A case supporting the proposal that cardiac filling pressure is the limiting factor in adjusting to heat stress.
Progressively increasing heat stress ultimately results in heat stroke, a medical emergency leading to death if not treated properly. Initially in heat stress, enormous increases in blood flow and volume in skin (and muscle if exercising) are achieved by the diversion of blood away from the splanchnic bed, kidneys, and probably fat and muscle, and in some species such as man, there is also an increase in cardiac output. The onset of heat stroke is thought to involve a decrease in central venous pressure, which is defended by constriction in both arterioles and veins of the skin via low-pressure baroreceptors in the cardiopulmonary region. Body heat loss is thereby reduced and the consequent rise in body temperature causes death due to thermally evoked critical changes in central nervous system activity and/or fatal embolization following disseminated intravascular coagulation and erythrocyte sphering. Evidence is presented, which supports the proposal that cardiac filling pressure is the limiting factor in adjusting to heat stress.
D000222:Adaptation, Physiological; D001833:Body Temperature Regulation; D002302:Cardiac Output; D002496:Central Venous Pressure; D006359:Heat Exhaustion / Q000209:etiology / Q000503:physiopathology; D006358:Hot Temperature / Q000009:adverse effects*; D006801:Humans; D008955:Models, Cardiovascular; D012039:Regional Blood Flow; D012867:Skin / Q000098:blood supply; D013312:Stress, Physiological / Q000503:physiopathology; D014661:Vasoconstriction