Metabolic alkalosis
Metabolic alkalosis is a primary rise in serum bicarbonate generated by acid loss or alkali retention (usually vomiting, nasogastric suction, or diuretic use) and sustained by a maintenance state, most often volume contraction, hypokalemia, or mineralocorticoid excess. The urine chloride level is the key diagnostic branch point, separating chloride-responsive (saline-responsive) causes, treated with isotonic saline and potassium repletion, from chloride-resistant causes driven by mineralocorticoid excess, treated with potassium repletion and correction of the underlying endocrine or genetic disorder.
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What this article covers
- Overview
Metabolic alkalosis is a primary rise in serum bicarbonate, distinguished from a compensatory rise for chronic respiratory acidosis by a concurrently elevated arterial or venous pH.
- Epidemiology
Chloride depletion is the most common cause overall: vomiting, nasogastric suction, and diuretic use, all producing a low urine chloride.
- Risk factors
Recurrent vomiting or nasogastric suction: the classic generation-phase trigger, with acid loss from the stomach.
- Pathophysiology
Generation occurs by acid loss or alkali gain: gastrointestinal acid loss (vomiting) removes hydrogen ions and leaves bicarbonate behind; a renal mineralocorticoid effect (primary or secondary to…
- Clinical features
Features are largely those of the underlying cause and its associated electrolyte disturbances rather than the alkalosis itself.
- Differential diagnosis
Vomiting or nasogastric suction (generation phase): low urine chloride with only slight extracellular fluid reduction, unlike the marked volume contraction of the maintenance phase of prolonged vomiting.
- Diagnosis
The diagnosis is established by a blood gas showing an elevated pH with an elevated serum bicarbonate (usually greater than 26 mEq/L), confirming a primary metabolic alkalosis rather than a…
- Management
First, treat the generation-phase cause when identifiable: stop vomiting (antiemetics, treat the underlying gastrointestinal disorder), discontinue nasogastric suction when no longer needed, and hold or adjust the offending diuretic.
- Complications
Cardiac arrhythmia, markedly increased by coexisting hypokalemia.
- Prognosis
Prognosis depends on the underlying cause: saline-responsive alkalosis from vomiting or diuretics resolves promptly with volume and potassium repletion once the trigger is removed.
- Prevention
Screen for primary hyperaldosteronism when resistant hypertension, hypokalemia (spontaneous or substantial on a low-dose thiazide), an incidentally found adrenal mass, family history of early-onset…
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Related articles
- Metabolic acidosis
Metabolic acidosis is a primary fall in serum bicarbonate that is first confirmed with an arterial or venous blood gas, then classified by the serum anion gap into an increased anion gap process (unmeasured organic anion, most often lactate) or a normal anion gap process (bicarbonate loss from the gut or kidney). The urine anion gap and clinical context localize the cause, and management targets the underlying disease, reserving intravenous sodium bicarbonate for severe acidemia (pH less than 7.1-7.2) or specific indications such as chronic kidney disease and renal tubular acidosis.
- Respiratory alkalosis
Respiratory alkalosis is a reduction in arterial Pco2 from increased alveolar ventilation, most often driven by sepsis, hepatic failure, anxiety, hyperventilation, pregnancy, or salicylate toxicity, presenting with tachypnea, lightheadedness, and paresthesia. Diagnosis rests on arterial blood gas confirmation of a primary fall in Pco2 with the expected compensatory drop in bicarbonate, and management targets the underlying driver rather than the blood gas itself, with acetazolamide or controlled hypoventilation reserved for rare severe alkalemia with hemodynamic compromise.
- Respiratory acidosis
Respiratory acidosis is retention of arterial carbon dioxide from impaired alveolar ventilation, producing hypercapnia and a low pH that is buffered acutely and partially corrected over 3 to 5 days by renal bicarbonate reabsorption. Management corrects the underlying ventilatory mechanism, escalating from treatment of the precipitant to noninvasive and then invasive mechanical ventilation based on the degree of acidosis, mental status, and hemodynamic stability.
- Cushing syndrome
Cushing syndrome is the clinical state of chronic glucocorticoid excess from any cause, most often exogenous glucocorticoid use, diagnosed by demonstrating loss of normal cortisol suppression or diurnal rhythm with at least two of three screening tests. Treatment targets the underlying source: withdrawal or tapering of exogenous steroid, transsphenoidal surgery for a pituitary cause, or adrenalectomy for an adrenal or ectopic tumor, with steroidogenesis inhibitors reserved for persistent or unresectable disease.