Metabolic alkalosis ammonium chloride

The pH-buffering of extracellular fluid depends in part on the carbon dioxide/ bicarbonate equilibrium so that the intake of sodium bicarbonate is followed by a brief alkalosis and an increased excretion of sodium carbonate in the urine. Depending on its carbonate concentration, the pH of the urine may rise to 8.07. Large doses (80—100 g/day) of sodium bicarbonate were needed if the pH of stomach contents was to be maintained at 4 or over in patients with duodenal ulcers8. Oxidation of organic anions in the body to carbon dioxide and water permits the use of sodium citrate, lactate or tartrate instead of sodium bicarbonate. In an analogous manner the ingestion of ammonium chloride induces a brief acidosis as a result of the metabolic conversion of ammonia to urea and lowers the pH of the urine. 

Ammonium chloride has a limited role in the treatment of metabolic alkalosis. The liver converts ammonium chloride to urea and free hydrochloric acid ... 

Ammonium chloride, an acid-forming salt (4 to 12 g p.o. daily), is indicated in metabolic alkalosis. In addition, as an acidifying agent, it has been used as an expectorant. 

Diuretic therapy is a common iatrogenic origin of metabolic disturbances of acid-base physiology. Diuretics are administered for their naturetic properties particularly in patients with cardiac, hepatic, pulmonary and renal disease, to rid the body of excess extracellular fluid. When the loss of sodium is matched by losses of other extracellular electrolytes in proportion to their extracellular concentrations, no disturbance of acid-base balance occurs. In cases where there is a disproportionate loss of bicarbonate, the result is metabolic acidosis. Conversely when there is an exaggeration of loss of ammonium or chloride ions by comparison with sodium, this leads to metabolic alkalosis. 

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