Metabolic Alkalosis
Not yet clinically reviewed
This protocol was migrated from the earlier Pharmapedia and Ward Guide apps for educational use. Follow your hospital's own policies and consult seniors when in doubt.
Introduction
Metabolic alkalosis is initiated by increased pH and HCO3 −, which can result from loss of H+ via the gastrointestinal (GI) tract (e.g., nasogastric suctioning, vomiting) or kidneys (e.g., diuretics, Cushing syndrome) or from gain of bicarbonate (e.g., administration of bicarbonate, acetate, lactate, or citrate).
- Metabolic alkalosis is maintained by abnormal renal function that prevents the kidneys from excreting excess bicarbonate.
- The respiratory response is to increase Paco2 by hypoventilation.
Clinical Presentation
No unique signs or symptoms are associated with mild to moderate metabolic alkalosis. Some patients complain of symptoms related to the underlying disorder (e.g., muscle weakness with hypokalemia or postural dizziness with volume depletion) or have a history of vomiting, gastric drainage, or diuretic use.
- Severe alkalemia (pH >7.60) can be associated with cardiac arrhythmias and neuromuscular irritability.
Treatment
Aim treatment at correcting the factor(s) responsible for maintaining the alkalosis and depends on whether the disorder is sodium chloride responsive or resistant.