Respiratory acidosis is primary increase in carbon dioxide partial pressure (Pco2) with or without compensatory increase in bicarbonate (HCO3−); pH is usually low but may be near normal. Cause is a decrease in respiratory rate and/or volume (hypoventilation), typically due to CNS, pulmonary, or iatrogenic conditions. Respiratory acidosis can be acute or chronic; the chronic form is asymptomatic, but the acute, or worsening, form causes headache, confusion, and drowsiness. Signs include tremor, myoclonic jerks, and asterixis. Diagnosis is clinical and with ABG and serum electrolyte measurements. The cause is treated; oxygen (O2) and mechanical ventilation are often required.
Respiratory acidosis is carbon dioxide (CO2) accumulation (hypercapnia) due to a decrease in respiratory rate and/or respiratory volume (hypoventilation). Causes of hypoventilation (discussed under Ventilatory Failure) include
Hypoxia typically accompanies hypoventilation.
Respiratory acidosis may be acute or chronic. Distinction is based on the degree of metabolic compensation; CO2 is initially buffered inefficiently, but over 3 to 5 days the kidneys increase HCO3− reabsorption significantly.
Symptoms and signs depend on the rate and degree of Pco2 increase. CO2 rapidly diffuses across the blood-brain barrier. Symptoms and signs are a result of high CO2 concentrations (low CNS pH) in the CNS and any accompanying hypoxemia.
Acute (or acutely worsening chronic) respiratory acidosis causes headache, confusion, anxiety, drowsiness, and stupor (CO2 narcosis). Slowly developing, stable respiratory acidosis (as in COPD) may be well tolerated, but patients may have memory loss, sleep disturbances, excessive daytime sleepiness, and personality changes. Signs include gait disturbance, tremor, blunted deep tendon reflexes, myoclonic jerks, asterixis, and papilledema.
Recognition of respiratory acidosis and appropriate renal compensation (see Acid-Base Disorders : Diagnosis) requires ABG and measurement of serum electrolytes. Causes are usually obvious from history and examination. Calculation of the alveolar-arterial (A-a) O2 gradient (inspired Po2 − [arterial Po2+5⁄4 arterial Pco2]) can help distinguish pulmonary from extrapulmonary disease; a normal gradient essentially excludes pulmonary disorders.
Treatment is provision of adequate ventilation by either endotracheal intubation or noninvasive positive pressure ventilation (for specific indications and procedures, see Overview of Respiratory Failure). Adequate ventilation is all that is needed to correct respiratory acidosis, although chronic hypercapnia generally must be corrected slowly (eg, over several hours or more), because too-rapid Pco2lowering can cause a posthypercapnic “overshoot” alkalosis when the underlying compensatory hyperbicarbonatemia becomes unmasked; the abrupt rise in CNS pH that results can lead to seizures and death. Any potassium and chloride deficits are corrected.
Sodium bicarbonate is almost always contraindicated, because of the potential for paradoxical acidosis within the CNS. One exception may be in cases of severe bronchospasm, in which HCO3− may improve responsiveness of bronchial smooth muscle to beta-agonists.
Respiratory acidosis involves a decrease in respiratory rate and/or volume (hypoventilation).
Common causes include impaired respiratory drive (eg, due to toxins, CNS disease), and airflow obstruction (eg, due to asthma, COPD, sleep apnea, airway edema).
Recognize chronic hypoventilation by the presence of metabolic compensation (elevated HCO3−) and clinical signs of tolerance (less somnolence and confusion than expected for the degree of hypercarbia).
Treat the cause and provide adequate ventilation, using tracheal intubation or noninvasive positive pressure ventilation as needed.