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The Nina, the Pinta, and heart rate variability: the search for prognostic indicators after cardiac arrest.

More than 500 years ago, Christopher Columbus set sail west across the Atlantic searching for better trade routes with East Asia. Although Columbus and his team never found the route to the Orient, they opened an age of European exploration of the Americas and popularized use of the prevailing trade winds for transcontinental travel (1). In this issue of Critical Care Medicine, Tiainen and colleagues (2) set out to study heart rate variability as a potential indicator of prognosis after cardiac arrest. Although one parameter of heart rate variability at 48 hours had prognostic implications for patients treated with therapeutic hypothermia, this report stands out as the first to carefully study electrocardiographic data during therapeutic hypothermia in patients who had already experienced a cardiac arrest. As with Columbus, these secondary discoveries may be the results better remembered. Therapeutic hypothermia has evolved from a novel intervention to a standard treatment for cardiac arrest survivors with encephalopathy (3– 6). Although most deaths are due to hypoxic-ischemic brain injury and not recurrent cardiovascular events (7, 8), concerns regarding the safety or potential adverse events associated with hypothermia may contribute to clinician reluctance to implement this important therapy (9, 10). Two recent reviews guiding efforts to predict outcome after cardiac arrest do not include data from patients treated with hypothermia (11, 12), but do note the potential confounding effect from the 24 hours of hypothermia and the increased use of sedation and neuromuscular blockade associated with it (13). Tiainen and colleagues provide the best existing data regarding adverse electrocardiographic events during hypothermia and describe a tool that may improve prognostic efforts. As part of the Hypothermia after Cardiac Arrest study, 70 consecutive adult patients resuscitated from out-of-hospital ventricular fibrillation at Helsinki University Hospital were randomly assigned either to therapeutic hypothermia or to normothermia (2). Twenty-four hour electrocardiographic recordings were performed on days 1, 2, and 14, and frequency and time domain assessments of heart rate variability were performed. Premature ventricular beats were increased in the hypothermia-treated group during the first two recordings, but no difference was noted in the occurrence of ventricular tachycardia or fibrillation for patients treated with hypothermia or normothermia. Defibrillation was required by only one patient during hypothermia (compared with two patients in the normothermic group). Two of 36 patients had mean heart rates 50 during hypothermia, and one of these received a temporary pacemaker that fired for 5 minutes. In multivariate analysis, preserved heart rate variability seemed to predict a favorable outcome. By careful documentation of electrocardiographic activity among cardiac arrest survivors treated with hypothermia and normothermia, Tiainen et al have added to previous work in neuroprognostication after cardiac arrest (14, 15). Of perhaps greater applicability, their study expands our understanding of the safety of hypothermia among patients with complex cardiac conditions. Therapeutic hypothermia was recently shown to be safe and beneficial in patients with cardiogenic shock treated with intra-aortic balloon pumps and in conjunction with percutaneous coronary intervention (16, 17). The present study confirms that ventricular arrhythmias are common, but not more prevalent in patients receiving hypothermia, and that bradycardia is common but rarely requires treatment. These findings increase our understanding and are based on data from more reliable monitoring than in existing reports. Just as Europeans provided information facilitating further exploration of the “new world” 500 years ago, Tiainen’s group provides data that advances our understanding of therapeutic hypothermia. We can only hope that many other investigators will travel these waters to discover better and safer ways of providing this important therapy and to furnish us with tools to better predict outcomes. Richard R. Riker, MD, FCCP David B. Seder, MD Gilles L. Fraser, PharmD, FCCM Neurosciences Institute Maine Medical Center Portland, Maine