Prolonged exposure to elevated ambient temperatures can result in heat cramps, heat exhaustion, or heat stroke.
Heat cramps result from loss of electrolytes through sweating. Cramping of voluntary muscles, usually in association with vigorous exercise, is the hallmark sign. Heat-dissipating mechanisms are able to maintain normal core body temperature.
Heat exhaustion is probably the most common hyperthermic syndrome. Its onset is sudden, with prostration and collapse, and it results from a failure of the cardiovascular system to compensate for hypovolemia, secondary to water depletion. After a period of collapse, which is usually brief, equilibrium is spontaneously reestablished if the victim is able to rehydrate.
Heat stroke is associated with high ambient temperatures and high humidity. Thermoregulatory mechanisms fail, sweating ceases, and core body temperature rises. In the clinical setting, a rectal temperature of 106°F or higher is considered a grave prognostic sign, and the mortality rate for such patients exceeds 50%. The underlying mechanism is marked generalized peripheral vasodilation with peripheral pooling of blood and a decreased effective circulating blood volume. Necrosis of the muscles and myocardium may occur. Arrhythmias, disseminated intravascular coagulation, and other systemic effects are common. Elderly people, persons with cardiovascular disease, and otherwise healthy people undergoing physical stress (such as young athletes and military recruits) are prime candidates for heat stroke.
• Malignant hyperthermia, although similar sounding, is not caused by exposure to high temperatures. It is a genetic condition resulting from mutations in genes such as RYR1 that control calcium levels in skeletal muscle cells. In affected individuals, exposure to certain anesthetics during surgery may trigger a rapid rise in calcium levels in skeletal muscle, which in turn leads to muscle rigidity and increased heat production. The resulting hyperthermia has a mortality rate of approximately 80% if untreated, but this falls to less than 5% if the condition is recognized and muscle relaxants are administered promptly.
Prolonged exposure to low ambient temperature leads to hypothermia. The condition is seen all too frequently in homeless alcoholics, in whom wet or inadequate clothing and dilation of superficial blood vessels, occurring as a result of the ingestion of alcohol, hasten the lowering of body temperature. At about 90°F, loss of consciousness occurs, followed by bradycardia and atrial fibrillation at lower core temperatures.
Chilling or freezing of cells and tissues causes injury by two mechanisms:
Direct effects probably are mediated by physical disruptions within cells and high salt concentrations incident to the crystallization of the intra-and extracellular water.
Indirect effects are the result of circulatory changes, which vary depending on the rate and the duration of the temperature drop. Slowly developing, prolonged chilling may induce vasoconstriction and increased permeability, leading to edema. Such changes are typical of “trench foot.” This condition developed in soldiers who spent long periods of time in waterlogged trenches during the First World War (1914–1918), frequently causing gangrene that necessitated amputation. Alternatively, with sudden sharp drops in temperature, the vasoconstriction and increased viscosity of the blood in the local area may cause ischemic injury and degenerative changes in peripheral nerves. In this situation, the vascular injury and increased permeability with exudation only become evident with rewarming. If the period of ischemia is prolonged, hypoxic changes and infarction of the affected tissues (e.g., gangrene of toes or feet) may result.