Question
What is the precise cellular mechanism by which prolonged, uncorrected severe hypothermia (< 30°C / 86°F) causes cold diuresis, and what is its impact on intravascular volume?
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Cold diuresis is primarily driven by peripheral vasoconstriction. In response to core hypothermia, the body shunts blood away from the extremities to the central circulation. This sudden increase in central blood volume is sensed by baroreceptors as relative hypervolemia. Consequently, the secretion of Antidiuretic Hormone (ADH/Vasopressin) from the posterior pituitary is inhibited, while Atrial Natriuretic Peptide (ANP) is released. This shuts down water reabsorption in the renal collecting ducts, causing a profound, inappropriate diuresis that severely depletes actual intravascular volume, worsening shock upon rewarming.
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