Severe Bradycardia of Profound Hypothermia in the Dog

Abstract

Mongrel dogs (70) were cooled, either in cold air or in ice water, to rectal temperatures as low as 16[degree]C. ECG was continuously monitored by use of a cathode ray tube. Many dogs had arterial blood pressure recorded by kymograph. All were vigorously respired with either 100% O2 or room air after receiving intravenous Sodium Pentothal. In 85% the sinus node ceased to act at 19[degree]C and after a period of asystole a nodal rhythm was instituted spontaneously at a much slower rate (5-9/minute from 25 to 30 minutes). In 15% of the animals ventricular fibrillation developed. Severe brady-cardia was readily relieved by rewarming; if not rewarmed a cardiac death resulted in 45 minutes to 1 hour. Vagotomy failed 10444-10451 B0DY TEMPERATURE REGULATION [Vol. 30] 1026 to accelerate the heart rate 60% of the time and atropine 90%. Epinephrine relieved bradycardia but resulted in a much higher incidence of ventricular fibrillation. It is not believed that vagal tone played a significant role in the production of bradycardia; rather, factors in the heart muscle itself were responsible.