THE CIRCULATORY RESPONSES TO HYPERTHERMIA INDUCED BY RADIANT HEAT 1

Abstract

The changes in the cardiovascular system were studied in anesthetized dogs during acute hyperthermia induced by intense radiant heat and during the return of body temp. from 42[degree]C to normal. During the warming period the O2 consumption increased markedly, rising to about 150% of normal at 42[degree]C. The cardiac output was progressively reduced. As a consequence the arteriovenous oxygen difference was increased. The blood pressure was maintained at relatively normal levels in the face of an apparent increase in the capacity of the vascular bed and a coincident decreased cardiac output, indicating an active vasoconstriction process. The heart rate increased progressively with hyperthermia and the right auricular pressure tended to fall. During the recooling period the O2 consumption, respiratory rates and heart rates returned toward normal levels. The cardiac output and right auricular pressure continued to decline significantly even after the body temp. had returned to control levels. The blood pressure was maintained in most of the animals. No significant changes were found in the pulmonary arterial pressure. During hyperthermia the heart appears to be able to cope with the venous return. It is concluded that the circulatory changes occurring in acute hyperthermia depend upon an increased demand for blood by the tissues which leads to an increase in the volume of the vascular bed. Since the circulating blood volume and venous return do not increase proportionately and may even decrease, a marked reduction in cardiac output occurs. If the blood pressure and the circulation are to be maintained, vasoconstriction must occur. Failure of the vasomotor centers to compensate for the progressively reduced cardiac output prepares the ground for peripheral vascular collapse.