Metabolic Alkalosis

Chapter: Metabolic Alkalosis
McMaster Section Editor(s): Christine M. Ribic, Karen C.Y. To
Section Editor(s) in Interna Szczeklika: Franciszek Kokot, Robert Drabczyk
McMaster Author(s): Karen C.Y. To
Author(s) in Interna Szczeklika: Franciszek Kokot, Edward Franek
Additional 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) Hypokalemia.

2) 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).

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

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 (see Standard Electrocardiogram), 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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