Ventilatory Support for the Post-CPR Patients
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Transcript of Ventilatory Support for the Post-CPR Patients
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
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