnography is used for
adults applications now include recommendations
for confirming tracheal tube placement and for
monitoring CPR quality and detecting ROSC based
on end-tidal carbon dioxide (PETCO2) values
PROGNOSTIC INDICATORS IN THE ADULT POSTARREST
PATIENT TREATED WITH THERAPEUTIC HYPOTHERMIA
2010 (New) In adult postndashcardiac arrest patients
treated with therapeutic hypothermia it is
recommended that clinical neurologic signs
electrophysiologic studies biomarkers and imaging
be performed where available at 3 days after
cardiac arrest
Hypothermia
ILCOR Advisory statement (2003)
Unconscious adult patients with spontaneous
circulation after out-of-hospital cardiac arrest
should be cooled to 32-34degC for 12-24 hrs when the
initial rhythm was ventricular fibrillation (VF)
Such cooling may also be beneficial for other
rhythms or in-hospital cardiac arrests
Hypothermia
Cooling
Retard enzymatic suppress production of free
radicals
Reduction of O2 demand in low-flow regions
Protection of membrane fluidity
Reduction of intracellular acidosis
Decrease in cerebral edema and ICP
2010 (New) Advanced life support training
should include training in teamwork
Why Resuscitation skills are often performed
simultaneously and healthcare providers must be
able to work collaboratively to minimize
interruptions in chest compressions Teamwork and
leadership skills continue to be important
particularly for advanced courses that include ACLS
and PALS providers
MONITORING DURING CPR
Physiologic parameters
Monitoring of PETCO2 (35 to 40 mmHg)
Coronary perfusion pressure (CPP) (15mmHg)
Central venous oxygen saturation (ScvO2)
Abrupt increase in any of these parameters is a
sensitive indicator of ROSC that can be monitored
without interrupting chest compressions
Quantitative waveform capnography
If Petco2 lt10 mm Hg attempt to improve CPR
quality
Intra-arterial pressure
If diastolic pressure lt20 mm Hg attempt to improve
CPR quality
If ScvO2 is lt 30 consider trying to improve the
quality of CPR
HIGH QUALITY CPR
Chest compressions of adequate rate 100min
A compression depth of at least 2 inches (5 cm) in
adults and in children a compression depth of at
least 15 inches [4 cm] in infants
Complete chest recoil after each compression
Minimizing interruptions in chest compressions
Avoiding excessive ventilation
If multiple rescuers are available rotate the task of
compressions every 2 minutes
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
CARDIOPULMONARY RESUSCITATION (CPR)
Cardiopulmonary resuscitation (CPR) is a series of
life saving actions that improve the chance of
survival following cardiac arrest
KEY CHANGES FROM THE
2005 BLS GUIDELINES
Immediate recognition of SCA based on assessing
unresponsiveness and absence of normal breathing
ldquoLook Listen and Feelrdquo removed from the BLS
algorithm
Encouraging Hands-Only (chest compression only)
CPR
Sequence change CAB rather than ABC
Health care providers continue effective chest
compressions CPR until return of spontaneous
circulation or termination of resuscitative efforts
A CHANGE FROM A-B-C TO C-A-B
o 2010 (New) ldquoLook listen and feelrdquo was removed from the CPR sequence After delivery of 30 compressions the lone rescuer opens the victimrsquos airway and delivers 2 breaths
2005 (Old) ldquoLook listen and feelrdquo was used to assess breathing after the airway was opened
2010 (New) Initiate chest compressions before ventilations
2005 (Old) The sequence of adult CPR began with opening of the airway checking for normal breathing and then delivery of 2 rescue breaths followed by cycles of 30 chest compressions and 2 breaths
2010 (New) It is reasonable for lay rescuers and
healthcare providers to perform chest
compressions at a rate of at least100min
2005 (Old) Compress at a rate of about 100mi
2010 (New) The adult sternum should be
depressed at least 2 inches (5 cm)
2005 (Old) The adult sternum should be depressed
approximately 1 to 2 inches (approximately 4 to 5
cm)n
2005 (Old) Cricoid pressure should be used only if
the victim is deeply unconscious and it usually
requires a third rescuer not involved in rescue
breaths or compressions
2010(new)routine use of cricoid pressure in
cardiac arrest is not recommended
17
CRICOID PRESSURE
ThyroidCartilage
Cricoid
2005 TO 2010 CHANGES
Component of CPR 2005 ECC recommendations
2010 ECC Recommendations
DEPTH OF COMPRESSION
1 frac12 - 2 inches Greater than 2 inches
RATE 100 MINUTE At least 100 MIN
VENTILATION 8-10 MINUTE 8-10 MINUTE
CHEST RECOIL 100 100
INTURUPTIONS Minimized Less than 10 seconds goal
PULSE CHECK HCP Only HCP only Checking for ldquoDEFNITE pulserdquo
2010 (New) The precordial thump should not be
used for un witnessed out-of-hospital cardiac arrest
The precordial thump may be considered for
patients with witnessed monitored unstable VT
(including pulse less VT) if a defibrillator is not
immediately ready for use but it should not delay
CPR and shock delivery
SUMMARY OF KEY ISSUES AND MAJOR CHANGES
The major changes in advanced cardiovascular life support
(ACLS) for 2010 include the following
bull Quantitative waveform capnography is recommended for
confirmation and monitoring of endotracheal tube placement
and CPR quality
bull The traditional cardiac arrest algorithm was simplified and an
alternative conceptual design was created to emphasize the
importance of high-quality CPR
bull There is an increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
bull Atropine is no longer recommended for routine use in the
management of pulse less electrical activity (PEA)asystole
CAPNOGRAPHY RECOMMENDATION
2010 (New) Continuous quantitative waveform
capnography is now recommended for intubated
patients throughout the per arrest period When
quantitative waveform capnography is used for
adults applications now include recommendations
for confirming tracheal tube placement and for
monitoring CPR quality and detecting ROSC based
on end-tidal carbon dioxide (PETCO2) values
PROGNOSTIC INDICATORS IN THE ADULT POSTARREST
PATIENT TREATED WITH THERAPEUTIC HYPOTHERMIA
2010 (New) In adult postndashcardiac arrest patients
treated with therapeutic hypothermia it is
recommended that clinical neurologic signs
electrophysiologic studies biomarkers and imaging
be performed where available at 3 days after
cardiac arrest
Hypothermia
ILCOR Advisory statement (2003)
Unconscious adult patients with spontaneous
circulation after out-of-hospital cardiac arrest
should be cooled to 32-34degC for 12-24 hrs when the
initial rhythm was ventricular fibrillation (VF)
Such cooling may also be beneficial for other
rhythms or in-hospital cardiac arrests
Hypothermia
Cooling
Retard enzymatic suppress production of free
radicals
Reduction of O2 demand in low-flow regions
Protection of membrane fluidity
Reduction of intracellular acidosis
Decrease in cerebral edema and ICP
2010 (New) Advanced life support training
should include training in teamwork
Why Resuscitation skills are often performed
simultaneously and healthcare providers must be
able to work collaboratively to minimize
interruptions in chest compressions Teamwork and
leadership skills continue to be important
particularly for advanced courses that include ACLS
and PALS providers
MONITORING DURING CPR
Physiologic parameters
Monitoring of PETCO2 (35 to 40 mmHg)
Coronary perfusion pressure (CPP) (15mmHg)
Central venous oxygen saturation (ScvO2)
Abrupt increase in any of these parameters is a
sensitive indicator of ROSC that can be monitored
without interrupting chest compressions
Quantitative waveform capnography
If Petco2 lt10 mm Hg attempt to improve CPR
quality
Intra-arterial pressure
If diastolic pressure lt20 mm Hg attempt to improve
CPR quality
If ScvO2 is lt 30 consider trying to improve the
quality of CPR
HIGH QUALITY CPR
Chest compressions of adequate rate 100min
A compression depth of at least 2 inches (5 cm) in
adults and in children a compression depth of at
least 15 inches [4 cm] in infants
Complete chest recoil after each compression
Minimizing interruptions in chest compressions
Avoiding excessive ventilation
If multiple rescuers are available rotate the task of
compressions every 2 minutes
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
KEY CHANGES FROM THE
2005 BLS GUIDELINES
Immediate recognition of SCA based on assessing
unresponsiveness and absence of normal breathing
ldquoLook Listen and Feelrdquo removed from the BLS
algorithm
Encouraging Hands-Only (chest compression only)
CPR
Sequence change CAB rather than ABC
Health care providers continue effective chest
compressions CPR until return of spontaneous
circulation or termination of resuscitative efforts
A CHANGE FROM A-B-C TO C-A-B
o 2010 (New) ldquoLook listen and feelrdquo was removed from the CPR sequence After delivery of 30 compressions the lone rescuer opens the victimrsquos airway and delivers 2 breaths
2005 (Old) ldquoLook listen and feelrdquo was used to assess breathing after the airway was opened
2010 (New) Initiate chest compressions before ventilations
2005 (Old) The sequence of adult CPR began with opening of the airway checking for normal breathing and then delivery of 2 rescue breaths followed by cycles of 30 chest compressions and 2 breaths
2010 (New) It is reasonable for lay rescuers and
healthcare providers to perform chest
compressions at a rate of at least100min
2005 (Old) Compress at a rate of about 100mi
2010 (New) The adult sternum should be
depressed at least 2 inches (5 cm)
2005 (Old) The adult sternum should be depressed
approximately 1 to 2 inches (approximately 4 to 5
cm)n
2005 (Old) Cricoid pressure should be used only if
the victim is deeply unconscious and it usually
requires a third rescuer not involved in rescue
breaths or compressions
2010(new)routine use of cricoid pressure in
cardiac arrest is not recommended
17
CRICOID PRESSURE
ThyroidCartilage
Cricoid
2005 TO 2010 CHANGES
Component of CPR 2005 ECC recommendations
2010 ECC Recommendations
DEPTH OF COMPRESSION
1 frac12 - 2 inches Greater than 2 inches
RATE 100 MINUTE At least 100 MIN
VENTILATION 8-10 MINUTE 8-10 MINUTE
CHEST RECOIL 100 100
INTURUPTIONS Minimized Less than 10 seconds goal
PULSE CHECK HCP Only HCP only Checking for ldquoDEFNITE pulserdquo
2010 (New) The precordial thump should not be
used for un witnessed out-of-hospital cardiac arrest
The precordial thump may be considered for
patients with witnessed monitored unstable VT
(including pulse less VT) if a defibrillator is not
immediately ready for use but it should not delay
CPR and shock delivery
SUMMARY OF KEY ISSUES AND MAJOR CHANGES
The major changes in advanced cardiovascular life support
(ACLS) for 2010 include the following
bull Quantitative waveform capnography is recommended for
confirmation and monitoring of endotracheal tube placement
and CPR quality
bull The traditional cardiac arrest algorithm was simplified and an
alternative conceptual design was created to emphasize the
importance of high-quality CPR
bull There is an increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
bull Atropine is no longer recommended for routine use in the
management of pulse less electrical activity (PEA)asystole
CAPNOGRAPHY RECOMMENDATION
2010 (New) Continuous quantitative waveform
capnography is now recommended for intubated
patients throughout the per arrest period When
quantitative waveform capnography is used for
adults applications now include recommendations
for confirming tracheal tube placement and for
monitoring CPR quality and detecting ROSC based
on end-tidal carbon dioxide (PETCO2) values
PROGNOSTIC INDICATORS IN THE ADULT POSTARREST
PATIENT TREATED WITH THERAPEUTIC HYPOTHERMIA
2010 (New) In adult postndashcardiac arrest patients
treated with therapeutic hypothermia it is
recommended that clinical neurologic signs
electrophysiologic studies biomarkers and imaging
be performed where available at 3 days after
cardiac arrest
Hypothermia
ILCOR Advisory statement (2003)
Unconscious adult patients with spontaneous
circulation after out-of-hospital cardiac arrest
should be cooled to 32-34degC for 12-24 hrs when the
initial rhythm was ventricular fibrillation (VF)
Such cooling may also be beneficial for other
rhythms or in-hospital cardiac arrests
Hypothermia
Cooling
Retard enzymatic suppress production of free
radicals
Reduction of O2 demand in low-flow regions
Protection of membrane fluidity
Reduction of intracellular acidosis
Decrease in cerebral edema and ICP
2010 (New) Advanced life support training
should include training in teamwork
Why Resuscitation skills are often performed
simultaneously and healthcare providers must be
able to work collaboratively to minimize
interruptions in chest compressions Teamwork and
leadership skills continue to be important
particularly for advanced courses that include ACLS
and PALS providers
MONITORING DURING CPR
Physiologic parameters
Monitoring of PETCO2 (35 to 40 mmHg)
Coronary perfusion pressure (CPP) (15mmHg)
Central venous oxygen saturation (ScvO2)
Abrupt increase in any of these parameters is a
sensitive indicator of ROSC that can be monitored
without interrupting chest compressions
Quantitative waveform capnography
If Petco2 lt10 mm Hg attempt to improve CPR
quality
Intra-arterial pressure
If diastolic pressure lt20 mm Hg attempt to improve
CPR quality
If ScvO2 is lt 30 consider trying to improve the
quality of CPR
HIGH QUALITY CPR
Chest compressions of adequate rate 100min
A compression depth of at least 2 inches (5 cm) in
adults and in children a compression depth of at
least 15 inches [4 cm] in infants
Complete chest recoil after each compression
Minimizing interruptions in chest compressions
Avoiding excessive ventilation
If multiple rescuers are available rotate the task of
compressions every 2 minutes
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
A CHANGE FROM A-B-C TO C-A-B
o 2010 (New) ldquoLook listen and feelrdquo was removed from the CPR sequence After delivery of 30 compressions the lone rescuer opens the victimrsquos airway and delivers 2 breaths
2005 (Old) ldquoLook listen and feelrdquo was used to assess breathing after the airway was opened
2010 (New) Initiate chest compressions before ventilations
2005 (Old) The sequence of adult CPR began with opening of the airway checking for normal breathing and then delivery of 2 rescue breaths followed by cycles of 30 chest compressions and 2 breaths
2010 (New) It is reasonable for lay rescuers and
healthcare providers to perform chest
compressions at a rate of at least100min
2005 (Old) Compress at a rate of about 100mi
2010 (New) The adult sternum should be
depressed at least 2 inches (5 cm)
2005 (Old) The adult sternum should be depressed
approximately 1 to 2 inches (approximately 4 to 5
cm)n
2005 (Old) Cricoid pressure should be used only if
the victim is deeply unconscious and it usually
requires a third rescuer not involved in rescue
breaths or compressions
2010(new)routine use of cricoid pressure in
cardiac arrest is not recommended
17
CRICOID PRESSURE
ThyroidCartilage
Cricoid
2005 TO 2010 CHANGES
Component of CPR 2005 ECC recommendations
2010 ECC Recommendations
DEPTH OF COMPRESSION
1 frac12 - 2 inches Greater than 2 inches
RATE 100 MINUTE At least 100 MIN
VENTILATION 8-10 MINUTE 8-10 MINUTE
CHEST RECOIL 100 100
INTURUPTIONS Minimized Less than 10 seconds goal
PULSE CHECK HCP Only HCP only Checking for ldquoDEFNITE pulserdquo
2010 (New) The precordial thump should not be
used for un witnessed out-of-hospital cardiac arrest
The precordial thump may be considered for
patients with witnessed monitored unstable VT
(including pulse less VT) if a defibrillator is not
immediately ready for use but it should not delay
CPR and shock delivery
SUMMARY OF KEY ISSUES AND MAJOR CHANGES
The major changes in advanced cardiovascular life support
(ACLS) for 2010 include the following
bull Quantitative waveform capnography is recommended for
confirmation and monitoring of endotracheal tube placement
and CPR quality
bull The traditional cardiac arrest algorithm was simplified and an
alternative conceptual design was created to emphasize the
importance of high-quality CPR
bull There is an increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
bull Atropine is no longer recommended for routine use in the
management of pulse less electrical activity (PEA)asystole
CAPNOGRAPHY RECOMMENDATION
2010 (New) Continuous quantitative waveform
capnography is now recommended for intubated
patients throughout the per arrest period When
quantitative waveform capnography is used for
adults applications now include recommendations
for confirming tracheal tube placement and for
monitoring CPR quality and detecting ROSC based
on end-tidal carbon dioxide (PETCO2) values
PROGNOSTIC INDICATORS IN THE ADULT POSTARREST
PATIENT TREATED WITH THERAPEUTIC HYPOTHERMIA
2010 (New) In adult postndashcardiac arrest patients
treated with therapeutic hypothermia it is
recommended that clinical neurologic signs
electrophysiologic studies biomarkers and imaging
be performed where available at 3 days after
cardiac arrest
Hypothermia
ILCOR Advisory statement (2003)
Unconscious adult patients with spontaneous
circulation after out-of-hospital cardiac arrest
should be cooled to 32-34degC for 12-24 hrs when the
initial rhythm was ventricular fibrillation (VF)
Such cooling may also be beneficial for other
rhythms or in-hospital cardiac arrests
Hypothermia
Cooling
Retard enzymatic suppress production of free
radicals
Reduction of O2 demand in low-flow regions
Protection of membrane fluidity
Reduction of intracellular acidosis
Decrease in cerebral edema and ICP
2010 (New) Advanced life support training
should include training in teamwork
Why Resuscitation skills are often performed
simultaneously and healthcare providers must be
able to work collaboratively to minimize
interruptions in chest compressions Teamwork and
leadership skills continue to be important
particularly for advanced courses that include ACLS
and PALS providers
MONITORING DURING CPR
Physiologic parameters
Monitoring of PETCO2 (35 to 40 mmHg)
Coronary perfusion pressure (CPP) (15mmHg)
Central venous oxygen saturation (ScvO2)
Abrupt increase in any of these parameters is a
sensitive indicator of ROSC that can be monitored
without interrupting chest compressions
Quantitative waveform capnography
If Petco2 lt10 mm Hg attempt to improve CPR
quality
Intra-arterial pressure
If diastolic pressure lt20 mm Hg attempt to improve
CPR quality
If ScvO2 is lt 30 consider trying to improve the
quality of CPR
HIGH QUALITY CPR
Chest compressions of adequate rate 100min
A compression depth of at least 2 inches (5 cm) in
adults and in children a compression depth of at
least 15 inches [4 cm] in infants
Complete chest recoil after each compression
Minimizing interruptions in chest compressions
Avoiding excessive ventilation
If multiple rescuers are available rotate the task of
compressions every 2 minutes
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
o 2010 (New) ldquoLook listen and feelrdquo was removed from the CPR sequence After delivery of 30 compressions the lone rescuer opens the victimrsquos airway and delivers 2 breaths
2005 (Old) ldquoLook listen and feelrdquo was used to assess breathing after the airway was opened
2010 (New) Initiate chest compressions before ventilations
2005 (Old) The sequence of adult CPR began with opening of the airway checking for normal breathing and then delivery of 2 rescue breaths followed by cycles of 30 chest compressions and 2 breaths
2010 (New) It is reasonable for lay rescuers and
healthcare providers to perform chest
compressions at a rate of at least100min
2005 (Old) Compress at a rate of about 100mi
2010 (New) The adult sternum should be
depressed at least 2 inches (5 cm)
2005 (Old) The adult sternum should be depressed
approximately 1 to 2 inches (approximately 4 to 5
cm)n
2005 (Old) Cricoid pressure should be used only if
the victim is deeply unconscious and it usually
requires a third rescuer not involved in rescue
breaths or compressions
2010(new)routine use of cricoid pressure in
cardiac arrest is not recommended
17
CRICOID PRESSURE
ThyroidCartilage
Cricoid
2005 TO 2010 CHANGES
Component of CPR 2005 ECC recommendations
2010 ECC Recommendations
DEPTH OF COMPRESSION
1 frac12 - 2 inches Greater than 2 inches
RATE 100 MINUTE At least 100 MIN
VENTILATION 8-10 MINUTE 8-10 MINUTE
CHEST RECOIL 100 100
INTURUPTIONS Minimized Less than 10 seconds goal
PULSE CHECK HCP Only HCP only Checking for ldquoDEFNITE pulserdquo
2010 (New) The precordial thump should not be
used for un witnessed out-of-hospital cardiac arrest
The precordial thump may be considered for
patients with witnessed monitored unstable VT
(including pulse less VT) if a defibrillator is not
immediately ready for use but it should not delay
CPR and shock delivery
SUMMARY OF KEY ISSUES AND MAJOR CHANGES
The major changes in advanced cardiovascular life support
(ACLS) for 2010 include the following
bull Quantitative waveform capnography is recommended for
confirmation and monitoring of endotracheal tube placement
and CPR quality
bull The traditional cardiac arrest algorithm was simplified and an
alternative conceptual design was created to emphasize the
importance of high-quality CPR
bull There is an increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
bull Atropine is no longer recommended for routine use in the
management of pulse less electrical activity (PEA)asystole
CAPNOGRAPHY RECOMMENDATION
2010 (New) Continuous quantitative waveform
capnography is now recommended for intubated
patients throughout the per arrest period When
quantitative waveform capnography is used for
adults applications now include recommendations
for confirming tracheal tube placement and for
monitoring CPR quality and detecting ROSC based
on end-tidal carbon dioxide (PETCO2) values
PROGNOSTIC INDICATORS IN THE ADULT POSTARREST
PATIENT TREATED WITH THERAPEUTIC HYPOTHERMIA
2010 (New) In adult postndashcardiac arrest patients
treated with therapeutic hypothermia it is
recommended that clinical neurologic signs
electrophysiologic studies biomarkers and imaging
be performed where available at 3 days after
cardiac arrest
Hypothermia
ILCOR Advisory statement (2003)
Unconscious adult patients with spontaneous
circulation after out-of-hospital cardiac arrest
should be cooled to 32-34degC for 12-24 hrs when the
initial rhythm was ventricular fibrillation (VF)
Such cooling may also be beneficial for other
rhythms or in-hospital cardiac arrests
Hypothermia
Cooling
Retard enzymatic suppress production of free
radicals
Reduction of O2 demand in low-flow regions
Protection of membrane fluidity
Reduction of intracellular acidosis
Decrease in cerebral edema and ICP
2010 (New) Advanced life support training
should include training in teamwork
Why Resuscitation skills are often performed
simultaneously and healthcare providers must be
able to work collaboratively to minimize
interruptions in chest compressions Teamwork and
leadership skills continue to be important
particularly for advanced courses that include ACLS
and PALS providers
MONITORING DURING CPR
Physiologic parameters
Monitoring of PETCO2 (35 to 40 mmHg)
Coronary perfusion pressure (CPP) (15mmHg)
Central venous oxygen saturation (ScvO2)
Abrupt increase in any of these parameters is a
sensitive indicator of ROSC that can be monitored
without interrupting chest compressions
Quantitative waveform capnography
If Petco2 lt10 mm Hg attempt to improve CPR
quality
Intra-arterial pressure
If diastolic pressure lt20 mm Hg attempt to improve
CPR quality
If ScvO2 is lt 30 consider trying to improve the
quality of CPR
HIGH QUALITY CPR
Chest compressions of adequate rate 100min
A compression depth of at least 2 inches (5 cm) in
adults and in children a compression depth of at
least 15 inches [4 cm] in infants
Complete chest recoil after each compression
Minimizing interruptions in chest compressions
Avoiding excessive ventilation
If multiple rescuers are available rotate the task of
compressions every 2 minutes
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
2010 (New) It is reasonable for lay rescuers and
healthcare providers to perform chest
compressions at a rate of at least100min
2005 (Old) Compress at a rate of about 100mi
2010 (New) The adult sternum should be
depressed at least 2 inches (5 cm)
2005 (Old) The adult sternum should be depressed
approximately 1 to 2 inches (approximately 4 to 5
cm)n
2005 (Old) Cricoid pressure should be used only if
the victim is deeply unconscious and it usually
requires a third rescuer not involved in rescue
breaths or compressions
2010(new)routine use of cricoid pressure in
cardiac arrest is not recommended
17
CRICOID PRESSURE
ThyroidCartilage
Cricoid
2005 TO 2010 CHANGES
Component of CPR 2005 ECC recommendations
2010 ECC Recommendations
DEPTH OF COMPRESSION
1 frac12 - 2 inches Greater than 2 inches
RATE 100 MINUTE At least 100 MIN
VENTILATION 8-10 MINUTE 8-10 MINUTE
CHEST RECOIL 100 100
INTURUPTIONS Minimized Less than 10 seconds goal
PULSE CHECK HCP Only HCP only Checking for ldquoDEFNITE pulserdquo
2010 (New) The precordial thump should not be
used for un witnessed out-of-hospital cardiac arrest
The precordial thump may be considered for
patients with witnessed monitored unstable VT
(including pulse less VT) if a defibrillator is not
immediately ready for use but it should not delay
CPR and shock delivery
SUMMARY OF KEY ISSUES AND MAJOR CHANGES
The major changes in advanced cardiovascular life support
(ACLS) for 2010 include the following
bull Quantitative waveform capnography is recommended for
confirmation and monitoring of endotracheal tube placement
and CPR quality
bull The traditional cardiac arrest algorithm was simplified and an
alternative conceptual design was created to emphasize the
importance of high-quality CPR
bull There is an increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
bull Atropine is no longer recommended for routine use in the
management of pulse less electrical activity (PEA)asystole
CAPNOGRAPHY RECOMMENDATION
2010 (New) Continuous quantitative waveform
capnography is now recommended for intubated
patients throughout the per arrest period When
quantitative waveform capnography is used for
adults applications now include recommendations
for confirming tracheal tube placement and for
monitoring CPR quality and detecting ROSC based
on end-tidal carbon dioxide (PETCO2) values
PROGNOSTIC INDICATORS IN THE ADULT POSTARREST
PATIENT TREATED WITH THERAPEUTIC HYPOTHERMIA
2010 (New) In adult postndashcardiac arrest patients
treated with therapeutic hypothermia it is
recommended that clinical neurologic signs
electrophysiologic studies biomarkers and imaging
be performed where available at 3 days after
cardiac arrest
Hypothermia
ILCOR Advisory statement (2003)
Unconscious adult patients with spontaneous
circulation after out-of-hospital cardiac arrest
should be cooled to 32-34degC for 12-24 hrs when the
initial rhythm was ventricular fibrillation (VF)
Such cooling may also be beneficial for other
rhythms or in-hospital cardiac arrests
Hypothermia
Cooling
Retard enzymatic suppress production of free
radicals
Reduction of O2 demand in low-flow regions
Protection of membrane fluidity
Reduction of intracellular acidosis
Decrease in cerebral edema and ICP
2010 (New) Advanced life support training
should include training in teamwork
Why Resuscitation skills are often performed
simultaneously and healthcare providers must be
able to work collaboratively to minimize
interruptions in chest compressions Teamwork and
leadership skills continue to be important
particularly for advanced courses that include ACLS
and PALS providers
MONITORING DURING CPR
Physiologic parameters
Monitoring of PETCO2 (35 to 40 mmHg)
Coronary perfusion pressure (CPP) (15mmHg)
Central venous oxygen saturation (ScvO2)
Abrupt increase in any of these parameters is a
sensitive indicator of ROSC that can be monitored
without interrupting chest compressions
Quantitative waveform capnography
If Petco2 lt10 mm Hg attempt to improve CPR
quality
Intra-arterial pressure
If diastolic pressure lt20 mm Hg attempt to improve
CPR quality
If ScvO2 is lt 30 consider trying to improve the
quality of CPR
HIGH QUALITY CPR
Chest compressions of adequate rate 100min
A compression depth of at least 2 inches (5 cm) in
adults and in children a compression depth of at
least 15 inches [4 cm] in infants
Complete chest recoil after each compression
Minimizing interruptions in chest compressions
Avoiding excessive ventilation
If multiple rescuers are available rotate the task of
compressions every 2 minutes
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
2005 (Old) Cricoid pressure should be used only if
the victim is deeply unconscious and it usually
requires a third rescuer not involved in rescue
breaths or compressions
2010(new)routine use of cricoid pressure in
cardiac arrest is not recommended
17
CRICOID PRESSURE
ThyroidCartilage
Cricoid
2005 TO 2010 CHANGES
Component of CPR 2005 ECC recommendations
2010 ECC Recommendations
DEPTH OF COMPRESSION
1 frac12 - 2 inches Greater than 2 inches
RATE 100 MINUTE At least 100 MIN
VENTILATION 8-10 MINUTE 8-10 MINUTE
CHEST RECOIL 100 100
INTURUPTIONS Minimized Less than 10 seconds goal
PULSE CHECK HCP Only HCP only Checking for ldquoDEFNITE pulserdquo
2010 (New) The precordial thump should not be
used for un witnessed out-of-hospital cardiac arrest
The precordial thump may be considered for
patients with witnessed monitored unstable VT
(including pulse less VT) if a defibrillator is not
immediately ready for use but it should not delay
CPR and shock delivery
SUMMARY OF KEY ISSUES AND MAJOR CHANGES
The major changes in advanced cardiovascular life support
(ACLS) for 2010 include the following
bull Quantitative waveform capnography is recommended for
confirmation and monitoring of endotracheal tube placement
and CPR quality
bull The traditional cardiac arrest algorithm was simplified and an
alternative conceptual design was created to emphasize the
importance of high-quality CPR
bull There is an increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
bull Atropine is no longer recommended for routine use in the
management of pulse less electrical activity (PEA)asystole
CAPNOGRAPHY RECOMMENDATION
2010 (New) Continuous quantitative waveform
capnography is now recommended for intubated
patients throughout the per arrest period When
quantitative waveform capnography is used for
adults applications now include recommendations
for confirming tracheal tube placement and for
monitoring CPR quality and detecting ROSC based
on end-tidal carbon dioxide (PETCO2) values
PROGNOSTIC INDICATORS IN THE ADULT POSTARREST
PATIENT TREATED WITH THERAPEUTIC HYPOTHERMIA
2010 (New) In adult postndashcardiac arrest patients
treated with therapeutic hypothermia it is
recommended that clinical neurologic signs
electrophysiologic studies biomarkers and imaging
be performed where available at 3 days after
cardiac arrest
Hypothermia
ILCOR Advisory statement (2003)
Unconscious adult patients with spontaneous
circulation after out-of-hospital cardiac arrest
should be cooled to 32-34degC for 12-24 hrs when the
initial rhythm was ventricular fibrillation (VF)
Such cooling may also be beneficial for other
rhythms or in-hospital cardiac arrests
Hypothermia
Cooling
Retard enzymatic suppress production of free
radicals
Reduction of O2 demand in low-flow regions
Protection of membrane fluidity
Reduction of intracellular acidosis
Decrease in cerebral edema and ICP
2010 (New) Advanced life support training
should include training in teamwork
Why Resuscitation skills are often performed
simultaneously and healthcare providers must be
able to work collaboratively to minimize
interruptions in chest compressions Teamwork and
leadership skills continue to be important
particularly for advanced courses that include ACLS
and PALS providers
MONITORING DURING CPR
Physiologic parameters
Monitoring of PETCO2 (35 to 40 mmHg)
Coronary perfusion pressure (CPP) (15mmHg)
Central venous oxygen saturation (ScvO2)
Abrupt increase in any of these parameters is a
sensitive indicator of ROSC that can be monitored
without interrupting chest compressions
Quantitative waveform capnography
If Petco2 lt10 mm Hg attempt to improve CPR
quality
Intra-arterial pressure
If diastolic pressure lt20 mm Hg attempt to improve
CPR quality
If ScvO2 is lt 30 consider trying to improve the
quality of CPR
HIGH QUALITY CPR
Chest compressions of adequate rate 100min
A compression depth of at least 2 inches (5 cm) in
adults and in children a compression depth of at
least 15 inches [4 cm] in infants
Complete chest recoil after each compression
Minimizing interruptions in chest compressions
Avoiding excessive ventilation
If multiple rescuers are available rotate the task of
compressions every 2 minutes
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
17
CRICOID PRESSURE
ThyroidCartilage
Cricoid
2005 TO 2010 CHANGES
Component of CPR 2005 ECC recommendations
2010 ECC Recommendations
DEPTH OF COMPRESSION
1 frac12 - 2 inches Greater than 2 inches
RATE 100 MINUTE At least 100 MIN
VENTILATION 8-10 MINUTE 8-10 MINUTE
CHEST RECOIL 100 100
INTURUPTIONS Minimized Less than 10 seconds goal
PULSE CHECK HCP Only HCP only Checking for ldquoDEFNITE pulserdquo
2010 (New) The precordial thump should not be
used for un witnessed out-of-hospital cardiac arrest
The precordial thump may be considered for
patients with witnessed monitored unstable VT
(including pulse less VT) if a defibrillator is not
immediately ready for use but it should not delay
CPR and shock delivery
SUMMARY OF KEY ISSUES AND MAJOR CHANGES
The major changes in advanced cardiovascular life support
(ACLS) for 2010 include the following
bull Quantitative waveform capnography is recommended for
confirmation and monitoring of endotracheal tube placement
and CPR quality
bull The traditional cardiac arrest algorithm was simplified and an
alternative conceptual design was created to emphasize the
importance of high-quality CPR
bull There is an increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
bull Atropine is no longer recommended for routine use in the
management of pulse less electrical activity (PEA)asystole
CAPNOGRAPHY RECOMMENDATION
2010 (New) Continuous quantitative waveform
capnography is now recommended for intubated
patients throughout the per arrest period When
quantitative waveform capnography is used for
adults applications now include recommendations
for confirming tracheal tube placement and for
monitoring CPR quality and detecting ROSC based
on end-tidal carbon dioxide (PETCO2) values
PROGNOSTIC INDICATORS IN THE ADULT POSTARREST
PATIENT TREATED WITH THERAPEUTIC HYPOTHERMIA
2010 (New) In adult postndashcardiac arrest patients
treated with therapeutic hypothermia it is
recommended that clinical neurologic signs
electrophysiologic studies biomarkers and imaging
be performed where available at 3 days after
cardiac arrest
Hypothermia
ILCOR Advisory statement (2003)
Unconscious adult patients with spontaneous
circulation after out-of-hospital cardiac arrest
should be cooled to 32-34degC for 12-24 hrs when the
initial rhythm was ventricular fibrillation (VF)
Such cooling may also be beneficial for other
rhythms or in-hospital cardiac arrests
Hypothermia
Cooling
Retard enzymatic suppress production of free
radicals
Reduction of O2 demand in low-flow regions
Protection of membrane fluidity
Reduction of intracellular acidosis
Decrease in cerebral edema and ICP
2010 (New) Advanced life support training
should include training in teamwork
Why Resuscitation skills are often performed
simultaneously and healthcare providers must be
able to work collaboratively to minimize
interruptions in chest compressions Teamwork and
leadership skills continue to be important
particularly for advanced courses that include ACLS
and PALS providers
MONITORING DURING CPR
Physiologic parameters
Monitoring of PETCO2 (35 to 40 mmHg)
Coronary perfusion pressure (CPP) (15mmHg)
Central venous oxygen saturation (ScvO2)
Abrupt increase in any of these parameters is a
sensitive indicator of ROSC that can be monitored
without interrupting chest compressions
Quantitative waveform capnography
If Petco2 lt10 mm Hg attempt to improve CPR
quality
Intra-arterial pressure
If diastolic pressure lt20 mm Hg attempt to improve
CPR quality
If ScvO2 is lt 30 consider trying to improve the
quality of CPR
HIGH QUALITY CPR
Chest compressions of adequate rate 100min
A compression depth of at least 2 inches (5 cm) in
adults and in children a compression depth of at
least 15 inches [4 cm] in infants
Complete chest recoil after each compression
Minimizing interruptions in chest compressions
Avoiding excessive ventilation
If multiple rescuers are available rotate the task of
compressions every 2 minutes
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
2005 TO 2010 CHANGES
Component of CPR 2005 ECC recommendations
2010 ECC Recommendations
DEPTH OF COMPRESSION
1 frac12 - 2 inches Greater than 2 inches
RATE 100 MINUTE At least 100 MIN
VENTILATION 8-10 MINUTE 8-10 MINUTE
CHEST RECOIL 100 100
INTURUPTIONS Minimized Less than 10 seconds goal
PULSE CHECK HCP Only HCP only Checking for ldquoDEFNITE pulserdquo
2010 (New) The precordial thump should not be
used for un witnessed out-of-hospital cardiac arrest
The precordial thump may be considered for
patients with witnessed monitored unstable VT
(including pulse less VT) if a defibrillator is not
immediately ready for use but it should not delay
CPR and shock delivery
SUMMARY OF KEY ISSUES AND MAJOR CHANGES
The major changes in advanced cardiovascular life support
(ACLS) for 2010 include the following
bull Quantitative waveform capnography is recommended for
confirmation and monitoring of endotracheal tube placement
and CPR quality
bull The traditional cardiac arrest algorithm was simplified and an
alternative conceptual design was created to emphasize the
importance of high-quality CPR
bull There is an increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
bull Atropine is no longer recommended for routine use in the
management of pulse less electrical activity (PEA)asystole
CAPNOGRAPHY RECOMMENDATION
2010 (New) Continuous quantitative waveform
capnography is now recommended for intubated
patients throughout the per arrest period When
quantitative waveform capnography is used for
adults applications now include recommendations
for confirming tracheal tube placement and for
monitoring CPR quality and detecting ROSC based
on end-tidal carbon dioxide (PETCO2) values
PROGNOSTIC INDICATORS IN THE ADULT POSTARREST
PATIENT TREATED WITH THERAPEUTIC HYPOTHERMIA
2010 (New) In adult postndashcardiac arrest patients
treated with therapeutic hypothermia it is
recommended that clinical neurologic signs
electrophysiologic studies biomarkers and imaging
be performed where available at 3 days after
cardiac arrest
Hypothermia
ILCOR Advisory statement (2003)
Unconscious adult patients with spontaneous
circulation after out-of-hospital cardiac arrest
should be cooled to 32-34degC for 12-24 hrs when the
initial rhythm was ventricular fibrillation (VF)
Such cooling may also be beneficial for other
rhythms or in-hospital cardiac arrests
Hypothermia
Cooling
Retard enzymatic suppress production of free
radicals
Reduction of O2 demand in low-flow regions
Protection of membrane fluidity
Reduction of intracellular acidosis
Decrease in cerebral edema and ICP
2010 (New) Advanced life support training
should include training in teamwork
Why Resuscitation skills are often performed
simultaneously and healthcare providers must be
able to work collaboratively to minimize
interruptions in chest compressions Teamwork and
leadership skills continue to be important
particularly for advanced courses that include ACLS
and PALS providers
MONITORING DURING CPR
Physiologic parameters
Monitoring of PETCO2 (35 to 40 mmHg)
Coronary perfusion pressure (CPP) (15mmHg)
Central venous oxygen saturation (ScvO2)
Abrupt increase in any of these parameters is a
sensitive indicator of ROSC that can be monitored
without interrupting chest compressions
Quantitative waveform capnography
If Petco2 lt10 mm Hg attempt to improve CPR
quality
Intra-arterial pressure
If diastolic pressure lt20 mm Hg attempt to improve
CPR quality
If ScvO2 is lt 30 consider trying to improve the
quality of CPR
HIGH QUALITY CPR
Chest compressions of adequate rate 100min
A compression depth of at least 2 inches (5 cm) in
adults and in children a compression depth of at
least 15 inches [4 cm] in infants
Complete chest recoil after each compression
Minimizing interruptions in chest compressions
Avoiding excessive ventilation
If multiple rescuers are available rotate the task of
compressions every 2 minutes
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
2010 (New) The precordial thump should not be
used for un witnessed out-of-hospital cardiac arrest
The precordial thump may be considered for
patients with witnessed monitored unstable VT
(including pulse less VT) if a defibrillator is not
immediately ready for use but it should not delay
CPR and shock delivery
SUMMARY OF KEY ISSUES AND MAJOR CHANGES
The major changes in advanced cardiovascular life support
(ACLS) for 2010 include the following
bull Quantitative waveform capnography is recommended for
confirmation and monitoring of endotracheal tube placement
and CPR quality
bull The traditional cardiac arrest algorithm was simplified and an
alternative conceptual design was created to emphasize the
importance of high-quality CPR
bull There is an increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
bull Atropine is no longer recommended for routine use in the
management of pulse less electrical activity (PEA)asystole
CAPNOGRAPHY RECOMMENDATION
2010 (New) Continuous quantitative waveform
capnography is now recommended for intubated
patients throughout the per arrest period When
quantitative waveform capnography is used for
adults applications now include recommendations
for confirming tracheal tube placement and for
monitoring CPR quality and detecting ROSC based
on end-tidal carbon dioxide (PETCO2) values
PROGNOSTIC INDICATORS IN THE ADULT POSTARREST
PATIENT TREATED WITH THERAPEUTIC HYPOTHERMIA
2010 (New) In adult postndashcardiac arrest patients
treated with therapeutic hypothermia it is
recommended that clinical neurologic signs
electrophysiologic studies biomarkers and imaging
be performed where available at 3 days after
cardiac arrest
Hypothermia
ILCOR Advisory statement (2003)
Unconscious adult patients with spontaneous
circulation after out-of-hospital cardiac arrest
should be cooled to 32-34degC for 12-24 hrs when the
initial rhythm was ventricular fibrillation (VF)
Such cooling may also be beneficial for other
rhythms or in-hospital cardiac arrests
Hypothermia
Cooling
Retard enzymatic suppress production of free
radicals
Reduction of O2 demand in low-flow regions
Protection of membrane fluidity
Reduction of intracellular acidosis
Decrease in cerebral edema and ICP
2010 (New) Advanced life support training
should include training in teamwork
Why Resuscitation skills are often performed
simultaneously and healthcare providers must be
able to work collaboratively to minimize
interruptions in chest compressions Teamwork and
leadership skills continue to be important
particularly for advanced courses that include ACLS
and PALS providers
MONITORING DURING CPR
Physiologic parameters
Monitoring of PETCO2 (35 to 40 mmHg)
Coronary perfusion pressure (CPP) (15mmHg)
Central venous oxygen saturation (ScvO2)
Abrupt increase in any of these parameters is a
sensitive indicator of ROSC that can be monitored
without interrupting chest compressions
Quantitative waveform capnography
If Petco2 lt10 mm Hg attempt to improve CPR
quality
Intra-arterial pressure
If diastolic pressure lt20 mm Hg attempt to improve
CPR quality
If ScvO2 is lt 30 consider trying to improve the
quality of CPR
HIGH QUALITY CPR
Chest compressions of adequate rate 100min
A compression depth of at least 2 inches (5 cm) in
adults and in children a compression depth of at
least 15 inches [4 cm] in infants
Complete chest recoil after each compression
Minimizing interruptions in chest compressions
Avoiding excessive ventilation
If multiple rescuers are available rotate the task of
compressions every 2 minutes
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
SUMMARY OF KEY ISSUES AND MAJOR CHANGES
The major changes in advanced cardiovascular life support
(ACLS) for 2010 include the following
bull Quantitative waveform capnography is recommended for
confirmation and monitoring of endotracheal tube placement
and CPR quality
bull The traditional cardiac arrest algorithm was simplified and an
alternative conceptual design was created to emphasize the
importance of high-quality CPR
bull There is an increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
bull Atropine is no longer recommended for routine use in the
management of pulse less electrical activity (PEA)asystole
CAPNOGRAPHY RECOMMENDATION
2010 (New) Continuous quantitative waveform
capnography is now recommended for intubated
patients throughout the per arrest period When
quantitative waveform capnography is used for
adults applications now include recommendations
for confirming tracheal tube placement and for
monitoring CPR quality and detecting ROSC based
on end-tidal carbon dioxide (PETCO2) values
PROGNOSTIC INDICATORS IN THE ADULT POSTARREST
PATIENT TREATED WITH THERAPEUTIC HYPOTHERMIA
2010 (New) In adult postndashcardiac arrest patients
treated with therapeutic hypothermia it is
recommended that clinical neurologic signs
electrophysiologic studies biomarkers and imaging
be performed where available at 3 days after
cardiac arrest
Hypothermia
ILCOR Advisory statement (2003)
Unconscious adult patients with spontaneous
circulation after out-of-hospital cardiac arrest
should be cooled to 32-34degC for 12-24 hrs when the
initial rhythm was ventricular fibrillation (VF)
Such cooling may also be beneficial for other
rhythms or in-hospital cardiac arrests
Hypothermia
Cooling
Retard enzymatic suppress production of free
radicals
Reduction of O2 demand in low-flow regions
Protection of membrane fluidity
Reduction of intracellular acidosis
Decrease in cerebral edema and ICP
2010 (New) Advanced life support training
should include training in teamwork
Why Resuscitation skills are often performed
simultaneously and healthcare providers must be
able to work collaboratively to minimize
interruptions in chest compressions Teamwork and
leadership skills continue to be important
particularly for advanced courses that include ACLS
and PALS providers
MONITORING DURING CPR
Physiologic parameters
Monitoring of PETCO2 (35 to 40 mmHg)
Coronary perfusion pressure (CPP) (15mmHg)
Central venous oxygen saturation (ScvO2)
Abrupt increase in any of these parameters is a
sensitive indicator of ROSC that can be monitored
without interrupting chest compressions
Quantitative waveform capnography
If Petco2 lt10 mm Hg attempt to improve CPR
quality
Intra-arterial pressure
If diastolic pressure lt20 mm Hg attempt to improve
CPR quality
If ScvO2 is lt 30 consider trying to improve the
quality of CPR
HIGH QUALITY CPR
Chest compressions of adequate rate 100min
A compression depth of at least 2 inches (5 cm) in
adults and in children a compression depth of at
least 15 inches [4 cm] in infants
Complete chest recoil after each compression
Minimizing interruptions in chest compressions
Avoiding excessive ventilation
If multiple rescuers are available rotate the task of
compressions every 2 minutes
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
CAPNOGRAPHY RECOMMENDATION
2010 (New) Continuous quantitative waveform
capnography is now recommended for intubated
patients throughout the per arrest period When
quantitative waveform capnography is used for
adults applications now include recommendations
for confirming tracheal tube placement and for
monitoring CPR quality and detecting ROSC based
on end-tidal carbon dioxide (PETCO2) values
PROGNOSTIC INDICATORS IN THE ADULT POSTARREST
PATIENT TREATED WITH THERAPEUTIC HYPOTHERMIA
2010 (New) In adult postndashcardiac arrest patients
treated with therapeutic hypothermia it is
recommended that clinical neurologic signs
electrophysiologic studies biomarkers and imaging
be performed where available at 3 days after
cardiac arrest
Hypothermia
ILCOR Advisory statement (2003)
Unconscious adult patients with spontaneous
circulation after out-of-hospital cardiac arrest
should be cooled to 32-34degC for 12-24 hrs when the
initial rhythm was ventricular fibrillation (VF)
Such cooling may also be beneficial for other
rhythms or in-hospital cardiac arrests
Hypothermia
Cooling
Retard enzymatic suppress production of free
radicals
Reduction of O2 demand in low-flow regions
Protection of membrane fluidity
Reduction of intracellular acidosis
Decrease in cerebral edema and ICP
2010 (New) Advanced life support training
should include training in teamwork
Why Resuscitation skills are often performed
simultaneously and healthcare providers must be
able to work collaboratively to minimize
interruptions in chest compressions Teamwork and
leadership skills continue to be important
particularly for advanced courses that include ACLS
and PALS providers
MONITORING DURING CPR
Physiologic parameters
Monitoring of PETCO2 (35 to 40 mmHg)
Coronary perfusion pressure (CPP) (15mmHg)
Central venous oxygen saturation (ScvO2)
Abrupt increase in any of these parameters is a
sensitive indicator of ROSC that can be monitored
without interrupting chest compressions
Quantitative waveform capnography
If Petco2 lt10 mm Hg attempt to improve CPR
quality
Intra-arterial pressure
If diastolic pressure lt20 mm Hg attempt to improve
CPR quality
If ScvO2 is lt 30 consider trying to improve the
quality of CPR
HIGH QUALITY CPR
Chest compressions of adequate rate 100min
A compression depth of at least 2 inches (5 cm) in
adults and in children a compression depth of at
least 15 inches [4 cm] in infants
Complete chest recoil after each compression
Minimizing interruptions in chest compressions
Avoiding excessive ventilation
If multiple rescuers are available rotate the task of
compressions every 2 minutes
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
PROGNOSTIC INDICATORS IN THE ADULT POSTARREST
PATIENT TREATED WITH THERAPEUTIC HYPOTHERMIA
2010 (New) In adult postndashcardiac arrest patients
treated with therapeutic hypothermia it is
recommended that clinical neurologic signs
electrophysiologic studies biomarkers and imaging
be performed where available at 3 days after
cardiac arrest
Hypothermia
ILCOR Advisory statement (2003)
Unconscious adult patients with spontaneous
circulation after out-of-hospital cardiac arrest
should be cooled to 32-34degC for 12-24 hrs when the
initial rhythm was ventricular fibrillation (VF)
Such cooling may also be beneficial for other
rhythms or in-hospital cardiac arrests
Hypothermia
Cooling
Retard enzymatic suppress production of free
radicals
Reduction of O2 demand in low-flow regions
Protection of membrane fluidity
Reduction of intracellular acidosis
Decrease in cerebral edema and ICP
2010 (New) Advanced life support training
should include training in teamwork
Why Resuscitation skills are often performed
simultaneously and healthcare providers must be
able to work collaboratively to minimize
interruptions in chest compressions Teamwork and
leadership skills continue to be important
particularly for advanced courses that include ACLS
and PALS providers
MONITORING DURING CPR
Physiologic parameters
Monitoring of PETCO2 (35 to 40 mmHg)
Coronary perfusion pressure (CPP) (15mmHg)
Central venous oxygen saturation (ScvO2)
Abrupt increase in any of these parameters is a
sensitive indicator of ROSC that can be monitored
without interrupting chest compressions
Quantitative waveform capnography
If Petco2 lt10 mm Hg attempt to improve CPR
quality
Intra-arterial pressure
If diastolic pressure lt20 mm Hg attempt to improve
CPR quality
If ScvO2 is lt 30 consider trying to improve the
quality of CPR
HIGH QUALITY CPR
Chest compressions of adequate rate 100min
A compression depth of at least 2 inches (5 cm) in
adults and in children a compression depth of at
least 15 inches [4 cm] in infants
Complete chest recoil after each compression
Minimizing interruptions in chest compressions
Avoiding excessive ventilation
If multiple rescuers are available rotate the task of
compressions every 2 minutes
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
Hypothermia
ILCOR Advisory statement (2003)
Unconscious adult patients with spontaneous
circulation after out-of-hospital cardiac arrest
should be cooled to 32-34degC for 12-24 hrs when the
initial rhythm was ventricular fibrillation (VF)
Such cooling may also be beneficial for other
rhythms or in-hospital cardiac arrests
Hypothermia
Cooling
Retard enzymatic suppress production of free
radicals
Reduction of O2 demand in low-flow regions
Protection of membrane fluidity
Reduction of intracellular acidosis
Decrease in cerebral edema and ICP
2010 (New) Advanced life support training
should include training in teamwork
Why Resuscitation skills are often performed
simultaneously and healthcare providers must be
able to work collaboratively to minimize
interruptions in chest compressions Teamwork and
leadership skills continue to be important
particularly for advanced courses that include ACLS
and PALS providers
MONITORING DURING CPR
Physiologic parameters
Monitoring of PETCO2 (35 to 40 mmHg)
Coronary perfusion pressure (CPP) (15mmHg)
Central venous oxygen saturation (ScvO2)
Abrupt increase in any of these parameters is a
sensitive indicator of ROSC that can be monitored
without interrupting chest compressions
Quantitative waveform capnography
If Petco2 lt10 mm Hg attempt to improve CPR
quality
Intra-arterial pressure
If diastolic pressure lt20 mm Hg attempt to improve
CPR quality
If ScvO2 is lt 30 consider trying to improve the
quality of CPR
HIGH QUALITY CPR
Chest compressions of adequate rate 100min
A compression depth of at least 2 inches (5 cm) in
adults and in children a compression depth of at
least 15 inches [4 cm] in infants
Complete chest recoil after each compression
Minimizing interruptions in chest compressions
Avoiding excessive ventilation
If multiple rescuers are available rotate the task of
compressions every 2 minutes
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
Hypothermia
Cooling
Retard enzymatic suppress production of free
radicals
Reduction of O2 demand in low-flow regions
Protection of membrane fluidity
Reduction of intracellular acidosis
Decrease in cerebral edema and ICP
2010 (New) Advanced life support training
should include training in teamwork
Why Resuscitation skills are often performed
simultaneously and healthcare providers must be
able to work collaboratively to minimize
interruptions in chest compressions Teamwork and
leadership skills continue to be important
particularly for advanced courses that include ACLS
and PALS providers
MONITORING DURING CPR
Physiologic parameters
Monitoring of PETCO2 (35 to 40 mmHg)
Coronary perfusion pressure (CPP) (15mmHg)
Central venous oxygen saturation (ScvO2)
Abrupt increase in any of these parameters is a
sensitive indicator of ROSC that can be monitored
without interrupting chest compressions
Quantitative waveform capnography
If Petco2 lt10 mm Hg attempt to improve CPR
quality
Intra-arterial pressure
If diastolic pressure lt20 mm Hg attempt to improve
CPR quality
If ScvO2 is lt 30 consider trying to improve the
quality of CPR
HIGH QUALITY CPR
Chest compressions of adequate rate 100min
A compression depth of at least 2 inches (5 cm) in
adults and in children a compression depth of at
least 15 inches [4 cm] in infants
Complete chest recoil after each compression
Minimizing interruptions in chest compressions
Avoiding excessive ventilation
If multiple rescuers are available rotate the task of
compressions every 2 minutes
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
2010 (New) Advanced life support training
should include training in teamwork
Why Resuscitation skills are often performed
simultaneously and healthcare providers must be
able to work collaboratively to minimize
interruptions in chest compressions Teamwork and
leadership skills continue to be important
particularly for advanced courses that include ACLS
and PALS providers
MONITORING DURING CPR
Physiologic parameters
Monitoring of PETCO2 (35 to 40 mmHg)
Coronary perfusion pressure (CPP) (15mmHg)
Central venous oxygen saturation (ScvO2)
Abrupt increase in any of these parameters is a
sensitive indicator of ROSC that can be monitored
without interrupting chest compressions
Quantitative waveform capnography
If Petco2 lt10 mm Hg attempt to improve CPR
quality
Intra-arterial pressure
If diastolic pressure lt20 mm Hg attempt to improve
CPR quality
If ScvO2 is lt 30 consider trying to improve the
quality of CPR
HIGH QUALITY CPR
Chest compressions of adequate rate 100min
A compression depth of at least 2 inches (5 cm) in
adults and in children a compression depth of at
least 15 inches [4 cm] in infants
Complete chest recoil after each compression
Minimizing interruptions in chest compressions
Avoiding excessive ventilation
If multiple rescuers are available rotate the task of
compressions every 2 minutes
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
MONITORING DURING CPR
Physiologic parameters
Monitoring of PETCO2 (35 to 40 mmHg)
Coronary perfusion pressure (CPP) (15mmHg)
Central venous oxygen saturation (ScvO2)
Abrupt increase in any of these parameters is a
sensitive indicator of ROSC that can be monitored
without interrupting chest compressions
Quantitative waveform capnography
If Petco2 lt10 mm Hg attempt to improve CPR
quality
Intra-arterial pressure
If diastolic pressure lt20 mm Hg attempt to improve
CPR quality
If ScvO2 is lt 30 consider trying to improve the
quality of CPR
HIGH QUALITY CPR
Chest compressions of adequate rate 100min
A compression depth of at least 2 inches (5 cm) in
adults and in children a compression depth of at
least 15 inches [4 cm] in infants
Complete chest recoil after each compression
Minimizing interruptions in chest compressions
Avoiding excessive ventilation
If multiple rescuers are available rotate the task of
compressions every 2 minutes
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
Quantitative waveform capnography
If Petco2 lt10 mm Hg attempt to improve CPR
quality
Intra-arterial pressure
If diastolic pressure lt20 mm Hg attempt to improve
CPR quality
If ScvO2 is lt 30 consider trying to improve the
quality of CPR
HIGH QUALITY CPR
Chest compressions of adequate rate 100min
A compression depth of at least 2 inches (5 cm) in
adults and in children a compression depth of at
least 15 inches [4 cm] in infants
Complete chest recoil after each compression
Minimizing interruptions in chest compressions
Avoiding excessive ventilation
If multiple rescuers are available rotate the task of
compressions every 2 minutes
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
HIGH QUALITY CPR
Chest compressions of adequate rate 100min
A compression depth of at least 2 inches (5 cm) in
adults and in children a compression depth of at
least 15 inches [4 cm] in infants
Complete chest recoil after each compression
Minimizing interruptions in chest compressions
Avoiding excessive ventilation
If multiple rescuers are available rotate the task of
compressions every 2 minutes
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
SOME THINGS REMAIN IMPORTANT
RATE
DEPTH
RELEASE
UNINTERRUPTED
DECREASED VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
CHEST COMPRESSIONS
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
CHEST COMPRESSIONS
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum
Technique
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
COMPRESSION RATE (AT LEAST 100
MINUTE)
Rate per minute is NOT a function of ldquospeedrdquo of compressions only but a function of both speed ands minimizing no-flow periods (discussed later) for a total compressionsminute
Compressions rates as high as 130 resulted in favorable outcomes
Compression rates lt87minute saw rapid drop off in ROSC
NEW RECOMMENDATION At LEAST100minute
Better too fast than too slow
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
COMPRESSION DEPTH (AT LEAST 2
INCHES)
Previous studies show that only about 27 of
compressions were deep enough (Wik 2005)
0 (none) were too deep
NEW GIUDELINES The adult sternum should be
depressed at least 2 inches (5 cm) with chest
compression and chest recoilrelaxation times
approximately equal
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
COMPRESSION RATEhellip
Percent segments
within 10 cpm
of AHA Guidelines
31
369
Abella et al 2005 Circulation
76
75
58
42
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
COMPLETE RELEASERECOIL (FULL)
Complete Recoil essential to reduce intrathoracic pressure between compressions
Reducing recoil improves hemodynamic in arrest and improves Coronary Perfusion Pressure (CPP)
Incomplete chest wall recoil can be reduced during CPR by using electronic recording devices that provide real-time feedback
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
Small studies showed
improvement but a
Cochrane Meta- review of
over 1000 patients did
not
ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb LOE B)
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
MECHANICAL PISTON DEVICES
LUCAS THUMPER ETC
In 3 Studies the use of a mechanical piston device for CPR improved end-tidal CO2 and mean arterial pressure during adult cardiac arrest resuscitation
No long term benefit over manual CPR discovered (yet)
There is insufficient evidence to support or refute the routine use of mechanical piston devices in the treatment of cardiac arrest
Use of such devices during specific cercumstances when manual CPR is difficult may be done (Class IIb LOE C)
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
INTURRUPTIONS
Pausing for procedures
intubation IV pulse check etc)
Pausing for rhythm analysis
Pausing to charge clear and shock
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
KEY POINT
ldquohellipHigh-quality CPR is important not only at the onset but throughout the course of resuscitation Defibrillation and advanced care should be interfaced in a way that minimizes any interruptionin CPRrdquo
AHA 2010 Guidelines
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
AIRWAY
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
AIRWAY AND VENTILATIONS
Opening airway ndash Head tilt chin lift or jaw thrust
The untrained rescuer will provide Hands-Only
(compression-only) CPR
The Health care provider should open the airway
and give rescue breaths with chest compressions
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
AIRWAY Assess the airway ensuring it is
- open
- clear
Jaw thrust can be used
Look in mouth for obstruction teeth tongue vomit
foreign object
Ensure airway is clear
If airway obstructed with fluid (vomit or blood) roll patient onto their side amp clear airway or use suction if available
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
AIRWAY
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
RESCUE BREATHS
By mouth-to-mouth or bag-mask
Deliver each rescue breath over 1 second
Give a sufficient tidal volume to produce visible
chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
After advanced airway is placed rescue breaths
given asynchronus with compression
1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
OPEN AIRWAY
Head tilt chin lift + jaw thrust
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
55
OPENING THE AIRWAY
Jaw thrust Head tiltndashchin lift
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
56
THE OROPHARYNGEAL AIRWAY
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
MOUTH TO POCKET MASK
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
61
MOUTH-TO-MASK VENTILATION
Fingers jaw thrust upward Fingers head tiltndashchin lift
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
62
BAG-MASK VENTILATION
Keymdashventilation volume ldquoenough to produce obvious chest riserdquo
1-Person difficult less effective
2-Personeasier more effective
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
BAGVALVEMASK
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
64
EQUIPMENT FOR INTUBATION
Laryngoscope with several blades
Tracheal tubes
Malleable stylet
10-mL syringe
Magill forceps
Water-soluble lubricant
Suction unit catheters and tubing
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (ldquolook uprdquo) aligns axis A relative to B
Flex-the-neck-on-shoulders (ldquolook downrdquo) aligns axis B relative
to C
C
ABA
B
C
TracheaPharynx
Mouth
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
SECURING THE AIRWAY
Perform chest compressions with a 302 compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases Do not delay or
interrupt compressions early in
CPR for a secure airway
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag use one hand and only bring the fingertips
together
DO NOT increase volume
back
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to deliver breaths after tube placement
back
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator ventilation into trachea through side openings = B
C = tracheal tube ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff inflated through catheter = E
F = esophageal cuff inflated through catheter = G
H = teeth marker blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
COMBITUBE
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophagealtracheal cuff
H = teeth markers insert until marker lines
at level of teeth
D
A
D
B F
H
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
Advanced Airways
Once advanced airway in place donrsquot interrupt chest compression for
ventilation and avoid over ventilation 8-10 breathsm
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
LARYNGEAL MASK AIRWAY
LMA
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
79
LMA IN POSITION
Once the LMA is in position a clear secure airway is present
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
80
ANATOMIC DETAIL
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
CRICOID PRESSURE (REALLY)
Cricoid pressure in no arrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation
However it also may impede ventilation and interfere with placement of a supraglottic airway or intubation
If cricoid pressure is used in special circumstances during cardiac arrest the pressure should be adjusted relaxed or released if it impedes ventilation or advanced airway placement
The routine use of cricoid pressure in cardiac arrest is not recommended
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
FIO2 (DURING ARREST)
Use of 100 inspired oxygen (FIO210) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
FIO2 (POST ARREST)
Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury
Exact FiO2 recommendations have not been
determined
In the post arrest phase if equipment is available
titration of FiO2 to SPO2 04 is recommended
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
PASSIVE O2 DELIVERY DURING ARREST
Passive O2 delivery via ETT has been reviewed
In theory because ventilation requirements are lower than normal during cardiac arrest oxygen supplied by passive delivery is likely to be sufficient for several minutes after onset of cardiac arrest with a patent upper airway
The studies involved resulted in improved outcomes but it is unsure what role (if any) passive O2 had
At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
ETT
There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest
Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions intubation frequently is associated with interruption of compressions for many seconds
Placement of a supraglottic airway is a reasonable alternative to endotracheal intubation and can be done successfully without interrupting chest compressions
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
ETT (MORAL OF STORY)
There are two pitfalls of ETT placement
1- Interruption of CPR
2- Poor Placement practices
Therefore Place during CPR if possible and
optimize first attempt (bougie etc)
If you CANT do this then use a supraglottic
airway
If you cant do this perhaps you should not be a
paramedic Hmmmmmmhelliphellip
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
87
CONFIRMATION
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
COMPRESSION-VENTILATION RATIO
Ventilation rate = 12min
Compression rate = 78min
Large amplitude waves = ventilations
Small amplitude waves = compressions
Each strip records 16 seconds of time
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
REALITY SUCKShellip
Compression Ventilation Ratio 21
47-48 Breaths a minute
47 Nails in a coffin
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
PROLONGED VENTILATIONS
1048707Ventilation Duration = 436 seconds breath
1048707Ventilation Rate = 11 breaths minute
1048707 time under Positive Pressure = 80
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
DECREASING VENTILATION
CPR with Advanced Airway 8 ndash 10 breathsminute
Post-resuscitation 10 ndash 12min
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
TREATABLE CAUSES OF CARDIAC ARREST
THE HrsquoS AND TrsquoS
Hrsquos Trsquos
Hypoxia Toxins
Hypovolemia Tamponade (cardiac)
Hydrogen ion(acidosis) Tension pneumothorax
Hypo-hyperkalemia Thrombosis pulmonary
Hypothermia Thrombosis coronary
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
HYPOKALEMIA FLAT ST SEGMENTS
See a normal EKGhellip
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
HYPOKALEMIA PROMINENT U WAVES
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
HYPERKALEMIA PEAKED T WAVES
See a normal EKGhellip
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
TREATMENT OF HYPERKALEMIA
Antagonize membrane effects of K +
IV Calcium onset 1-2 min duration 30-60 min
Drive K+ into cells
Insulin (remember to give with glucose)
Beta agonists (high dose) ndash like albuterol
Remove K+ from the body
Kayexalate- binds K+ in gut onset 1-2 hours
Diuretics- only work if renal function remains
Hemodialysis- depends on availability
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
ELECTRICAL ALTERNANS THE EKG FINDING
OF TAMPONADE
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
TREATMENT OF TAMPONADE PERICARDIOCENTESIS
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
TENSION PNEUMOTHORAX
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
TREATMENT OF TENSION PTX
Oxygen
Insert a large-bore (ie 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib) at the midclavicular line
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
Arrest Rhythms
Shockable rhythms
VF
Pulseless VT
Non shockable rhythms
PEA
Asystole
Electrical therapies in ACLS
Cardiversion Defibrillation for Tachyarrhythmias
Unsynchronized = defibrillation (Uses higher energy levels and delivers shock immediately)
Synchronized delivers shock at peak of QRS complex (Avoids delivering shock during repolarization)
Pacing for brady arrhythmias
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
PRE‐CORDIAL THUMP
bull No prospective studies so far
bull Rationale is to convert mechanical energy to
electrical energy
bull In all successful cases the thump was given
within first 10s
bull More likely to be successful in converting VT to
sinus rhythm
bull Much less likely for VF
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
PRE‐CORDIAL THUMP
bull Consider as an option for witnessed sudden
collapse and defibrillator NOT immediately
available
bull Thump may cause deterioration
ndash Rate acceleration of VT
ndash Conversion of VT to VF
ndash Complete Heart Block
ndash A systole
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
PRE‐CORDIAL THUMP
bull Only by trained healthcare providers immediately
confirm cardiac arrest
bull Use ulnar edge of tightly clenched fist
bull Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
bull After that immediately retract the fist
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
DEFIBRILLATION
Defibrillation is defined as termination of VF for at
least 5 seconds following the shock
Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
Defibrillation Sequence
Turn the AED on
Follow the AED prompts
Resume chest compressions immediately after the shock(minimize interruptions)
Shock Energy
Biphasic Manufacturer recommendation (eg initial dose of 120-200 J) if unknown use maximum available
Second and subsequent doses should be equivalent and higher doses may be considered
Monophasic 360 J
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
Defibrillation technique
Defibrillation Sequence
Action Announcements
1 Switch on
2 Place coupling padsgel in correct position
3 Apply paddles
4 Check ECG rhythm and confirm no pulse
5 Select non-synchronized (VF) setting
6 Charge to required energy level Charging
7 Ensure no-one is in contact with anything touching the patient
Stand clear
8 Press paddle buttons simultaneouslyShocking
now
9eturn to ALS algorithm for further steps
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
CAUTION IN USE OF AED
Donrsquot apply pads over pacemakers
Donrsquot apply pads over skin patchesmedications
Be cautious around water
NEVER attach to anyone not in cardiac arrest
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR then pulse check and
re-analyze if necessary
DEFIBRILLATION
These measures reduce ldquono flow timerdquo Why is it
important to reduce the amount of time when
compressions are not performed
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
WHAT NEXT
Commence CPR immediately after delivering
the shock
Use a ratio of 30 compressions to 2 breaths
Follow the voice prompts amp continue CPR until
signs of life return
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
Evidence from 2 well-conducted prepost design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
If 1 shock fails to eliminate VF the incremental
benefit of another shock is low and resumption of
CPR is likely to confer a greater value than another
shock
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
CARDIAC ARREST
Cardiac arrest can be caused by 4 rhythms
1 Ventricular fibrillation(VF)
2 Pulseless ventricular tachycardia (VT)
3 Pulseless electric activity (PEA) and
4 Asystole
How to recognise cardiac arrest
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
VF Pulseless VT
Witnessed arrest
2 rescue breaths then
Defibrillate
Unwitnessed arrest
5 cycles of CPR (2 min)
then
Defibrillate
200 Joules for biphasic
machines
360 Joules for monophasic
machines
Single shock (not 3 shocks)
followed by CPR
No gap between chest
compression and shock
delivery
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
VENTRICULAR FIBRILLATION
Fine VF
Coarse VF
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
VENTRICULAR FIBRILLATION
Rate Cannot be determined because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
VENTRICULAR TACHYCARDIA
Treat the following as VF
Pulse less monomorphic VT
Pulse less polymorphic VT
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beatsmin typically 200 to 250 beatsmin
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 012 sec or more there is a gradual alteration in the
amplitude and direction of the QRS complexes a
typical cycle consists of 5 to 20 QRS complexes
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beatsmin
Rhythm Essentially regular
P waves Usually not seen if present they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 012 sec or more often difficult to differentiate
between the QRS and the T wave
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
MONOMORPHIC VENTRICULAR TACHYCARDIA
Signs and symptoms associated with VT vary
Sustained VT does not always produce signs of
hemodynamic instability
VT may occur with or without pulses
Treatment is based on signs and symptoms and the
type of VT
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
WHAT IS THIS RHYTHM
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
ASYSTOLE PROTOCOL
Check another lead
Is it on paddles
Power on
Check lead and cable connections
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible but atrial activity may
be seen (ie ldquoP-waverdquo asystole)
Rhythm Ventricular not discernible atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
ldquoP-Waverdquo Asystole
Asystole
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 143
THE RESUSCITATION TEAM
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
GOALS OF THE RESUSCITATION TEAM
To re-establish spontaneous circulation and
respiration
To preserve vital organ function during resuscitation
Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
CRITICAL TASKS OF RESUSCITATION
1 Chest compressions
2 Airway management
3 ECG monitoring and defibrillation
4 Vascular access and medication administration
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
TEAM LEADER RESPONSIBILITIES
Assesses the patient
Orders emergency care in accordance with protocols
Considers reasons for cardiac arrest
Supervises team members
Evaluates the adequacy of chest compressions
Ensures that the patient receives appropriate oxygen therapy
Evaluates the adequacy of ventilation
Ensures safe and correct defibrillation when it is indicated
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
TEAM LEADER RESPONSIBILITIES
Ensures the correct choice and placement of vascular access
Confirms proper positioning of an advanced airway
Ensures correct drug dose and route of administration
Ensures the safety of all team members
Problem solves
Decides when to terminate resuscitation efforts
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
Copyright copy 2012 by Mosby an imprint of Elsevier Inc 148
TEAM MEMBER RESPONSIBILITIES
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
AIRWAY TEAM MEMBER
Manual airway maneuvers
Oral airway
Nasal airway
Oxygen-delivery devices
Bag-mask ventilation
Suctioning
Advanced airway placement
If within scope of practice
Waveform capnography exhaled
carbon dioxide detector and
esophageal detector device
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
The ACLS or BLS team member who is responsible
for CPR must be able to do the following
Properly perform CPR
Provide chest compressions of adequate rate force
and depth in the correct location
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
ELECTROCARDIOGRAPHYDEFIBRILLATION
TEAM MEMBER
Synchronized versus unsynchronized shocks
Pad or paddle placement
Safety precautions
Indications for and complications of transcutaneous
pacing
Problem solving with regard to equipment failure
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
KEY CONCEPTS REVISITEDhellip
Avoid Hyperventilation
Push hard and fast allow complete chest recoil minimal
interruptions
Compress chest depth of 15 to 2 inches at a rate of 100
compressions per minute
Compression to ventilation ratio 302 after advanced
airway no need to interrupt compression
Turing defibrillator onhellip
5 Hs and 5 Tshellip
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
EPINEPHRINE
Indications
Cardiac arrest
VF VT a systole PEA
Symptomatic bradycardia
After atropine alternative to dopamine
Severe hypotension
When atropine and pacing fail hypotension accompanying
bradycardia phosphodiesterase enzyme inhibitors
Anaphylaxis severe allergic reactions
Combine with large fluid volume corticosteroids
antihistamines
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
EPINEPHRINE
Precautions
May increase myocardial ischemia angina and oxygen demand
High doses do not improve survival may be detrimental
Higher doses may be needed for poisondrug induced shock
Dosing
Cardiac arrest 1 mg (110000) IVIO every 3-5 min
High dose up to 02 mgkg for specific drug ODrsquos
Infusion of 2-10 mcgmin
Endotracheal of 2-25 times normal dose
SQIM 03-05 mg
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
VASOPRESSORS
Drug Therapy
Epinephrine IVIO Dose 1 mg every 3-5 minutes
Vasopressin IVIO Dose 40 units can replace first
or second dose of epinephrine
Amiodarone IVIO Dose First dose 300 mg bolus
Second dose 150 mg
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
Continuous quantitative waveform capnography is
recommended
Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)asystole
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia
Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
Narrow regular 50 ndash 100 J
Narrow irregular Biphasic ndash 120 ndash 200 J and
Monophasic ndash 200 J
Wide regular ndash 100 J
Wide irregular ndash defibrillation dose
Adenosine 6 mg rapid iv push follow with NS
flush Second dose 12 mg
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
INITIAL OBJECTIVES OF POSTndash CARDIAC
ARREST CARE
Optimize cardiopulmonary function and vital organ
perfusion
After out-of-hospital cardiac arrest transport patient
to an appropriate hospital with a comprehensive
postndashcardiac arrest treatment
Transport the in-hospital postndash cardiac arrest patient
to an appropriate critical-care unit
Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest
THANK YOU
THANK YOU