The patient who's been vomiting for three days doesn't just need fluids — their pH is climbing because they're losing acid they can't replace. Knowing why changes everything you do next.
Metabolic alkalosis occurs when pH rises above 7.45 due to excess bicarbonate (HCO₃⁻ above 26 mEq/L) or loss of hydrogen ions. The two most testable causes are prolonged vomiting or nasogastric suctioning (loss of hydrochloric acid from the stomach) and overuse of loop or thiazide diuretics (which cause chloride and potassium wasting). Both mechanisms create a chloride-responsive alkalosis — the kidneys want to excrete the excess bicarb but can't without adequate chloride. This is why normal saline, not D5W, is the cornerstone IV fluid. Hypokalemia almost always accompanies metabolic alkalosis because the kidneys trade potassium for hydrogen ions trying to correct pH, and low potassium itself perpetuates the alkalosis. Expected ABG pattern: pH above 7.45, HCO₃⁻ above 26, with respiratory compensation showing a rising PaCO₂ (the body hypoventilates to retain CO₂ and lower pH). Signs include confusion, muscle twitching, tingling, hypoventilation, and possible seizures. Nursing priorities: replace chloride and potassium, monitor I&O closely, assess respiratory rate and depth for compensatory shallow breathing, and address the underlying cause.
Key Distinctions
Don't confuse the slow, shallow breathing of compensatory hypoventilation in metabolic alkalosis with respiratory depression from opioids — the mechanism and intervention differ entirely. Students commonly mistake metabolic alkalosis symptoms (tingling, muscle twitching) for hypocalcemia; both can coexist, but the primary driver here is elevated pH. Chloride-responsive alkalosis (vomiting, NG suction, diuretics) corrects with saline; chloride-resistant alkalosis (Cushing's, hyperaldosteronism) does not.
Clinical Pearl
Vomiting steals acid, diuretics steal chloride and potassium — all roads to metabolic alkalosis run through what the body loses, not what it gains.