Clinical Note

Heat Stroke and Heat Exhaustion

In a dry environment, the normal individual can withstand an ambient temperature of up to 150°F for several hours, but, as discussed earlier, heat loss in this circumstance depends on the evaporation of sweat, which is progressively diminished as the relative humidity rises. When the evaporative heat losses cannot match body heat production plus conductive and radiative heat input, the body temperature rises. When it reaches 40 to 41.5°C (104 to 107°F), the temperature integrative center in the hypothalamus ceases to function, and a state of heat pyrexia (heat stroke) ensues. Heat stroke is a medical emergency because the normal reflexes are lost; in spite of the high body temperature, sweating ceases and death ensues rapidly unless the body is immediately cooled by ice water baths and supportive medical care. Heat stroke is usually observed in the setting of physical exertion in a hot environment, and it may occur very precipitously or be preceded by the symptoms of heat collapse described later. Heat stroke is generally recognized by the presence of dry skin due to the absence of sweating after collapse; however, in an individual who collapses while working or exercising, the skin may still be sweaty. Thus, the most important diagnostic criterion is a body core temperature in excess of 40° C because above this temperature normal physiological temperature regulation is lost and intervention is imperative.

Heat exhaustion (heat collapse) also occurs in the setting of a hot environment, but it results from circulatory problems rather than from an increase in body temperature. Severe sweating leads to a decrease in extracellular fluid volume due to NaCl and water losses. The resulting decrease in plasma volume is further complicated by vasodilation, which keeps a larger blood volume in the cutaneous circulation. If venous return is sufficiently compromised, the situation is quite analogous to mild circulatory shock. In this state, the body core temperature is not necessarily elevated, and the collapse might be regarded as protective, although potentially dangerous, because the activity that produces heat ceases. The collapse is preceded by weakness, vertigo, headache, and sometimes by vomiting. The period of collapse is usually brief and the recovery spontaneous if the individual is removed from the hot environment and given fluids. Heat exhaustion and collapse are frequently seen in the elderly, who may be less well hydrated or less aware of their dehydration because of a diminished ability to care for themselves; however, even trained athletes may experience heat collapse, especially when exercising heavily in hot and humid conditions. The chances of developing heat stroke or collapse are also increased by certain drugs that inhibit sweating and/or vasodilation, including atropine, scopolamine, phenothiazides, mono-amine oxidase inhibitors, and glutethimide.

extreme, these effects can lead to heat exhaustion (see the clinical note).

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