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Metabolic alkalosis, presentation and treatment

Metabolic alkalosis, pathophysiology, presentation and treatmentMetabolic alkalosis is initiated by increased pH and HCO3−, which can result from loss of H+ via the gastrointestinal (GI) tract (eg, nasogastric suctioning, vomiting) or kidneys (eg, diuretics, Cushing syndrome) or from gain of bicarbonate (eg, 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.


• 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.


• Aim treatment at correcting the factor(s) responsible for maintaining the alkalosis and depends on whether the disorder is sodium chloride responsive or resistant.


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