21-19: Metabolic Alkalosis

ESSENTIALS OF DIAGNOSIS

GENERAL CONSIDERATIONS

Metabolic alkalosis is characterized by high serum HCO₃^– levels. The development of metabolic alkalosis requires its “generation” from loss of acid or gain of alkali, and its “maintenance” from the kidney’s inability to excrete excess bicarbonate.

The causes of metabolic alkalosis are classified into two groups based on chloride responsiveness and are generally distinguished using urine chloride values (Table 21–15). The compensatory increase in PCO₂ rarely exceeds 55 mm Hg; higher PCO₂ values imply a superimposed primary respiratory acidosis.

A. Chloride-Responsive Metabolic Alkalosis (U_Cl^– less than 20 mEq/L)

Chloride-responsive metabolic alkalosis involves the loss of chloride and extracellular volume. In vomiting and nasogastric suction, loss of acid (HCl) generates the alkalosis and volume contraction from chloride loss maintains the alkalosis. Distally acting diuretics that cause chloride loss, eg, loop and thiazide diuretics, are a common cause of metabolic alkalosis. U_Cl^– levels can be unreliable in these settings since these diuretics increase U_Cl^–. These disorders cause concurrent hypokalemia, which can exacerbate metabolic alkalosis by stimulating H⁺ secretion and ammoniagenesis. In respiratory acidosis, the kidneys compensate by increasing renal HCO₃^– retention, which causes volume expansion and hence NaCl excretion. If the hypercapnia is corrected rapidly, the kidneys will attempt to correct the alkalosis by excreting HCO₃^–; if sufficient Cl^– is unavailable, bicarbonaturia will halt and metabolic alkalosis will persist. This process has been termed posthypercapneic metabolic alkalosis.

In alkalosis, bicarbonaturia causes obligatory sodium excretion as the accompanying cation and U_Na levels are unreliable markers of extracellular volume.

B. Chloride-Unresponsive Alkalosis (U_Cl^– more than 20 mEq/L)

1. Excess mineralocorticoid ...