Effects of heat stress on autonomic control of the circulation in humans

 

Craig G. Crandall

Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas, and Department of Internal Medicine, University of Texas Southwestern Medical Center at Dallas, TX, USA

 

Whole-body heat stress causes pronounced reductions in systemic vascular resistance primarily associated with cutaneous vasodilation necessary to dissipate heat.  In order to maintain blood pressure in the face of marked decreases in systemic vascular resistance, cardiac output must increase along with increases in vascular resistance from non-cutaneous beds.  These responses have resulted in heat stress being termed a “hyperadrenergic state”.  Orthostasis (i.e., upright posture) in humans presents another hyperadrenergic state, given increases in sympathetic neural activity and associated increases in vascular resistance that accompany this condition.  A combination of the aforementioned conditions (i.e., heat stress with orthostasis) leads to consistent reductions in orthostatic tolerance; however, the mechanisms by which this occurs are not entirely clear.  The objective of the presentation is to provide evidence that heat stress-induced orthostatic intolerance may result from a combination of factors including an attenuated reserve to increase vascular resistance of non-cutaneous beds, a shift in the operating position on a Frank-Starling curve to the steep portion of the curve, an elevation in cerebral vascular resistance secondary to reductions in PaCO₂ and perhaps sympathetically-mediated vasoconstriction, and an attenuated cutaneous vasoconstrictor responsiveness.  Identification of the mechanisms responsible for heat stress-induced alterations in blood pressure control could lead to improved care for individuals, such as military personnel, experiencing a hemorrhagic injury while heat stressed.

 

Key words: Hyperthermia, Orthostatic tolerance, Autonomic nervous system, Cerebral blood flow