Elevated serum bicarbonate from H+ loss or HCO3 gain, subdivided by chloride responsiveness.
Also known as: metabolic alkalosis, alkalemia, contraction alkalosis, saline-responsive alkalosis, saline-resistant alkalosis
Overview
A primary acid-base disorder characterized by elevated serum bicarbonate (>26-28 mEq/L) and arterial pH >7.45, resulting from either net loss of hydrogen ions, net gain of bicarbonate, or loss of fluid containing chloride in excess of bicarbonate (contraction alkalosis). Classified by urine chloride: saline-responsive (UCl <20 mEq/L) and saline-resistant (UCl >20 mEq/L).
Epidemiology
Among the most common acid-base disturbances in hospitalized patients. Often iatrogenic (diuretics, nasogastric suction, transfusion of citrate-rich blood products). Mortality of severe metabolic alkalosis (pH >7.55) approaches 45-65% in critically ill patients — reflects severity of underlying illness.
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Question 1RenalMedium
A 48-year-old woman is evaluated for hypertension that remains poorly controlled on three antihypertensive agents. She reports no vomiting, diarrhea, or diuretic use. Blood pressure is 168/102 mm Hg and she has no edema. Laboratory studies show sodium 144 mEq/L, potassium 2.9 mEq/L, chloride 96 mEq/L, and bicarbonate 33 mEq/L; arterial pH is 7.49. A spot urine chloride is 38 mEq/L. Which of the following is the most appropriate next diagnostic test?
ARepeat arterial blood gas analysis
BGenetic testing for Gitelman syndrome
COvernight dexamethasone suppression
DPlasma aldosterone-to-renin ratio
Reveal answer & full explanation
Correct answer: D — Plasma aldosterone-to-renin ratio
ARepeat arterial blood gas analysis
BGenetic testing for Gitelman syndrome
COvernight dexamethasone suppression
DPlasma aldosterone-to-renin ratio✓
Why Plasma aldosterone-to-renin ratio is correct
This patient has a saline-resistant metabolic alkalosis (high pH, high HCO3) with hypokalemia, hypertension, and a urine chloride >20 mEq/L, which points away from chloride-depletion causes (vomiting, diuretics) and toward mineralocorticoid excess.
The combination of hypertension + hypokalemic alkalosis is the classic screen for primary hyperaldosteronism; an aldosterone-to-renin ratio >20 (with elevated aldosterone) supports the diagnosis and is the correct next step before adrenal imaging or confirmatory testing.
Why the others are wrong
Repeat arterial blood gas analysis — useful only to exclude a sampling artifact; the alkalosis here is internally consistent (high pH with appropriately high HCO3) and the diagnostic question is the underlying cause, not confirmation of the disturbance.
Overnight dexamethasone suppression — screens for Cushing syndrome, a much less common cause of mineralocorticoid-excess alkalosis; it is pursued only when cushingoid features are present or aldosterone testing is unrevealing.
Genetic testing for Gitelman syndrome — Bartter/Gitelman cause saline-resistant alkalosis but with NORMAL blood pressure; hypertension makes a tubulopathy unlikely, and genetic testing is reserved for young normotensive patients with unexplained alkalosis.
Question 2RenalMedium
A 34-year-old woman with hyperemesis gravidarum has been vomiting for 5 days and has had a nasogastric tube to low suction for 2 days. Vitals: BP 98/62 mm Hg, HR 104/min, with dry mucous membranes. Labs: Na 138 mEq/L, K 2.9 mEq/L, Cl 88 mEq/L, HCO3 38 mEq/L. Arterial pH is 7.52. Urine chloride is 8 mEq/L. The elevated bicarbonate persists despite the initial insult having stopped. Which of the following best explains the maintained alkalosis?
Why Chloride depletion forces renal bicarbonate reabsorption is correct
Vomiting and NG suction lose HCl-rich fluid, generating the alkalosis and depleting chloride and volume.
Maintenance is the key: with chloride scarce, the proximal and distal nephron must reabsorb Na+ alongside another anion, so HCO3- reabsorption rises and the kidney cannot excrete the excess bicarbonate.
Volume depletion (BP 98/62, HR 104) adds secondary hyperaldosteronism and enhanced proximal Na/HCO3 reabsorption, but the urine chloride of 8 mEq/L (<20) marks this as a saline-responsive, chloride-depleted process.
Isotonic saline plus KCl repairs the chloride and volume deficits, after which the kidney can excrete HCO3- and correct the pH.
Why the others are wrong
Aldosterone excess promotes distal sodium-for-hydrogen exchange: this is the mechanism of saline-RESISTANT alkalosis (Conn syndrome, Cushing); those patients are volume-expanded and hypertensive with urine chloride >20 mEq/L, the opposite of this hypovolemic, hypotensive picture.
Hypokalemia stimulates renal ammoniagenesis and acid excretion: hypokalemia does contribute to maintaining alkalosis, but it is a secondary perpetuator here; the dominant driver in a vomiting, chloride-depleted patient with urine Cl 8 mEq/L is chloride depletion, and KCl is given precisely because Cl- (not just K+) must be restored.
Bicarbonate gain from metabolism of transfused citrate load: citrate-load alkalosis occurs with massive transfusion or CRRT, neither of which is present; this patient's bicarbonate came from H+ loss, not exogenous alkali.
Per standard acid-base teaching, urine chloride is the single most useful test to subclassify metabolic alkalosis: <20 mEq/L indicates the saline-responsive, chloride-depletion mechanism.
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Trousseau and Chvostek signs (functional hypocalcemia)
Hyperreflexia, fasciculations
Volume status varies — depleted in saline-responsive, expanded in mineralocorticoid excess
Hypertension in mineralocorticoid-excess states
Classic findings
Vomiting patient with hypochloremic, hypokalemic metabolic alkalosis and low urine chloride. Hypertensive patient with hypokalemic alkalosis and aldosterone:renin ratio >20 suggests primary hyperaldosteronism.
Differential diagnosis
Respiratory acidosis (compensated) — Chronic hypercapnia raises HCO3, but pH is low or low-normal — not alkalotic
Laboratory error / contamination — Air bubble in ABG sample can falsely lower PaCO2 and raise pH; repeat sample if implausible
Mixed acid-base disorder — Use anion gap, delta-delta, and expected compensation to detect coexisting disturbances
Bartter syndrome — Genetic loop-diuretic-like defect — hypokalemic, hypochloremic alkalosis with normotension and hypercalciuria
Replace potassium (KCl) and magnesium aggressively — both perpetuate alkalosis when depleted
Saline-resistant with mineralocorticoid excess: surgical removal of adenoma, OR mineralocorticoid receptor antagonist (spironolactone, eplerenone), OR ENaC blocker (amiloride, triamterene) for Liddle syndrome
Discontinue exogenous alkali (excessive antacids, bicarbonate-containing dialysate, citrate from transfusion or CRRT)
Persistent vomiting / NG suction
IV normal saline with KCl
H2 blocker (famotidine) or PPI (pantoprazole, omeprazole) to reduce HCl loss
Antiemetic — ondansetron, metoclopramide
Diuretic-induced
Discontinue or reduce diuretic if clinically feasible
Replace K and Mg; add K-sparing diuretic (spironolactone, eplerenone, amiloride)
If diuretic necessary (e.g., heart failure), accept mild alkalosis and treat aggressively
Primary hyperaldosteronism
Adrenalectomy for aldosterone-producing adenoma
Spironolactone or eplerenone for bilateral adrenal hyperplasia
Address HTN aggressively
Severe alkalosis with edema or renal failure (cannot tolerate saline)
Hypoventilation with hypoxemia — particularly dangerous in patients with underlying lung disease
Difficulty weaning from mechanical ventilation
Increased mortality in critically ill patients (especially pH >7.55)
PANCE pearls
Urine chloride is the single most useful test to subclassify metabolic alkalosis — vomiting and recent diuretic use can both lower it; consider timing.
You cannot fully correct metabolic alkalosis until chloride, potassium, and magnesium deficits are repaired.
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