Metabolic alkalosis is the most common acid-base disorder, typically developing after hospitalization in critically ill patients, but it is not most frequently present upon admission, unlike metabolic acidosis [1, 2].

Metabolic alkalosis is a primary acid-base disorder characterized by an increase in serum HCO3 (>26 mEq/L), a high pH (>7.45), and a compensatory increase in PaCO2 due to alveolar hypoventilation. Hypochloremia and hypokalemia are commonly encountered electrolyte imbalances in metabolic alkalosis.

Respiratory compensation: Hypoventilation, which occurs as a respiratory compensation in metabolic alkalosis, is a relatively slow process compared to the hyperventilation response that occurs in metabolic acidosis. Hypoventilation-induced hypoxia is a limiting factor for compensatory mechanisms in metabolic alkalosis because severe hypoxia (PO2 <60 mm Hg) is a potent stimulus to increase alveolar ventilation, offsetting this protective respiratory response.

Comparison with chronic respiratory acidosis: Increased HCO3 and increased PaCO2 are also features of chronic respiratory acidosis, but the differentiating feature is a low pH.

For a proper understanding of the pathogenesis of metabolic alkalosis, it is important to know the two distinct phases involved in sustaining metabolic alkalosis: 1. Generation of metabolic alkalosis and 2. Maintenance of metabolic alkalosis, as summarized in Table 32.1.

Mechanisms leading to the primary increase in plasma HCO3 can involve one or more of the following:

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