Pathophysiology
Clinical meaning
Metabolic alkalosis is characterized by a primary increase in serum bicarbonate (HCO3- >26 mEq/L) with a compensatory increase in PaCO2 (hypoventilation - the lungs retain CO2 to lower pH). Two mechanisms generate metabolic alkalosis: (1) Loss of hydrogen ions (H+) - vomiting/NG suction loses HCl from the stomach, leaving excess bicarbonate; (2) Gain of bicarbonate - excessive NaHCO3 administration, contraction alkalosis. Contraction alkalosis occurs when ECF volume contracts (dehydration from diuretics) and bicarbonate becomes more concentrated because the kidneys preferentially reabsorb sodium over bicarbonate to maintain volume. Classification by chloride responsiveness guides treatment: Chloride-responsive (urine Cl- <20 mEq/L): caused by vomiting, NG suction, diuretics (thiazide/loop), post-hypercapnia. Treatment: IV normal saline (chloride replacement allows kidneys to excrete excess bicarbonate). Chloride-resistant (urine Cl- >20 mEq/L): caused by primary hyperaldosteronism (Conn syndrome), Cushing syndrome, severe hypokalemia, Bartter/Gitelman syndromes. Treatment: address the underlying hormone excess or potassium deficit; saline alone is ineffective.