Abstract
Exertional heat exhaustion (HEX) is the most prevalent form of heat illness in athletic, industrial, and military settings. The common etiological features include dehydration, high ambient temperature/humidity/solar radiation with slow air movement, and strenuous/prolonged exercise. The fundamental pathophysiology of HEX involves total body water and whole-body sodium deficits, mild hyperthermia, and great cardiovascular strain. Although some authorities believe that HEX represents only postural hypotension leading to collapse, numerous clinical and physiological publications have described HEX in a variety of scenarios and concluded that HEX involves more than postural hypotension per se. Recognition of HEX focuses on great fatigue or muscular weakness, mild rectal temperature elevation, nausea, vomiting, and the signs and symptoms that reflect dehydration (i.e., whole-body sodium and body water deficits) plus circulatory insufficiency (e.g., hypotension, ashen skin). When HEX patients collapse and/or exhibit altered mental status, severe HEX is indicated; they have reached the limits of cardiovascular compensation, and hyperthermia adds additional stress to existing cardiovascular insufficiency. Mild HEX with no other symptoms may be treated with rest and leg elevation, but severe HEX cases that involve large fluid losses and tachycardia at rest should be treated by judicious administration of intravenous fluid, under supervision of a physician. Exercise-heat acclimatization across 8–10 days improves orthostatic intolerance, enhances cardiovascular stability, reduces salt losses in sweat and urine, and expands plasma (extracellular) volume; the resulting adaptations improve heat tolerance and enhance ability to work and exercise in the heat.
Keywords
Dehydration Sodium Salt depletion Water depletion Hyperthermia Collapse Exercise Orthostatic intolerance Fluid-electrolyte SweatReferences
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