The changes in the cardiovascular system that develop in chronic heart failure obviously affect thermoregulation. A constant, normal body temperature is the consequence of a regulated balance between heat production and heat loss. Both sides of this balance are altered in chronic heart failure. This article reviews fundamentals of human thermoregulation and the changes that are known to occur or may be expected in chronic heart failure.
The discussion begins with the question of how the pattern of distribution of the limited cardiac output of a heart failure patient among the major vasculatures might alter body temperatures and the dynamics of response to altered thermal conditions and exercise. A specific example is the known tendency for core temperature to fall when heart failure patients exercise. Then it focuses on the effects on the cutaneous vasculature in its role as a heat exchanger. Finally, overall responses to thermal stress are considered in terms of three zones of thermoregulation:
The upper boundary of the zone of hypothermia must extend to include environments that, at worst, are annoyingly chilly for people with normal cardiovascular systems but cause shivering in heart failure patients. The cardiac stress associated with the onset of shivering is likely to be compounded by increased thermal stress through enhanced rate of decline of core temperature and a consequent stimulus for still more shivering.
In the neutral zone, characterized by the range of skin temperatures over which core temperature is maintained by control of skin blood flow, long-term physiological adaptations in the control of systemic vascular resistance must alter the normal body temperature. Pharmacological interventions have the potential to deprive the patient of the ability to maintain thermal balance; elimination of cutaneous vasoconstriction could result in a 2° C decline in Tc in what would normally be a neutral environment.
In the zone of hyperthermia, in which warm environments cause elevated skin temperatures (hyperthermia due to endogenous heat production, i.e., exercise, is not discussed in this review), thermal steady states are possible in which the combined stimuli of elevated skin and core temperatures elicit reflex sweating and cutaneous vasodilation adequate to achieve thermal balance. The vasodilator component of this response is also undoubtedly influenced by the physiological changes and pharmacological interventions associated with heart failure and its treatment. Nonetheless, a vasodilator response can be elicited that has been shown experimentally to result in improvement of cardiac output similar to that observed with pharmacological vasodilator treatment but possibly with the difference that the increase in cardiac output is entirely diverted to the cutaneous vasculature.
skin blood flow, cutaneous vasculature, core temperature, thermal compartments, hypothermia, hyperthermia, shivering inefficiency, afterload reduction