Metabolic alkalosis results from loss of acid, retention of base, or renal mechanisms associated with decreased serum levels of potassium and chloride.
Loss of acid
Causes of critical acid loss include vomiting, nasogastric tube drainage or lavage without adequate electrolyte replacement, fistulas, and the use of steroids and certain diuretics (furosemide, thiazides, and ethacrynic acid).
Hyperadrenocorticism is another cause of severe acid loss. Cushing’s disease, primary hyperaldosteronism, and Bartter’s syndrome, for example, all lead to retention of sodium and chloride and urinary loss of potassium and hydrogen.
Retention of base
Excessive retention of base can result from excessive intake of bicarbonate of soda or other antacids (usually for treatment of gastritis or peptic ulcer), excessive intake of absorbable alkali (as in milk-alkali syndrome), administration of excessive amounts of I.V. fluids with high concentrations of bicarbonate or lactate, or respiratory insufficiency—all of which cause chronic hypercapnia from high levels of plasma bicarbonate.
Signs and symptoms
Signs and symptoms of metabolic alkalosis result from the body’s attempt to correct the acid-base imbalance, primarily through hypoventilation. Others include irritability, picking at bedclothes (carphology), twitching, confusion, nausea, vomiting, and diarrhea (which aggravates alkalosis).
Cardiovascular abnormalities—such as atrial tachycardia—and respiratory disturbances—such as cyanosis and apnea—also occur. In the alkalotic patient, diminished peripheral blood flow during repeated blood pressure checks may provoke carpopedal spasm in the hand—a possible sign of impending tetany (Trousseau’s sign). Uncorrected metabolic alkalosis may progress to seizures and coma.
A blood pH greater than 7.45 and a bicarbonate level above 29 mEq/L confirm the diagnosis. A partial pressure of carbon dioxide greater than 45 mm Hg indicates attempts at respiratory compensation. Serum electrolyte levels show a potassium level of 3.5 mEq/L and a chloride level of 98 mEq/L. Other characteristic findings include:
- urine pH of about 7 (usually)
- urinalysis revealing alkalinity after the renal compensatory mechanism begins to excrete bicarbonate
- electrocardiography that may show a low T wave merging with a P wave and atrial tachycardia.
The goal of treatment is to correct the underlying cause of metabolic alkalosis. Therapy for severe alkalosis may include cautious administration of ammonium chloride I.V. to release hydrogen chloride and restore the concentration of extracellular fluid and chloride levels.
Potassium chloride and normal saline solution (except in the presence of heart failure) are usually sufficient to replace losses from gastric drainage. Electrolyte replacement with potassium chloride and discontinuation of diuretics correct metabolic alkalosis resulting from potent diuretic therapy.