KEY POINTS
• Therapeutic hypothermia decreases energy use and oxygen consumption in the brain and heart and glucose consumption during the early stages of cardiac arrest.
• The patient is cooled as quickly as possible, within 3 to 4 hours, to a target temperature of 32°C to 34°C, and rewarming begins 24 hours after the initiation of hypothermia.
• Hypothermia is induced with cooling blankets and mattresses in conjunction with ice packs and, in some cases, cooled IV fluids. Other methods include ice lavage, surface cooling helmets, and endovascular heat-exchange catheters.
• Passive rewarming techniques are simply to remove the cooling device or to discontinue the cooling method and allow the patient to return to normal temperature. Active rewarming techniques use warming blankets or warmed IV fluids.
Cardiac arrest is common in the United States; it accounts for approximately 325,000 deaths every year.1 Many patients with cardiac arrest in whom a return of spontaneous circulation is achieved ultimately have a poor functional outcome as a result of hypoxic-ischemic injuries sustained during and after the arrest. Despite many years of data analysis and improvements in CPR techniques and advanced cardiac life support protocols, the American Heart Association reports that median survival to discharge after sudden cardiac arrest is 6.4%.1 Only 11% to 48% of patients who survive the acute event are discharged from the hospital with a good neurologic outcome.2 Over the years, the prognosis after sudden cardiac arrest has remained unchanged in spite of massive educational efforts and improved technological advances. However, mild therapeutic hypothermia as a possible treatment modality has promising outcomes.
Actively cooling a patient to 32°C to 34°C, termed induced therapeutic hypothermia, is a technique that has been used for more than half a century to protect the brain from ischemia caused by a cessation of normal cardiac mechanical function. Introduced in the 1950s, induced therapeutic hypothermia was used to prevent potentially devastating ischemia to the brain during cardiac surgery. Soon after, clinicians used therapeutic hypothermia as treatment after an out-of-hospital cardiac arrest (OHCA). The practice was quickly abandoned, however, because of difficulties in attaining and maintaining the lower body temperature and an uncertainty about its benefits.
Therapeutic hypothermia was reevaluated in the early 1980s because animal studies showed that hypothermia reduced postarrest neuronal damage.3-5 The encouraging results found with animal models led to a resurgence of human clinical trials in the 1990s. The results of two milestone studies that demonstrated improved neurologic function and survival after sudden cardiac arrest in patients treated with the technique were published in 2002.6,7 The International Liaison Committee on Resuscitation included therapeutic hypothermia in its published recommendations in 2003, and in 2005, the American Heart Association included 12 to 24 hours of therapeutic hypothermia in its formal recommendations for treating survivors of OHCA. Hypothermia has emerged as an effective mode of neuroprotection after cardiac arrest and a preventive technique for other neurologic conditions that result from cardiac arrest, such as traumatic brain injury, stroke, and anoxic brain injury.
REVIEW OF KEY STUDIES
A thorough review of the data for mild hypothermia after cardiac arrest is beyond the scope of this article. However, a discussion and brief synopsis of the major studies that support the use mild therapeutic hypothermia is worthwhile.
Cerebral ischemia may persist for hours after resuscitation, and the use of hypothermia may decrease the multifactorial effects. The stage was initially set by two landmark studies that evaluated the efficacy of therapeutic hypothermia after cardiac arrest (Table 1).
