Renal, Fluids, Electrolytes & Acid-Base · Topic 21 of 22

Metabolic Alkalosis

Renal & electrolytes · acid–base

Metabolic Alkalosis

Too much bicarbonate, held by the kidneys. Check urine chloride: under 20 means saline and potassium will fix it.

Key numbers

Primary bicarbonate rise with pH above 7.45HCO₃⁻ > 28 mEq/L

Expected PaCO₂ rise: about 0.7 per mEqΔPaCO₂ ≈ 0.7 × ΔHCO₃⁻

Urine chloride under 20 = chloride-responsiveUrine Cl⁻ < 20 mEq/L

pH above 7.6: dialysis or IV HClpH > 7.6

01 · Defined byPrimary bicarbonate rise with pH above 7.45

Metabolic alkalosis is a primary rise in serum bicarbonate (above about 28 mEq/L) with pH above 7.45; it persists only because the kidneys keep reabsorbing bicarbonate, usually driven by volume depletion, chloride depletion or hypokalemia.

02 · Defined byUrine chloride under 20 = chloride-responsive

Order a urine chloride when the cause is unclear: below 20 mEq/L means chloride-responsive alkalosis (vomiting, NG suction, prior diuretics); above 20 mEq/L suggests chloride-resistant alkalosis (mineralocorticoid excess, severe hypokalemia, Bartter or Gitelman).

03 · DoGive IV 0.9% saline plus potassium chloride

Treat chloride-responsive alkalosis with IV 0.9% saline and potassium chloride: restoring volume, chloride and potassium removes the stimulus for renal bicarbonate reabsorption, and the kidneys excrete the excess.

What it is

Core idea

Aldosterone maintains alkalosis and causes hypokalemiaVolume contraction raises aldosterone, which increases distal sodium reabsorption with potassium and hydrogen ion loss — so hypokalemia is both a cause and a consequence of metabolic alkalosis.

Causes & risk factors

Why it happens

Most common: diuretics, vomiting, NG suctionThe most common causes are diuretic use and volume depletion with loss of gastric acid and chloride from recurrent vomiting or nasogastric suction.

Posthypercapnic alkalosis after rapid ventilationLowering PaCO₂ quickly in chronic hypercapnia leaves the compensatory bicarbonate behind, producing posthypercapnic metabolic alkalosis; lower PaCO₂ gradually and correct chloride and potassium deficits.

Presentation

What you'll see

Low ionized calcium: tetany, seizures, arrhythmiasSevere alkalemia increases protein binding of calcium, lowering ionized calcium: headache, lethargy, neuromuscular excitability, delirium, tetany and seizures; with hypokalemia it lowers the threshold for angina and arrhythmias.

Diagnosis & monitoring

Work-up

Expected PaCO₂ rise: about 0.7 per mEq must knowExpected respiratory compensation: PaCO₂ rises about 0.7 mmHg (0.6–0.75) for each 1 mEq/L rise in bicarbonate, rarely above 55 mmHg. A higher PaCO₂ means added respiratory acidosis; a lower one, added respiratory alkalosis.

Do right now

In this order

First moves

Expected PaCO₂ rise: about 0.7 per mEqΔPaCO₂ ≈ 0.7 × ΔHCO₃⁻

→

Urine chloride under 20 = chloride-responsiveUrine Cl⁻ < 20 mEq/L

→

Give IV 0.9% saline plus potassium chloride

Why each step

Expected PaCO₂ rise: about 0.7 per mEqExpected respiratory compensation: PaCO₂ rises about 0.7 mmHg (0.6–0.75) for each 1 mEq/L rise in bicarbonate, rarely above 55 mmHg. A higher PaCO₂ means added respiratory acidosis; a lower one, added respiratory alkalosis.

Urine chloride under 20 = chloride-responsiveOrder a urine chloride when the cause is unclear: below 20 mEq/L means chloride-responsive alkalosis (vomiting, NG suction, prior diuretics); above 20 mEq/L suggests chloride-resistant alkalosis (mineralocorticoid excess, severe hypokalemia, Bartter or Gitelman).

Give IV 0.9% saline plus potassium chlorideTreat chloride-responsive alkalosis with IV 0.9% saline and potassium chloride: restoring volume, chloride and potassium removes the stimulus for renal bicarbonate reabsorption, and the kidneys excrete the excess.

Management

Orders

Chloride-resistant: treat cause, replete K⁺ and Mg²⁺Chloride-resistant alkalosis does not respond to saline: treat the cause, replete potassium and magnesium, and use a mineralocorticoid receptor antagonist (spironolactone, eplerenone) or amiloride for mineralocorticoid excess.

Acetazolamide when saline is not an optionAcetazolamide 250–375 mg orally or IV once or twice daily increases bicarbonate excretion; it suits volume-overloaded patients with diuretic-induced alkalosis and posthypercapnic alkalosis, but worsens potassium and phosphate losses.

pH above 7.6: dialysis or IV HClSevere alkalemia (pH above 7.6) may need urgent correction: hemodialysis or hemofiltration, especially with volume overload or renal failure; central-line dilute hydrochloric acid is reserved for kidney failure when dialysis is impossible.

Chloride-responsive or chloride-resistant?

Commonly confused

Urine chloride	< 20 mEq/L
Typical causes	Vomiting, NG suction, prior diuretic use, posthypercapnia
Blood pressure clue	Volume depleted
Treatment	IV 0.9% saline plus KCl

More detail

Reference

Show 8 reference facts

In critically ill patients, severe metabolic alkalosis with arterial pH of 7.55 or higher is associated with significantly increased mortality.

Contraction alkalosis: loss of sodium chloride and water (diuretics, sweat in cystic fibrosis) concentrates an unchanged amount of bicarbonate in a smaller extracellular volume.

Milk-alkali (calcium-alkali) syndrome from calcium carbonate antacids or supplements causes hypercalcemia with alkalosis; hypercalcemia suppresses PTH and increases bicarbonate reabsorption. Volume expansion is the first treatment.

Alkali loading can overshoot: lactate or ketoacids regenerate bicarbonate once the acidosis resolves, worsened by bicarbonate therapy, and sodium bicarbonate given with hypokalemia worsens alkalosis.

Run 0.9% saline about 50–100 mL/h above ongoing losses until urine chloride exceeds 25 mEq/L and urine pH normalizes after the initial bicarbonaturia.

Urine chloride and potassium are not diagnostic in stage 4–5 chronic kidney disease.

Gitelman syndrome (young adults) adds hypomagnesemia and hypocalciuria; Bartter syndrome presents in early childhood with renal salt wasting — both mimic chronic diuretic use.

In ventilated patients with metabolic alkalosis, carbonic anhydrase inhibitors improved blood gases and shortened mechanical ventilation by about 27 hours in a meta-analysis (2 trials); the effect on mortality was uncertain (low-certainty evidence).

Pearl

Vomiting, NG suction and diuretics cause most cases — and the alkalosis persists only while volume, chloride or potassium stay low.

Sources · Merck Manual Professional — Metabolic Alkalosis (Mar 2025) · Merck Manual Professional — Acid-Base Disorders (table: Primary Changes and Compensations) · Do C, Vasquez PC, Soleimani M. Metabolic Alkalosis Pathogenesis, Diagnosis, and Treatment: Core Curriculum 2022. Am J Kidney Dis 2022 · Tanios BY et al. Carbonic anhydrase inhibitors in patients with respiratory failure and metabolic alkalosis: systematic review and meta-analysis. Crit Care 2018 · Merck Manual Professional — Respiratory Acidosis (posthypercapnic overshoot alkalosis) · Starter sheet built from the verified AGACNP fact map (facts reviewed 2026-10-15).