Effect of hypothermia on transthoracic defibrillation in a swine model

Induced hypothermia (H) appears a promising intervention to protect the heart and brain after resuscitation from cardiac arrest. However, the influence of H on transthoracic defibrillation energy requirements is not well documented. In 39 swine (21.4 ± 1.3(S.E.) kg) hypothermia was induced by surrounding the head, thorax and abdomen with ice. The swine were divided into four groups: (1) normothermia (N) followed by severe H (30 °C) ( n = 10), (2) severe H followed by N ( n = 10), (3) N followed by moderate H (33 °C) ( n = 10) and (4) moderate H followed by N ( n = 9). After 30 s of electrically induced ventricular fibrillation (VF), the swine were defibrillated (biphasic waveform) at energies of 20 J, 30 J, 50 J and 100 J in random order in both N and H conditions. For pigs in Group 1 (N followed by severe H), shock success in terminating VF was higher during hypothermia (odds ratio 4.09 (95% CI: 2.21, 5.58; p < 0.0001), despite the fact that impedance rose from 39 ± 3 Ω (N) to 42 ± 3 Ω (H) ( p < 0.001) and current fell from 22 ± 8 (N) to 21 ± 7 A (H) ( p < 0.001). There were no significant differences in the shock success between N and H for the other groups. Post-defibrillation ventricular asystole occurred less often during hypothermia compared to normothermia ( p = 0.0002). Severe H facilitated transthoracic defibrillation in this swine model. Since impedance rose and current fell during H, the improved shock success must be due to a hypothermia-induced change in the mechanical or electrophysiologic properties of the myocardium. Moderate hypothermia did not alter the energy requirement for defibrillation.