Myxedema coma pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]
Overview
Pathophysiology
A normal body core temperature is preserved in compensated hypothyroidism because of neurovascular adaptations, including chronic peripheral vasoconstriction, mild diastolic hypertension, and diminished blood volume. The hypothyroid heart also compensates by performing more work at a given amount of oxygen through better coupling of ATP to contractile events. These adaptations to thyroid hormone deficiency maintain homeostasis, albeit at a precarious balance. A further reduction in blood volume (e.g., secondary to gastrointestinal bleeding or the use of diuretics) may disrupt this precarious balance, which homeostatic mechanisms are no longer able to restore. Likewise, the already compromised ventilatory drive may progress to respiratory failure by intercurrent pulmonary infection. Impairment in central nervous system function can be provoked further by stroke, the use of sedatives, and hyponatremia (a common phenomenon in severe hypothyroidism).