Metabolic Alkalosis Nursing Care Plan 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.
Metabolic alkalosis results from the loss of acid, retention of base with decreased serum levels of potassium and chloride. Other causes may include:
Nasogastric tube drainage or lavage without adequate electrolyte replacement
Use of diuretics
Excessive intake of alkali (i.e., milk, baking soda, antacid)
Signs and Symptoms
Manifestations of metabolic alkalosis result from the body’s attempt to correct the acid-base imbalance, primarily through hypoventilation. Other manifestations may include:
Picking at bedclothes (carphology)
Cardiovascular abnormalities (i.e., atrial tachycardia).
Uncorrected metabolic alkalosis may progress to seizures and coma.
CONFIRMING DIAGNOSIS: Blood pH level greater than 7.45 and bicarbonate levels above 29 mEq/L confirms Metabolic Alkalosis.
Urinalysis shows urine pH is usually about 7.0.
Electrocardiogram may show low T wave, merging with a U wave and atrial or sinus tachycardia.
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 sub-acute unit.
Plans of care specific to predisposing factor
Fluid and electrolyte imbalances
Respiratory acidosis (primary carbonic acid excess)
Respiratory alkalosis (primary carbonic acid deficit)
May exhibit: Tachycardia, irregularities/dysrhythmias
May report: Diarrhea (with high chloride content)
Use of potassium-losing diuretics (Diuril, Hygroton, Lasix, Edecrin)
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
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.
Provide information about condition/prognosis and treatment needs as appropriate.
Physiological balance restored.
Free of complications.
Condition, prognosis, and treatment needs understood.
Plan in place to meet needs after discharge.
The following are the possible nursing diagnosis for Respiratory Acidosis:
Ineffective Tissue Perfusion
Risk for Injury
Nursing Care Plan
Main Article: Metabolic Alkalosis Nursing Care Plan
Nursing Interventions & Considerations
Dilute potassium when giving via I.V. containing potassium salts. Monitor the infusion rate to prevent damage and watch out for signs of phlebitis.
Watch for signs of muscle weakness, tetany or decreased activity. Monitor vital signs frequently and record intake and output to evaluate respiratory, fluid and electrolyte status.
These are general interventions for patients with Metabolic Alkalosis.
- Display serum bicarbonate and electrolytes WNL.
- Be free of symptoms of imbalance, e.g., absence of neurological impairment/irritability.
|Monitor respiratory rate, rhythm, and depth.||Hypoventilation is a compensatory mechanism to conserve carbonic acid and represents definite risks to the individual (hypoxemia and respiratory failure).|
|Assess level of consciousness and neuromuscular status, strength, tone, movement; note presence of Chvostek’s or Trousseau’s signs.||The CNS may be hyperirritable (increased pH of CNS fluid), resulting in tingling, numbness, dizziness, restlessness, or apathy and confusion. Hypocalcemia may contribute to tetany (although occurrence is rare).|
|Monitor heart rate and rhythm.||Atrial and ventricular ectopic beats and tachy dysrhythmias may develop.|
|Record amount and source of output. Monitor intake and daily weight.||Helpful in identifying source of ion loss and potassium and HCl are lost in vomiting and GI suctioning.|
|Restrict oral intake and reduce noxious environmental stimuli; use intermittent and low suction during NG suctioning; irrigate gastric tube with isotonic solutions rather than water.||Limits gastric losses of HCl, potassium, and calcium.|
|Provide seizures and safety precautions as indicated. Pad side rails, protect the airway, put bed in low position and frequent observation.||Changes in mentation and CNS or neuromuscular hyperirritability may result in patient harm, especially if tetany or convulsions occur.|
|Encourage intake of foods and fluids high in potassium and possibly calcium (dependent on blood level), canned grapefruit and apple juices, bananas, cauliflower, dried peaches, figs, and wheat germ.||Useful in replacing potassium losses when oral intake permitted.|
|Review medication regimen for use of diuretics, such as thiazides (Diuril, Hygroton), furosemide (Lasix), and ethacrynic acid (Edecrin).||Discontinuation of these potassium-losing drugs may prevent recurrence of imbalance.|
|Instruct patient to avoid use of excessive amounts of sodium bicarbonate.||Ulcer patients can cause alkalosis by taking baking soda and milk of magnesia in addition to prescribed alkaline antacids.|
|Assist with identification and treatment of underlying disorder.||Addressing the primary condition (prolonged vomiting and/or diarrhea, hyper aldosteronism, Cushing’s syndrome) promotes correction of the acid-base disorder.|
|Monitor laboratory studies as indicated: ABGs/pH, serum electrolytes (especially potassium), and BUN.||Evaluates therapy needs and effectiveness and monitors renal function.|
|Administer medications as indicated:||Correcting sodium, water, and chloride defects may be all that is needed to permit kidneys to excrete bicarbonate and correct alkalosis, but must be used with caution in patients with HF or renal insufficiency.|
|Sodium chloride PO/Ringer’s solution IV unless contraindicated||Hypokalemia is frequently present. Chloride is needed so kidney can absorb sodium with chloride, enhancing excretion of bicarbonate.|
|Ammonium chloride or arginine hydrochloride||Although used only in severe cases, ammonium chloride may be given to increase amount of circulating hydrogen ions. Monitor administration closely to prevent too rapid a decrease in pH, hemolysis of RBCs. Note: May cause rebound metabolic acidosis and is usually contraindicated in patients with renal or hepatic failure.|
|Acetazolamide (Diamox)||A carbonic anhydrase inhibitor that increases renal excretion of bicarbonate.|
|Spironolactone (Aldactone)||Effective in treating chloride-resistant alkalosis, e.g., Cushing’s syndrome.|
|Avoid or limit use of sedatives or hypnotics.||If respirations are depressed, may cause hypoxia and respiratory failure.|
|Encourage fluids IV/PO.||Replaces extracellular fluid losses, and adequate hydration facilities removal of pulmonary secretions to improve ventilation.|
|Administer supplemental O2 as indicated and respiratory treatments to improve ventilation.||Respiratory compensation for metabolic alkalosis is hypoventilation, which may cause decreased Pao2 levels or hypoxia.|
|Prepare patient for and assist with dialysis as needed.||Useful when renal dysfunction prevents clearance of bicarbonate.|
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