THE EFFECTS OF HIGH TEMPERATURE ON THE HEART AND CIRCULATION IN INTACT ANIMALS

Abstract

The successive changes which take place in the heart and circulation when the blood temperature of an anesthetized dog is first lowered and then raised to a lethal point were studied. The course of events was arbitrarily divided into 4 stages. There is first the interval of recovery from previous cooling. The only significant observation during this period was that cooling lengthens the duration of systole much more than can be accounted for by slowing alone. As blood temperature returns from 33[degree] to 37[degree] this disparity disappears. The initial stage extends to the point at which cardiac abnormalities are first recognized. Respiration and heart rate increase progressively, while S.A. node remains the pacemaker. The P-R interval is slightly abbreviated; the QRS complex is smaller and often bifurcated. The central pulse curves indicate that the duration of systole and the velocity of ejection are reduced. These effects are attributable to high temperature. Now the alveolar and blood CO2 are much decreased, and a condition of mild alkalosis exists. The S.A. node still controls the rhythm and A-V conduction time is further shortened. The heart rate reaches its maximum[long dash]300 per min. in some cases; systolic and diastolic pressures decline progressively. The arterial pressure curves suggest a low total peripheral resistance. Durations of systole and systolic ejection are reduced more than can be accounted for by the rapid rate, suggesting decreased venous return and decreased intraventricular tension. Alternation frequently develops but may disappear as the temperature increases further. During the critical stage heart rate suddenly drops, due to A-V block and ventricular rhythm. Cardiac irregularity occurs before the cessation of respiration. The S.A. node is very resistant to high temperature and remains the pacemaker until very near the end. Systolic and diastolic pressures fall rapidly and pulse pressure is small. The duration of systole suddenly increases as the heart finally fails. The cessation of the circulation is precipitated by direct changes in the heart, regardless of whether terminal asphyxia supervenes or whether this is prevented by artificial respiration.