Therapeutic hypothermia after cardiac arrest in adults: mechanism of neuroprotection, phases of hypothermia, and methods of cooling.

Sudden cardiac arrest is the main manifestation of ischemic heart diseases, which is the leading cause of death worldwide. Each year an estimated 300,000 people suffer from cardiac arrest in the United States, with a variable incidence ranging from 36/100,000 to 128/100,000. Approximately 7.9% of cardiac arrest victims survive to hospital discharge in the United States, whereas fewer than half of patients dmitted to hospital achieve a favorable outcome. Permanent severe brain damage ccounts for the high mortality after successful resuscitation in the hospital. Mild hypothermia, defined here as a reduction of core temperature to 32°C to 34°C, s the only proven therapy to improve survival and neurologic outcome after sudden ardiac arrest in clinical trials, and recommended by the American Heart Association AHA) as the routine intervention for selected comatose adult victims of witnessed ut-of-hospital cardiac arrest. This article addresses the mechanism of neurorotection, phases of hypothermia, and cooling methods.