A 22-year-old woman with recurrent vomiting develops a metabolic alkalosis with serum bicarbonate of 38 mEq/L and urine chloride less than 10 mEq/L. The factor chiefly responsible for perpetuating the alkalosis is:

• A Extracellular volume depletion sustaining proximal bicarbonate reabsorption via the renin-angiotensin system ✓
• B Direct loss of chloride causing distal tubular sodium reabsorption with bicarbonate excretion
• C Respiratory hypoventilation driven by the raised bicarbonate concentration alone
• D Increased aldosterone secretion secondary to suppressed renin activity

Explanation

Vomiting removes HCl, generating alkalosis, but the kidney could normally excrete the excess bicarbonate rapidly. Volume contraction around the remaining bicarbonate plus angiotensin II stimulation of proximal Na-H exchange keeps bicarbonate reabsorbed, maintaining the alkalosis. Hence the term contraction alkalosis and the very low urine chloride, which marks volume depletion. Aldosterone rises WITH renin in volume depletion, so option D states the opposite relationship.

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

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