The induction of mild hypothermia improves systolic function of the resuscitated porcine heart at no further sympathetic activation

Abstract

Mild hypothermia (MH) after cardiac arrest attenuates hypoxic brain injury and improves survival. As MH increases contractility in normal hearts, we hypothesized that MH improves cardiovascular function after cardiac arrest. In 16 anaesthetized pigs (64 ± 2 kg), ventricular fibrillation was induced electrically for 5 min. At 10 min after resuscitation and return of spontaneous circulation (ROSC), pigs were assigned to normothermia (NT, 38°C, n = 8) or MH (33°C, n = 8, intravascular cooling). At ROSC 6 h vs. baseline, heart rate (HR) was unchanged in NT, but decreased in MH. Cardiac output (CO, l min(-1)) decreased in MH (3.5 ± 0.2 vs. 5.5 ± 0.4, P < 0.05) more than in NT (4.8 ± 0.4 vs. 5.7 ± 0.4, P = ns). Mixed venous oxygen saturation decreased in NT (56 ± 2 vs. 66 ± 3%, P < 0.05), but remained constant in MH (64 ± 2 vs. 65 ± 2%) due to a 35% decrease of whole body oxygen consumption. Left ventricular (LV) dP/dt(max) (mmHg s(-1)) decreased in NT (1163 ± 97 vs. 1665 ± 134, P < 0.05), but was preserved in MH (1602 ± 102 vs. 1603 ± 96), whereas LV relaxation was profoundly slowed during MH. Pressure-volume analysis confirmed improved LV systolic function during MH, but also demonstrated decreased LV end-diastolic distensibility, which was further potentiated by right atrial pacing at baseline HR. MH did not increase plasma catecholamine levels. Spectral analysis of heart rate variability revealed reduced sympathetic activation during MH. The induction of MH after cardiac resuscitation improves systolic myocardial function without further sympathetic activation. A reduced metabolism during MH outweighs a decreased CO and thereby acts favourably on systemic oxygen supply/demand balance.