In heat stroke (core temperature >40°C), the failure of sweating is due to:

• A Depletion of eccrine gland acetylcholine stores from sustained cholinergic stimulation
• B Peripheral sweat gland fatigue/failure from sustained maximal stimulation, combined with systemic inflammatory response impairing hypothalamic thermostasis ✓
• C Central hypothalamic set-point reset by pyrogens to a fever response, inhibiting sweating
• D Sympathetic adrenergic override suppressing cholinergic sweat gland activity

Explanation

In exertional heat stroke, sustained maximal eccrine gland activity leads to sweat gland exhaustion/anhidrosis. Additionally, the systemic inflammatory cascade (cytokines, endotoxin from gut ischemia) impairs thermoregulatory center function. In classic heat stroke (elderly, non-exertional), failure of eccrine glands and cardiovascular insufficiency prevent adequate heat dissipation. This differs from fever where the hypothalamic set-point is actively raised by pyrogens — in heat stroke the set-point remains normal but heat dissipation mechanisms fail. Sweat glands are innervated by cholinergic sympathetic fibers, not adrenergic ones, so sympathetic override reducing sweating is not the mechanism.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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Written and medically reviewed by the StethoPrep medical team.