Study on mechanism of ventricular fibrillation in deep hypothermia
Sano, A.
Nihon Kyobu Geka Gakkai 28(1): 35-47
1980
ISSN/ISBN: 0369-4739 PMID: 7365304 Document Number: 158622
Experimental studies were performed on dogs for investigation of the mechanism of ventricular fibrillation which is the most serious complication in deep hypothermia. Hypothermia was induced by surface cooling after the animals were anesthetized with ether (E group), neuroleptoanesthesia (N group) or sodium pentobarbital (C group). Another group (EC group) received simply ether anesthesia in normothermia. Physiological measurements were performed using intracardiac catheter electrode and special stimulator. Arrhythmia developed in 40% in C group, 36% in N and 25% in E, respectively, although ventricular fibrillation developed only in 1 of N group. Ventricular extrasystole developed in 40% in C group, 73% in the N and 44% in E, respectively. Ventricular fibrillation threshold elevated during hypothermia and recovered after rewarming. Its elevation was most significant in E group, though not elevated in EC group. Diastolic excitability threshold elevated or fell under 25.degree. C and heart stand-still ensued in most of the former, though extrasystole developed in most of the latter. Refractory period prolonged gradually in progress of hypothermia and its change was most significant in both C and E groups at 30 and 25.degree. C. Conduction time prolonged gradually in progress of hypothermia, though less significant compared to prolongation of refractory period. This difference increased gradually in progress of hypothermia, though slight in E group. Marked acidosis developed in E group, though incidence of arrhythmia was lowest and elevation of ventricular fibrillation threshold was highest. Hypothermic ventricular fibrillation is evidently initiated by increased ectopic autonomic activity, that is, abnormal excitability of myocardium at a local area.