10.4 Acid-Base Imbalance

Interpreting ABGs

Arterial blood gas values can be interpreted to indicate one of four conditions: respiratory acidosis, respiratory alkalosis, metabolic acidosis, or metabolic alkalosis. Once this interpretation is made, conditions can further be classified as compensated, partially compensated, or uncompensated, depending on whether an internal compensatory mechanism is attempting to correct the imbalance in the body. Compensation is indicated by certain changes in ABG values.

A simple way to remember how to interpret ABG values is the acronym ROME, which stands for Respiratory Opposite, Metabolic Equal. This means that the respiratory component (PaCO₂) moves in the opposite direction of the pH if the respiratory system is causing the imbalance. If the metabolic system is causing the imbalance, the metabolic component (HCO₃) moves in the same direction as the pH.

Pathophysiology of Metabolic Acidosis

A common cause of metabolic acidosis is diabetic ketoacidosis. In diabetic ketoacidosis, acids called ketones, a byproduct of anaerobic metabolic due to a lack of insulin, are detected and excreted in the urine. Another common cause in hospitalized patients is lactic acidosis, which can be caused by impaired tissue oxygenation. Metabolic acidosis can also be caused by increased loss of bicarbonate due to severe diarrhea or from renal disease that impairs the kidneys’ ability to eliminate acid.

Clinical Manifestations of Metabolic Acidosis

Nurses may first suspect that a patient has metabolic acidosis because the patient has rapid breathing; this occurs as the lungs try to remove excess CO₂ to resolve the acidosis. Other signs and symptoms of metabolic acidosis include

• confusion
• decreased level of consciousness
• electrolyte disturbances that can progress to circulatory collapse and death if not treated promptly
• GI distress: diarrhea
• hypotension

Medical Therapies and Related Care

It is important to quickly notify the provider of suspected metabolic acidosis so that an ABG measurement can be ordered, a sample collected, and treatment prescribed (based on the cause of the metabolic acidosis) to allow acid levels to improve. Treatment includes IV fluids to improve hydration status, tight glucose management, and circulatory support. When the pH drops below 7.1, IV sodium bicarbonate is often prescribed to help neutralize the acids in the blood.

Pathophysiology of Metabolic Alkalosis

Metabolic alkalosis has a variety of causes, including prolonged vomiting and nasogastric suctioning. This is because gastric secretions have high levels of hydrogen ions: as acid is lost, the pH level of the bloodstream increases. Excessive urinary loss (due to diuretics or excessive mineralocorticoids) can cause metabolic alkalosis due to loss of hydrogen ions in the urine. Intravenous administration of sodium bicarbonate can also cause metabolic alkalosis due to increased levels of bases introduced into the body.

Metabolic alkalosis can also happen when hydrogen ions shift into cells due to hypokalemia. Recall that hypokalemia refers to low levels of potassium in the bloodstream. When this happens, potassium ions shift out of cells and into the bloodstream to maintain a normal level of serum potassium for optimal cardiac function. However, as the potassium ions (K⁺) move out of cells, H⁺ moves into the cells from the bloodstream to maintain electrical neutrality. This transfer of ions causes the pH in the bloodstream to rise resulting in metabolic alkalosis.

Clinical Manifestations of Metabolic Alkalosis

A nurse may first suspect that a patient has metabolic alkalosis because they may have a decreased respiratory rate; this is the result of the lungs trying to retain additional CO₂ to increase the acidity of the blood and resolve the alkalosis. The patient may also be confused due to the altered pH level. The nurse should report signs of suspected metabolic alkalosis because the condition, if uncorrected, can result in hypotension and cardiac dysfunction. Additionally, any fluid loss from the stomach level and above results in loss of acids and eventual alkalosis, whereas fluid losses below the stomach result in loss of bases and eventual acidosis. For example, prolonged vomiting can result in alkalosis and prolonged diarrhea can result in acidosis.

Medical Therapies and Related Care

Treatment for metabolic alkalosis is prescribed on the basis of the ABG results and the suspected cause. For example, orders may include treating the cause of the vomiting, stopping the GI suctioning, or stopping the administration of diuretics. If hypokalemia is also present, it should be promptly treated. If bicarbonate is being administered, it should be stopped. Patients with kidney disease or severe imbalances may require dialysis.

Pathophysiology of Respiratory Alkalosis

Respiratory alkalosis is caused by hyperventilation that can occur due to anxiety, panic attacks, pain, fear, head injuries, or mechanical ventilation. Overdoses of salicylates and other toxins can also cause respiratory alkalosis initially; the condition often progresses to metabolic acidosis in later stages. Acute asthma exacerbations, pulmonary embolisms, or other respiratory disorders can initially cause respiratory alkalosis as the lungs breathe faster in an attempt to increase oxygenation, which decreases the PaCO₂. After a while, however, these hypoxic disorders cause respiratory acidosis, as respiratory muscles tire, breathing slows, and CO₂ builds up in the blood.

Clinical Manifestations of Respiratory Alkalosis

Patients experiencing respiratory alkalosis often report feelings of shortness of breath, dizziness or light-headedness, chest pain or tightness, paresthesia, and palpitations. These symptoms result from decreased CO₂ levels. Respiratory alkalosis is not fatal, but it is important to recognize that underlying conditions such as asthma exacerbation or pulmonary embolism can be life-threatening, so treatment of these underlying conditions is essential.

Medical Therapies and Related Care

As the body’s pH level increases, the kidneys attempt to compensate for the shortage of hydrogen ions by reabsorbing bicarbonate before it can be excreted in the urine. This is a slow process, so additional treatment may be necessary to address the underlying cause of hyperventilation. Acute management of patients who are hyperventilating should focus on patient reassurance, an explanation of the symptoms the patient is experiencing, and the removal of any stressors.

Pathophysiology of Respiratory Acidosis

Respiratory acidosis is typically caused by a medical condition such as an acute asthma exacerbation, COPD, or an acute heart failure exacerbation causing pulmonary edema; these conditions all decrease the exchange of oxygen and CO₂ at the alveolar level. Respiratory acidosis can also be caused by decreased ventilation from anesthesia, the consumption of alcohol, or the administration of medications such as opioids and sedatives.

Chronic respiratory diseases, such as COPD, often cause chronic respiratory acidosis that is fully compensated for by the kidneys retaining HCO₃⁻. Because the CO₂ levels build up over time, the body adapts to elevated PaCO₂ levels, and they are better tolerated. However, in acute respiratory acidosis, the body does not have time to adapt to elevated CO₂ levels, causing mental status changes associated with hypercapnia. Acute respiratory acidosis is caused by acute respiratory conditions, such as an asthma attack or heart failure exacerbation with pulmonary edema, when the lungs suddenly are not able to ventilate adequately. As breathing slows and respirations become shallow, less CO₂ is excreted by the lungs and PaCO₂ levels quickly rise.

Clinical Manifestations of Respiratory Acidosis

Signs and symptoms of hypercapnia vary depending upon the level and rate of CO₂ accumulation in arterial blood. Patients with mild to moderate hypercapnia may be anxious or complain of mild dyspnea, daytime sluggishness, headaches, or hypersomnolence. Patients with higher levels of CO₂ or rapidly developing hypercapnia may develop delirium, paranoia, depression, and confusion that can progress to seizures and coma as levels continue to increase. Individuals with normal lung function typically exhibit a depressed level of consciousness when the PaCO₂ is greater than 75 to 80 mm Hg, whereas patients with chronic hypercapnia may not develop symptoms until the PaCO₂ is greater than 90 to 100 mm Hg.

Medical Therapies and Related Care

When a patient demonstrates signs of potential hypercapnia, the nurse should assess airway, breathing, and circulation. Urgent assistance should be sought, especially if the patient is in respiratory distress. The provider should order an ABG measurement and prescribe treatments based on assessment findings and potential causes. Treatment for respiratory acidosis typically involves improving ventilation and respiration by removing airway restrictions, reversing oversedation, administering nebulizer treatments, or increasing the rate and depth of respiration by using a bilevel positive airway pressure (BiPAP) or continuous positive airway pressure (CPAP) device. BiPAP and CPAP devices provide noninvasive positive pressure ventilation to increase the depth of respiration, remove CO₂, and oxygenate the patient. If these noninvasive interventions are not successful, the patient will likely need to be intubated and receive mechanical ventilation support.

Recognizing and Analyzing Cues

For patients presenting with signs and symptoms indicating the presence of an acid-base imbalance, one of the first interventions is to obtain an ABG measurement. The respiratory therapist (RT) often performs this, which highlights the importance of interdisciplinary collaboration and teamwork. On the basis of the findings of the ABG sample, the nurse, RT, and provider will work together to determine the next step and develop an appropriate plan of care for the patient.

Prioritizing Hypotheses, Generating Solutions, and Taking Action

The main nursing interventions for patients with acid-base imbalances include

• closely monitoring respiratory and neurological status for deviations from baseline that would indicate worsening of the imbalance
• monitoring and recording accurate intake and output
• monitoring and treating the specific acid-base imbalance
• monitoring vital signs

Evaluation of Nursing Care for Patients with Acid-Base Imbalances

After diagnosis of and initiation of treatment for an acid-base imbalance, it is important for the nurse to evaluate patient outcomes to determine whether treatment was effective and if further intervention is necessary. After treatment, signs that would indicate the patient’s condition is improving include

• normal ABG values
• normal serum electrolyte levels
• regular breathing pattern and adequate oxygenation

Compensation

Various compensatory mechanisms exist to maintain blood pH within a narrow range, including buffers, respiration, and renal mechanisms. Although compensatory mechanisms usually work very well, when one of these mechanisms is not working properly (e.g., as in kidney failure or respiratory disease), they have their limits. If the pH and bicarbonate to carbonic acid ratio are changed too drastically, the body may not be able to compensate. Moreover, extreme changes in pH can denature proteins. Extensive damage to proteins in this way can result in disruption of normal metabolic processes, serious tissue damage, and, ultimately, death.