Ventilatory Support for the Ventilatory Support for the Post-CPR PatientsPost-CPR Patients

台北榮民總醫院台北榮民總醫院呼吸治療科主治醫師呼吸治療科主治醫師

連德正連德正

OutlineOutline

Postresuscitation syndrome Respiratory problems after CPR Effects of mechanical ventilation on

cardiovascular system Ventilatory support for cardiogenic and

noncardiogenic pulmonary edema (ARDS) Hyperventilation for ischemic brain

Postresuscitation SyndromePostresuscitation Syndrome

Introduced by Negovsky in 1972 Hypotheses of pathogenic factors

– reperfusion failure– reoxygenation injury– cerebral intoxication from derangement of

extracerebral organs– change in blood cell activity and coagulation

abnormalities

Negovsky Negovsky ResuscitationResuscitation 1972;1:1 1972;1:1Safar Safar Crit Care MedCrit Care Med 1988;13:932 1988;13:932

Stages of Postresuscitation Stages of Postresuscitation Syndrome (I)Syndrome (I)

Stage I: 0-10 hrs– rapid changes of cerebral and systemic hemodynamics– initiation of immune response (hyperreactivity of T and B

lymphocytes)– metabolic derangement leading to catabolism (3-7 d)

Stage II: 10-24 hrs– normalization of CV function, persistent brain dysfunction, impaired

microcirculation– cause of death: recurrent cardiac arrest, increased bleeding, brain and

lung edema

Stages of Postresuscitation Stages of Postresuscitation Syndrome (II)Syndrome (II)

Stage III: 1-3 days– normalization of systemic indices (brain too)– increased intestinal permeability leading to bacteremia

and pulmonary, hepatic, pancreatic and renal insufficiency

Stage IV: > 3 days– localized or generalized infection– prolonged metabolic derangement in severe cases

Postresuscitation Syndrome and Multiorgan Postresuscitation Syndrome and Multiorgan Dysfunction Syndrome (MODS)Dysfunction Syndrome (MODS)

Systemic ischemiaSystemic ischemia&&

ReperfusionReperfusion

CV & BrainCV & BrainDysfunctionDysfunction MODSMODS

OutcomeOutcome

SIRSSIRS

DeathDeath RecoveryRecovery

Estimated Fate for Cardiac Arrest Estimated Fate for Cardiac Arrest Patient (< 4 min)Patient (< 4 min)

CardiacCardiacarrestarrest

ROSCROSC25%25%

No No ROSCROSC75%75%

RecoveryRecovery 7%7%

PRSPRS18%18%

Alive 3%Alive 3%

DeadDead15%15%

ROSC: recovery of spontaneous ROSC: recovery of spontaneous circulationcirculation

PRS: postresuscitation syndromePRS: postresuscitation syndrome

Possible Respiratory ProblemsPossible Respiratory Problems after CPR after CPR

Deadspace ventilation due to low CO Respiratory muscle hypoperfusion and fatigue Increased oxygen consumption Cardiogenic pulmonary edema (impaired heart

function) ARDS due to shock and/or sepsis

Indications for Mechanical Indications for Mechanical Ventilation Ventilation

Inadequate ventilation to maintain pH Inadequate oxygenation refractory to O2

therapy Excessive workload of respiratory

muscles Cardiovascular support

Reduction in Respiratory OReduction in Respiratory O22 Consumption Consumption

by Mechanical Ventilationby Mechanical Ventilation

Respiratory Respiratory OO22 consumption consumption

NormalNormal VentilatoryVentilatoryFailureFailure

ControlledControlledVentilationVentilation

ShockShock(Spontaneous(SpontaneousVentilation)Ventilation)

Influence of Ventilatory Support on Influence of Ventilatory Support on Respiratory Muscle PerfusionRespiratory Muscle Perfusion

LactateLactate

NormalNormal ShockShock(Controlled(ControlledVentilation)Ventilation)

Mechanisms by Which Positive Pressure Mechanisms by Which Positive Pressure Ventilation Alters CV FunctionVentilation Alters CV Function

Reduction of stress Hydrostatic mechanisms Humoral mechanisms Redistribution of systemic blood flow

DeGent DeGent Crit Care ClinCrit Care Clin 1993;9:377 1993;9:377

Mechanisms by Which Positive Pressure Mechanisms by Which Positive Pressure Ventilation Alters CV Function (I)Ventilation Alters CV Function (I)

Decreased work of breathing Reversal of hypoxemia Reduction of hypercapnia

Reduced CO and Reduced CO and myocardial workmyocardial work

Reduction of stressReduction of stress

Mechanisms by Which Positive Pressure Mechanisms by Which Positive Pressure Ventilation Alters CV Function (II)Ventilation Alters CV Function (II)

Direct (change in Paw and Palv)– Starling resistor phenomenon– ventricular interdependence

Indirect (change in Ppl)– chronotropic effects– reduced venous return (preload)– reduced LV afterload, but increased RV afterload– impedance to ventricular diastolic filling

Hydrostatic mechanismsHydrostatic mechanisms

Starling Resistor PhenomenonStarling Resistor Phenomenon

PalvPalv

Ventricular InterdependenceVentricular Interdependence

PrvRV S LV

LV

PERI

RV

PperiPITP

R Lung L Lung

S

Transmission of Alveolar Pressure to Transmission of Alveolar Pressure to Pleural Pressure (Indirect Effects)Pleural Pressure (Indirect Effects)

Decreased transmission – Reduced CL e.g. lung edema, ARDS, pneumonia…

– Increased CCW e.g. muscle relaxant, open wounds

Increased transmission – Increased CL e.g. emphysema

– Reduced CCW e.g. obesity, ascites…..

----------- = ----------------------------- = ------------------ PplPpl

PalvPalv

CCLL

CCLL + C + CCWCW

Chronotropic Effects of Positive Chronotropic Effects of Positive Pressure Ventilation (PPV)Pressure Ventilation (PPV)

Hyperinflation HR but usually unaffectedunaffected when circulatory

volume and ventricular function are normal. Fluid overload: PPV tachycardia Hypovolemia: PPV tachycardia Irritable ventricle: PPV ectopy

Vagus n.Vagus n.

Immediate Effects of PPV on Immediate Effects of PPV on PreloadPreload

The effects are transient. Reduced VR Reduced RV preload

Reduced RV output Blood squeezed out of lungs Increased LV preload Increased LV output

Venous ReturnVenous Return AOAO

RARA RVRV

PAPALUNGSLUNGS LALA LVLV

Venous ReturnVenous Return AOAO

RARA RVRV

PAPALUNGSLUNGS LALA LVLV

Mechanical InspirationMechanical Inspiration

ExpirationExpiration

Overall Effects of PPV on Preload Overall Effects of PPV on Preload (Steady) (Steady)

Decreased LV and RV preload– fluid overload: increased stroke volume

– hypovolemia or septic shock: reduced stroke volume

StrokeStrokeVolumeVolume

PreloadPreload

Effects of PPV on AfterloadEffects of PPV on Afterload

RV afterload (overall: increased)– increased: Starling resistor phenomenon

– decreased: RV compression, pulmonary vasodilation due to increased lung volume

LV afterload: decreased due to LV and thoracic aorta compression

Mechanisms by Which Positive Pressure Mechanisms by Which Positive Pressure Ventilation Alters CV Function (III)Ventilation Alters CV Function (III) Humoral mechanisms ( fluid retention)

– antidiuretic hormone– plasma aldosterone– plasma renin activity

Redistribution of systemic blood flow– moderate PEEP renal blood flow urine amount– high PEEP renal blood flow reversed by

SIMV, low-dose dopamine and stopping PEEP

Positive Pressure VentilationPositive Pressure Ventilation in AMI with Cardiogenic Shock in AMI with Cardiogenic Shock

PPV may reduce preload, afterload and work of breathing, rests respiratory muscles, and decrease myocardial work and ischemia.

Swan-Ganz catheter to rule out hypovolemia is indicated if shock persists after PPV.

Small increments of PEEP (2-3 cm H2O)

Positive Pressure Ventilation inPositive Pressure Ventilation in Cardiogenic Pulmonary Edema Cardiogenic Pulmonary Edema

PPV may reduce preload, afterload and work of breathing, rests respiratory muscles, and decrease sympathetic tone and myocardial work.

Moderate PEEP is adequate. Prompt reduction of PEEP after treatment

such as diuretic and inotropics.

Basic Principles in the Ventilatory Basic Principles in the Ventilatory Management of ARDSManagement of ARDS

Accomplish effective gas exchange Avoid complications

– reduced cardiac output

– barotrauma

– oxygen toxicity

– ventilator-induced lung injury (VILI)

Ventilator-Induced Ventilator-Induced Lung Injury (VILI)Lung Injury (VILI)

In severe ARDS, no more than 1/3 alveoli remain patent (heterogeneous, small lung)

PTA> 30-35 cm H2O stretch injury of bronchioles and A-C membrane by shear forces

Supported by most animal studies and some controlled clinical reports

Transalveolar Pressure (PTransalveolar Pressure (PTATA))

1010 10 10 00 0 0 -10-10 -10 -10

PPTATA = P = Palvalv - P - Pplpl = 30 cm H = 30 cm H22O O

4040 3030 2020

PPpltplt P Palvalv P PTATA

If PEEP Is Insufficient in the If PEEP Is Insufficient in the Early Stage of ARDSEarly Stage of ARDS Atelectasis parenchymal infiltration of

activated neutrophils Phasic atelectasis "Milking" action

– depletion of surfactant

– spreading of mediators to less involved alveoli

Phasic atelectasis Stretch injury

mediatorsmediators

"Milking" Action due to Phasic "Milking" Action due to Phasic AtelectasisAtelectasis

surfactantsurfactant

Lung Protective Strategies by PLung Protective Strategies by Pflexflex

Static Pressure

Vol

FRC

TLC

PPflexflex

Keep PEEP above lower Pflex to avoid alveolar

underrecruitmentunderrecruitment Keep tidal breathing

between upper and lower Pflex to avoid alveolar

overdistensionoverdistension

Limitations of PflexLimitations of Pflex

Time consuming and technique dependent With certain risks such as hypoxemia Requiring sedation and paralysis Difficulty to identify the exact point of inflection May overestimate the PEEP (maintenance P <

opening P) Lack of clinical data to validate its efficacy

Determination of PEEP by PaODetermination of PEEP by PaO22 or SpO or SpO22

Keep PaO2 55-80 mm Hg or SpO2 88-95%

Increasing or decreasing PEEP step by step

FiOFiO22 PEEPPEEP FiOFiO22 PEEPPEEP

0.30.3 5 5 0.80.8 14 140.40.4 5 5 0.9 0.9 14 140.40.4 8 8 0.90.9 16 160.50.5 8 8 0.90.9 18 180.50.5 10 10 1.01.0 18 180.60.6 10 10 1.01.0 20 200.70.7 10 10 1.01.0 22 220.70.7 12 12 1.01.0 24 240.70.7 14 14 ...34...34

ARDS network ARDS network NEJMNEJM 2000;342:1301 2000;342:1301

Ventilator-Induced Multiple Organ Ventilator-Induced Multiple Organ FailureFailure

Shear-stress injury in ARDS by MV may induce not only lung injury, but also the production of pro-inflammatory mediators and cellular injury (biotrauma).

Biotrauma may lead to the development of multiorgan failure.

Slutsky Slutsky AJRCCMAJRCCM 1998;157:1721 1998;157:1721Ranieri Ranieri JAMAJAMA 1999; 282:54 1999; 282:54

Ventilation with Lower VVentilation with Lower VTT vs. Traditional vs. Traditional

VVTT for ALJ and ARDS for ALJ and ARDS

A multicenter (10), randomized trial with n =432 vs. 429, average PaO2/FiO2 = 136 (83% < 200)..

Physioslogic parameters on day 1:

ARDS network ARDS network NEJMNEJM 2000;342:1301 2000;342:1301

VT 6 ml/kg 12 ml/kg

Pplat cmH2O 25 33PEEP cmH2O 9.4 8.6RR 29 16PaCO2 mmHg 40 35pH 7.38 7.41PaO2/FiO2 158 176

Ventilation with Lower VVentilation with Lower VTT vs. Traditional vs. Traditional

VVTT for ALJ and ARDS for ALJ and ARDSARDS network ARDS network NEJMNEJM 2000;342:1301 2000;342:1301

150

155

160

165

170

175

180

day 1 day 3 day 7

PaO

2 / F

iO2

lower t id a lvolumestraditional tidalvolumes

Ventilation with Lower VVentilation with Lower VTT vs. Traditional vs. Traditional

VVTT for ALJ and ARDS for ALJ and ARDSARDS network ARDS network NEJMNEJM 2000;342:1301 2000;342:1301

0.00.10.20.30.40.50.60.70.80.91.0

0 20 40 60 80 100 120 140 160 180Days after Randomization

Pro

portio

n of

Pat

ient

s

Lower VT Survival

Lower VT Discharge

Traditional VT Survival

Traditional VT Discharge

Ventilation with Lower VVentilation with Lower VTT vs. Traditional vs. Traditional

VVTT for ALJ and ARDS for ALJ and ARDSARDS network ARDS network NEJMNEJM 2000;342:1301 2000;342:1301

0.0

0.5

1.0

1.5

2.0

2.5

3.0

Traditional VT Lower VT

IL-6

(pg

/ml)

d1

d3

Main Outcome of Ventilation with Lower VMain Outcome of Ventilation with Lower VTT

vs. Traditional Vvs. Traditional VTT for ALJ and ARDS for ALJ and ARDSARDS network ARDS network NEJMNEJM 2000;342:1301 2000;342:1301

Lower VLower VTT Traditional Traditional P ValueP Value VVTT

Mortality beforeMortality before 31.0 31.0%% 39.8%39.8% 0.007 0.007 dischargedischargeBreathing withoutBreathing without 65.7% 65.7% 55.0%55.0% < 0.001< 0.001 assistance by d 28assistance by d 28No. of ventilator-No. of ventilator- 12 ± 11 12 ± 11 10 ± 1110 ± 11 0.007 0.007 free days, to d 28free days, to d 28Barotrauma to d 28Barotrauma to d 28 10% 10% 11%11% 0.43 0.43No. of days withoutNo. of days without failure of other organfailure of other organ 15 ± 11 15 ± 11 12 ± 1112 ± 11 0.006 0.006

Comparison of Randomized Trials of Comparison of Randomized Trials of Lower VLower VTT in ARDS in ARDS

Authors/yearAuthors/year N N BenefitBenefit Pplat (cmHPplat (cmH22O)O)

Amato/1998Amato/1998 53 53 yes yes 38 vs. 2438 vs. 24

Stewart/1998Stewart/1998 120120 no no 28 vs. 2028 vs. 20

Brochard/1998Brochard/1998 116116 no no 32 vs. 2632 vs. 26

Brower/1999Brower/1999 52 52 no no 31 vs. 2531 vs. 25

ARDSNET/2000ARDSNET/2000 861861 yes yes 37 vs. 2637 vs. 26

References: 1.References: 1. NEJMNEJM 338:347 2. 338:347 2. NEJMNEJM 338:355 338:355 3. 3. AJRCCMAJRCCM 158:1831 4. 158:1831 4. CCMCCM 27:1492 5. 27:1492 5. NEJMNEJM 342:1301 342:1301

Problems of Permissive HypercapniaProblems of Permissive Hypercapnia

Acute– intracellular acidosis– nervous dysfunction– intracranial pressure increase– muscular weakness– cardiovascular dysfunction

Chronic- depressed ventilatory drive

alveolar collapse and impaired oxygenation

Ventilatory Strategy for ARDSVentilatory Strategy for ARDSPplt > 35 cmH2O or High FiO2 with SaO2 < 90%

Sedation & Paralysis

SaO2 < 90% SaO2 > 90% SaO2 < 90%Pplt > 35 cmH2O Pplt > 35 cmH2O Pplt < 35 cmH2O

PCIRV PermissiveHypercapnia

PEEP

PC 1:1, Higher PEEP & Lower VT

Good Candidates for PEEPGood Candidates for PEEP Hypoxemia in spite of high FiO2

Diffuse acute pulmonary disease Poorly compliant lungs or presence of lower Pflex

Adequate cardiac reserve with normal to increased intravascular volume

A tendency to atelectasis Acute cardiogenic pulmonary edema or ARDS Increased LV afterload Severe airflow obstruction with difficult triggering

Hyperventilation for Traumatic Hyperventilation for Traumatic Brain InjuryBrain Injury

Routine hyperventilation should be avoided during the first 24 hours after severe TBI.

Intermittent hyperventilation may be helpful for transient IICP with acute neurological deterioration.

Prolonged hyperventilation may be necessary for refractory IICP. Weaning is required.

SjvO2, A-VDO2 and CBF may help to identify ischemia if PaCO2 < 30 mmHg is needed.

Guidelines by American Association of Neurosurgeons 1995Guidelines by American Association of Neurosurgeons 1995Crit Care ClinCrit Care Clin 1997;13:163 1997;13:163

PaCOPaCO22 and Cerebral Blood Flow in and Cerebral Blood Flow in

Global Cerebral IschemiaGlobal Cerebral Ischemia

In animals, the response of the cerebral blood flow to hyper or hypocapnia is attenuated or abolished after global ischemia.

In dogs, hypercapnia delayed electrophysiologic recovery and hyperventilation improved the brain histopathology score after 15 min of cardiac arrest.

No similar studies available in human. No definite conclusion yet.

Brian Brian AnesthesiologyAnesthesiology 1998;88:1365 1998;88:1365

PaCOPaCO22 and Cerebral Blood Flow in and Cerebral Blood Flow in

Focal Cerebral IschemiaFocal Cerebral Ischemia

Hyperventilation does not improve outcome in humans and can exacerbate ischemia in animals.

In a minority of patients (10%), hyperventilation can increase blood flow.

Brian Brian AnesthesiologyAnesthesiology 1998;88:1365 1998;88:1365

Not to Prolong Dying ProcessNot to Prolong Dying ProcessPurpose ofPurpose of CPR and Mechanical VentilationCPR and Mechanical Ventilation