RT 230Unit A-

Indication, Setup and Monitoring of CMV

INDICATIONS FOR CMV

ApneaAcute ventilatory failure: A PCO2 of more

than 50mmHg with a pH of less than 7.25 Impending acute ventilatory failure

Based on lab data and clinical findings indicating that pt is progressing towards ventilatory failure

Quick tip: acute hypercapnic failure ph drops 0.8 for every 10mm hg rise in co2 chronic hupercapnic ph drops 0.03 for every 10 mmhg rise in co2

Clinical problems often resulting in impending ventilatory failure Pulmonary abnormalities

RDS=Respiratory Distress Syndrome Pneumonia Pulmonary emboli

Mechanical ability of lung to move air=muscle fatigue Ventilatory muscle fatigue Chest injury Thoracic abnormalities=scoliosis, kyphoscoliosis

Neurologic disease=GB, MG Pleural disease=pleurasy

Clinical evaluation Vital signs: Pulse and BP increase Ventilatory parameters

VT decreases RR increases Accessory muscle use increases

Paradoxical breathing (abdomen out, rib cage in) Retractions may be noted Development of impending acute vent failure may

demonstrate Progressive muscle weakness in pt with Neurologic

disease Increasing fatigue

ABGs demonstrating a trend toward failure

9am 10am11am12pm1pm pH 7.58 7.53 7.46 7.38 7.35 PCO2 22 28 35 42 48

HCO3 21 22 23 24 24

PO2 60 55 50 43 40

Non-responsive hypoxemia

PaO2 less than 50% on an FIO2 greater than 50%

PEEP is indicatedREFRACTORY HYPOXEMIA

PHYSIOLOGIC EFFECTS OF POSITIVE PRESSURE VENTILATION

Increased mean intrathoracic pressureDecreased venous return

Thoracic pump is eliminated*** Pressure gradient of flow to right side of heart is

decreased Right ventricular filling is impaired

Give fluid

Decreased cardiac output Caused by decreased venous return Give drugs and fluid

Monitor I and O. Normal urine output 1000-1500 cc/24 hours

THORACIC PUMP

The "thoracic pump" is the thoracic cavity, the diaphragm, the lungs, and the heart.

The diaphragm moves down, pressure in the cavity decreases and venous blood rushes through the vena cava via the right heart into the lungs. Pulmonary blood vessels expand dramatically, filling with blood, air and blood meeting across the very thin alveolar surface. The deeper the inhalation, the more negative the pressure, the more blood flows, and the fuller the lungs become.

THORACIC PUMP

As the diaphragm moves up the pressure in the thoracic cavity reverses. Pulmonary blood vessels shrink ejecting an equal volume of blood out of the pulmonary veins into the left heart. The left heart raises the pressure and checks and regulates the flow. The more

complete the exhalation, the more positive the pressure becomes and the more blood is ejected from the lungs.

Decrease exhalation, more pressure in cavity decrease CO

EFFECTS OF PPV CONT.

Increased intracranial pressure Blood pools in periphery and cranium because of

decreased venous return Increased volume of blood in cranium increases

intracranial pressure

Decreased urinary outputPPV could cause 30-50% decrease renal

output Decreased CO results in decreased renal blood flow

Alters filtration pressures and diminishes urine formation

Decreased venous return and decreased atrial pressure are interpreted as a decrease in overall blood volume ADH is increased and urine formation is decreased

ADH=VASOPRESSIN

Roughly 60% of the mass of the body is water, and despite wide variation in the amount of water taken in each day, body water content remains incredibly stable. Such precise control of body water and solute concentrations is a function of several hormones acting on both the kidneys and vascular system, but there is no doubt that antidiuretic hormone is a key player in this process.

Antidiuretic hormone, also known commonly as arginine vasopressin

The single most important effect of antidiuretic hormone is to conserve body water by reducing the loss of water in urine. A diuretic is an agent that increases the rate of urine formation.

high concentrations of antidiuretic hormone cause widespread constriction of arterioles, which leads to increased arterial pressure.

Retention of fluids will cause EDEMA

EFFECTS OF PPV CONT.

Decreased work of breathing Force to ventilate is provided by the ventilator

Increased deadspace ventilation Positive pressure distends conducting airways &

inhibits venous return The portion of VT that is deadspace increases Greater percentage of ventilation goes to apices

Increased intrapulmonary shunt Ventilation to gravity dependent areas is decreased Perfusion to gravity dependent areas increase Shunt fraction increases from 2-5% to 10%

A pulmonary shunt is a physiological condition which results when the alveoli of the lung are perfused with blood as normal, but ventilation (the supply of air) fails to supply the perfused region. In other words, the ventilation/perfusion ratio (the ratio of air reaching the alveoli to blood perfusing them) is zero. A pulmonary shunt often occurs when the alveoli fill with fluid, causing parts of the lung to be unventilated although they

are still perfused. Intrapulmonary shunting is the main cause of hypoxemia (inadequate blood oxygen) in pulmonary edema and conditions such as pneumonia in which the lungs become consolidated.The shunt fraction is the percentage of blood put out by the heart that is not completely oxygenated. A small degree of shunt is normal and may be described as 'physiological shunt'. In a normal healthy person, the physiological shunt is rarely over 4%; in pathological conditions such as pulmonary contusion, the shunt fraction is significantly greater and even breathing 100% oxygen does not fully oxygenate the blood.[1]

EFFECTS OF PPV CONT.

Respiratory rate, VT, Inspiratory time, and flow rate can be controlled

May cause stress ulcers and bleeding in GI tract

16

COMPLICATIONS OF MECHANICAL VENTILATION

Complications related to pressure Ventilator-associated lung injury (VALI)

High pressures are associated with barotrauma Pneumothorax, pneumomediastinum,

pneumopericardium, subcutaneous emphysema Pneumothorax has decreased chest movement,

hyperresonance to percussion, on affected side If tension pneumothorax: medical emergency

Relieved by needle insertion, then chest tube Use 100% oxygen to speed reabsorption.

Placing patient on CMV

Establish airway Select VT 8‑12ml/kg of ideal body weight Select mode ‑ a/c sensitivity at minimal to not self

cycle Set pressure limit 10cmH2O above delivery pressure Set sigh volume 1‑1/2 to 2 times VT Sigh pressure 10cmH2O above sigh delivery pressure Rate as ordered PEEP as ordered: exp. resist, insp. hold, etc. Set spirometer 100 cc less than patient volume

check for function (turn on)

Modes Control

All of WOB is taken over by ventilator Sedation is required Control mode is useful

During ARDS, especially if high PEEP is required or inverse I:E ratio

Assist Patient is able to control ventilatory rate Should not be used for continuous mechanical

ventilation if pt is apneic

Assist/control Pt able to control vent rate as long as spontaneous

rate > backup rate Machine performs majority of WOB Sedation is often required to prevent

hyperventilation Is useful during early phase of vent support where

rest is required Useful for long term for pt not ready to wean

SIMV In between positive press breaths pt can breathe

spontaneously Useful for long term for pt not ready to wean Used as weaning technique for short-term vent

dependent pt

PS Vent functions as constant pressure generator

Positive pressure is set Pt initiates breath, a predetermined pressure is

rapidly established Pt ventilates spont, establishes own rate, VT, peak flow

and I:E Can be used independently/CPAP/SIMV Indicated to reduce work imposed by ETT, 5 to 20cm

H2O Can be used for weaning

A set IPS (12ml/kg VT) achieved by adjusting IPS level then slowly reducing as clinical status improves

To overcome resistance of ETT, IPS should meet Raw To determine amount of PS needed: [(PIP – Plateau

pressure) / Ventilatory inspiratory flow] x spontaneous peak inspiratory flow

IBWEstimated ideal body weight in (kg)Males: IBW = 50 kg + 2.3 kg for each inch over 5 feet.Females: IBW = 45.5 kg + 2.3 kg for each inch over 5 fee.

1 Kilogram = 2.20462262 Pounds

MONITORING CMV

Observation Look at patient!

Make a good visual assessment Start with patient, trace circuit back to ventilator

Check and drain tubing Check connections

Check patient Suctioning, position, etc. BP Spontaneous RR Heart rate and all vital signs

Check machine settings VT (set, exhaled, corrected) f (assisted, set, spontaneous) Pressure limit: 10 above delivery pressure PEEP if applicable: Check BP! Peak Insp. Pressure (PIP): Keep as low as possible I:E ratio for proper flow FiO2: Keep as low as possible to prevent Oxygen

Toxicity yet keep them adequately oxygenated Check all apnea alarms and settings. Check set VT to exhaled VT for any lost volumes

If difference is greater than 100 cc, check for leak.

Compliance

Measures distensibility of lung – how much does the lung resist expansion.

Relationship between Volume and Pressure

High compliance equals lower PIP thus easier ventilation and less side effects of CMV

Disease states resulting in low compliance include the Adult Respiratory Distress Syndrome (ARDS), pulmonary edema, pneumonectomy, pleural effusion, pulmonary fibrosis, and pneumonia among others.

Emphysema is a typical cause of increased lung compliance.

YOU MUST KNOW

Dynamic = VT (corrected or exhaled)

PIP – PEEP

Always subtract out PEEP Consistently use exhaled or corrected VT

Used to assess volume/pressure relationships during breathing – any changes in RR will effect it

CDYN decreases as RR increases which may cause V/Q mismatch which may cause hypoxemia

May reflect change due to change in flow due to turbulence instead of compliance

Normal = 30 – 40 cmH2O

VERY IMPORTANT Static = VT (corrected or exhaled)

Plateau – PEEP

Always subtract out PEEP Always consistently use either VT exhaled or VT

corrected Will not change due to change in flow, more

accurate Measured pressure to keep airways open with no gas

flow. Normal values very with pt, but usually above 80

cmh2o will show lung overdistention

Importance to follow trends in patient compliance Decreased C = stiffer lung = less compliant = higher

ventilating pressures = you need a ventilator with high internal resistance to deliver volumes using square wave.

High compliance = possible Emphysema

STATIC VS DYNAMIC COMPLIANCE Decrease in CDYN with no change in CST indicates

worsening airway resistance Causes

Bronchospasm Secretions Kinked/Occluded ETT Inappropriate flow and/or sensitivity settings

If both CDYN and CST worsen, not likely to be an airway problem Causes

Pulmonary Edema ARDS Tension Pneumothorax Atelectasis Fibrosis Pneumonia Obesity Patient Position

RAW = PIP – Pplat

Flow (L/sec.) Airway Resistance

Impedance to ventilation by movement of gas through the airways thus the smaller the airway the more resistance which will increase WOB (causing respiratory muscle and patient fatigue)

Example: ETT, Ventilator Circuit, Bronchospasm

Airway Resistance & Compliance Decreased Compliance + Increased Airway

Resistance = High PIP, Decreased Volumes and significant increase in WOB

Very difficult to wean a patient until problems are resolved

PATIENT STABILITY

Vital signs Pulse – normal, weak, thready, bounding, rate, etc. BP – hypo/hypertensive – directly related to CO Respirations – tachypnea, bradypnea, hyperpnea,

hypopnea, rate, etc. Color – dusky, pale, gray, pink, cyanotic

Auscultation ‑ bilateral, etc. Are they bilateral, amount of air moving, rales, rhonchi

or wheezing Are they Vesicular (normal) or Adventitious (abnormal) Describe what you hear: fine, course, high-pitched,

low-pitched, etc. And the location where you heard it: bilateral bases,

posterior bases, right upper anterior lobe, laryngeal, upper airway, etc.

HEMODYNAMIC MONITORING

BTFDC Also known as

Balloon Tipped Flow Directed Catheter Swan-Ganz Catheter Pulmonary Artery Catheter

Done by inserting a BTFDC into R atrium, thru R ventricle, and into pulmonary artery

SvO2 is drawn from the distal port of a BTFDC Used to monitor tissue oxygenation and the amount of

O2 consumed by the body

CATHETERS AND INSERTION SITES

PA PRESSURE WAVEFORMS

CVP 

Monitors fluid levels, blood going to the right side of heart

Normal = 2 – 6 mmHg (4 – 12 cmH2O) Increased CVP = right sided heart failure (cor

pulmonale), hypervolemia (too much fluid) Decreased CVP = hypovolemia (too little fluid),

hemorrhage, vasodilation (as occurs with septic shock)

PAP Pulmonary Artery Pressure = B/P lungs Monitors blood going to lungs via Swan-Ganz catheter

(BTFDC) Normal 25/8 (mmHg) Increased PAP= COPD, Pulmonary Hypertension, or

Pulmonary Embolism

PCWP Pulmonary Capillary Wedge Pressure monitors blood

moving to the L heart Balloon is inflated to cause a wedge Normal PCWP = 8 mmHg Range is 4 – 12 mmHg Increased PCWP = L heart failure, CHF Measure backflow resistance

Cardiac Output Expressed as QT or CO (QT= Greek alphabet, 1050 BC

scientist used qt had cardiac output expression) Normal = 5 LPM Range 4 – 8 LPM Decreased CO = CHF, L heart failure, High PEEP effects

I & O Needs to be monitored closely to prevent fluid

imbalance due to increased ADH production and decreased renal perfusion

Fluid imbalance can develop into pulmonary edema and hypertension

CARDIAC OUTPUT (CO)

The amount of blood pumped out of the left ventricle in 1 minute is the CO

A product of stroke volume and heart rate Stroke volume: amount of blood ejected

from the left ventricle with each contraction Normal stroke volume: from 60 to 130 ml Normal CO: from 4 to 8 L/min at rest Fick CO: Vo2/Cao2-Cvo2 C(a-v)O2 could decrease if CO is increased

due to less oxygen needs to be extracted from each unit of blood that passes

Fick MethodThe Fick method requires that you be able to measure the A-V oxygen content difference and requires that you be able to measure the oxygen consumption. An arterial blood gas from a peripheral artery provides the blood for the CaO2 measurement or calculation while blood from the distal PA port of a Swan-Ganz catheter provides the blood for the CvO2 measurement or calculation

Dilution methods mathematically calculate (using calculus) the cardiac output based on how fast the flowing blood can dilute a marker substance introduced into the circulation normally via a pulmonary artery catheter. (injecting a dye in prox port of Swanz. Not really used anymore due to infections

MEASURES OF CARDIAC OUTPUT AND PUMP FUNCTION

MEASURES OF CARDIAC OUTPUT AND PUMP FUNCTION (CONT’D)

Cardiac workA measurement of the energy spent

ejecting blood from the ventricles against aortic and pulmonary artery pressures

It correlates well with the amount of oxygen needed by the heart

Normally cardiac work is much higher for the left ventricle

MEASURES OF CARDIAC OUTPUT AND PUMP FUNCTION (CONT’D) Ventricular stroke work

A measure of myocardial work per contraction It is the product of stroke volume times the

pressure across the vascular bed Ventricular volume

Estimated by measuring end-diastolic pressure

Ejection fraction The fraction of end-diastolic volume ejected

with each systole; normally 65% to 70%; drops with cardiac failure

Measures of Cardiac Output and Pump Function (cont’d)

DETERMINANTS OF PUMP FUNCTION

Preload Created by end-diastolic volume The greater the stretch on the myocardium

prior to contraction the greater the subsequent contraction will be

When preload is too low, SV and CO will drop This occurs with hypovolemia Too much stretch on the heart can also reduce

SV

Afterload Two components: peripheral vascular resistance

and tension in the ventricular wall Created by end systolic volume Increases with ventricular wall distention and

peripheral vasoconstriction As afterload increases, so does the oxygen

demand of the heart Decreasing afterload with vasodilators may help

improve SV but can cause BP to drop if the blood volume is low

Determinants of Pump Function

Ventilation Patient Parameters

Spontaneous VT

Is it adequate for patient? Spontaneous volumes should be between 5 – 8 ml/Kg

of Ideal Body Weight (IBW)

Spontaneous VC 10 – 15 ml/Kg IBW

NIF/MIP/MIF/NIP -20 to -25 cmH2O within 20 seconds

ABGS

PaO2 represents oxygenation – adjust with PEEP or FiO2

PaCO2 represents ventilation – adjust with VT or RR

pH represents Acid/Base status pH acid: High CO2 (respiratory cause) or low HCO3

(Metabolic cause) pH alkaline: Low CO2 (respiratory cause) or high HCO3

(Metabolic cause)

Draw ABGs To stabilize With any change in ventilator settings change only one

vent setting at a time With any change in patient condition

VENTILATOR ALARMS

Appropriate for each patientUsually 10 higher/lower than set

parameterFor pressure and RR settingsVT alarms 100 ml higher/lower than set VT

Adjust all alarms for patient safety.

X‑RAY WHEN INDICATED FOR

Tube placement: 2 – 4 cm above carinaPossible pneumothoraxTo check for disease process reversal, or

lack of, for treatment purposes and weaning

FREQUENCY OF VENTILATOR CHECKS

Must be done as often as required by the patients condition unstable patients continuous to hourly

In general patients and ventilators need evaluation Q1-Q4h

With every vent check, patient assessment should take place

Use VT exhaled for calculations. Corrected VT = exhaled vt-tubing lost volume Tubing volume lost factor 1-8 cc x pressure Exhaled vt 650= pip-peep x (3) = 60 650-60=590 corrected vt

WAVEFORM ANALYSIS

Three wave forms typically presented together Pressure Flow Volume

Plotted versus time Horizontal axis is time Vertical axis is variable

Other common wave forms: Pressure vs Volume Flow vs Volume

Pressure vs Time Assessment Patient Effort: Negative pressure deflection at

beginning of inspiration indicates patient initiated breath

Peak & Plateau Pressures Adequacy of inspiratory flow: If pressure rises slowly,

or if curve is concave, flow is inadequate to meet patient’s demand.

Flow vs Time Assessment Inspiratory flow patterns Air Trapping – a.k.a. AutoPEEP – expiratory flow fails to

reach baseline prior to delivery of next breath

Airway Resistance Lower slope (smaller angle) indicative of high

resistance to flow Steeper slope (greater angle) indicative of lower

resistance to flow Also increased resistance manifests itself as

decreased peak expiratory flowrate (depth of expiratory portion of flow pattern) with more gradual return to baseline as expiratory flow meets with resistance

Bronchodilator = increased peak expiratory flow rate with quicker return to baseline

Volume vs Time Assessment VT = peak value reached during inspiration Air Trapping = fails to reach baseline before

commencement of next breath Identifying breath type

Larger volumes = mechanical breaths Smaller volumes = spontaneous breaths

Pressure vs Volume Loop Volume on vertical axis Pressure on horizontal axis Positive pressure on right of vertical axis

Indicates mechanical breath Application of positive pressure to the lung Tracing is in a “counter-clockwise” rotation

Subambient pressure to the left of the vertical axis Indicates a spontaneous breath Spontaneous inspiration is to the left of the vertical

axis – subatmospheric pressure at start of inspiration (Intrapulmonary pressure = -3 cmH2O)

Spontaneous expiration is to the left of the vertical axis – +3 cmH2O intrapulmonary pressure on expiration

Tracing is in a “clockwise” rotation Useful in helping diagnosing

Alveolar Overdistension = looks like bird’s beak, or the “Partridge Family” symbol

Increased RAW = looks “pregnant” or “fat” Decreased compliance = looks “lazy” or like it’s

lying down

Flow vs Volume Loop Helpful in assessing changes in RAW, such as after the

administration of a bronchodilator Flow on vertical axis Volume on horizontal axis Inspiration is top part of loop, expiration on bottom When RAW improved, expiratory flows are greater and

the slope of the expiratory flow is greater

To determine patient effort, use the following curves Pressure vs Time Pressure vs Volume Loop Volume vs Time All show subambient drops in pressure/volume when

patient initiates the breath

To determine Auto-PEEP, use Volume vs Time Flow vs Time Pressure vs Volume Loop For all curves, ask “does the exhalation reach baseline

before the next breath starts

To determine the adequacy of inspiratory flow Pressure vs Time = concave or slow rise to pressure

means inadequate flow on inspiration Volume vs Time = Too slow flow = increased I – Time =

decreased E-Time = AutoPEEP Volume vs Pressure = Slope is shallow, may look

similar to loop associated with increased RAW

If you detect the patient actively working during mechanical breath, increase the flow to help meet the patient’s demand and decrease the WOB

To assess changes in compliance, use Pressure vs Volume Loop

Steeper slope = increased compliance, or larger volume at lower pressure

Shallow slope = decreased compliance, or smaller volume at higher pressure

To assess changes in RAW, use Pressure vs Volume Loop

Space – “hysteresis” – between inspiratory and expiratory portions of loop

“Bowed” appearance – inspiratory portion more rounded and distends toward the pressure axis

Flow vs Volume Loop Observe peak flow on Flow-Volume Loop Increased RAW = Decreased Peak Flow

UNIT B

Acute & Critical Care

PEEP/CPAP

PEEP – Positive End Expiratory PressureDefinition

Application of pressure above atmospheric at the airway throughout expiration

Goal To enhance tissue oxygenation Maintain a PaO2 above 60 mmHg with least amount of

supplemental oxygen Recruit alveoli DECREASE (PA-a)02

Don’t forget (PA-a)02 will increase with v/q or shunt

HOW TO ACHIVE CPAP/PEEP

A. Exhaling through a spring tension diaphragm

B. Exhaling through a column of water C. Exhaling through a partially inflated

exhalation valve (mushroom type) D. A continuous flow through the circuit

Indications Cardiogenic pulmonary edema

Left sided heart failure Prevents transudation of fluid Improves gas exchange

ARDS Increases lung compliance Decreases intrapulmonary shunting Increases FRC

Refractory hypoxemia PaO2 < 50 mmHg with an FIO2 >50%

Increase FRC Opens collapsed alveoli Increases reserve

Contraindications Unilateral lung disease Hypovolemia Hypotension Untreated pneumothorax Increased ICP

Hazards All of the effects of CMV are magnified Increased intrathoracic pressure Decreased venous return Increased ADH Decreased blood pressure Decreased cardiac output Loss of thoracic pump Barotrauma

Physiological effects Baseline pressure increases Increased intrapleural pressures Increased FRC—recruiting collapsed alveoli Dead space—increased in non-uniform lung disease

and healthy lungs by distending alveoli Increased alveolar volumes Can increase compliance Cardiovascular

Decrease venous return Decrease cardiac output Decrease blood pressure

Decreases intrapulmonary shunt Increases mixed venous value (PvO2)--Drawn from

pulmonary artery via Swan-Ganz Increased intracranial pressures Decrease in A-a gradient (A-a DO2)

Increased PaO2

Decrease in FIO2, which causes a decrease in PAO2

INITIATION AND MONITORING OF PEEP

Start off at 5 cmH2O and increase by 3 to 5 cmH2O increments

Adjust sensitivity With an increase in baseline pressure the sensitivity must

be increased or the patient will have to increase inspiratory effort to initiate a breath

Monitor Blood pressure: First thing you look at when adding PEEP Cardiac output: Goal is least cardiac embarrassment with

the best PaO2 and least FIO2

Pulse If the patient is hypoxemic their heart rate is probably

increased With addition of PEEP the hypoxemia should resolve

and pulse should decrease to normal level

PaO2: Goal is best PaO2 with the lowest possible FIO2

MAINTENANCE LEVEL OF PEEP

PEEP trial Used to determine best level of PEEP This is the pressure at which cardiac output and total

lung compliance is maximized,the VD/VT is minimal, and the best PaO2 and PvO2, and the lowest P(A‑a)O2 are obtained

Optimal Peep Level at which physiological shunt (Qs/Qt) is

lowest without detrimental drop in cardiac output A C(A-V)O2 of less than 3.5 vol% should reflect

adequate CO Fick’s law CO = VO2/C(a-v)O2

Cardiac output and C(a-v)O2 are inversely related

Best oxygenation with lease cardiac issues

CPAP

Physiologically the same as PEEP Used in spontaneously breathing patients Maintains continuous positive airway pressure during

inspiration and expiration

Accomplished by a continuous flow of gas or a demand valve System flow must be enough to meet patient’s

peak inspiratory demands

Used to treat OSA CPAP delivered via mask or nasal pillows

No machine breaths, all spontaneous ventilation

NPPV (BIPAP)

Similar to CPAP Delivers two levels of pressure during the inspiratory-

expiratory cycle Delivers higher pressure on inspiration Delivers lower pressure on exhalation Less resistance to exhalation

Two levels of pressure EPAP

Constant pressure delivered during exhalation Same as CPAP Adjust for oxygenation

IPAP Constant pressure delivered during inspiration Same as IPPB Adjust for ventilation

The difference between the two pressures is known as pressure support

Used to treat OSA Better tolerated than traditional CPAP Delivered with mask or nasal pillows

Used in acute respiratory failure Can prevent or delay intubation and CMV Improves ventilation and oxygenation Improves patient comfort

RULES OF PUTTING PATIENT ON PEEP

Obtain order Set‑up PEEP and make additional changes

(i.e., sensitivity)Monitor patient for hazards, BP, CO if

availableMonitor for "optimal/best PEEP"

60-60 Rule: to improve oxygenation increase fio2 to 60% then start adding peep (to prevent o2 toxicity). To remove peep go down to 60% and then start removing peep

IMV/SIMV

Definitions IMV: Intermittent Mandatory Ventilation

Patient receives set number of mechanical breaths from the ventilator. In between those breaths, the patient can take their own spontaneous breaths at a rate and VT of their choice.

SIMV: Synchronized Intermittent Mandatory Ventilation Same as IMV, except the mechanical breaths are

synchronized with the patient’s spontaneous respiratory rate. Helps improve patient/ventilator synchrony and helps prevent “breath stacking” (where the vent delivers the machine set VT on top of the patient’s spontaneous VT)

IMV Advantages

Prevents muscle atrophy – makes patient assume an increasing, self-regulating role in their own respirations, helping to rebuild respiratory muscles

Allows patient to reach baseline ABGs – baseline means the patient’s baseline ABGs Chronic CO2 retainer ABGs do not have a normal

PaCO2 of 40 Decreases mean intrathoracic pressure – the lower the

IMV/SIMV rate, the lower the intrathoracic pressure Avoids decreased venous return – lower intrathoracic

pressure = greater venous return Avoids cardiac embarrassment – greater venous return

= less decrease in cardiac output and blood pressure

May avoid positive fluid balance Allows normalization of ADH production Helps avoid cardiac embarrassment

Psychological encouragement Some patients may exhibit anxiety, especially those

who have been on the vent for several days or weeks

Do not tell the patient they will never need the vent again

Some patients become encouraged by progress, being able to do more for themselves

Weaning gradually – re-evaluate if weaning takes several days

May allow decreased use of pharmacological agents – e.g., morphine, diprivan, versed, etc. If patient is too sedated, won’t be able to breathe

spontaneously and participate in weaning May be the only way to correct respiratory alkalosis on

patient who is “over-breathing” the vent in A/C mode Patient’s spontaneous VT will most likely be smaller

than that of the set VT on mechanical ventilator

Candidates for IMV/SIMV

IMV/SIMV is great for weaning patient from CMV Allows patient to assume increased responsibility for

providing own respirations, with diminishing mechanical support

Allows patient to re-build respiratory muscle strength

Patient must be stable. Not ideal for unstable patient. Consider patient unstable if Fever – causes increased O2 consumption and

increased CO2 production, thereby increasing WOB Unstable cardiac status Unresolved primary problem that caused them to be

on the vent in the first place

Problems of IMV Fighting the ventilator – patient becomes

out of phase – or synch – with the ventilator

Stacking of breaths is not necessarily a problem Patient will normally synchronize self with ventilator

rate

Patient disconnection from gas source (with external IMV circuit)

Other problems of CMV

Benefits of SIMV – Synchronized IMV Prevents stacking of breaths (pt can breath

spontaneously through demand valve)May help patient to become in phase with

ventBreath stacking could be prevented just by

increase inspiratory flow

INSPIRATORY PRESSURE SUPPORT (IPS)

Commonly referred to simply as “Pressure Support”

During spontaneous breathing, the ventilator functions as a constant pressure generator Pressure develops rapidly in the ventilator system and

remains at the set level until spontaneous inspiratory flow rates drop to 25% of the peak inspiratory flow (or specific flow rate)

This mode may be used Independently With CPAP With SIMV With any spontaneous ventilatory mode

Not with any full support modes, such as Control or A/C

PS is used to overcome the increased resistance of the ET tube and vent circuit Pouiselle’s Law: decrease the diameter of a tube by ½,

increase the resistance of flow through that tube by 16 times

If you apply/use PS, do not set less than 5 cmH2O of PS — least amount needed to overcome resistance of ET tube and vent circuit

If PS is set at a level higher than RAW, you will be adding to patient volumes, rather than just helping overcome the increased resistance from the ET tube and vent circuit

Can be used to help wean patient from vent and help rebuild respiratory muscle strength

MANAGEMENT OF VENTILATORS BY ABGS

Pressure Control VentilationCan be used as CMV or SIMV In SIMV mode, the machine breaths are

delivered at the preset pressure while the spontaneous breaths are delivered with PS

PC-CMV (a.k.a., PCV) used to decrease shear forces that damage alveoli whenever the peak or plateau pressures meet or exceed 35cm H2O Help prevent damage to alveoli from excessively high

ventilating pressures Shear forces damage alveoli when they collapse

(because closing volumes are above FRC) and then are forced back open again with the next breath. Damage occurs as this cycle is repeated over time: alveoli collapses, then is reinflated, collapses, reinflated, etc.

Also used when permissive hypercapnia is desired (treatment of ARDS) When the PaCO2 is allowed to rise through a planned

reduction in PPV, which allows for a reduction in the mean intrathoracic pressure, which results in less incidence of barotrauma and other commonly associated complications of PPV

The gradual increase in PaCO2 is accomplished by a reduction of the mechanical VT (by decreasing the pressure) and usually does not affect the oxygenation

PC-IRV: Pressure Controlled Inverse Ratio Ventilation Pressure controlled ventilation with an I:E ratio > 1:1. Causes mean airway pressure to rise with the I:E ratio Usually used on patients with severe hypoxemia where

high FIO2s and PEEP have failed to improve oxygenation

Causes intrinsic PEEP (a.k.a. auto-PEEP), which is what causes the mean airway pressure to increase, which is the mechanism for alveolar recruitment and improved arterial oxygenation

While an increase in oxygenation does occur at the lung, a resultant decrease in cardiac output (due to the increased mean intrathoracic pressures) may result in an overall decrease in tissue oxygenation. Care must be exercised to maintain adequate cardiac output in order to maintain adequate tissue oxygenation

Because it’s not a natural way to breath (backwards from the way we normally breath), most patients must be either heavily sedated (Diprivan, Versed) or must be paralyzed with a paralytic drug (such as Pavulon or Norcuron)

APRV: Airway Pressure Release Ventilation Related to PC-IRV except that patient breathes

spontaneously throughout periods of raised and lowered airway pressure.

APRV intermittently decreases or releases the airway pressure from an upper CPAP (IPAP) level to a lower CPAP (EPAP) level

The airway pressure release usually lasts 1.5 seconds or shorter, allowing the gas to passively leave the lungs to eliminate CO2

I:E ratio is usually > 1:1, but differs from PC-IRV in that it allows spontaneous breathing

Because patient is breathing spontaneously, there is less need for sedation

Usually has lower peak airway pressure than PC-IRV Originally proposed as a treatment for severe

hypoxemia, but appears to be more useful in improving alveolar ventilation rather than oxygenation.

END TIDAL CO2 MONITORING (PETCO2)

Measures CO2 level at end exhalation, when CO2 levels are highest in exhaled breath

Two methods of collection Sidestream – typically used for non-intubated patients Mainstream – typically used for intubated patients and

more commonly seen and used Probe is placed between the patient wye of vent

tubing and the patient’s ETT Infrared light measures CO2 levels Inspired gas should have value of zero PETCO2 content should be within 2 – 5 mmHg of

patient’s PaCO2 Difference will be greater on a patient with larger

amounts of air trapping, e.g. Emphysema

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CAPNOMETRY (CONT.)

End-tidal CO2 monitoring is for trending Not absolute—can vary from breath to breath; similar to

pulse oximetry Look at the trend. Is the patient’s PETCO2 increasing or

decreasing over a period of time? Similar activity should then be also occurring with the PaCO2

When setup, correlate the PETCO2 readings with current ABGs PaCO2. This will give you an idea of how much less the PETCO2 is reading than the PaCO2, giving you a good idea of future trends of the PETCO2 will relate to the PaCO2

CHEST TUBE DRAINAGE SYSTEMS Chest tube placed high in thoracic cavity

to drain air Second or third intercostal space at midclavicular line Incision made right over the rib Chest tube advanced towards anterior apex of lung.

Chest tube placed low in thoracic cavity to drain fluid (e.g., pleural effusion) Placement is in fourth intercostal space (or lower) at

midaxillary line Patient is placed lying on side with affected side “up” Once incision is made, tube is advanced posteriorly,

toward the base of the lung so gravity can help drain the fluid

Three chamber chest tube drainage system is most common Left chamber is the suction control chamber Level of water determines how much suction is applied

to the chest cavity, regardless of how much the suction is set on the suction regulator on the wall

Middle chamber is the water seal chamber Usually no more than 2 cmH2O Too much and you increase difficulty of air or fluid to

drain Too little and you risk an air leak

Bubbles in water seal indicate that a leak in the lung is still present Spontaneous breathing patients with leak will have

bubbles on exhalation Intubated, mechanically ventilated patients with

leak will have bubbles on inspiration Continuous bubbling could be a sign of a leak in

your chest tube drainage system and must be corrected immediately! Clamp chest tube briefly where it exits patient’s chest. If

bubbling stops, leak is in your patient (intrathoracic). If bubbling persists, then you must check your chest

tube drainage system for leaks Move clamp down tubing in 10cm (approx. 4 inch)

increments (working from patient to chest tube drainage system), briefly clamping as you go until bubbling stops

Right chamber is the drainage collection chamber This is where the fluid drained from the patient is

collected

ALI=ACUTE LUNG INJURY OR ARDS

Definition agreed upon in 1994 at the American – European Consensus Conference on ARDS

ALI Definition: a syndrome of acute and persistent lung inflammation with increased vascular permeability. Characterized by: Bilateral radiographic infiltrates A ratio PaO2/FIO2 between 201 and 300 mmHg,

regardless of the level of PEEP. The PaO2 is measured in mmHg and the FIO2 is expressed as a decimal between 0.21 and 1.00

No clinical evidence of an elevated left atrial pressure. If measured, the PCWP is 18 mmHg or less

ARDS Definition: same as ALI, except the hypoxia is worse. Requires a PaO2/FIO2 ratio of 200 mmHg or less, regardless of the level of PEEP. ARDS is ALI in its most extreme stateMortality rate between 40 and 60%

--varies from source to source Down from about 20 years ago when ARDS was

almost certain death sentence with approximately 90% mortality rate.

Current Protective Lung StrategiesLower VTs with ALI/ARDS patients: about 6

ml/Kg IBW to avoid “volutrauma” from alveolar over distension

Sufficient PEEP to prevent alveolar collapse at end expiration, yet not so much that cardiac status is compromised

Permissive hypercapnia when treating ALI/ARDS

PaO2 > 65 mmHg

PIP < 35cm H2O If your PIP is greater than 35cm H2O, consider using

PCV

Closed suctioning system to maintain PEEP

Do not “bag” ALI/ARDS patient to “recruit more alveoli”; could lead to barotrauma or volutrauma

Monitor: Patient must be monitored closely as condition can change relatively quickly!

Things to monitor: I&OCardiac outputBPPIPPPLAT

Pulse OxFIO2

VT

VE

CSTPETCO2

WaveformsA-a Gradient

Renal vasoconstriction, due to hypoxemia, reduces urinary output. Resolution of the hypoxemic state relieves the renal vasoconstriction, thus increasing urinary output.

MANAGEMENT OF ABGS WITH CMV

ABG normal pH values Normal range = 7.35 – 7.45 “Normal” = 7.40

PaCO2

High PaCO2 will cause a low pH, thus causing respiratory acidosis

Low PaCO2 will cause a high pH, thus causing respiratory alkalosis

pH needs to be corrected so that drugs being given to patient will be metabolized

PaCO2 and Ventilation ABG normal PaCO2 values

PaCO2/Ventilation = 35 – 45 “Normal” = 40

High PaCO2 represents hypoventilation or the patient is under ventilated or retaining CO2

Low PaCO2 represents hyperventilation or the patient is over ventilated or blowing off CO2

CO2 represents how well your patient is ventilating. You would adjust VT, f, or remove dead space if on ventilator

PaCO2 & pH Calculations PaCO2 and pH have a direct relationship. Starting at a PaCO2 of 40

If PaCO2 increases by 20 mmHg, pH decreases by 0.10

If PaCO2 decreases by 10 mmHg, pH increases by 0.10

To increase PaCO2 decrease VA The PaCO2 is inversely proportional to VA providing

that CO2 production remains constant VA = (VT – VD)f

To decrease VA (increase PaCO2) Decrease VT (keep in normal range) Decrease f (will not blow off as much CO2) Increase VD (only in control mode – 50cc per link of

large bore tubing)

To decrease PaCO2 increase VA VA = (VT – VD)f To increase VA (decrease PaCO2)

Increase VT (keep in normal range) Increase f (will blow off more CO2) Decrease VD

Dead Space = Ventilation without perfusion Anatomical dead space averages about 1 ml per pound Alveolar dead space is alveoli that are ventilated but

not perfused Physiological dead space is the sum of the above

Normally, this is approximately 1/3 of the VT, or between 20 and 40% for spontaneously breathing, non-intubated patient

Normal for patient on ventilator is 40 – 60%

Formulas for VD/VT, Desired VT, & Desired f VD/VT = PaCO2 – PetCO2 PaCO2 Gives the portion/percentage of VT not taking place in

gas exchange.

STRATEGIES TO ALTER VENTILATION

Always adjust VT first, but remember to keep it in the normal range (8 – 12 ml/kg of ideal body weight) If PaCO2 is high, patient is on SIMV, and the patient is

taking spontaneous breaths and the volumes are low, initiate Pressure Support to increase spontaneous volumes.

If you cannot adjust VT up or down because it would place the VT out of normal range, then change f (rate)

Change Mechanical Rate Doing this alters Alveolar Ventilation If your rate exceeds 20 bpm, auto-PEEP may develop

(patients with very stiff lungs. e.g., ARDS—may require higher f)

Increase f = decreased PaCO2 (hyperventilate)

Decrease f = increased PaCO2 (hypoventilate)

Add or remove VDMech only in control mode Add VDMech to increase PaCO2

Decrease VDMech to decrease PaCO2

Cut ETT to proper length to decrease dead space

Use low compliance vent circuit to decrease dead space

Large VT and slow f are preferred to small VT and rapid f because Alveolar Ventilation is increased Distribution of inspired gas is improved Ventilation/Oxygenation is improved Mean intrathoracic pressure is reduced

PAO2 & OXYGENATION

PaO2/Oxygenation norm = 80 – 100

If PaO2 is below 60, the patient has hypoxemia

For patients that are hypoxic and on a ventilator, adjust the FIO2 to > 50% then start adding PEEP

When the patient improves, decrease FIO2 to 40 – 50%, then start removing PEEP to prevent O2 toxicity

To increase PaO2 (in any mode)

Increase FIO2 if hypoxemia is caused by low V/Q ratio to > 50%, then add PEEP to prevent oxygen toxicity. () What is oxygen toxicity? How does it effect the

patient?

When hypoxemia is present due to lung injury or physiological shunting (as in disease states like ARDS), add PEEP or CPAP

PaO2 can be altered by either reducing or increasing PaCO2 levels by controlling VT

By reducing PaCO2 levels (hyperventilation), PaO2 levels increase (RBCs can carry more O2)

Works the opposite way, too—increasing PaCO2 levels (hypoventilation), PaO2 levels decrease (RBCs carry less O2)

TWO INDICES OF OXYGENATION

a/A Ratio PaO2/PAO2

O2 from alveoli to blood Divide PaO2 by PAO2

Normal = > 60%

A-a Gradient P(A-a)O2

Difference between alveolar and arterial PO2

Also known as: - D(A-a)O2

Subtract PaO2 from PAO2

Normal: - On 21%: 10 – 15 - On 100%: 65 On 100%, every 50 mmHg difference equals approx.

2% shunt If under 300, you have V/Q mismatch so increase FiO2

If over 300, you have a shunt, so add PEEP or CPAP

First calculate PAO2

Unless told otherwise PBAR = 760 PH2O = 47 RQ = 0.8

(Pb-PH2O)fio2-(Paco2x1.25)

If FiO2 is greater than 60%, omit RQ from PAO2 formula

PaO2 is obtained from an ABG

To decrease PaO2 (in any mode)

Decrease FIO2

Decrease PEEP gradually If FIO2 > 50% with PEEP, decrease FIO2 to 40 – 50% first

(to reduce O2 toxicity) If patient remains stable and has an adequate PaO2,

start to reduce PEEP slowly

Increase PaCO2 (Dalton’s Law)Monitor patient at all times for signs of

hypoxemia

MANIPULATION OF ABGS IN CONTROL MODE

To increase PaCO2 Decrease VT

Decrease f Increase VD

To decrease PaCO2

Increase VT

Increase f Decrease VD

MANIPULATION OF ABGS IN A/C

To increase PaCO2 Decrease VT: May be ineffective as pt. may increase f Decrease f: Patient can increase assisting to override Never add VD in any mode but control

To decrease PaCO2 Increase VT Increase f above assist rate

If ineffective, change to control or IMV modes

MANIPULATION OF ABGS IN SIMV/IMV

To increase PaCO2 Decrease VT – only to ranges for patient

Not best choice Decrease f

Best choice towards weaning Never add VD in this mode Will increase patient’s WOB and they will eventually

fail

To decrease PaCO2 Increase VT ‑ stay within normal range Increase f (blow off CO2) Increase minute ventilation

May need to add PS to augment spontaneous volumes

Do not look at just the numbers and values

Always assess your patient with every ventilator change.

You are treating a patient, not a machine!