julie m. waters rn ms ccrn clinical nurse educator for critical care providence health care march...
TRANSCRIPT
JULIE M. WATERS RN MS CCRNCLINICAL NURSE EDUCATOR FOR CRITICAL
CAREPROVIDENCE HEALTH CARE
MARCH 2015
Hitting the Target:Does Temperature Management
Matter After Cardiac Arrest?
What do they have in common?
Hit the target every time
Objectives
Describe the impact of thermoregulation in patients after cardiac arrest
Discuss the current state of targeted temperature management in cardiac arrest patients
Identify key principles in the clinical management of patients receiving targeted temperature management
Cardiac Arrest - Dismal
Cardiac Arrest≈300K
Hospital Dischar
ge≈60K
Long Term Recovery
≈30K
80% Mortalit
y50%
NeuroInjury
Cardiac Arrest - Management
Major Goals: Determine and treat the cause of the cardiac arrest
Etiology determines therapy Minimize brain injury Manage cardiovascular dysfunction Manage problems resulting from global ischemia and
reperfusion injury
Baseline Neurological Exam
Determine the likely cause, possible clinical course, and need for interventions
Neurological injury is the most common cause of death in patients with out-of-hospital
cardiac arrest
Consider Targeted Temperature Management for:
Patients who can not follow commands or demonstrate purposeful movement
Definitions for today…..
Controlled Normothermia 36-37.5°C
Temperature Control No higher than 36°C
Therapeutic Hypothermia Decrease core temp to 32-34°C
Targeted Temperature Management (TTM) Maintaining body temp 33-36°C
Historical Perspective
Ancient Greece – Hippocrates1812 Napoleon’s soldiers19th Century “Russian Method of
Resuscitation”
Early Methods of Cooling
Make use of the environment
Pack in ice
Problems with Early Hypothermia
Goal was deep hypothermia (30 C)Duration of cooling varied widely (from 2-10
days)ICUs didn’t exist, monitoring was limitedCooling methods weren’t very reliable
1945: positive effects of TH in severe head injury 1950: improved neuro function in cardiac surgery
with TH Then …………..........
Outcome Hypothermia (n = 43)
Normothermia (n = 34)
Discharge to home or a rehab facility
39% (21/43) 26% (9/34)
Mortality* 51% 68%
* Did not reach statistical significance
Outcome Hypothermia (n = 137)
Normothermia (n = 138)
Positive Neurological
Recovery
55% (75/136) 39% (54/137)
Mortality at 6 months
41% 55%
2010 Updated AHA Guidelines
WHY?.........Ischemia
Perman et al. Clinical Applications of Targeted Temperature Management. Chest 2014; 145(2):386-393.
Abnormal Electrical Depolarization
Blood-Brain Barrier Disruption
Free Oxygen Radical Formation
Neurotransmitter Release
Increased Levels of Excitotoxins
Destabilized Cell Membranes
Mitochondrial Failure
Slide A. Lawrence 2015
Neuronal Damage
Increased temp in the neurologically injured brain or ischemic/anoxic brain…
Cellular Derangements
Cellular Damage
Cell Death
Ischemic Brain Injury
Injury occurs within 4-6 minutes without perfusion
Initial insult followed by a cascade of events
Damage occurs from hours to daysCan be re-triggered by new ischemiaAll processes are temperature dependent
Stimulated by fever Mitigated by hypothermia
Possible Mechanisms of Action
Reduction of cerebral metabolic demand 6-8% for every 1 decrease in temp Reduced 02 and glucose needs more
closely match reduced blood flow Less CO2 and lactate production
Ischemic cell
¯ Oxygen & glucose ¯ ATP
Disruption of Na-K ATP pump
Excitatory Neurotransmitt
ers (glutamate)
CalciumInflux
Degradation enzymes (carpase,
lipase)
Cellular Apoptosis
Mitochondrial
Dysfunction
X
J. Dirks 2013
ReperfusionInjury
(Inflammatory Response)
↑ Vascular Permeability
(edema)
Disruption of Blood-brain
Barrier
Activation of Coagulation
Microthrombi formation
Cellular Hyperactivity
Temperature in brain
X
J. Dirks 2013
Other Benefits of Hypothermia
Reduction in intracranial pressure
Suppression of epileptic activity
Improved tolerance of recurrent ischemia
Design of Study
International trial - 939 unconscious adults after OHCA targeting either 33°or 36°
Blind study - between 2010-2013 36 ICUs across 10 countries in the EU and AUSAll patients were sedated and ventilated and
had feedback cooling devices All patients had 72 hrs of temp intervention
post ROSC to prevent fever
Summary of Findings
How can this be?
Considerations
All had good post arrest care, 2/3 had angiography, strict rules outlined for prognostication and withdrawal of care
The population included OHCA primary cardiac arrest patients with all rhythms (shockable and nonshockable)80% were Vfib/Vtach and 20% PEA/Asystole
73% of patients received bystander CPR
December 2013
State of the Therapy
All Comatose Post-Arrest Patients
Active control of patient’s temp between 32-36°C
Active avoidance of fever
TTM Recommendations - Patient Specific?
36°C 33°CDuration: 24 hours Duration: 24 hours
Uncomplicated patient with some motor response
Patient with loss of motor response or brainstem reflex
No malignant EEG patterns
Malignant EEG patterns
No evidence of cerebral edema on CT
CT changes suggestive of cerebral
edemaRittenberger JC UpToDate: Post-Cardiac Arrest Management in Adults. Last updated 2/2015
Questions to be Answered
What is the optimal temperature? TTM trial was neutral 33C based on extensive lab evidence and 2 RCTs
What is the optimal duration?What is the optimal injury measurement for post-
arrest? We can’t tell who will have significant post-arrest injury
currentlyHow should we tailor therapy to each patient?
Different presenting rhythms: VF/VT vs PEA/Asystole Different length of down time Severity of presenting illness or comorbiditiesOnly get one shot to modify neurological
injury
Indications and Contraindications
Indications ANY patient not following commands after cardiac
arrestContraindications
Advanced directive against aggressive therapyConsiderations
Active noncompressible bleeding (36°C)
Nielsen trial showed no statistically significant differences in adverse events between 33°C and 36°C
Phases of TTM
1. Induction2. Maintenance3. Rewarming4. Controlled Normothermia
Induction
Temperature Measurement Core Temp 2 Sites Registered Temp + Lag Time = Overshoot
Site of Temperature Measurement
Variation from Core
Temperature
Average Lag Time
Best Practice: Advantage Disadvantage
Pulmonary Artery Catheter
Gold Standard Complex insertion
Esophagus <0.1 C⁰ 5 mins(range 3-10)
Most rapid and accurate reflection of gold standard Temp fluctuates according to depth of probe, accurate placement is key
Bladder <0.2 C⁰ 20 mins(range 10-60)
Easy insertion, low risk dislodgement Accuracy influenced by low U.O., Long lag time, movement of sensor
Rectum <0.3 C⁰ 15 mins(range10-40)
Easy insertion High risk of dislocation, influenced by stool in rectum, long lag time
Rapid Induction is Key at 33°C
35-38 C⁰
33.5 C⁰
FAST
ICEDSALIN
E
ICE PACKS
MEDSCOOLING PADS
Target Temp 36°C
If < 36°C:Controlled rewarm at
0.25°C/ hour
Infusion of Ice-Cold Fluids
Rapidly infuse 30ml/kg (1-3L) of cold (4◦C) isotonic saline via pressure bag
↓ Body temp > 2 ◦C per hour 1L of fluids over 15 minutes can
↓ body temp ≈ 1.0 ◦C Caution in patients with:
Heart failure Severe renal dysfunction Pulmonary edema
If clinically indicated – make the volume cold
Conventional Cooling
Adequate although tricky
DisadvantagesLack of feedback loop makes
maintenance difficultHigh incidence of over coolingExtreme nursing vigilance requiredEffect of temperature fluctuations and
excessive hypothermia on patient outcomes is unknown
Surface Cooling Thermostatically Controlled Devices
DisadvantagesCover patient’s
surface area 40-90%
Risk skin lesionsAdvantages
Easy and fast time to administration
Nurse-driven protocols
Core CoolingIntravascular Cooling Devices
DisadvantagesTime and expertise to initiate
therapyRisk of catheter-related thrombosis
AdvantagesRapid cooling ratesReliable maintenance of core
temperature
Intravascular VS Surface Cooling
Findings: comparable in terms of cooling effectiveness and automatic
temperature feedback controlStudy
Time to device deployment were comparable No significant differences in survival to final
hospital discharge with good neurological function
No difference in rate of shivering No device specific injuries were noted
TФmte O, et al. A comparison of intravascular and surface cooling techniques in comatose cardiac arrest survivors. Crit Care Med 2011; 39(3):443-449.
Thermoregulatory Defenses
BehavioralAutonomic
Vasoconstriction
Shivering
Normal……………. 37°C
Vasoconstriction…..36.5°C
Shivering…..…….35.5°C
Below shivering…..34°C
Threshold
**Still see shivering at 36°C
Shivering
↑ heat production by 600%↑ oxygen consumption 2-3x↑ CO2 production 2-3x↑ metabolic rate 2-5xLinked to ↑risk of morbid cardiac
eventsImpedes induction of TTM and
eliminates possible neuroprotective benefits
Who is likely to shiver?
>60% patients undergoing TTM experience shivering
Young MalesLow Magnesium levels <1.7mg/dLPatients with a difficult-to-
extinguish shivering response had a higher odds of neurological intact survival
How to assess for shivering
Early detectionObserve for piloerectionPalpation of the mandible for
vibrationsIdentifying ECG artifact Resistance to cooling
Objective Indicators
Look for increase in patient’s tempLook at water tempWhat does it indicate the patient is
doing?
Bedside Shivering Assessment Scale*
Score Definition
0 None: no shivering noted on palpation of the masseter, neck, or chest wall
1 Mild: shivering localized to the neck and/or thorax only
2 Moderate: shivering involves gross movement of the upper extremities (in addition to neck and thorax)
3 Severe: shivering involves gross movements of the trunk and upper and lower extremities
*Badjatia N et al, Metabolic impact of shivering during therapeutic temperature modulation: Stroke 2008; 39:3242-3247.
Goal is BSAS ≤ 1
How to combat shivering:Pharmacological &
Nonpharmacological
Surface WarmingSkin temperature influences at least 20% of
the shivering thresholdWorks by countering the feedback loop from
the skin temp to the hypothalamusEffective adjunct in suppressing the
shivering reflexAir-circulating blanket
Insulation of cutaneous thermoregulators on face, hands and feet
Pharmacological
Goal: Pharmacological induction of thermal tolerance
Avoid a cooling-related stress response through pharmacological impairment
Combination of drugs to prevent excessive toxicity
Vasodilation with sedation & analgesiaSedation is importantMonitor efficacy and potency due to
decreased metabolism and elimination of drugs
Miscellaneous Drugs
Acetaminophen Inhibits cyclooxygenase-mediated prostaglandin
synthesis 650-1000mg Q 4-6 H (IV/PO/PR)
Buspirone Acts on 5-HTLA receptor; lowers shiver threshold 20-30mg PO Q 8 H
Magnesium Sulfate Peripheral vasodilation & Facilitates the cooling
process Decreased time to goal temperature Possible direct neuroprotective effects 500mg – 1 gm/hr to reach goal Mg level 3-4mg/dL
Opioids
FENTANYLo 25-50 mcg/hr IV
MORPHINEMEPERIDINE
25-50mg IV Q 1 H One of the most effective anti-shivering
drugs Lowering of the seizure threshold????? Caution in renal failure
Sedation
Dexmedetomidine Dose 0.2-1.5mcg/kg/hr (off-label) Bradycardia & Hypotension
Propofol 50-75 mcg/kg/min Anti-seizure effect Hypotension
Midazolam/Benzodiazepines 2-10 mg/hr Complicates neuro evaluation Less hypotension
Paralytics
Muscles may stop – Brain is still working Advantages
Very effective; quickest method to stop shivering Help achieve goal temp quickly Do not cause hypotension
Considerations May not be able to detect seizure activity
Consider continuous EEG ↑risk of critical illness polyneuromyopathy May mask incomplete sedation Only use as long as needed…….stop/restart TOF does NOT correlate in TH
Combination Agents
Buspirone & MeperidineBuspirone & DexmedetomidineDexmedetomidine & Meperidine
Benefit from combination therapy-
Whether methods or drugs
*Seder DB et al, CCM 2009; 37(7):S211-S222
Columbia Anti-Shivering ProtocolStep Intervention Dose
0 Baseline AcetaminophenBuspironeMagnesium SulfateSkin Counterwarming
650-100mg Q 4-6 h30mg Q 8 h0.5-1 mg/h IV (Goal 3-4 mg/dl)43⁰C/MAX Temp
1 Mild Sedation
Dexmedetomidine OROpioid
0.2-1.5 mcg/kg/hFentanyl starting dose 25mcg/hMeperidine 50-100mg IM or IV
2 Moderate Sedation
Dexmedetomidine AND Opioid
Doses as above
3 Deep Sedation
Propofol 50-75 mcg/kg/min
4 NMB Vecuronium 0.1mg/kg IVChoi HA et al. NeuroCrit Care 2011; 14:389-394.
5.1% of
patients
18% of patients
November 2013
Physiological Impact of Hypothermia
Patients require ICU care to: Maintain hemodynamic stability Ensure adequate oxygenation Correct fluid/electrolyte derangements Prevent complications (infection or bleeding) Deliver safe, controlled cooling and re-
warming Manage shivering
Immunologic:Impaired leukocyte functionCutaneous vasoconstriction
Increased risk of infection if
hypothermia maintained >24
hrs
Systemic Effects of Hypothermia
Hematologic:Depressed clotting
enzyme reactionsImpaired platelet
functionMild
coagulopathy, possible bleeding
Systemic Effects of Hypothermia
Systemic Effects of Hypothermia
HemodynamicSlight increase in contractility (mild hypothermia) then
decrease (moderate-deep)
TH not associated with increased need for vasopressor support
CO = demand
Typical EKG Changes
BradycardiaProlonged PR,
QRS, QTcOsborne waves
(a dome or hump occurring at the R-ST junction (J point) on the ECG)
From: Krantz MJ, Lowery CM. “Giant Osborne Waves in Hypothermia” N Engl J Med 2005; 352:184
Bradycardia usually
well tolerated
33°C
Systemic Effects of Hypothermia
“Cold Diuresis”: Electrolytes:Vasoconstriction increases venous returnIntracellular shifts of electrolytes during
temperature manipulation renal losses due to tubular dysfunction
HypovolemiaLoss of electrolytes(potassium, magnesium,
phosphate)
33°C
Metabolic:Decreased cellular metabolism
O2 & glucose consumption fat metabolism CO2 production
insulin sensitivity
ABGs: O2, CO2, acidosisGlucose: Goal 140-180
mg/dL
Systemic Effects of Hypothermia
Induction Phase
Rapid identification and implementationRapidly cool to 33°CIf <36°C – controlled rewarm at 0.25°C/hr
Maintenance Phase
Maintain target temperature for 24 hours
• Monitor EKG changes• Maintain fluid status• Watch for infection• Monitor for bleeding• Electrolyte monitoring• Monitor for skin breakdown• Avoid hyperglycemia
Rewarming Phase
Rapid rewarming can negate the benefits of TTM
Controlled rate of rewarming to 37°C ≤0.5°C / hour Most suggest 0.25°C / hour
Monitor for Electrolyte abnormalities Cerebral edema Seizures Shivering
Controlled Normothermia Phase
Fever during the first 72 hours after ROSC has been associated with poor outcome
For patients unable to follow commands: maintain normothermia (<37.5°C) for an additional 48 hours after rewarming
Rebound fevers after therapy stopped
Neuroprognostication
Drug clearance is decreased so sedatives may be present 48-72 hours Decisions regarding withdrawal of care must be delayed until adequate clinical exam can be performed Patient’s temperature must be at 35˚C before declaration of brain death can be made
72 hours
Summary
TTM has been shown to improve outcomes in patients after cardiac-arrest
TTM is considered the standard of care for comatose survivors after cardiac-arrest (VF/VT)
TTM is best implemented as a protocol-driven therapy
Shivering must be controlled Stratifying patients based on organ system
dysfunction may be the way to determine 33 vs 36
33°C
36°C
What is my target
temperature?
Questions?
[email protected] “The odds of hitting your
target go up dramatically when you aim at it.”
M. Pancoast