Acid-Base Imbalances: Metabolic Acidosis and Alkalosis
Acid-Base Imbalances: Metabolic Acidosis and Alkalosis; Respiratory Acidosis and Alkalosis
|Mean LOS:||4.7 days|
|Description:||MEDICAL: Nutritional and Miscellaneous Metabolic Disorders with Major CC|
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, a pH below 7.35, results from any nonpulmonary condition that leads to an excess of acids over bases. Renal patients with chronic acidemia may show signs of skeletal problems as calcium and phosphate are released from bone to help with the buffering of acids. Children with chronic acidosis may show signs of impaired growth. Metabolic alkalosis, a pH above 7.45, results from any nonpulmonary condition that leads to an excess of bases over acids. Metabolic alkalosis results from one of two mechanisms: an excess of bases or a loss of acids. Patients with a history of congestive heart failure and hypertension who are on sodium-restricted diets and diuretics are at greatest risk for metabolic alkalosis. Metabolic alkalosis can also be caused by prolonged vomiting, hyperaldosteronism, and diuretic therapy.
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. 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 chronic pulmonary disease patients 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. Improper use of mechanical ventilators 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.
See Table 1.
|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) suctioning|
|Other: ingestion of bicarbonates, carbonates, acetates, citrates, and lactates found in total parenteral nutrition solutions, Ringer’s 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, 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): 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.|
A number of inherited disorders can result in acid-base imbalances. Bartter’s 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’s syndrome is inherited in an autosomal recessive pattern. Metabolic acidosis is often seen with inborn errors of metabolism, such as Gaucher disease (autosomal recessive transmission).
Gender, ethnic/racial, 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 the elderly are at greater risk because of associated fluid imbalances. Young women are at an increased risk of metabolic acidosis because of the popular fad diets of starvation. Ethnicity and race have no known effects on the risk for acid-base imbalance.
Metabolic alkalosis is a common disorder of adult hospitalized patients. Elderly patients are at risk for metabolic alkalosis because of their delicate fluid and electrolyte status. Young women who practice self-induced vomiting to lose weight are also at risk for developing metabolic alkalosis. Finally, middle-aged men and women 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. The elderly 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. The elderly are at an increased risk for respiratory alkalosis because of the high incidence of pulmonary disorders, specifically pneumonia, in the elderly population. Identification of a respiratory alkalosis may be more difficult in the older patient because the early symptoms of increased respirations and altered neurological status may be attributed to other disease processes.
Global health considerations
No data are available.
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 intravenous (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 she or he has 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.
Metabolic Acidosis.Inspect the patient’s skin, noting if it feels warm. Note a flushed appearance. Assess the patient’s breathing pattern for Kussmaul’s respirations, 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 P-R 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 Chvostek’s and Trousseau’s signs (see Hypocalcemia, p. 568). 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 Q-T 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’s 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’s or Trousseau’s sign may indicate hypocalcemia (see Hypocalcemia, p. 568), which may occur from lower amounts of ionized calcium during periods of alkalosis.
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’s feeling powerless and plan care to support all psychological needs.
|Test||Normal Result||Abnormality With Condition||Explanation|
|Arterial blood gases||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
DiagnosisAltered health maintenance related to acid-base imbalances
OutcomesKnowledge: Diet; Disease process; Health behaviors; Medication: Treatment regime; Nutritional status; Electrolyte and acid-base balance
InterventionsAcid-base management; Acid-base monitoring; Health education; Risk identification; Teaching: Disease process; Referral; Medication management; Nutritional management
Planning and implementation
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 (< 7.2). Sodium bicarbonate may be administered by intravenous drip or by intravenous 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, post–chronic 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.
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 anti-anxiety 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.
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 hours) 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
Heidari, K., Hatamabadi, H., Ansarian, N., Alavi-Moghaddam, M., Amini, A., Safari, S., …Vafaee, A. (2013). Correlation between capillary and arterial blood gas parameters in an ED. American Journal of Emergency Medicine, 31(2), 326–329.
- Capillary blood gases (CBGs) are sometimes used as an alternative to arterial blood gases (ABGs) since the risks associated with arterial blood sampling are minimized, capillary sampling is more convenient, patients report less pain, and the blood volume necessary is lower.
- In one study among 187 patients in an emergency department, CBGs and ABGs demonstrated statistically significant (p < 0.001) correlations as follows: PaO2 (0.77), PaCO2 (0.73), SaO2 (0.52), HCO3 (0.90), and pH (0.78).
- Recognition by care providers that correlations between CBGs and ABGs vary among PaO2, PaCO2, SaO2, HCO3, and pH, which may also be affected by the location of the capillary sampling, is critical to planning and decision-making.
- Physical findings: Flushed, dry, warm skin; mental status (presence of disorientation or confusion); respiratory rate and pattern, breath sounds; cardiac rhythm and rate, blood pressure, quality of pulses, urine output; level of consciousness, orientation, ability to concentrate, motor strength, and seizure activity (if seizures are present, the following information should be charted: time the seizure began, parts of the body involved in the seizure, progression of the seizure, type of body movements, pupil size and reaction, eye movements, vital signs during seizure, and postictal state)
- Response to therapy: Medications, activity, interventions
- Laboratory values: ABGs and serum potassium, calcium, sodium, chloride, and magnesium
Discharge and home healthcare guidelines
The patients at highest risk for a recurrence of acid-base imbalances are those who consume large quantities of thiazide diuretics, antacids, and licorice, as well as those who have chronic renal, pulmonary, cardiac, and neurological disorders and IDDM. Make sure these patients understand the importance of maintaining the prescribed treatment regimen. Teach patients on diuretic therapy the signs and symptoms of the associated fluid and electrolyte disturbances of hypovolemia and hypokalemia. Teach patients the action, dose, and side effects of all medications. Teach the patient with mild to moderate anxiety progressive muscle relaxation, therapeutic breathing, and visualization techniques to control anxiety.