What Is the Use of Hypothermia for Neuroprotection After Out-of-Hospital Cardiac Arrest? | Ten Points to Remember

Kim F, Bravo PE, Nichol G.
Stroke 2015;Jan 6:[Epub ahead of print].

The following are 10 points to remember about the use of hypothermia after out-of-hospital cardiac arrest (OHCA):

  1. Survival to hospital discharge after OHCA ranges from 10.7% to 31.7%. The most common cause of death among patients hospitalized after OHCA is neurological injury.
  2. Reperfusion injury occurs in the brain and heart during and after restoration of blood flow. It includes release of pro-inflammatory and anti-inflammatory cytokines, which contribute to poor capillary perfusion, tissue ischemia, and microcirculatory dysfunction. Long-term prognosis is correlated with the extent of reperfusion injury.
  3. Hypothermia after reperfusion reduces production of deleterious glutamate, oxygen free radicals and inflammatory molecules, cerebral oxygen demand, intracranial pressure, and the final extent of neurological injury.
  4. Induced hypothermia, started 4-8 hours after resuscitation, is associated with improved neurological outcome compared with normothermia.
  5. Guidelines on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care recommend that: comatose adult patients with restoration of spontaneous circulation (ROSC) after out-of-hospital ventricular fibrillation (VF) cardiac arrest should be cooled to 32°C to 34°C for 12-24 hours (Class I, Level of Evidence [LOE] B). Induced hypothermia also may be considered for comatose adult patients with ROSC after in-hospital cardiac arrest of any initial rhythm or after OHCA with an initial rhythm of pulseless electric activity or asystole (Class IIb, LOE B).
  6. In a Seattle and King County trial, 1,359 adult patients successfully resuscitated from OHCA were randomized to prehospital cooling versus standard of care—cooling upon arrival to the hospital, irrespective of the presenting rhythm. Prehospital cooling was initiated by emergency medical system (EMS) providers via rapid infusion of ≤2 L of 4°C normal saline after ROSC. Survival and favorable neurological outcome at the time of hospital discharge were not significantly different between the groups. The prehospital use of rapid cold saline infusion was associated with more episodes of re-arrest en route, acidosis, and pulmonary edema on admission.
  7. Taken together with another randomized study, the available data do not support the use of EMS-initiated rapid infusion of cold crystalloids as a means to achieve faster cooling rates after ROSC in patients with or without VF arrest.
  8. The Pre-ROSC IntraNasal Cooling Effectiveness study showed that a transnasal evaporative cooling device during active cardiopulmonary resuscitation (CPR) was feasible, relatively safe, and reduced the core temperature by nearly 2 hours faster than hospital-based cooling. Larger randomized trials are ongoing to assess the effect of intra-arrest induced hypothermia on clinically important outcomes.
  9. In the TTM (Targeted Temperature Management) trial of 939 patients with OHCA randomized to hospital-initiated cooling to a target temperature of 33°C or 36°C, there was no difference in survival. Patients in either group had a good overall prognosis and perhaps insufficient neurological or cardiac injury to benefit from induced hypothermia.
  10. The quality and timing of bystander CPR, the performance and training of EMS, and care by emergency and intensive care units are all critical elements and direct determinants of survival and functional outcomes. Prehospital-induced hypothermia might still benefit patients with OHCA in areas with less optimal EMS systems than those where the clinical trials were conducted.

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