Heat stress means perceived discomfort and physiologic strains during heat exposure. A series of physiologic events occur to adapt heat. These events include thermoregulation (with acclimatization), an acute-phase response, and production of heat shock proteins. If these sequence of actions fails to prevents body from high temperature, heat stress progresses to heat stroke. Thermoregulation, acclimatization, acute phase responses, and heat shock proteins are the important factors in response to heat stroke. Hypothalamus is the center of thermoregulation. Increase in the peripheral body temperature will activate sympathetic response through thermoregulatory action of hypothalamus to deliver more blood flow by vasodilation of surface cutaneous veins. This increase in blood flow will cause sweating. The elevated blood temperature will cause tachycardia, increase in cardiac output, and increase in minute ventilation.  Blood shift from internal organs to the skin may cause decreased visceral perfusion and predispose them to ischemia. Increased sweating will cause loss of salt and water up to 2 liters per hour. Therefore, dehydration may worsen thermoregulation.
Heat stroke pathophysiology
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