Abstract P198: The Induction of Mild Hypothermia is Associated With Cardiac Diastolic Dysfunction
The induction of mild hypothermia (MH) has become guideline therapy after cardiac arrest. Experimental data in vitro and in normal hearts indicate that MH induces diastolic dysfunction. In 16 anaesthetized pigs (64±2 kg), ventricular fibrillation (VF, 5 min) was induced electrically. 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 device). Data are reported at 6h after ROSC vs control. Heart rate (HR, bpm) was unchanged in NT (86±6 vs 90±3) but lower in MH (59±4 vs 86±6, p<0.05). LV maximum pressure (mmHg) decreased in both groups (NT: 84±2 vs 111±4; MH: 93±6 vs 110±4). CO was lower in MH than in NT, but was balanced by a simultaneous reduction of whole body oxygen consumption, such that mixed venous oxygen saturation (%) decreased in NT (56±2 vs 66±3, p<0.05), but not in MH (64±2 vs 65±2). LV dP/dtmin (mmHg/sec) decreased in NT (−1538±65 vs −2386±145, p<0.05); this decrease was pronounced in MH (−811±87 vs −2307±155, p<0.05 vs control and NT). The isovolumic relaxation constant τ was unchanged in NT (38±2 vs 38±1), but prolonged drastically in MH (171±21 vs 41±3, p<0.05). The end-diastolic pressure-volume relationship (aortic balloon catheter inflation) was unchanged in NT, but shifted leftwards in MH. This shift was potentiated when MH animals were paced (right atrial probe) at baseline heart rate. In resuscitated hearts, MH induces pronounced diastolic dysfunction, characterized by slowed active relaxation and reduced end-diastolic distensibility. These data indicate that MH should be applied with caution when pre-existing severe diastolic dysfunction is suspected.