Acid-Base Imbalances: Metabolic Acidosis and Alkalosis; Respiratory Acidosis and Alkalosis

The hydrogen ion concentration ([H⁺]) of the body, described as the pH or negative log of the [H⁺], is maintained in a narrow range to promote health and homeostasis. The body has many regulatory mechanisms that counteract even a slight deviation from normal pH. An acid-base imbalance can alter many physiological processes and lead to serious problems or, if left untreated, to coma and death. A pH below 7.35 is considered acidosis and above 7.45 is alkalosis. Alterations in hydrogen ion concentration can be metabolic or respiratory in origin or they may have a mixed origin.

Metabolic acidosis results from any nonpulmonary condition that leads to an excess of acids as compared to bases and can have long-term consequences. For example, damaged kidneys in patients with renal failure lead to decreased acid excretion and chronic acidemia. Skeletal problems then occur as calcium and phosphate are released from bone to help with the buffering of acids. Loss of bicarbonate in patients with severe diarrhea or with gastrointestinal fistulae can also lead to metabolic acidosis. Metabolic alkalosis results from any nonpulmonary condition that leads to an excess of bases over acids. Metabolic alkalosis results from one of two mechanisms: loss of acids or excess of bases. Prolonged vomiting, hyperaldosteronism, and diuretic therapy lead to loss of acids. Patients with a history of heart failure and hypertension who are on sodium-restricted diets and diuretics may develop metabolic alkalosis from increased urinary acid secretion. Ingestion or infusion of bases such as sodium bicarbonate can also lead to metabolic alkalosis.

Respiratory acidosis is a pH imbalance that results from alveolar hypoventilation and an accumulation of carbon dioxide. It can be classified as either acute or chronic. Acute respiratory acidosis is associated with a sudden failure in ventilation, such as conditions like obstructive sleep apnea and pneumothorax. Chronic respiratory acidosis is seen in patients with chronic pulmonary disease in whom long-term hypoventilation results in a chronic elevation (> 45 mm Hg) of Paco₂ levels (hypercapnia), which renders the primary mechanism of inspiration, an elevated Paco₂, unreliable. The major drive for respiration in patients with chronic pulmonary disease then becomes a low oxygen level (hypoxemia). Respiratory alkalosis is a pH imbalance that results from the excessive loss of carbon dioxide through hyperventilation (Paco₂< 35 mm Hg). Respiratory alkalosis is the most frequently occurring acid-base imbalance of hospitalized patients. When the central respiratory center is stimulated by anxiety, pain, or fever, respiratory alkalosis may occur. Improper use of mechanical ventilators with a rapid respiratory rate per minute can cause iatrogenic respiratory alkalosis, whereas secondary respiratory alkalosis may develop from hyperventilation stimulated by metabolic or respiratory acidosis. Patients with respiratory alkalosis are at risk for hypokalemia, hypocalcemia, and hypophosphatemia.

Causes ⬆ ⬇

See Table 1.

Table 1 Common Causes of Acid-Base Disorders

ACID-BASE DISORDER		COMMON CAUSES
Metabolic acidosis		Decreased acid excretion: chronic renal disease results in decreased acid excretion and is the most common cause of chronic metabolic acidosis
		Excessive acid production: oxygen tissue deprivation with shock and cardiopulmonary arrest, vigorous exercise (transient), prolonged periods of fever, ketoacidosis in insulin-dependent diabetics, alcoholic ketoacidosis, and ingestion of drugs and chemicals (methanol, ethylene glycol, aspirin)
		Underproduction of bicarbonate: pancreatitis
		Excessive loss of bicarbonate: severe diarrhea; intestinal obstruction; small bowel, pancreatic, ileostomy, or biliary fistula drainage
		Hyperchloremic acidosis, an increase in the extracellular concentration of chloride, also promotes bicarbonate loss
Metabolic alkalosis		Most common: vomiting and nasogastric (NG) suction
		Other: ingestion of bicarbonates, carbonates, acetates, citrates, and lactates found in total parenteral nutrition solutions, Ringer lactate, and sodium bicarbonate administration; rapid administration of stored blood and volume expanders with high citrate and acetate levels; excessive intake of antacids, which are composed of sodium bicarbonate or calcium carbonate; loss of acids (gastric fluid loss, diuretic therapy, excessive mineralocorticoid release); hypercalcemia; diuretic therapy; aldosterone excess
Respiratory acidosis		Depression of respiratory center in the medulla: head injury, drug ingestion (anesthetics, opiates, barbiturates, ethanol)
		Decreased amount of functioning lung tissue: bronchial asthma, chronic bronchitis, emphysema, pneumonia, hemothorax, pneumothorax, pulmonary edema
		Airway obstruction: foreign body aspiration, obstructive sleep apnea, bronchospasm, laryngospasm
		Disorders of the chest wall: flail chest, impaired diaphragm movement (pain, splinting, chest burns, tight chest or abdominal dressings)
		Abdominal distention: obesity, ascites, bowel obstruction
		Disorders of respiratory muscles: severe hypokalemia, amyotrophic lateral sclerosis, Guillain-Barré syndrome, poliomyelitis, myasthenia gravis, drugs (curare, succinylcholine)
Respiratory alkalosis		Hyperventilation due to hypoxemia (a decrease in the oxygen content of blood) or improper ventilator settings: anemia; hypotension; high altitudes; and pulmonary disease, such as pneumonia, interstitial lung disease, pulmonary vascular disease, and acute asthma
		Direct stimulation of the central respiratory center: anxiety, pain, fever, sepsis, salicylate ingestion, head trauma, central nervous system (CNS) disease (inflammation, lesions)
Examples of mixed disorders		Respiratory acidosis and metabolic alkalosis: chronic obstructive pulmonary disease (COPD) produces chronically elevated Paco₂ levels and high HCO₃ levels as a compensatory mechanism. If the chronically elevated Paco₂ is rapidly decreased, as it would be with aggressive mechanical ventilation, HCO₃ levels remain elevated, causing metabolic alkalosis.
		Respiratory alkalosis and metabolic acidosis: salicylate ingestion directly stimulates the respiratory center, resulting in an increased rate and depth of breathing; ingestion of large amounts of salicylates can also produce metabolic acidosis; respiratory alkalosis results from the “blowing off” of CO₂

Genetic Considerations ⬆ ⬇

A number of inherited disorders can result in acid-base imbalances. Bartter syndrome (a group of several disorders of impaired salt reabsorption in the thick ascending loop of Henle) results in metabolic alkalosis along with hypokalemia and hyperaldosteronism. Bartter syndrome is inherited in an autosomal recessive pattern. Liddle syndrome is inherited in an autosomal dominant pattern and results in metabolic alkalosis due to dysregulation of the epithelial sodium channel. Metabolic acidosis is often seen with inborn errors of metabolism, such as Gaucher disease (autosomal recessive transmission) or from mutations in the pyruvate dehydrogenase complex genes (autosomal recessive or X-linked inheritance).

Sex and Life Span Considerations ⬆ ⬇

Metabolic acidosis occurs primarily in patients with insulin-dependent diabetes mellitus (IDDM) and chronic renal failure regardless of age. Metabolic acidosis from severe diarrhea can occur at any age, but children and older adults are at greater risk because of associated fluid imbalances. Young people are at an increased risk of metabolic acidosis because of popular fad diets that lead to starvation.

Metabolic alkalosis is a common disorder of adult hospitalized patients. Older patients are at risk for metabolic alkalosis because of their delicate fluid and electrolyte status. Young people who practice self-induced vomiting to lose weight are also at risk for developing metabolic alkalosis. Finally, middle-aged people with chronic hypercapnia respiratory failure are at risk for metabolic alkalosis if their Paco₂ levels are rapidly decreased with mechanical ventilation, corticosteroids, or antacids.

Patients of all ages are at risk for acute respiratory acidosis when an injury or illness results in alveolar hypoventilation. Older adults are at high risk for electrolyte and fluid imbalances, which can lead to respiratory depression. Patients with COPD are at highest risk for chronic respiratory acidosis. The typical COPD patient is a middle-aged man with a history of smoking. Older children and adults are at risk for respiratory alkalosis with large-dose salicylate ingestion. Older adults are at an increased risk for respiratory alkalosis because of the high incidence of pulmonary disorders, specifically pneumonia, in their population. Identification of respiratory alkalosis may be more difficult in older patients because the early symptoms of increased respirations and altered neurological status may be attributed to other disease processes.

Health Disparities and Sexual/Gender Minority Health ⬆ ⬇

Ethnicity, race, and sexual/gender minority status have no known effect on the risk for acid-base imbalance.

Global Health Considerations ⬆ ⬇

No data are available.

Assessment ⬆ ⬇

ASSESSMENT

History

Metabolic Acidosis

Establish a history of renal disease, IDDM, or hepatic or pancreatic disease. Determine if the patient has experienced seizure activity, starvation, shock, acid ingestion, diarrhea, nausea, vomiting, anorexia, or abdominal pain or dehydration. Ask if the patient has experienced dyspnea with activity or at rest, as well as weakness, fatigue, headache, or confusion.

Metabolic Alkalosis

Establish a history of prolonged vomiting, NG suctioning, hypercalcemia, hypokalemia, or hyperaldosteronism. Determine if the patient has been taking thiazide diuretics, has been receiving potassium-free IV infusions, eats large quantities of licorice, or regularly uses nasal sprays. Elicit a history of lightheadedness; agitation; muscle weakness, cramping, and twitching or tingling; or circumoral (around the mouth) paresthesia. Ask the patient if they have experienced anorexia, nausea, or vomiting.

Respiratory Acidosis

Establish a history of impaired ventilation or breathlessness. The initial manifestations of respiratory acidosis involve changes in a patient's behavior. Investigate early signs of confusion, impaired judgment, lack of motor coordination, and restlessness. Determine if the patient has experienced headache, lethargy, blurred vision, confusion, or nausea.

Respiratory Alkalosis

Establish a history of hyperventilation from anxiety or mechanical overventilation. Early manifestations involve changes in neurological and neuromuscular status due to decreased Paco₂ levels (hypocapnia), which may lead to decreased cerebral perfusion. Determine if the patient has experienced lightheadedness, anxiety, inability to concentrate, or confusion. Elicit a patient history of muscle cramps, spasms, tingling (paresthesia) of the extremities, and circumoral numbness. Other possible symptoms are nausea and vomiting, caused by a low potassium level.

Physical Examination

Metabolic Acidosis

Inspect the patient's skin, noting if it feels warm. Note a flushed appearance. Assess the patient's breathing pattern for Kussmaul breathing, a compensatory mechanism that the body uses to attempt to balance the pH by blowing off carbon dioxide. Check for an increased heart rate caused by stimulation of the sympathetic nervous system. To detect changes in cardiac performance, use a cardiac monitor for patients with a pH less than 7 and a potassium level greater than 5 mEq/L. Assess for changes in heart rate, ventricular ectopics, T-wave configuration, QRS, and PR intervals. Include neurological status checks at least every 4 hours or more frequently if the patient is confused or lethargic.

Metabolic Alkalosis

The patient with metabolic alkalosis demonstrates signs associated with the accompanying electrolyte imbalances. If hypocalcemia is present, the patient may demonstrate positive Chvosteks and Trousseau signs (see Hypocalcemia, p. 614). Hypocalcemia and hypokalemia affect muscle strength and irritability. Assess the strength of the patient's hand grasps. Observe the patient's gait for unsteadiness, and note the presence of any hyperactive reflexes, such as spasms and seizures. Observe the patient's breathing patterns for a compensatory decrease in the rate and depth of breathing. Use continuous cardiac monitoring, and check for an increased heart rate or ventricular dysrhythmias. Assess the patient for atrial tachycardias, ventricular dysrhythmias, and a prolonged QT interval.

Respiratory Acidosis

Assess the patient for an increased heart rate. As Pao₂ decreases and Paco₂ increases, the sympathetic nervous system is stimulated, resulting in a release of catecholamines, epinephrine, and norepinephrine, which causes an increase in heart rate and cardiac output. Note cardiovascular abnormalities, such as tachycardia, hypertension, and atrial and ventricular dysrhythmias. During periods of acute respiratory acidosis, monitor the cardiac rhythm continuously. Take the patient's pulse, noting a bounding quality that may occur with hypercapnia. If the cause of the respiratory acidosis is respiratory center depression or respiratory muscle paralysis, respirations are slow and shallow. As respiratory acidosis worsens and respiratory muscles fail, the rate of respirations decreases.

Respiratory Alkalosis

The hallmark sign of respiratory alkalosis is hyperventilation; the patient may be taking 40 or more respirations per minute and may manifest a breathing pattern that is reminiscent of Kussmaul breathing caused by diabetic acidosis. Check the patient for an increased heart rate caused by hypoxemia. Test the patient's hand grasps for signs of weakness. Observe the patient's gait for unsteadiness, and note any indications of hyperactive reflexes such as spasms, tetany, and seizures. The presence of a positive Chvostek or Trousseau sign may indicate hypocalcemia (see Hypocalcemia, p. 614), which may occur from lower amounts of ionized calcium during periods of alkalosis.

Psychosocial

Acid-base imbalances frequently affect patients with both acute and chronic illnesses. Their response to yet another problem is at best unpredictable. Neurological changes such as confusion, agitation, or psychosis are upsetting if they occur, as are electrolyte disturbances. Anticipate the patient feeling powerless and plan care to support all psychological needs.

Diagnostic Highlights

Test	Normal Result	Abnormality With Condition	Explanation
Arterial blood gases (ABGs)	pH 7.35–7.45; Pao₂ 80–100 mm Hg; Paco₂ 35–45 mm Hg; SaO₂> 95%; HCO₃ 22–26 mEq/L	Metabolic acidosis: pH < 7.35; HCO₃< 22 mEq/L; metabolic alkalosis: pH > 7.45; HCO₃> 26 mEq/L; respiratory acidosis: pH < 7.35; Paco₂> 45 mm Hg; respiratory alkalosis: pH > 7.45; Paco₂< 35 mm Hg	Hydrogen ion concentration varies based on condition

Other Tests: Electrocardiogram; serum electrolyte levels (sodium, chloride, calcium, potassium, magnesium); glucose; lactate; total protein; blood urea nitrogen; creatinine; urine pH

Primary Nursing Diagnosis ⬆ ⬇

Diagnosis

DiagnosisRisk for electrolyte imbalance as evidenced by compromised pulmonary and/or renal function

Outcomes

OutcomesMetabolic acidosis severity; Metabolic alkalosis severity; Metabolic function; Acute respiratory acidosis severity; Acute respiratory alkalosis severity; Respiratory status; Electrolyte & acid/base balance; Electrolyte balance

Interventions

InterventionsAcid-base management: Metabolic acidosis, Metabolic alkalosis, Respiratory acidosis, Respiratory alkalosis; Acid-base monitoring; Electrolyte monitoring

Planning and Implementation ⬆ ⬇

PLANNING AND IMPLEMENTATION

Collaborative

General

The highest priority for all patients with acid-base imbalances is to maintain the adequacy of airway, breathing, and circulation. An important focus for collaborative treatment is to deliver oxygen, remove carbon dioxide, and monitor gas exchange. Treatment is focused on correcting the cause and restoring fluids and electrolytes to a normal range. Provide constant cardiac monitoring for patients with hypokalemia, hypocalcemia, and hypomagnesemia. Consult with a dietitian to provide foods that can help restore electrolyte balance and increase oral intake. If a patient demonstrates impaired physical mobility, consult a physical therapist to evaluate the patient's abilities and to recommend needed strengthening exercises and assist devices.

Metabolic Acidosis

Sodium bicarbonate may be administered to treat normal anion gap metabolic acidosis, but it is controversial in treating increased anion gap metabolic acidosis. Research has shown that administering sodium bicarbonate may inhibit hemoglobin release of oxygen to the tissues, thus increasing the acidosis. Sodium bicarbonate is recommended if the pH is greatly reduced (< 7.1). Sodium bicarbonate may be administered by IV drip or by IV push. Overmedication of sodium bicarbonate may cause metabolic alkalosis, fluid volume overload, hypokalemia, and worsened acidosis. Potassium-sparing diuretics, amphotericin B, and large quantities of isotonic saline solutions should not be administered to patients with suspected renal failure. These drugs may contribute to the development of metabolic acidosis.

Metabolic Alkalosis

Pharmacologic therapy may include IV saline solutions, potassium supplements, histamine antagonists, and carbonic anhydrase inhibitors. IV saline solutions (0.9% or 0.45%) may be used to replace lost volume and chloride ions. Causes of metabolic alkalosis that respond favorably to saline therapy include vomiting, NG suctioning, postchronic hypercapnia, and diuretic therapy. The causes of metabolic alkalosis that do not respond favorably to the administration of saline include hypokalemia and mineralocorticoid excess. Potassium chloride is used to treat hypokalemia in a patient with metabolic alkalosis. Dietary supplements of potassium are not effective unless chloride levels are stabilized.

Histamine H₂ receptor antagonists, particularly cimetidine and ranitidine, reduce the production of hydrochloric acid in the stomach and may prevent the occurrence of metabolic alkalosis in patients with NG suctioning and vomiting. In severe cases of metabolic alkalosis (pH > 7.55), IV hydrochloric acid may be indicated.

The carbonic anhydrase inhibitor acetazolamide (Diamox) is useful for correcting metabolic alkalosis in patients with congestive heart failure who cannot tolerate fluid volume administration. Acetazolamide promotes the renal excretion of bicarbonate. Severe metabolic alkalosis may require the administration of weak acid solutions. Because acetazolamide promotes the excretion of potassium, it is not given until serum potassium levels are evaluated as safe.

Potassium-sparing diuretics, such as spironolactone, may be used if diuretics are needed. Anticonvulsants are usually not needed because the risk for seizures decreases as fluid and electrolyte imbalances are corrected.

Respiratory Acidosis

Although oxygen therapy is required to treat the hypoxemia that accompanies respiratory acidosis, a fraction of inspired air (Fio₂) of less than 0.40 is desirable. Oxygen concentrations greater than 0.80 are toxic to the lung over a 5- to 6-day time period. Caution: The use of oxygen for patients with COPD and hypercapnia may remove the stimulus for respiration and result in respiratory depression. If the Paco₂ is greater than 60 mm Hg or the Pao₂ is less than 50 mm Hg with high levels of supplemental oxygen, intubation and mechanical ventilation are required. Pharmacologic therapy for respiratory acidosis depends on the cause and severity of acidosis. The administration of sodium bicarbonate is controversial for a pH greater than 7.0. If the pH is below 7.0, sodium bicarbonate administration is recommended. Bronchodilators may be used to decrease bronchospasms. Antibiotics are prescribed for respiratory infections, but sedatives that depress respirations are limited.

Respiratory Alkalosis

Because the most common cause of respiratory alkalosis is anxiety, reassurance and sedation may be all that are needed. Pharmacologic therapy most likely includes the administration of antianxiety medications and potassium supplements. Benzodiazepines, commonly used to control acute anxiety attacks, are administered intramuscularly or intravenously. If the anxiety is more severe and the respiratory alkalosis is pronounced, rebreathing small amounts of exhaled air with a paper bag or a rebreather mask helps increase arterial Paco₂ levels and decrease arterial pH. If the cause of the hyperventilation is hypoxemia, oxygen therapy is needed. Overventilation by mechanical ventilation can be easily remedied by decreasing the respiratory rate or tidal volume. If ventilator changes do not decrease the pH, dead space can be added to the ventilator tubing. Dead space provides a smaller volume of air so that less CO₂ can be expired.

Independent

For patients who are acutely ill, the priority is to maintain a patent airway, which can be managed through positioning or the use of an oral airway or endotracheal tube. Position the patient in a semi-Fowler position to allow for optimal chest wall expansion, patient comfort, and adequate gas exchange. Aggressive pulmonary hygiene techniques are used to mobilize secretions and increase alveolar ventilation. These measures should include turning, coughing, and deep breathing every 2 hours; postural drainage and percussion every 4 hours; and sitting up in a chair twice per day.

Orient a confused patient to person, time, and place. Use clocks, calendars, family photos, and scheduled rest periods to help maintain orientation. Assist the patient in using hearing aids and glasses to ensure an accurate interpretation of surroundings. Consider using restraints according to hospital policy if the risk for injury is high. Remove the restraints every 2 hours to allow for range-of-motion exercises. Incorporate the patient's normal sleep routines into the care plan. Schedule collaborative activities to allow at least two 1-hour rest periods during the day and one 4-hour rest period at night.

Provide assistance as needed in feeding, bathing, toileting, and dressing. Provide frequent mouth care (every 2 hr) to ensure patient comfort. If the patient is able to swallow, offer sips of water or ice chips every hour. Avoid lemon glycerine swabs, which may cause dryness. The patient is not discharged until the cause of the acid-base alteration has been resolved; in many patients, however, underlying organ diseases may not be resolved.

Evidence-Based Practice and Health Policy

Lo, K., Garvia, V., Stempel, J., Ram, P., & Rangaswami, J. (2020). Bicarbonate use and mortality outcome among critically ill patients with metabolic acidosis: A meta analysis. Heart & Lung, 49, 167–174.

The authors studied the role of sodium bicarbonate in the treatment of severe acidosis in the intensive care unit (ICU) setting.
They studied all available articles in several healthcare databases and located 202 articles addressing bicarbonate use in ICUs. Five studies evaluated mortality.
Following advanced analysis, the authors found that mortality was not improved by the use of bicarbonate in severe acidosis unless actual bicarbonate loss is the primary mechanism for acidosis.

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DRG Information ⬇

Introduction ⬆ ⬇

Causes ⬆ ⬇

Genetic Considerations ⬆ ⬇

Sex and Life Span Considerations ⬆ ⬇

Health Disparities and Sexual/Gender Minority Health ⬆ ⬇

Global Health Considerations ⬆ ⬇

Assessment ⬆ ⬇

Primary Nursing Diagnosis ⬆ ⬇

Planning and Implementation ⬆ ⬇

Documentation Guidelines ⬆ ⬇

Discharge and Home Healthcare Guidelines ⬆