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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


  • 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


  • 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

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