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Multiple Organ Failure after CPR

Multiple Organ Failure after CPR. 唐高駿 Gau-Jun Tang, MD, MHS 台北榮民總醫院 重症加護 中心. LIVING CELL. (Cerebral and Extracerebral Tissues) Ischemic Anoxia Mitochondrial Energy Failure. Primary Injury. Tissue Lactacidosis : vasoparalysis osmolality tissue pH. Ionic Fluxes

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Multiple Organ Failure after CPR

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  1. Multiple Organ Failure after CPR • 唐高駿 • Gau-Jun Tang, MD, MHS • 台北榮民總醫院 • 重症加護中心

  2. LIVING CELL (Cerebral and Extracerebral Tissues) Ischemic Anoxia Mitochondrial Energy Failure Primary Injury Tissue Lactacidosis : vasoparalysis osmolality tissue pH Ionic Fluxes K+ efflux* Na+ influx H2O influx cytotoxic edema Ca++ influx* Lipid Peroxidation : membrane phospholipids phospholipase free fatty acids +O2 Free Radicals protease proteolysis leakage of lysosomes

  3. Electrical pump failure Outflux of potassium influx of sodium Voltage dependent Ca channel activate Large uncontrollable Ca influx

  4. The relationship of lactate to shock, SIRS and MODS

  5. Bacteria translocation Shock Vasodilation Hepatic failure Tissue perfusion Capillary Leak ARDS DIC Bacteria Renal failure Endotoxermea Bacteremia Intestine mucosa Bacterial Translocation

  6. Activation of inflammation

  7. Brain is very vulnerable to ischemia and hypoxia High metabolic rate 60% electrophysiological activity membrane potential neurotransmitter synthesis and uptake 2% body weigh 15% cardiac output jugular vein oxygen saturation 55-70

  8. PANORGANIC DEATH CLINICAL DEATH CIRCULATORY ARREST ? APPROXIMATE TIME, MIN. 5 10 15 20 RESTORATION OF CIRCULATION APNEA UNCONSCIOUS SPONTANEOUS BREATHING UNCONSCIOUS SPONTANEOUS BREATHING CONSCIOUS SPONTANEOUS BREATHING CONSCIOUS OR STUPOR NEUROL NORMAL NEUROL DEFICIT VEGETATIVE STATE EEG ABNORMAL BRAIN DEATH EEG ISOELECTRIC

  9. Cessation of circulation 10 seconds Unconsciousness 15-25 sec Isoelectric 2 to 4 minutes Glucose and glycogen store of the brain are depleted 3 to 5 minutes ATP is exhausted Electrical pump failure

  10. Lung • Injury to rib cage and intrathoracic viscera • chest compression • Aspiration pneumonia • 24%, 96 patients • Rello, Clin Infect Dis, 1995 • Pulmonary edema • 30% • Dohi, Crit Care Med, 1983 • Similar to ARDS

  11. massive pneumoperitoneum gastric disruption

  12. pneumothorax results from a break in the parietal pleura

  13. Barotrauma

  14. Kidney • Acute tubular necrosis (ATN) • Hypotension • Hypovolumea • Shock • Poor renal perfusion

  15. Hepatic changes after cardiac arrest • Markedly elevated transaminases 20 to 100 times of normal • Jaundice appeared 2 or 3 days latter • Albumin lost • Biopsy • central lobular necrosis with • centrilobular congestion, hemorrhage & necrosis • acute inflammation • cholestasis

  16. Coagulopathy • Increased blood coagulability • microvascular thrombosis • small emboli in pulmoanry circuit • consumption of Hageman facor • acitivation of intrinsic pathway

  17. Coagulopathy • Formation of fibrin • Formation of thrombin antithrombin complex • figrin monomers • Fibrolytic process was not activated • D- dimer • plasminogen activator inhibitor • Bottiger, Circulation, 1995

  18. Acute adrenal insufficiency • hyponatremia • hyperkalemia • hypotension • weakness or fatigue • Pathology • bilateral adrenal cortex hemorrhage

  19. Sick euthyroid syndrome • Thyroxine (T4) level is low • Thyrotropin (TSH) normal • No sign or sympatom of hypothyroidism • No treatment is indicated

  20. Postresuscitation myocardial dysfunction • Global impairment in myocardial function • last for hrs, days or weeks • myocardial stunning • Low BP • CI • SVI • LVSWI

  21. Circulation failure • CNS dysfunction • Renal failure • Hepatic dysfunction • Gut failure • Lactic acidosis • Presence of Anarobic respiration • Related to mortality

  22. TCA Cycle Pyruvic acid (3C) Coenzyme A Acetyl Co A (2C) Oxaloacetic acid (4C) citric acid (6C) NADH + H+ NAD NAD+ Malic acid (4C) H2O NADH + H+ Fumaric acid (4C) CO2 FADH2 FAD a-ketoglutaric acid (5C) CoA-SH NAD+ Succinic acid (4C) NADH + H+ Succinyl CoA (4C) CO2 ATP

  23. Vascular failureEndothelial and cell membrane disruption

  24. Gastrointestinal failure Stress ulcer Achaculus Cholecystitis Poor perfusion of mucosa

  25. Tonometer catheter

  26. Tonometer

  27. Determinant of Cardiac output and Blood pressure

  28. Cardiac failure • Treatment underlying disease • Myocaridal infarction • cardiac tamponade • aortic dissection • pulmonary embolism • pneumothorax • hypovolumia

  29. Circulatory support • Optimize preload • Dobutamine • (5-15 ug/kg/min) • Vasopressor action • dopamine (5-20 ug/kg/min) • norepinephrine, Epinephrine • increase in myocardial consumption • milrinone • phosphodiasterase inhibitor

  30. Hemodynamic management CVP/PCWP Volume (NL or High) (Low) Volume Flow Cardiac Output (Low) (NL or High) Volume, Dobutamine O2 Transport O2 Uptake (Low) (NL or High) Tissue oxygenation Volume Lactate (NL) (High) Observe supranormal VO2

  31. Mechanical supportIABP, ECMO

  32. Respiration Endotracheal tube Mechanical ventilation PEEP Oxygen Keep PaCO2 30 to 35 mmHg

  33. How we protect the Brain? Adequate cerebral blood flow Adequate oxygen in the blood

  34. No flow Cardiac arrest Incomplete ischemia CPR No reflow BP normal, vasospasma Ischemic penumbra (缺血半影) Transition zone between infarct and normal brain Ischemia Electrical silence No cytolysis Brain ischemia

  35. Cerebral metabolism matched well with blood flow Carbon dioxide Oxygen Hypothermia Anesthetics Cerebral blood flow dependent on cerebral perfusion pressure Regulation of cerebral blood flow

  36. Autoregulation of cerebral blood flow Lost after extended hypoxemia or hypercarbia cerebral blood flow depend on cerebral perfusion pressure Cerebral perfusion pressure = mean arterial pressure - intracranial pressure Maintain cerebral perfusion pressure

  37. Mean arterial pressure Maintaining a normal or slightly elevated mean arterial pressure Hypertension after arrest Reducing intracranial pressure head elevated to 30 increase cerebral venous drainage hyperventilation PaCO2 25-30 Reduce cerebral blood flow Optimize cerebral perfusion pressure

  38. Hypertension SBP 150-200mmHg 1 to 5 min Normal or hypertension, absolutely no hypotension Hematocrit: 33~35 mg % Glucose Lactic acidosis 100 至 200 g/dl Brain Protection

  39. Seizures phenobarbital, phenytoin, diazepam Hyperthermia Barbiturate coma EEG isoelectric Clinical not significant ? Reduce metabolism also reduce cerebral blood flow Hypothermia Reduce cerebral metabolism

  40. Moderate Hypothrmia (28-32) protect the brain during heart surgery Deep Hypothermia (<25) cardiac arrest Hypothermia

  41. Head-neck-trunk surface Nasopharyngeal Esophagogastric IV cold infusion Venovenous shunt with pump, heat exchange Arteriovenous shunt, heat exchange Peritoneal cold lavage Intracarotid cold flush Cardiopulmonary bypass Rapid brain cooling methods:

  42. 加護病房中對CPR後昏迷病患之處理 • 將血中值維持正常 • Hematocrit 30%-35% • Electrolytes normal • Plasma COP >15 mmHg • Serum albumin >3g/dl • Serum osmolality 280-330 mOsm/liter • Glucose 100-300mg/dl

  43. 加護病房中對CPR後昏迷病患之處理 • 使用高滲透壓液體以降低腦壓 • 正常體溫或適量的低體溫(>34ºC) • 避免高燒 • 靜脈注射 • 不要單獨給予葡萄糖水 • 使用葡萄糖水5%-10% 在0.25%-0.5% 的生理食鹽水中靜脈方式給予 • 給予營養輸液 (24 to 48 hr)

  44. 維持顱內恆定 • 必須排除出血或腦瘤(電腦斷層) • 監測ICP • 維持ICP<15mmHg • 降低CO2 • 腦脊髓液引流 • Mannitol 0.5g/kg iv plus 0.3g/kg/hr iv, short-term;or mannitol 1g/kg once iv • Loop diuretic (eg.furosemide,0.5-1.0mg/kg iv) • Thiopental or pentobarbital 2-5mg/kg iv;repeat as needed • Corticosteroid

  45. Electrolyte balance • Hypernatremea • Hyperosmolality • Hyperkelemea • Hypokelemea • Hypomegnesia

  46. Mg in head and spinal injury

  47. Mg++ as a Channel Blocker

  48. Post resuscitation • Heart failure • recurrent cardiac arrest • ischemia encephalopathy • intercurrent infection • multiple organ failure

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