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Heat-related illnesses include a spectrum of disorders ranging from heat syncope, muscle cramps, and heat exhaustion to medical emergencies such as heatstroke. The core body temperature is normally maintained within a very narrow range. Although significant levels of hypothermia are tolerated (Chap. 454), multiorgan dysfunction occurs rapidly at temperatures >41°–43°C. In contrast to heatstroke, the far more common sign of fever reflects intact thermoregulation.


Humans are capable of significant heat generation. Strenuous exercise can increase heat generation twentyfold. The heat load from metabolic heat production and environmental heat absorption is balanced by a variety of heat dissipation mechanisms. These central integrative dissipation pathways are orchestrated by the central thermostat, which is located in the preoptic nucleus of the anterior hypothalamus. Efferent signals sent via the autonomic nervous system trigger cutaneous vasodilation and diaphoresis to facilitate heat loss.

Normally, the body dissipates heat into the environment via four mechanisms. The evaporation of skin moisture is the single most efficient mechanism of heat loss but becomes progressively ineffective as the relative humidity rises to >70%. The radiation of infrared electromagnetic energy directly into the surrounding environment occurs continuously. (Conversely, radiation is a major source of heat gain in hot climates.) Conduction—the direct transfer of heat to a cooler object—and convection—the loss of heat to air currents—become ineffective when the environmental temperature exceeds the skin temperature.

Factors that interfere with the evaporation of diaphoresis significantly increase the risk of heat illness. Examples include dripping of sweat off the skin, constrictive or occlusive clothing, dehydration, and excessive humidity. While air is an effective insulator, the thermal conductivity of water is 25 times greater than that of air at the same temperature. The wet-bulb globe temperature is a commonly used index to assess the environmental heat load. This calculation considers the ambient air temperature, the relative humidity, and the degree of radiant heat.

The regulation of this heat load is complex and involves the central nervous system (CNS), thermosensors, and thermoregulatory effectors. The central thermostat activates the effectors that produce peripheral vasodilation and sweating. The skin surface is in effect the radiator and the principal location of heat loss, since skin blood flow can increase 25–30 times over the basal rate. This dramatic increase in skin blood flow, coupled with the maintenance of peripheral vasodilation, efficiently radiates heat. At the same time, there is a compensatory vasoconstriction of the splanchnic and renal beds.

Acclimatization to heat reflects a constellation of physiologic adaptations that permit the body to lose heat more efficiently. This process often requires one to several weeks of exposure and work in a hot environment. During acclimatization, the thermoregulatory set point is altered, and this alteration affects the onset, volume, and content of diaphoresis. The threshold for the initiation of sweating is lowered, and the amount of sweat increases, with a lowered ...

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