Acidosis, Respiratory

For further information, see CMDT Part 21-21: Respiratory Acidosis (Hypercapnia)

Key Features

• Low arterial pH (< 7.35), increased PCO₂ (> 48 mm Hg)

• Respiratory acidosis results from decreased alveolar ventilation 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 hypochloremia

  • When chronic respiratory acidosis is corrected suddenly, posthypercapnic metabolic alkalosis ensues until kidneys excrete excess HCO₃^– over 2–3 days

Clinical Findings

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

• Severe hypercapnia

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

  • Papilledema and pseudotumor cerebri may be seen

Diagnosis

• Low arterial pH (< 7.35), increased PCO₂ (> 48 mm Hg)

• Serum HCO₃^– is elevated (> 32 mEq/L or > 32 mmol/L) 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

• Administer naloxone, 0.04–2.0 mg every 2–3 minutes intravenously or subcutaneously (or intramuscularly) × 3 doses if needed, for possible opioid overdose

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