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  • High HCO3 with alkalemia.

  • Evaluate effective circulating volume by physical examination.

  • Urinary chloride concentration differentiates saline-responsive alkalosis from saline-unresponsive alkalosis.


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.

Table 21–15.Metabolic alkalosis.

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 ...

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