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As an example, administration of intravenous loop diuretics to induce rapid fluid removal in a markedly edematous patient often generates a metabolic alkalosis. The etiology of this metabolic alkalosis is multifactorial and includes stimulation of distal tubule hydrogen ion secretion and hypokalemia-related acid-base effects, but one component of the alkalosis is contraction [18,37]. Other disorders in which contraction alkalosis may be a major contributor to the acid-base derangement include sweat losses in cystic fibrosis, congenital chloride diarrhea, and, possibly, the loss of gastric secretions in patients with achlorhydria [10,38-40]. (See "Approach to chronic diarrhea in neonates and young infants (<6 months)", section on 'Evaluation for suspected congenital diarrheas and enteropathies'.)
Although contraction of the extracellular volume can, by itself, theoretically raise the serum bicarbonate, the pathophysiology of the alkalosis in disorders associated with a contraction alkalosis is always multifactorial and complicated. In addition to contraction alkalosis, such patients often have renal bicarbonate generation due to elevated aldosterone levels, combined with generous distal tubule salt and water delivery. Hypokalemia also frequently contributes to accelerated renal bicarbonate generation and/or reduced renal bicarbonate excretory capacity. The glomerular filtration rate is almost invariably reduced, and this also restricts the ability to excrete bicarbonate.
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