21-20: Metabolic Alkalosis

GENERAL CONSIDERATIONS

Metabolic alkalosis is characterized by high HCO₃^–. Abnormalities that generate HCO₃^– are called “initiation factors,” whereas abnormalities that promote renal conservation of HCO₃^– are called “maintenance factors.” Thus, metabolic alkalosis may persist even after the initiation factors have resolved.

The causes of metabolic alkalosis are classified into two groups based on “saline responsiveness” using the urine Cl^– as a marker for volume status (Table 21–15). Saline-responsive metabolic alkalosis is a sign of extracellular volume contraction and is much more commonly encountered than saline-unresponsive alkalosis, which implies excessive total body bicarbonate with either euvolemia or hypervolemia. The compensatory increase in PCO₂ rarely exceeds 55 mm Hg; higher PCO₂ values imply a superimposed primary respiratory acidosis.

A. Saline-Responsive Metabolic Alkalosis

Saline-responsive alkalosis is characterized by normotensive extracellular volume contraction (contraction alkalosis) and hypokalemia. Hypotension and orthostasis may be seen. In vomiting or nasogastric suction, loss of acid (HCl) initiates the alkalosis, but volume contraction from Cl^– loss maintains the alkalosis (due to increased proximal reabsorption of NaHCO₃ and secondary hyperaldosteronsim). Renal Cl^– reabsorption is high, and urine Cl^– is low (less than 20 mEq/L). In alkalosis, bicarbonaturia may force Na⁺ excretion as the accompanying cation even if volume depletion is present, and urine Cl^– is preferred to urine Na⁺ as a measure of extracellular volume. Diuretics are a common cause of metabolic alkalosis, but in this setting, the utility of urine Cl^– to assess volume is limited.

Metabolic alkalosis is generally associated with hypokalemia due to the direct effect of alkalosis on renal potassium excretion and secondary hyperaldosteronism from volume depletion. Hypokalemia exacerbates the metabolic alkalosis by increasing bicarbonate reabsorption in the ...