endocrine and metabolic disorders
Metabolic Alkalosis
Etiology of Metabolic Alkalosis
Metabolic alkalosis is bicarbonate (HCO3−) accumulation due to Acid loss Alkali administration —as occurs in Hypokalemia ) Renal HCO3−retention Regardless of initial cause, persistence of metabolic alkalosis indicates that the kidneys have increased their HCO3−reabsorption, because HCO3−is normally freely filtered by the kidneys and hence excreted. Volume depletion and hypokalemia are the most common stimuli for increased HCO3−reabsorption, but any condition that elevates aldosterone or mineralocorticoids (which enhance sodium [Na] reabsorption and potassium [K] and hydrogen ion [H+] excretion) can elevate HCO3−. Thus, hypokalemia is both a cause and a frequent consequence of metabolic alkalosis. Themost common causesof metabolic alkalosis are Diuretic use Volume depletion (particularly when involving loss of gastric acid and chloride [Cl] due to recurrent vomiting or nasogastric suction) Among otherare disorders that cause Bicarbonate excess Renal acid loss Metabolic alkalosis can be Chloride (Cl)-responsive: Involves loss or excess secretion of Cl; it typically corrects with IV administration of NaCl-containing fluid. Chloride-unresponsive: Does not correct with NaCl-containing fluids, and typically involves severe magnesium (Mg) and/or potassium (K) deficiency or mineralocorticoid excess. The 2 forms can coexist, eg, in patients with volume overload made hypokalemic by high-dose diuretics. 