therapeutic hypothermia for postresuscitation syndrome and lactate levels
DESCRIPTION
Therapeutic hypothermia for postresuscitation syndrome and lactate levelsTRANSCRIPT
THERAPEUTIC HYPOTHERMIA FOR POSTRESUSCITATION SYNDROME AND LACTATE
LEVELS
Sule AKIN, Assoc.Prof, MDBaskent University School of Medicine
Anestehsiology and Critical Care DepartmentAdana - TURKEY
2nd World Congress on BIOMARKERS & CLINICAL RESEARCH Baltimore, Maryland , USA. – 13 September 2011
THERAPEUTIC HYPOTHERMIA FOR POSTRESUSCITATION SYNDROME AND LACTATE
LEVELS
Sule AKIN, Assoc.Prof, MDBaskent University School of Medicine
Anestehsiology and Critical Care DepartmentAdana - TURKEY
HYPOTHERMIA
• Body Temperature < 35 C
THERAPEUTIC HYPOTHERMIA (TH)
Low Blood Flow
Tissue Ischemia
THERAPEUTIC HYPOTHERMIA
TH INDICATIONS IN CLINICS• Cardiopulmonary Resuscitation• Traumatic Brain Injury• Cerebral Infarct• Encephalitis • Bacterial Menengitis• Hepatic Encephalopathy• Herat Failure• Postoperative tachicardia• ARDS
Airway
Breathe
Circulate
Drugs
E.C.G.
Fluids
Gauge
Hypothermia
Intensive Care
1961
TH - MECHANISMSHİPOTERMİ
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 EdemaNeurol Clin 2008;22:487-506
Anesthesia and Analgesia 1959 38(6);423- 428
N Engl J Med 2002 Feb 21;346(8):557-63Treatment 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):549-56Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest.Hypothermia after Cardiac Arrest Study Group (HACA).
Resuscitation 2001 Dec;51(3):275-81Mild hypothermia induced by a helmet device: a clinical feasibility study.Hachimi-Idrissi S, Corne L, Ebinger G, Michotte Y, Huyghens L.
CHAIN OF SURVIVAL
“Chain of Survival Concept”
Circulation 83: 1832-1847, 1991Resuscitation 46: 29-71, 2000
CHAIN OF SURVIVAL
Out-of-hospital CPR, VF First 6 hours, 32-34 C
For 12-24 hours
CHAIN OF SURVIVAL
European Resuscitation Council Guidelines for Resuscitation 2010 Section 1. Executive summaryJerry 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 Group1Therapeutic HypothermiaThere 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
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
• Pregnancy
TH – ADVERSE EFFECTS
CARDIVASCULAR HEMATOLOGIC IMMUNOLOGIC METABOLIC
- Arrhythmia -Platelet dysfunction
-Coagulopathy
-Neutrophil dysfunction
- Infection
-Hypocalemia
-Hyperglisemia
-İleus
- Pancreatitis
• Increases due to cooling duration and intensity
POSTRESUSCITATION
SYNDROME (PRS)
POST CARDIAC ARREST
SYNDROME
SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS)
PRS
Cardiac arrest
ROSC (+)25%
ROSC (-) 75 %
Recovery 7%
PRS18%
Alive 3%
Dead15%
ROSC: Return Of Sontaneous Circulation
İSKEMİ
Blockage Muscle
Blood flow
ischemia
O2
Ca+2Necrosis
Apoptosis
Cell Death
Necrosis
Apoptosis
Cell Death
Inflammation
REPERFUSION
Clot DissolutionFlow Restoration
Oxidative Stress
Mitochondrial Resp. ChainNAD(P)H OxidasesNitric Oxide Synthesas
O2- , H2O2-, OH-, NO, ONO O-
O2
Mitokondri
İskemi
EkstrasellülerCa +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
PRS- TREATMENT STRATEGIES
PRS- TREATMENT STRATEGIES
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
Fagocytosis
Leucocyte
plug O2
radicals Ischemia
NO Adhesion molecules
Compleman activation
PGI2 TXA2 LTB4
Cytokines IL-1 IL-6
Vasoconstruction, thrombocyte aggregation, neutrophil chemotaxis
Ischemia/Reperfusion Injury
GLUCOSE
PyruvateOxygen (-)(anaerobic)
Oxygen (-)(anaerobic)
Acetyl CoA
CO2 + H2OOxygen (+)(aerobic)
PFK
LDHPDH
2 Lactate2 Etanol + H2O
KREB’S Cycle
2 ATP
36 ATP
GLUCOSE
PyruvateOxygen (-)(anaerobic)
Oxygen (-)(anaerobic)
Acetyl CoA
CO2 + H2OOxygen (+)(aerobic)
PFK
LDHPDH
2 Lactate2 Etanol + H2O
2 ATP
36 ATP
THERAPEUTIC HYPOTHERMIA FOR POSTRESUSCITATION SYNDROME AND LACTATE
LEVELS
Sule AKIN, Assoc.Prof, MDBaskent University School of Medicine
Anestehsiology and Critical Care DepartmentAdana - TURKEY