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🌱 來自: Etiologies-of-Metabolic-Alkalosis

summary of metabolic alkalosis

• Metabolic alkalosis: Metabolic alkalosis, which produces an elevation of the serum bicarbonate, is a relatively frequent clinical problem that is most commonly generated by excess loss of hydrogen ions from the gastrointestinal tract or in the urine, and/or by hydrogen ion movement into cells (table 1). An increased serum bicarbonate concentration may also result from alkali administration or extracellular fluid volume contraction around a relatively constant amount of extracellular bicarbonate (called a “contraction alkalosis”). Most patients with preserved renal function and normal volume status will rapidly excrete excess bicarbonate in the urine. Thus, for metabolic alkalosis to persist, there must be a reduction in the kidney’s ability to excrete the excess bicarbonate into the urine. (See ‘Introduction’ above.)

• Intracellular shift of hydrogen: Metabolic alkalosis can result from the shift of hydrogen ions into cells. This most often occurs in patients with hypokalemia and potassium deficits. (See ‘Intracellular shift of hydrogen’ above.)

• Gastrointestinal hydrogen loss: Gastrointestinal hydrogen loss can result from the removal of gastric secretions (vomiting or nasogastric suction) or, rarely, from the loss of acid-rich stool as in congenital chloridorrhea and villous adenoma. (See ‘Gastrointestinal hydrogen loss’ above.)

• Excessive renal hydrogen loss: An increase in renal acid excretion is usually due to sodium and water delivery to the distal nephron combined with increased mineralocorticoid activity. This occurs with primary mineralocorticoid excess, use of loop or thiazide diuretics, Bartter and Gitelman syndromes, and, to a lesser extent, with hypercalcemia due to the milk (or calcium)-alkali syndrome. (See ‘Excessive renal hydrogen loss’ above and ‘Primary mineralocorticoid excess’ above and ‘Loop or thiazide diuretics’ above and ‘Bartter and Gitelman syndromes’ above and ‘Hypercalcemia and the milk (or calcium)-alkali syndrome’ above.)

• Pendred syndrome: Individuals with Pendred syndrome may develop severe metabolic alkalosis if treated with a thiazide diuretic. (See ‘Pendred syndrome’ above.)

• Posthypercapnic alkalosis: Chronic respiratory acidosis should generate an appropriate increase in renal hydrogen secretion and bicarbonate reabsorption. The ensuing increase in the plasma bicarbonate concentration will raise the arterial pH toward normal. If the chronically elevated PCO2 is rapidly lowered, usually by mechanical ventilation, the plasma bicarbonate concentration may remain elevated, producing a posthypercapnic alkalosis. (See ‘Posthypercapnic alkalosis’ above.)

• Alkali administration: Alkali loads administered to a patient with an impaired renal capacity to excrete the bicarbonate (due to low effective arterial blood volume, chloride depletion, hypokalemia, or intrinsic renal disease) may produce metabolic alkalosis. The rapid administration of large alkali loads can cause short-term metabolic alkalosis. (See ‘Alkali administration’ above.)

• Contraction alkalosis: A contraction alkalosis occurs when there is loss of large volumes of fluids containing high concentrations of sodium chloride but relatively low concentrations of bicarbonate. The plasma bicarbonate concentration rises in this setting because there is contraction of the extracellular volume around a relatively constant quantity of extracellular bicarbonate. (See ‘Contraction alkalosis’ above.)