We thank Dr. Rincon for his comments about the role of induced hypothermia in the management of cardiac arrest. Our narrative review focused on the key modifications in the updated American Heart Association guidelines (1) for cardiopulmonary resuscitation and emergency cardiovascular care to highlight the most important practical changes to these 2 topics. In all forms of cardiac arrest, availability of high-quality, basic life-support skills has the highest impact on survival. Thus, the most critical determinant of survival from cardiac arrest is the presence of rescuers who are trained to push hard and fast, allowing full chest recoil while minimizing interruptions in compressions, and to defibrillate promptly when appropriate (1).

Induced hypothermia has the potential to play a critical role in the postresuscitative care of a small subset of cardiac arrest patients. We concur with Dr. Rincon's comment that increased awareness about and induction of therapeutic hypothermia in select patients could lead to better outcomes with advanced cardiovascular life support. In their updated 2005 guidelines, the American Heart Association identified induced hypothermia as one of several beneficial therapies in the postresuscitative care of cardiac arrest (2). Benefit of induced hypothermia was observed in a subset of patients who were initially comatose but hemodynamically stable after a witnessed ventricular fibrillation arrest (2, 3). In the HACA study (3), only 8% of cardiac arrest victims were eligible to receive induced hypothermia. Similar therapy may be beneficial for patients with nonventricular fibrillation arrest out of the hospital or for patients with in-hospital arrest (2). Further experimental studies and clinical trials are required to determine optimal methods, timing, duration, and intensity of cooling for achieving a measurable impact on cardiopulmonary resuscitation outcomes (1, 4).

Finally, we would like to thank several readers, particularly Dr. Smith, for pointing out an error in our article (5) about the mechanism of action of atropine, an acetylcholine-receptor blocker of the muscarinic type.