Causes
Metabolic alkalosis results from loss of acid or retention of base with decreased serum potassium and chloride. Causes include vomiting, nasogastric tube drainage or lavage without adequate electrolyte replacement, fistulas, steroids, diuretics, hyperadrenocorticism, and excessive intake of alkali (milk, baking soda, antacids).
Signs and Symptoms
Manifestations come from the body compensating, primarily through hypoventilation, and include irritability, picking at bedclothes (carphology), twitching, confusion, nausea, vomiting, diarrhea, and cardiovascular abnormalities such as atrial tachycardia.
Complications
Uncorrected metabolic alkalosis may progress to seizures and coma.
Laboratory Studies
A blood pH greater than 7.45 with bicarbonate above 29 mEq/L confirms metabolic alkalosis. Urinalysis usually shows a urine pH of about 7.0. ECG may show a low T wave merging with a U wave and atrial or sinus tachycardia.
Care Setting
This condition is a complication of a broader problem and may require inpatient care in a medical-surgical or subacute unit.
Related Concerns
Plans of care specific to predisposing factors, fluid and electrolyte imbalances, renal dialysis, respiratory acidosis (primary carbonic acid excess), and respiratory alkalosis (primary carbonic acid deficit).
Assessment
Circulation: tachycardia, irregularities or dysrhythmias, hypotension, cyanosis. Elimination: diarrhea (high chloride content), use of potassium-losing diuretics (Diuril, Hygroton, Lasix, Edecrin), laxative abuse. Food and fluid: anorexia, prolonged nausea and vomiting, high salt intake, excessive licorice ingestion, and recurrent indigestion or heartburn with frequent antacid or baking soda use. Neurosensory: tingling of fingers and toes, circumoral paresthesia, muscle twitching and weakness, dizziness, hypertonicity of muscles, tetany, tremors, convulsions, loss of reflexes, confusion, irritability, restlessness, belligerence, apathy, coma, and picking at bedclothes. Safety: recent transfusion of citrated blood. Respiration: hypoventilation (raises PCO2 and conserves carbonic acid) with periods of apnea. Teaching and learning: history of Cushing's syndrome or corticosteroid therapy.
Diagnostic Studies
Arterial pH is increased, higher than 7.45. Bicarbonate is increased, higher than 26 mEq/L (primary). PaCO2 is slightly increased, higher than 45 mm Hg (compensatory), and base excess is increased. Serum chloride is decreased, less than 98 mEq/L, disproportionately to serum sodium decreases if the alkalosis is hypochloremic. Serum potassium is decreased. Serum calcium is usually decreased; prolonged nonparathyroid hypercalcemia may be a predisposing factor. Urine pH is increased, higher than 7.0. Urine chloride less than 10 mEq/L suggests chloride-responsive alkalosis, while levels higher than 20 mEq/L suggest chloride resistance (StatPearls). ECG may show hypokalemic changes including peaked P waves, flat T waves, depressed ST segment, low T wave merging to P wave, and elevated U waves.
Priorities
Achieve homeostasis, prevent or minimize complications, and provide information about the condition, prognosis, and treatment needs.
Discharge Goals
Physiological balance restored, free of complications, condition and treatment needs understood, and a plan in place to meet needs after discharge.
Nursing Diagnosis
Possible nursing diagnoses for metabolic alkalosis include ineffective tissue perfusion, acute confusion, and risk for injury.
Nursing Interventions and Considerations
Dilute potassium when giving IV fluids containing potassium salts, monitor the infusion rate to prevent vessel damage, and watch for phlebitis. Watch for muscle weakness, tetany, or decreased activity. Monitor vital signs frequently and record intake and output to evaluate respiratory, fluid, and electrolyte status. Observe seizure precautions.
Frequently Asked Questions
What lab values confirm metabolic alkalosis? A blood pH above 7.45 with a serum bicarbonate above 26 to 29 mEq/L confirms it, often with a compensatory rise in PaCO2 above 45 mm Hg from hypoventilation (StatPearls).
What is the difference between chloride-responsive and chloride-resistant alkalosis? Urine chloride below 10 mEq/L points to chloride-responsive alkalosis, which corrects with isotonic saline and volume replacement. Urine chloride above 20 mEq/L points to chloride-resistant alkalosis, often tied to mineralocorticoid excess.
What are the most common causes? Loss of acid through vomiting or nasogastric suction without electrolyte replacement, potassium-losing diuretics, hyperadrenocorticism, and excessive alkali intake from antacids or baking soda.
Why does metabolic alkalosis cause neuromuscular symptoms? Alkalosis lowers ionized calcium, producing tingling, circumoral paresthesia, muscle twitching, tetany, and in severe cases seizures. Low potassium adds muscle weakness and dysrhythmia risk.
What are the priority nursing interventions? Replace fluid and electrolytes carefully, dilute IV potassium and watch the infusion site, monitor vital signs and intake and output, watch for tetany and dysrhythmias, and maintain seizure precautions.