The patient with metabolic alkalosis

Abstract

ABSTRACTMetabolic alkalosis defined by the increase of both plasma HCO3- level (>26 mmol/L) and blood arterial pH (>7.43) is quite frequent and usually accompanied by hypokalemia. Its pathogenesis requires both the generation of alkalosis and its maintenance. Generation may be due to excessive hydrogen ion loss by the gastrointestinal tract (e.g. vomiting) or by the kidney (e.g. use of loop diuretics) or may be due to exogenous base gain. Maintenance reflects the inability of the kidney to excrete the excess of bicarbonate because of hypovolemia, chloride depletion, hypokalemia, hyperaldosteronism, renal failure or a combination of these factors. The evaluation of volemic status and measurement of urinary Cl- and plasma levels of renin and aldosterone are crucial to identify the cause(s) of metabolic alkalosis. The cornerstone of treatment is the correction of existing depletions and the prevention of further losses. In vomiting-induced chloride depletion alkalosis, infusion of potassium chloride restores the excretion of bicarbonate by the kidney.