Determine the effects of hypothermia on defibrillation energy requirements and cardiac electrophysiology.
Prospective randomized acute intervention trial.
Medical center animal laboratory.
Fifteen domestic farm swine.
Swine were randomized to a hypothermia group (n = 8) or a control group (n = 7). All animals were instrumented with a transvenous defibrillation system connected to a defibrillator that delivers a biphasic-truncated waveform. Values for defibrillation energy requirements were measured at baseline (normothermia, 38–40°C) and during treatment with total body hypothermia (30°C) or no temperature change (sham). Hypothermia was induced by circulating ice-water through anterior and posterior surgical thermal blankets.
Measurements and Main Results
Defibrillation energy requirement values at 20%, 50%, and 80% were determined by using an up/down method. In the hypothermia group, defibrillation energy requirement values at baseline did not significantly change during hypothermia (defibrillation energy requirements 50% = 14 ± 2 J vs. 15 ± 2 J, respectively). Similarly, the defibrillation energy requirement values in the control group did not change from baseline to sham phase (defibrillation energy requirements 50% = 12 ± 1 J vs. 13 ± 1 J, respectively). Hypothermia profoundly affected cardiac electrophysiology, decreasing ventricular fibrillation threshold by 72%, conduction velocity by 25% (p < .01), and tissue excitability, while it prolonged ventricular repolarization and refractoriness by 7.5% to 15%, respectively (p < .05).
Total body cooling to 30°C was highly arrhythmogenic, although this unstable electrophysiological state did not alter ventricular defibrillation energy requirements. These data suggest that hypothermia may be used to slow metabolic processes without concern over the ability to successfully defibrillate and treat hypothermia-induced arrhythmias.