Abstract
Cardiac arrest is common and causes substantial morbidity and mortality. Despite advances in prevention and resuscitation, most patients remain unconscious and survival remains poor. Therapeutic hypothermia (32-34°C) has emerged as a potent neuroprotective modality following resuscitation. In early clinical trials, application of therapeutic hypothermia improved survival in patients with ventricular fibrillation (VF), which led to the recommended use of therapeutic hypothermia for patients resuscitated from VF. However, two recent clinical trials have challenged some assumptions. First, the use of paramedic-initiated rapid infusion of cold crystalloids as a mean to achieve faster cooling rates after resuscitation in patients with and without VF arrest did not improve survival. Second, once patients were admitted to the hospital, targeting their temperature to 33 versus 36°C for 36h (in addition to active hyperthermia prevention) after out-of-hospital cardiac arrest did not to change clinical outcomes, suggesting that 36°C may represent the target temperature instead of temperatures of less than 34°C.
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