Acidosis, Respiratory

Key Features

• Low arterial pH, increased PCO₂

• Respiratory acidosis results from hypoventilation and subsequent hypercapnia

• Acute respiratory failure

  • 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

  • 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 kidneys excrete excess HCO₃^– over 2–3 days

Clinical Findings

• Acute respiratory acidosis: somnolence, confusion, mental status changes, asterixis myoclonus

• Severe hypercapnia

  • Increases cerebral blood flow, cerebrospinal fluid pressure, and intracranial pressure

  • Papilledema and pseudotumor cerebri may be seen

Diagnosis

• Low arterial pH, increased PCO₂

• 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

• For all forms of respiratory acidosis, treatment must aim to improve ventilation