Each year in the United States, it is estimated that between 350,000 and 450,000 patients suffer witnessed out-of-hospital sudden cardiac arrest (OHSCA). Around 100,000 of these are subjected to resuscitation efforts and 40,000 of these survive to hospital discharge.¹ The incidence of OHSCA is estimated to be between 0.04% and 0.19%, and among patients in whom resuscitation is attempted, between 14% and 40% achieve return of spontaneous circulation (ROSC) and are admitted to the hospital.² Of these, just 7%-30% have good neurologic outcomes at hospital discharge.³ Concerted efforts targeting the resuscitated population may be able to improve these numbers.

In 2010, the Emergency Cardiac Care Committee of the American Heart Association (AHA) declared that doubling survival from cardiac arrest would be one of its “Impact Goals.” In the past, much effort has been focused on the initial objectives of post–cardiac arrest care, including optimizing cardiopulmonary function, triaging patients prehospital to critical care centers equipped for appropriate post–cardiac arrest care, and prevention of recurrent arrest by addressing precipitating factors. However, recent efforts have broadened to focus on secondary objectives of post–cardiac arrest care, such as rehabilitation care and optimizing mechanical ventilation to prevent lung injury.⁴

The focus of this article is on the essentials of one of these secondary objectives: therapeutic hypothermia in the post–cardiac arrest setting to optimize survival and neurologic outcomes.

Therapeutic Hypothermia

Therapeutic hypothermia is a relatively new concept for preservation of neurologic function in comatose patients after cardiac resuscitation. It entails cooling the patient’s core body temperature in a controlled way to maintain a range of 32-34°C for 24 hours in a critical care setting once the patient has been stabilized from resuscitation. Ideally, the cooling should begin within a few hours of arrest, though there is some lack of consensus on the ideal onset timeframe.⁴

Pathophysiology

After cardiorespiratory arrest, resuscitation reestablishes blood flow to a starved brain. Overall, it is clearly a good idea to restore the brain’s energy stores and function, but reperfusion can trigger some harmful chemical cascades. Reperfusion has been implicated in the generation of free radicals and other harmful chemical mediators that lead to “postresuscitation syndrome” and multifocal brain damage via neuronal apoptosis.⁵ During hypothermia, the ability to survive anoxic low-flow states is dramatically increased.⁶ Furthermore, it is postulated that therapeutic hypothermia can reduce processes that lead to tissue damage such as biosynthesis and the release and uptake of several catecholamines and neurotransmitters. Other beneficial effects include preserving the blood-brain barrier, protecting existing energy stores, restoring cerebral microcirculation, and potentially decreasing intracranial pressure.²