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Ventilatory Support for the Post-CPR Patients

Ventilatory Support for the Post-CPR Patients. 台北榮民總醫院 呼吸治療科主治醫師 連德正. Outline. Postresuscitation syndrome Respiratory problems after CPR Effects of mechanical ventilation on cardiovascular system Ventilatory support for cardiogenic and noncardiogenic pulmonary edema (ARDS)

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Ventilatory Support for the Post-CPR Patients

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  1. Ventilatory Support for the Post-CPR Patients 台北榮民總醫院 呼吸治療科主治醫師 連德正

  2. Outline • 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

  3. Postresuscitation Syndrome Negovsky Resuscitation 1972;1:1 Safar Crit Care Med 1988;13:932 • 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

  4. Stages of Postresuscitation 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

  5. Stages of Postresuscitation 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

  6. Postresuscitation Syndrome and Multiorgan Dysfunction Syndrome (MODS) Systemic ischemia & Reperfusion CV & Brain Dysfunction MODS SIRS Outcome Recovery Death

  7. Estimated Fate for Cardiac Arrest Patient (< 4 min) Recovery 7% ROSC 25% Cardiac arrest Alive 3% PRS 18% Dead 15% No ROSC 75% ROSC: recovery of spontaneous circulation PRS: postresuscitation syndrome

  8. Possible Respiratory Problems 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

  9. Indications for Mechanical Ventilation • Inadequate ventilation to maintain pH • Inadequate oxygenation refractory to O2 therapy • Excessive workload of respiratory muscles • Cardiovascular support

  10. Reduction in Respiratory O2 Consumption by Mechanical Ventilation Respiratory O2 consumption Controlled Ventilation Ventilatory Failure Normal

  11. Influence of Ventilatory Support on Respiratory Muscle Perfusion Lactate Shock (Spontaneous Ventilation) Shock (Controlled Ventilation) Normal

  12. Mechanisms by Which Positive Pressure Ventilation Alters CV Function • Reduction of stress • Hydrostatic mechanisms • Humoral mechanisms • Redistribution of systemic blood flow DeGent Crit Care Clin 1993;9:377

  13. Mechanisms by Which Positive Pressure Ventilation Alters CV Function (I) Reduction of stress • Decreased work of breathing • Reversal of hypoxemia • Reduction of hypercapnia Reduced CO and myocardial work

  14. Mechanisms by Which Positive Pressure Ventilation Alters CV Function (II) Hydrostatic mechanisms • 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

  15. Starling Resistor Phenomenon Palv

  16. Ventricular Interdependence PERI L Lung R Lung RV LV S Pperi PITP RV S LV Prv

  17. Transmission of Alveolar Pressure to Pleural Pressure (Indirect Effects) D Ppl D Palv CL CL + CCW • 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….. ----------- = ------------------

  18. Chronotropic Effects of Positive Pressure Ventilation (PPV) Vagus n. • Hyperinflation HR • but usually unaffected when circulatory volume and ventricular function are normal. • Fluid overload: PPV tachycardia • Hypovolemia: PPV tachycardia • Irritable ventricle: PPV ectopy

  19. Immediate Effects of PPV on Preload • The effects are transient. • Reduced VR Reduced RV preload Reduced RV output • Blood squeezed out of lungs • Increased LV preload • Increased LV output

  20. RA RV LA LV LUNGS PA AO Venous Return Mechanical Inspiration RA RV LA LV LUNGS PA Venous Return AO Expiration

  21. Stroke Volume Preload Overall Effects of PPV on Preload (Steady) • Decreased LV and RV preload • fluid overload: increased stroke volume • hypovolemia or septic shock: reduced stroke volume

  22. Effects 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

  23. Mechanisms by Which Positive Pressure 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

  24. Positive Pressure Ventilation 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)

  25. Positive Pressure Ventilation in 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.

  26. Basic Principles in the Ventilatory Management of ARDS • Accomplish effective gas exchange • Avoid complications • reduced cardiac output • barotrauma • oxygen toxicity • ventilator-induced lung injury (VILI)

  27. Ventilator-Induced 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 +

  28. Transalveolar Pressure (PTA) + + Pplt Palv PTA 20 40 30 10 10 0 0 -10 -10 PTA = Palv - Ppl = 30 cm H2O

  29. If PEEP Is Insufficient in the Early 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 + +

  30. "Milking" Action due to Phasic Atelectasis surfactant mediators

  31. Lung Protective Strategies by Pflex • Keep PEEP above lower Pflex to avoid alveolar underrecruitment • Keep tidal breathing between upper and lower Pflex to avoid alveolar overdistension Pflex TLC Vol FRC Static Pressure

  32. Limitations 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

  33. Determination of PEEP by PaO2 or SpO2 ARDS network NEJM 2000;342:1301 • Keep PaO2 55-80 mm Hg or SpO2 88-95% • Increasing or decreasing PEEP step by step FiO2 PEEP FiO2 PEEP 0.3 5 0.8 14 0.4 5 0.9 14 0.4 8 0.9 16 0.5 8 0.9 18 0.5 10 1.0 18 0.6 10 1.0 20 0.7 10 1.0 22 0.7 12 1.0 24 0.7 14 ...34

  34. Ventilator-Induced Multiple Organ Failure • 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 AJRCCM 1998;157:1721 Ranieri JAMA 1999; 282:54

  35. Ventilation with Lower VT vs. Traditional VT for ALJ and ARDS ARDS network NEJM 2000;342:1301 • A multicenter (10), randomized trial with n =432 vs. 429, average PaO2/FiO2 = 136 (83% < 200).. • Physioslogic parameters on day 1: VT 6 ml/kg 12 ml/kg Pplat cmH2O 25 33 PEEP cmH2O 9.4 8.6 RR 29 16 PaCO2 mmHg 40 35 pH 7.38 7.41 PaO2/FiO2 158 176

  36. Ventilation with Lower VT vs. Traditional VT for ALJ and ARDS ARDS network NEJM 2000;342:1301

  37. Ventilation with Lower VT vs. Traditional VT for ALJ and ARDS ARDS network NEJM 2000;342:1301

  38. Ventilation with Lower VT vs. Traditional VT for ALJ and ARDS ARDS network NEJM 2000;342:1301

  39. Main Outcome of Ventilation with Lower VT vs. Traditional VT for ALJ and ARDS ARDS network NEJM 2000;342:1301 Lower VT Traditional P Value VT Mortality before 31.0 % 39.8% 0.007 discharge Breathing without 65.7% 55.0% < 0.001 assistance by d 28 No. of ventilator- 12 ± 11 10 ± 11 0.007 free days, to d 28 Barotrauma to d 28 10% 11% 0.43 No. of days without failure of other organ 15 ± 11 12 ± 11 0.006

  40. Comparison of Randomized Trials of Lower VT in ARDS Authors/year N Benefit Pplat (cmH2O) Amato/1998 53 yes 38 vs. 24 Stewart/1998 120 no 28 vs. 20 Brochard/1998 116 no 32 vs. 26 Brower/1999 52 no 31 vs. 25 ARDSNET/2000 861 yes 37 vs. 26 References: 1.NEJM 338:347 2. NEJM 338:355 3. AJRCCM 158:1831 4. CCM 27:1492 5. NEJM 342:1301

  41. Problems of Permissive Hypercapnia alveolar collapse and impaired oxygenation • Acute • intracellular acidosis • nervous dysfunction • intracranial pressure increase • muscular weakness • cardiovascular dysfunction • Chronic- depressed ventilatory drive

  42. Ventilatory Strategy for ARDS Pplt > 35 cmH2O or High FiO2 with SaO2 < 90% PC 1:1, Higher PEEP & Lower VT Sedation & Paralysis SaO2 < 90% SaO2 > 90% SaO2 < 90% Pplt > 35 cmH2O Pplt > 35 cmH2O Pplt < 35 cmH2O PCIRV Permissive Hypercapnia PEEP

  43. Good 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

  44. Hyperventilation for Traumatic Brain 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 1995 Crit Care Clin 1997;13:163

  45. PaCO2 and Cerebral Blood Flow in Global Cerebral Ischemia Brian Anesthesiology 1998;88:1365 • 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.

  46. PaCO2 and Cerebral Blood Flow in Focal 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 Anesthesiology 1998;88:1365

  47. Not to Prolong Dying ProcessPurpose ofCPR and Mechanical Ventilation

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