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Respiratory acidosis is primary increase in P co 2 with or without compensatory increase in HCO 3 − ; pH is usually low but may be near normal. Cause is a decrease in respiratory rate, volume (hypoventilation), or both 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; O 2 and mechanical ventilation are often required.
Respiratory acidosis is CO 2 accumulation (hypercapnia) due to a decrease in respiratory rate, respiratory volume (hypoventilation), or both. Causes of hypoventilation (discussed under Ventilatory Failure, see Ventilatory Failure) include
Hypoxia typically accompanies hypoventilation.
Respiratory acidosis may be acute or chronic. Distinction is based on the degree of metabolic compensation; CO 2 is initially buffered inefficiently, but over 3 to 5 days the kidneys increase HCO 3 − reabsorption significantly.
Symptoms and signs depend on the rate and degree of P co 2 increase. CO 2 rapidly diffuses across the blood-brain barrier. Symptoms and signs are a result of high CNS CO 2 concentrations (low CNS pH) and any accompanying hypoxemia.
Acute (or acutely worsening chronic) respiratory acidosis causes headache, confusion, anxiety, drowsiness, and stupor (CO 2 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 ( 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) O 2 gradient (inspired P o 2 − [arterial P o 2 + 5 ⁄ 4 arterial P co 2 ]) 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 Respiratory Failure and Mechanical Ventilation). 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 P co 2 lowering 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 K + and Cl − deficits are corrected.
NaHCO 3 is almost always contraindicated, because HCO 3 − can be converted to P co 2 in serum but crosses the blood-brain barrier slowly, thus increasing serum pH without affecting CNS pH. One exception may be in cases of severe bronchospasm, in which HCO 3 − may improve responsiveness of bronchial smooth muscle to β-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 HCO 3 − ) 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.
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