Mechanism of Chloride Deficit in the Maintenance of Metabolic Alkalosis

Accessible online at: www.karger.com/journals/nef Metabolic alkalosis can be classified into two broad categories: chloride-responsive and chloride-resistant. Chloride-responsive metabolic alkalosis is characterized by reduced extracellular volume and can be corrected by administration of a chloride-containing solution, whereas chloride-resistant metabolic alkalosis is characterized by normal or expanded extracellular volume and, with some exceptions1, is not corrected by chloride administration. The term chloride depletion metabolic alkalosis has also been used to describe chloride-responsive alkalosis in order to emphasize the perceived pathogenetic role of chloride depletion. This discussion deals with the role played by chloride deficit in the maintenance of metabolic alkalosis and chloride replacement in its reversal. A typical clinical example of chloride depletion metabolic alkalosis is that due to vomiting or nasogastric suction. All observers agree that metabolic alkalosis of this type can be corrected readily by administration of NaCl or KCl [1–5]. Controversy exists, however, regarding the mechanism by which chloride administration corrects metabolic alkalosis. One school of thought (the volume school) attributes correction of metabolic alkalosis to the increased excretion of bicarbonate that follows the expansion of extracellular volume [6–8]. The other position (the