Metabolic Alkalosis

How to Cite This Chapter: To KCY, Kokot F, Franek E. Metabolic Alkalosis. McMaster Textbook of Internal Medicine. Kraków: Medycyna Praktyczna. Accessed March 03, 2021.
Last Updated: June 13, 2018
Last Reviewed: May 17, 2019
Chapter Information

Definition, Etiology, PathogenesisTop

Metabolic alkalosis is defined as an increase in blood pH to >7.45 due to a primary increase in the concentration of bicarbonate [HCO3] or other bases, or due to loss of H+.


1) Excessive loss of H+ or Cl through the gastrointestinal tract (vomiting, gastric suction, congenital chloride diarrhea), with urine (diuretics), and through the skin (cystic fibrosis).

2) Excessive intake of bases or potential bases: NaHCO3, sodium citrate or lactate, or calcium carbonate; posthypercapnic alkalosis.

3) Severe hypokalemia.

Metabolic alkalosis may result from the primary loss of H+, Cl, or K+, or from a shift of K+ from the extracellular to the intracellular compartment, which leads to hypokalemia.

Clinical Features and DiagnosisTop

Clinical manifestations depend on the underlying condition. Hypokalemia, depending on its severity, may manifest as muscle weakness and arrhythmia, while alkalosis may manifest as signs and symptoms of tetany or its equivalents (see Hypocalcemia).

Diagnostic criteria of metabolic alkalosis include pH >7.45, increase in [HCO3], increase in the partial pressure of carbon dioxide in arterial blood (PaCO2) (as a compensatory mechanism), and often hypokalemia.

Differential diagnosis of compensated metabolic alkalosis (with a normal pH) should include compensated respiratory acidosis (features of respiratory failure are present).


1. Treatment of the underlying condition is the mainstay of the management of metabolic alkalosis.

2. In patients with hypokalemia, correct potassium deficiency using KCl (see Hypokalemia).

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