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.
CARE SETTING
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.
RELATED CONCERNS
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)
CIRCULATION
May exhibit: Tachycardia, irregularities/dysrhythmias
Hypotension
Cyanosis
ELIMINATION
May report: Diarrhea (with high chloride content)
Use of potassium-losing diuretics (Diuril, Hygroton, Lasix, Edecrin)
Laxative abuse
FOOD/FLUID
May report: Anorexia, nausea/prolonged vomiting
High salt intake; excessive ingestion of licorice
Recurrent indigestion/heartburn with frequent use of antacids/baking soda
NEUROSENSORY
May report: Tingling of fingers and toes; circumoral paresthesia
Muscle twitching, weakness
Dizziness
May exhibit: Hypertonicity of muscles, tetany, tremors, convulsions, loss of reflexes
Confusion, irritability, restlessness, belligerence, apathy, coma
Picking at bedclothes
SAFETY
May report: Recent blood transfusions (citrated blood)
RESPIRATION
May exhibit: Hypoventilation (increases PCO2 and conserves carbonic acid), periods of apnea
TEACHING/LEARNING
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.
DIAGNOSTIC STUDIES
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.
NURSING PRIORITIES
1. Achieve homeostasis.
2. Prevent/minimize complications.
3. Provide information about condition/prognosis and treatment needs as appropriate.
DISCHARGE GOALS
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.
CARE SETTING
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.
RELATED CONCERNS
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)
CIRCULATION
May exhibit: Tachycardia, irregularities/dysrhythmias
Hypotension
Cyanosis
ELIMINATION
May report: Diarrhea (with high chloride content)
Use of potassium-losing diuretics (Diuril, Hygroton, Lasix, Edecrin)
Laxative abuse
FOOD/FLUID
May report: Anorexia, nausea/prolonged vomiting
High salt intake; excessive ingestion of licorice
Recurrent indigestion/heartburn with frequent use of antacids/baking soda
NEUROSENSORY
May report: Tingling of fingers and toes; circumoral paresthesia
Muscle twitching, weakness
Dizziness
May exhibit: Hypertonicity of muscles, tetany, tremors, convulsions, loss of reflexes
Confusion, irritability, restlessness, belligerence, apathy, coma
Picking at bedclothes
SAFETY
May report: Recent blood transfusions (citrated blood)
RESPIRATION
May exhibit: Hypoventilation (increases PCO2 and conserves carbonic acid), periods of apnea
TEACHING/LEARNING
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.
DIAGNOSTIC STUDIES
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.
NURSING PRIORITIES
1. Achieve homeostasis.
2. Prevent/minimize complications.
3. Provide information about condition/prognosis and treatment needs as appropriate.
DISCHARGE GOALS
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.
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