Abstract

The first step in the diagnosis of metabolic alkalosis is to determine the acid-base condition of the blood. This can be determined by looking at the arterial pH. Any value greater than 7.40 is considered alkalosis. The second step is to identify the primary cause of alkalosis. There are only two possibilities for alkalosis. Either the arterial PCO2 is decreased (respiratory alkalosis) or the plasma HCO3− is increased (metabolic alkalosis). Metabolic alkalosis is characterized by increased plasma HCO3− concentration and a compensatory increase in arterial PCO2. The next step is to determine the quantitative relationship between the change in the metabolic alkalosis and the change in the respiratory response. In an otherwise healthy individual with metabolic alkalosis, a 1 mEq/L increase in plasma HCO3− concentration should result in a 0.6 mmHg increase in arterial PCO2 (Δ PCO2 = 0.6 Δ HCO3−). If the patient’s blood gas agree with the predicated changes, a single disorder is most likely. If they do not, more than one disorder should be considered (mixed disorder). The next most important step is the determination of the cause of sustained metabolic alkalosis. The measurement of urinary chloride is useful in the differentiation between these disorders. The urinary chloride concentration is typically less than 15 mEq/L with hypovolemia and chloride depletion due to surreptitious vomiting or post diuretic therapy. In contrast, higher values are seen if the diuretic is still active, as in Bartter syndrome, Gitelman syndrome, severe hypokalemia, or primary aldosteronism.

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