Raising the Dead

Prehospital hypothermia for cardiac arrest victims


     Patients resuscitated from cardiac arrest today are treated with a variety of regimens, including pharmacological therapy, intra-aortic balloon pumps, extracorporeal membrane oxygenation and lengthy stays in state-of-the-art intensive care units. Despite all the treatments available, the success rate for resuscitation to hospital discharge has remained relatively unchanged over the last 50 years. In other words, while all the technological advances have increased survivability of sudden cardiac arrest, patients are not surviving long enough to be discharged from the hospital, and, if they do survive, many have significant neurological impairment.

     Three quarters of cardiac arrests occur in the prehospital setting, with fewer than 5% of those patients surviving to discharge. Of the surviving patients, only 2% will be discharged with minor to no neurological deficits (minor being defined as able to live at home and maintain a part-time job). Many EMS services boast cardiac arrest resuscitation rates nearing 20%; however, many of these patients never survive to discharge from the hospital.1,2 Increasing application of therapeutic hypothermia may help to bridge the gap.

THERAPEUTIC HYPOTHERMIA THROUGH THE AGES
     Therapeutic hypothermia induction is not new; it has actually been well documented throughout medical literature. The use of hypothermia was described by the ancient Egyptians, Greeks and Romans dating back to 2500 B.C. (the Ebers papyrus) and 1600 B.C. (the Smith papyrus). In 450 B.C., Hippocrates hypothesized about packing patients in snow, stating that the cold would be beneficial to them. In 1814, Baron Larrey, a battlefield surgeon in Napoleon's army at the invasion of Russia, found that injured soldiers who were placed next to campfires died sooner than those left in the cold. In the 1930s, Germany experimented with hypothermia in prison camps to learn about the effects of cold water on downed airmen. From the 1950s to 1990s, hypothermia was mentioned sporadically throughout medical literature; however, while benefits seemed clear, there had been an overall hesitation to use therapeutic hypothermia on patients because of numerous documented untoward effects. Research conducted soon found that the majority of detrimental effects were caused by moderate-to-deep hypothermia induction (temperatures ranging from 15°C to 25°C) and were potentiated by extended length of induction (several days at a time, up to 10 days).

     Several studies conducted in 2001 and 2002 demonstrated the efficacy of therapeutic hypothermia induction if mild hypothermia was induced (temperatures ranging from 32°C to 34°C) and maintained for a shorter time (one to two days, with a slow return to normal temperature).3 Considered among the benchmark studies of therapeutic hypothermia, two studies published in 2002 in the New England Journal of Medicine demonstrated that hypothermic patients had a better neurological outcome than the normothermic control group (55% versus 39%).4 The European and Australian Hypothermia After Cardiac Arrest (HACA) trial both showed that survivability nearly doubled with mild, shorter-term hypothermia induction and detrimental effects were limited (see Figure 1).5 Numerous studies from around the world were published shortly after the European and Australian studies that validated the efficacy of therapeutic hypothermia in the hospital setting.

     In 2003, physicians attending the Rocky Mountain Critical Care Conference globally agreed that therapeutic hypothermia should be introduced as a standard of care for post-cardiac arrest patients. Following the Advanced Life Support Task Force of the International Liaison Committee on Resuscitation (ILCOR) meeting in 2005, the American Heart Association (AHA) officially endorsed hypothermia induction for return of spontaneous circulation with adult patients.6 It gave prehospital therapeutic hypothermia induction a Class IIA endorsement for all ventricular fibrillation and ventricular tachycardia arrests, and a Class IIB endorsement for pulseless electrical activity and asystole arrests that were cardiac in origin.

This content continues onto the next page...