23-20: Respiratory Acidosis (Hypercapnia)

GENERAL CONSIDERATIONS

Respiratory acidosis results from hypoventilation and subsequent hypercapnia. Both pulmonary and extrapulmonary disorders can cause hypoventilation.

Acute respiratory acidosis is associated with only a modest increase in bicarbonate since serum bicarbonate is an ineffective buffer because of impaired elimination of carbon dioxide. After 6–12 hours, the primary increase in PCO₂ evokes a renal compensation to excrete more acid and to generate more HCO₃^–. Complete metabolic compensation by the kidney takes several days. In acute respiratory acidosis, HCO₃^– increases by 1 mEq/L for every 10 mm Hg increase in PCO₂.

Chronic respiratory acidosis is generally seen in patients with underlying lung disease, such as COPD. Renal excretion of acid as NH₄Cl results in compensatory metabolic alkalosis. In this situation, HCO₃^– increases by 3 mEq/L for every 10 mm Hg increase in PCO₂.

CLINICAL FINDINGS

A. Symptoms and Signs

With acute-onset respiratory acidosis, somnolence, confusion, mental status changes, asterixis, and myoclonus may develop. Severe hypercapnia increases cerebral blood flow, CSF pressure, and intracranial pressure; papilledema and seizures may be seen.

B. Laboratory Findings

Arterial pH is low and PCO₂ is increased. Serum HCO₃^– is elevated but does not fully correct the pH. Respiratory etiologies of respiratory acidosis usually have a wide A-a gradient; a relatively normal A-a gradient in the presence of respiratory acidosis is highly suggestive of global hypoventilation.

TREATMENT

If opioid overdose is a possible diagnosis or there is no other obvious cause for hypoventilation, the clinician should consider a diagnostic and therapeutic trial of intravenous naloxone (see Chapter 40). Noninvasive or mechanical ventilation may be necessary.