NCP Metabolic Alkalosis (Primary Base Bicarbonate Excess)

Metabolic alkalosis is characterized by a high pH (loss of hydrogen ions) and high plasma bicarbonate caused by excessive intake of sodium bicarbonate, loss of gastric/intestinal acid, renal excretion of hydrogen and chloride, prolonged hypercalcemia, hypokalemia, and hyperaldosteronism. Compensatory mechanisms include slow, shallow respirations to increase CO2 level and an increase of bicarbonate excretion and hydrogen reabsorption by the kidneys.


This condition does not occur in isolation but rather is a complication of a broader problem that may require inpatient care in a medical-surgical or subacute unit.


Plans of care specific to predisposing factors

Fluid and electrolyte imbalances

Renal dialysis

Respiratory acidosis (primary carbonic acid excess)

Respiratory alkalosis (primary carbonic acid deficit)

Patient Assessment Database (Dependent on Underlying Cause)


May exhibit: Tachycardia, irregularities/dysrhythmias




May report: Diarrhea (with high chloride content)

Use of potassium-losing diuretics (Diuril, Hygroton, Lasix, Edecrin)

Laxative abuse


May report: Anorexia, nausea/prolonged vomiting

High salt intake; excessive ingestion of licorice

Recurrent indigestion/heartburn with frequent use of antacids/baking soda


May report: Tingling of fingers and toes; circumoral paresthesia

Muscle twitching, weakness


May exhibit: Hypertonicity of muscles, tetany, tremors, convulsions, loss of reflexes

Confusion, irritability, restlessness, belligerence, apathy, coma

Picking at bedclothes


May report: Recent blood transfusions (citrated blood)


May exhibit: Hypoventilation (increases PCO2 and conserves carbonic acid), periods of apnea


History of Cushing’s syndrome; corticosteroid therapy

Discharge plan

DRG projected mean length of inpatient stay depends on underlying cause

May require change in therapy for underlying disease process/condition.

Refer to section at end of plan for postdischarge considerations.


Arterial pH: Increased, higher than 7.45.

Bicarbonate (HCO3): Increased, higher than 26 mEq/L (primary).

PaCO2: Slightly increased, higher than 45 mm Hg (compensatory).

Base excess: Increased.

Serum chloride: Decreased, less than 98 mEq/L, disproportionately to serum sodium decreases (if alkalosis is hypochloremia).

Serum potassium: Decreased.

Serum calcium: Usually decreased. Prolonged hypercalcemia (nonparathyroid) may be a predisposing factor.

Urine pH: Increased, higher than 7.0.

Urine chloride: Less than 10 mEq/L suggests chloride-responsive alkalosis, whereas levels higher than 20 mEq/L suggest chloride resistance.

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.


1. Achieve homeostasis.
2. Prevent/minimize complications.
3. Provide information about condition/prognosis and treatment needs as appropriate.


1. Physiological balance restored.
2. Free of complications.
3. Condition, prognosis, and treatment needs understood.
4. Plan in place to meet needs after discharge.

Because no current nursing diagnosis speaks clearly to metabolic imbalances, the following interventions are presented in a general format for inclusion in the primary plan of care.