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Therapeutic hypothermia for postresuscitation syndrome and lactate levels
- 1. THERAPEUTIC HYPOTHERMIA FOR POSTRESUSCITATION SYNDROME AND LACTATE LEVELS Sule AKIN, Assoc.Prof, MD Baskent University School of Medicine Anestehsiology and Critical Care Department Adana - TURKEY 2nd World Congress on BIOMARKERS & CLINICAL RESEARCH Baltimore, Maryland , USA. – 13 September 2011
- 2. THERAPEUTIC HYPOTHERMIA FOR POSTRESUSCITATION SYNDROME AND LACTATE LEVELS Sule AKIN, Assoc.Prof, MD Baskent University School of Medicine Anestehsiology and Critical Care Department Adana - TURKEY
- 5. HYPOTHERMIA • Body Temperature < 35 °C
- 6. THERAPEUTIC HYPOTHERMIA (TH)Low Blood Flow Tissue Ischemia THERAPEUTI C HYPOTHERMI A
- 7. TH INDICATIONS IN CLINICS • Cardiopulmonary Resuscitation • Traumatic Brain Injury • Cerebral Infarct • Encephalitis • Bacterial Menengitis • Hepatic Encephalopathy • Herat Failure • Postoperative tachicardia • ARDS
- 10. TH - MECHANISMS H POTERMİ İ Metabolic rate ↓ 1 °C ↓ CMRO2 6 %↓ Oxygen consumption ↓ Glutamate release Calcium shifts Mitocondrial disfunction Free oxygen radicals Exotoxicity Inflmmation cascade CELL DEATH BBB Impairment Brain Edema Neurol Clin 2008;22:487-506
- 11. Anesthesia and Analgesia 1959 38(6);423- 428
- 13. N Engl J Med 2002 Feb 21;346(8):557-63 Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. Bernard SA, Gray TW, Buist MD, Jones BM, Silvester W, Guttridge G, Smith K. N Engl J Med 2002 Feb 21;346(8):549-56 Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. Hypothermia after Cardiac Arrest Study Group (HACA). Resuscitation 2001 Dec;51(3):275-81 Mild hypothermia induced by a helmet device: a clinical feasibility study. Hachimi-Idrissi S, Corne L, Ebinger G, Michotte Y, Huyghens L.
- 14. CHAIN OF SURVIVAL “Chain of Survival Concept” Circulation 83: 1832-1847, 1991 Resuscitation 46: 29-71, 2000
- 16. Out-of-hospital CPR, VF First 6 hours, 32-34 °C For 12-24 hours
- 18. European Resuscitation Council Guidelines for Resuscitation 2010 Section 1. Executive summary Jerry P. Nolana, Jasmeet Soarb, David A. Zidemanc, Dominique Biarentd, Leo L. Bossaerte, Charles Deakinf, Rudolph W. Kosterg, Jonathan Wyllieh, Bernd Böttigeri, on behalf of the ERC Guidelines Writing Group1 Therapeutic Hypothermia There is good evidence supporting the use of induced hypothermia in comatose survivors of out-of- hospital cardiac arrest caused by VF. One randomised trial704 and a pseudorandomised trial669 demonstrated improved neurological outcome at hospital discharge or at 6 months in comatose patients after out-of-hospital VF cardiac arrest. Cooling was initiated within minutes to hours after ROSC and a temperature range of 32–34 C was◦ maintained for 12–24 h. Two studies with historical control groups showed improvement in neurological outcome after therapeutic hypothermia for comatose survivors of VF cardiac arrest.705–707 Extrapolation of these data to other cardiac arrests (e.g., other initial rhythms, in-hospital arrests, paediatric patients) seems reasonable but is supported by only lower level data. Out-of-hospital CPR, In –hospital CPR VF, PVT, Asistoly, PEA First 6 hours, 32-34 °C For 12-24 hours
- 19. TH – TO WHOM WE CAN’T APPLY?• Awake patients • Myoclonus, status epilepticus • Severe coagulopathy and active bleeding • Haemodynamic instability • Resistant arrhythmia • Septic shock • Delayed cases ( >12 hours) • Suspicious intracranial hemorrhage
- 20. TH – ADVERSE EFFECTS CARDIVASCULA R HEMATOLOGIC IMMUNOLOGIC METABOLIC - Arrhythmia -Platelet dysfunction -Coagulopat hy -Neutrophil dysfunction - Infection ↑ -Hypocalemia -Hyperglisemi a - leusİ - Pancreatitis • Increases due to cooling duration and intensity
- 23. SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS) PRS
- 24. Cardiac arrest ROSC (+) 25% ROSC (-) 75 % Recovery 7% PRS 18% Alive 3% Dead 15% ROSC: Return Of Sontaneous Circulation
- 26. Necrosis Apoptosis Cell Death Inflammatio n REPERFUSION Clot Dissolution Flow Restoration Oxidative Stress Mitochondrial Resp. Chain NAD(P)H Oxidases Nitric Oxide Synthesas O2- , H2O2- , OH- , NO, ONO O- O2 ↑
- 27. Mitokondri İskemi Ekstrasellüler Ca +2 Mitokondri Hasar verici ajan Endoplazmik retikulum Artmış sitozolik Ca +2 ATPaz Fosfolipaz Proteaz Endonükleaz ATP’de azalma Fosfolipidlerde azalma Membran ve sitoskletal proteinlerde parçalanma Nükleus kromatin hasarı Membran hasarı
- 30. Trombocyte activation (Trombosis + Vasoconstruction) Metabolism Changes (ATP lost) Tissue injury REPERFUSION (REOXYGENATION) PAF+TTB4 Free radicals Lipid peroxydation Endotel injury Chemotacytic factors Neutrophil accumulationDegredation of membrane integrity Fagocytosi s Leucocyte plug O2 radicals Ischemia NO ↓ Adhesion molecules Complema n activation PGI2 ↓ TXA2 ↑ LTB4 ↑ Cytokines IL-1 ↑ IL-6↑ Vasoconstruction, thrombocyte aggregation, neutrophil chemotaxis Ischemia/Reperfusion Injury
- 33. GLUCOSE Pyruvate Oxygen (-) (anaerobic) Oxygen (-) (anaerobic) Acetyl CoA CO2 + H2O Oxygen (+) (aerobic) PFK LDHPDH 2 Lactate2 Etanol + H2O KREB’S Cycle 2 ATP 36 ATP
- 34. GLUCOSE Pyruvate Oxygen (-) (anaerobic) Oxygen (-) (anaerobic) Acetyl CoA CO2 + H2O Oxygen (+) (aerobic) PFK LDHPDH 2 Lactate2 Etanol + H2O 2 ATP 36 ATP
- 37. THERAPEUTIC HYPOTHERMIA FOR POSTRESUSCITATION SYNDROME AND LACTATE LEVELS Sule AKIN, Assoc.Prof, MD Baskent University School of Medicine Anestehsiology and Critical Care Department Adana - TURKEY