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Joint Anesthesia/ ICU meeting Post cardiac arrest syndrome & Therapeutic hypothermia

Joint Anesthesia/ ICU meeting Post cardiac arrest syndrome & Therapeutic hypothermia. Dr Lee Wai Chuen Raymond A/C ICU TMH. Introduction. 70% of patients successfully resuscitated die before hospital discharge. Introduction. main causes of death: irreversible neurological injury

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Joint Anesthesia/ ICU meeting Post cardiac arrest syndrome & Therapeutic hypothermia

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  1. Joint Anesthesia/ ICU meetingPost cardiac arrest syndrome & Therapeutic hypothermia Dr Lee Wai Chuen Raymond A/C ICU TMH

  2. Introduction • 70% of patients successfully resuscitated die before hospital discharge

  3. Introduction • main causes of death: • irreversible neurological injury • uncontrollable cardiovascular failure • Severe multiple organ dysfunction syndrome

  4. Introduction • Dr. Vladimir Negovsky first described a systemic ‘‘post-resuscitation syndrome’’(Negovsky VA. The second step in resuscitation—–the treatment of the ‘post-resuscitation disease’. Resuscitation. 1972;1:1—7) • “Post-resuscitation” implies end of resuscitation, a new term post-cardiac arrest syndrome is suggested

  5. post-cardiac arrest syndrome • Organ injury by • ischaemia & hypoxia during cardiac arrest • reperfusion injury after ROSC • trigger a SIRS or sepsis-like syndrome • unregulated leukocyte production of cytokines • high levels of circulating cytokines, adhesion molecules, plasma endotoxin

  6. Early postarrest phase • early interventions might be most effective • intermediate phase • injury pathways are still active • aggressive treatment is typically instituted • Recovery phase • prognostication becomes more reliable • Ultimate outcomes are more predictable

  7. post-cardiac arrest syndrome • 4 components: (1) postarrest brain dysfunction (2) postarrest myocardial dysfunction (3) systemic ischemia/reperfusion response (4) Persistent precipitating pathology • individual components are potentially treatable

  8. post-cardiac arrest syndrome • Treatment of the global ischaemic brain damage and the dysfunctional heart during the reperfusion phase is the main challenge • The first intervention proved to be clinically effective is therapeutic hypothermia

  9. Post resuscitation care • 1. Optimising physiology • Body temperature • Blood pressure • Blood glucose • Acid-base status • Electrolytes (potassium) • 2. Revascularisation • Thrombolysis • PTCA • CABG • 3. Antiarrhythmic therapy • ICD • Beta blockers • Amiodarone • 4. Anticonvulsant therapy

  10. postarrest brain dysfunction

  11. postarrest brain dysfunction • unique vulnerability of the brain • limited tolerance of ischaemia • Unique response to reperfusion • in the hippocampus, cortex, cerebellum, corpus striatum, and thalamus degenerate over hours to days

  12. Hypoxic brain injury • Without blood flow, cerebral tissue oxygen tension declines continuously reaching 0 after 2 min • Neuronal energy(ATP) is depleted • Dysfunction of the cell membrane ion pumps → accumulation of calcium in cytosol • Release of excitatory amino acid • ischemia persists, neuronal necrosis throughout the brain • Permanent neurological injury occurs after 5 to 10 mins of no cerebral blood flow state

  13. postarrest brain dysfunction • initial reperfusion phase in the first few minutes • often hyperaemic • elevated CPP and impaired autoregulation • Hypertension (MAP >100 mmHg) in the first 5 min after ROSC was not associated with improved neurological outcome • exacerbate brain oedema & reperfusion injury • too much oxygen exacerbate neuronal injury • production of free radicals & mitochondrial injury

  14. postarrest brain dysfunction • delayed hypoperfusion in hours to days • hypotension, hypoxaemia, impaired cerebrovascular autoregulation, brain oedema • MAP during the first 2 h after ROSC was positively correlated with neurological outcome • cerebral perfusion varies with CPP instead of being linked to neuronal activity • CPP necessary to maintain optimal cerebral perfusion will vary among individual post-cardiac arrest patients at various time points after ROSC

  15. postarrest brain dysfunction • failure of cerebral microcirculatory reperfusion despite adequate CPP (no-reflow phenomenon) • Fixed and/or dynamic no reflow • intravascular thrombosis during cardiac arrest • edema of endothelium, blood cell sludging, leukocyte adhesion • persistent ischaemia & small infarctions • ? responsive to thrombolytic therapy • Thrombolysis in Cardiac Arrest (TROICA) trial, tenectaplase did not increase 30-day survival

  16. postarrest brain dysfunction • Cerebral edema • limited evidence that brain oedema or elevated ICP directly exacerbates post-cardiac arrest brain injury • early transient brain oedema • rarely associated with clinically relevant increases in ICP • delayed brain oedema, days to weeks after cardiac arrest • due to delayed hyperaemia • likely the consequence of severe ischaemic neurodegeneration

  17. postarrest brain dysfunction • Pyrexia • T >39 ◦C in first 72 h post cardiac arrest increased risk of brain death • T >37.8 ◦C was associated with increased in-hospital mortality • Unfavorable outcome increased for every degree Celsius that the peak temperature > 37◦C. • Hyperglycaemia • seizures

  18. postarrest brain dysfunction • Management: • avoided hyperventilation: normocarbia • Maintain oxygen saturation 94—98% • hypoxaemia is harmful • hyperoxia ass with worse neurological outcome • production of free radicals & mitochondrial injury • Anticonvulsants: no evidence to support prophylactic anticonvulsant • control of glucose: normoglycaemia

  19. Therapeutic hypothermia

  20. Therapeutic hypothermia • The Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002;346:549—56 • portion of patients with favorable neurological outcome increased by 40%

  21. Therapeutic hypothermia • The Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002;346:549—56 mortality reduced by 26%

  22. Therapeutic hypothermia • The Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002;346:549—56 • included a small subset of patients with inhospital cardiac arrest

  23. Therapeutic hypothermia • Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med 2002;346:557—63

  24. Therapeutic hypothermia • Holzer M, Bernard SA, Hachimi-Idrissi S, Roine RO, Sterz F Mu¨ llner M. Hypothermia for neuroprotection after cardiac arrest: systematic review and individual patient data metaanalysis. Crit Care Med 2005;33:414–8 • NNT to allow one additional patient with no or only minimal neurological damage is 6

  25. Therapeutic hypothermia • Arrich, HolzerM, HerknerH, MüllnerM. Hypothermia for neuroprotection in adults after cardiopulmonary resuscitation. Cochrane Database of Systematic Reviews 2009, Issue 4 • patients in the hypothermia group • more likely to reach a best cerebral performance categories score of one or two during hospital stay (RR, 1.55; 95% CI 1.22 to 1.96) • more likely to survive to hospital discharge (RR, 1.35; 95%CI 1.10 to 1.65)

  26. Therapeutic hypothermia • growing amount of data from nonrandomized studies reported benefit in comatose survivors of out-of-hospital non-VF arrest and all rhythm arrests

  27. Therapeutic hypothermia • therapeutic hypothermia has become more feasible and minimal side effects, it is widely used in the management of anoxic neurological injury whatever the presenting cardiac rhythm and include inhospital cardiac arrest

  28. Therapeutic hypothermia • Contraindications: • The patient can follow verbal commands; • More than 8 hrs have elapsed since ROSC; • life-threatening bleeding or infection • Cardiopulmonary collapse is imminent, despite vasopressor or mechanical hemodynamic support; • An underlying terminal condition exists

  29. Therapeutic hypothermia • physiological effects • reduces metabolism & cerebral oxygen demands • Metabolism is reduced by 6% to 10% /°C reduction • protection of ATP stores • decrease in apoptosis via • Reduction in calcium overload and glutamate release • Attenuates oxidative stress & lipid peroxidation • direct inhibition of apoptosis • antiapoptotic protein Bcl-is enhanced • proapoptotic factor BAX is suppressed

  30. Therapeutic hypothermia • physiological effects • reduction of brain edema and increase cerebral blood flow • Preservation of the blood brain barrier • inhibtion of coagulation cascades & inflammatory reactions improve cerebral reperfusion • inhibiting neutrophil infiltration31 and function • reducing lipid peroxidation and leukotriene production

  31. Therapeutic hypothermia • Uncertain areas: • inhospital cardiac arrest • treatment in children • cooling characteristics • “door-to-cool” time • target temperature • cooling rate • duration of hypothermia • cooling methods (external or internal)

  32. Cooling methods • Although there are great differences in efficacy and invasiveness among them, it currently not clear whether one particular technique should be preferred to the others. • No studies are available that have compared different cooling devices • the choice of the cooling method was at the physician’s discretion

  33. Active surface cooling 0.9°C per hr 1.2°C per hour Rare but serious skin complications

  34. Active surface cooling • Nasopharyngeal evaporative cooling with the Rhino-Chill-device (BeneChill, Inc, San Diego, USA) • spraying a convective coolant into the nasal cavity • cooling basal brain regions • cooling rate 1.4°C per hour • out-of-hospital use

  35. Active internal cooling No preference of choice of fluid Need muscle paralysis to avoid shivering cooling rate of 3.4°C per hour Compatible with other cooling devices

  36. Icy catheter & the CoolGard3000

  37. Icy catheter & the CoolGard 3000 • Endovascular cooling via a closed-loop indwelling catheter inserted into the femoral vein • Icy catheter with a CoolGard 3000 system: • temperature monitor, temperature control unit, heat exchange unit, a roller pump • saline circulate through the closed catheter membranes to facilitate steady achievement and maintenance of the desired body temperature • Feedback from a bladder thermister regulates the temperature of sterile saline • providing an extra infusion port to allow for central infusions

  38. Active internal cooling cooling rates of 0.8°C -1.2°C per hour Limited to the hospital setting Expensive delays the induction of hypothermia complications of central venous catheterization

  39. Active internal cooling • Venovenous cooling • uses a double lumen dialysis catheter inserted in the femoral vein • connected to a heat exchanger for rapid extracorporeal blood cooling • Total liquid ventilation with perflourcarbon • induce hypothermia effectively while allowing oxygenation and ventilation

  40. Cooling methods • cooling with the endovascular device or any other cooling method were similar except time to cooling & rewarming rates • water circulating blankets, adherent gel pads, and the intravascular cooling device are more efficient means of induction than ice packs and cold fluids or a surface air-cooling system • intravascular cooling device was the most effective at maintaining temperature

  41. Therapeutic hypothermia • 3 phases: • Induction • Maintenance • Rewarming • temperature normally decreases within the first hour after ROSC

  42. Therapeutic hypothermia • Rapid inductionphase: • as early as possible • 31% reduction of favorable neurological recovery per 1 hr delay • Active external cooling • Easy and fast • Can be given pre hospital • facilitated by concomitant neuromuscular blockade with sedation to prevent shivering

  43. Therapeutic hypothermia • Controlled maintenance phase • external or internal cooling devices, with continuous temperature feedback • avoid significant temperature fluctuation • cooling blankets or pads with water-filled circulating systems • Intravascular cooling catheters • 32°C-34°C for 12 to 24 hours • For asphyxia induced cardiac arrest ? Up to 72 hrs

  44. Therapeutic hypothermia • Controlled rewarming/Decooling phase • optimal rate of rewarming is not known • ≈ 0.25—0.5 ◦C/h or in 12-24 hrs • avoid an overshoot hyperthermia • Controlled, not passive rewarming • Maintain normothermia of < 37.5°C • associated with electrolyte shifts, vasodilation, “postresuscitation” syndrome • the most challenging period of postarrest care

  45. Therapeutic hypothermia • Monitoring: • Continuous Pulse Oximetry: • Peripheral cold-induced vasoconstriction, digital sensory may be inaccurate • forehead lacks sympathetic vasoconstrictive properties-> Forehead sensors

  46. Therapeutic hypothermia • Monitoring: • Temperature Source: • continuous feedback to the cooling device is required to maintain the desired temperature range and avoid overcooling • Core temperatures: Esophageal temperature • most practical, very accurate and reliable • Peripheral temperature: • lag behind core temperature • Bladder temperature: depends on adequate urine output

  47. therapeutic hypothermia • Complications • Shivering: • occurs between 34°C and 35.5°C • common during induction phase • Sedation, muscle relexant, Magnesium sulphate • increases SVR: reduces cardiac output • Arrhythmias: • Only occur < 31°C • bradycardia (slow AF) is most common

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