21-21: Respiratory Acidosis (Hypercapnia)

GENERAL CONSIDERATIONS

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

Acute respiratory failure is associated with severe acidosis and only a small increase in the plasma bicarbonate. 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.

Chronic respiratory acidosis is generally seen in patients with underlying lung disease, such as chronic obstructive pulmonary disease. Renal excretion of acid as NH₄Cl results in a compensatory metabolic alkalosis. When chronic respiratory acidosis is corrected suddenly, posthypercapnic metabolic alkalosis may persist until the kidneys excrete the excess bicarbonate over 2–3 days.

CLINICAL FINDINGS

A. Symptoms and Signs

With acute onset, somnolence, confusion, mental status changes, asterixis, and myoclonus may develop. Severe hypercapnia increases cerebral blood flow, cerebrospinal fluid pressure, and intracranial pressure; papilledema and idiopathic intracranial hypertension (pseudotumor cerebri) 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. If the disorder is chronic, hypochloremia is seen. Respiratory etiologies of respiratory acidosis usually have a wide A-a gradient; a relatively normal A-a gradient suggests a nonpulmonary (eg, central) etiology.

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 38). In all forms of respiratory acidosis, treatment is directed at the underlying disorder to improve ventilation.