Metabolic Alkalosis

ByJames L. Lewis III, MD, Brookwood Baptist Health and Saint Vincent’s Ascension Health, Birmingham
Reviewed/Revised Jul 2023
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Metabolic alkalosis is primary increase in bicarbonate (HCO) with or without compensatory increase in carbon dioxide partial pressure (P); pH may be high or nearly normal. Common causes include prolonged vomiting, hypovolemia, diuretic use, and hypokalemia. Renal impairment of HCO

(See also Acid-Base Regulation and Acid-Base Disorders.)

Etiology of Metabolic Alkalosis

Metabolic alkalosis is bicarbonate (HCO3) accumulation due to

  • Acid loss

  • Alkali administration

  • Intracellular shift of hydrogen ion (H+—as occurs in hypokalemia)

  • Renal HCO3 retention

Regardless of initial cause, persistence of metabolic alkalosis indicates that the kidneys have increased their HCO3 reabsorption, because HCO3 is normally freely filtered by the kidneys and hence excreted. Volume depletion and hypokalemia are the most common stimuli for increased HCO3 reabsorption, but any condition that elevates aldosterone or mineralocorticoids (which enhance sodium [Na] reabsorption and potassium [K] and hydrogen ion [H+] excretion) can elevate HCO3. Thus, hypokalemia is both a cause and a frequent consequence of metabolic alkalosis.

The most common causes of metabolic alkalosis are

  • Diuretic use

  • Volume depletion (particularly when involving loss of gastric acid and chloride [Cl] due to recurrent vomiting or nasogastric suction)

Among other causes of metabolic alkalosis are disorders that cause

  • Bicarbonate excess

  • Renal acid loss


Metabolic alkalosis can be

  • Chloride (Cl)-responsive: Involves loss or excess secretion of Cl; it typically corrects with IV administration of NaCl-containing fluid.

  • Chloride-unresponsive: Does not correct with NaCl-containing fluids, and typically involves severe magnesium (Mg) and/or potassium (K) deficiency or mineralocorticoid excess.

The 2 forms can coexist, eg, in patients with volume overload made hypokalemic by high-dose diuretics.

Symptoms and Signs of Metabolic Alkalosis

Symptoms and signs of mild alkalemia are usually related to the underlying disorder. More severe alkalemia increases protein binding of ionized calcium (Ca++), leading to hypocalcemia and subsequent headache, lethargy, and neuromuscular excitability, sometimes with delirium, tetany, and seizures. Alkalemia also lowers threshold for anginal symptoms and arrhythmias. Concomitant hypokalemia may cause weakness.

Diagnosis of Metabolic Alkalosis

  • Arterial blood gas (ABG) and serum electrolyte measurements

  • Diagnosis of cause (usually clinical)

  • Sometimes measurement of urinary Cl and K+

Recognition of metabolic alkalosis and appropriate respiratory compensation is discussed in Diagnosis of Acid-Base Disorders and requires measurement of ABG and serum electrolytes (including Ca and Mg).

Common causes can often be determined by history and physical examination. If history is unrevealing and renal function is normal, urinary Cl and K+ concentrations are measured (values are not diagnostic in stage 4 or 5 chronic kidney disease).

  • Urinary Cl < 20 mEq/L (< 20 mmol/L) indicates significant renal Cl reabsorption and hence a Cl-responsive cause (see table Causes of Metabolic Alkalosis)

  • Urinary Cl > 20 mEq/L (> 20 mmol/L) suggests a chloride-unresponsive form.

Urinary K and the presence or absence of hypertension help differentiate the chloride-unresponsive alkaloses.

  • Urinary K < 30 mEq/day (< 30 mmol/day) signifies hypokalemia or laxative misuse.

  • Urinary K > 30 mEq/day (> 30 mmol/day) in a patient without hypertension suggests diuretic abuse or Bartter syndrome or Gitelman syndrome.

  • Urinary K > 30 mEq/day (> 30 mmol/day) in a patient with hypertension requires evaluation for hyperaldosteronism, mineralocorticoid excess, and renovascular disease.

Tests in patients with hypertension typically include plasma renin activity and aldosterone and cortisol levels (see Diagnosis of Cushing Syndrome and Diagnosis of Primary Aldosteronism).

Treatment of Metabolic Alkalosis

  • Cause treated

  • IV 0.9% saline solution for chloride-responsive metabolic alkalosis

Underlying conditions are treated, with particular attention paid to correction of hypovolemia and hypokalemia.

Patients with chloride-responsive metabolic alkalosis are given 0.9% saline solution IV; infusion rate is typically 50 to 100 mL/hour greater than urinary and other sensible and insensible fluid losses until urinary Cl rises to > 25 mEq/L (> 25 mmol/L) and urinary pH normalizes after an initial rise from bicarbonaturia.

Patients with chloride-unresponsive metabolic alkalosis rarely benefit from rehydration alone.

Patients with severe metabolic alkalosis (eg, pH > 7.6) sometimes require more urgent correction of blood pH. Hemofiltration or hemodialysis3 excretion but may also accelerate urinary losses of K+ and phosphate (PO4); volume-overloaded patients with diuretic-induced metabolic alkalosis and those with posthypercapnic metabolic alkalosis may especially benefit.

In patients with severe metabolic alkalosis (pH > 7.6) and kidney failure who otherwise cannot or should not undergo dialysis, hydrochloric acid in a 0.1 to 0.2 normal solution IV is safe and effective but must be given through a central catheter because it is hyperosmotic and scleroses peripheral veins. Dosage is 0.1 to 0.2 mmol/kg/hour. Frequent monitoring of ABGs and electrolytes is needed.

Key Points

  • Metabolic alkalosis is bicarbonate (HCO3) accumulation due to acid loss, alkali administration, intracellular shift of hydrogen ion, or renal HCO3 retention.

  • The most common causes are volume depletion (particularly when involving loss of gastric acid and chloride (Cl) due to recurrent vomiting or nasogastric suction) and diuretic use.

  • Metabolic alkalosis involving loss or excess secretion of Cl is termed chloride-responsive.

  • Treat the cause and give patients with chloride-responsive metabolic alkalosis 0.9% saline IV.

  • Chloride-resistant metabolic alkalosis is due to increased aldosterone effect.

  • Treatment of chloride-resistant metabolic alkalosis involves correction of hyperaldosteronism.

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