WHILE ventricular fibrillation in the nonhibernating animal limits safe hypothermia below 20 C, its cause at this critical temperature range is now known.1-3 Of the many factors which seem to contribute to ventricular fibrillation at low body temperatures, little emphasis has been placed on the activity of the central nervous system. The relationship of anesthesia to cardiac abnormalities under hypothermia has been stressed, and of the barbiturate group, thiopental sodium has been less frequently associated with ventricular fibrillation than sodium pentobarbital.4 In hypothermia, the ventricular refractory period is prolonged and the recovery rate of diastolic excitability, as well as the response latency of the ventricles, are greatly increased; such changes might be important in initiating ventricular fibrillation.5 From results of dog heart-lung studies6 and oxygen-extraction studies, hypoxia does not seem to be a major cause of ventricular fibrillation. Penrod7 has shown that the arteriovenous oxygen
Battista AF. Phrenic and Cardiac Irregularities in the Hypothermic Cat. Arch Surg. 1967;95(1):30–37. doi:10.1001/archsurg.1967.01330130032007
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