Sections View Full Chapter Figures Tables Videos Annotate Full Chapter Figures Tables Videos Supplementary Content + Download Section PDF Listen ++ For further information, see CMDT Part 21-21: Respiratory Acidosis (Hypercapnia) + Key Features Download Section PDF Listen +++ ++ 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 Download Section PDF Listen +++ ++ 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 Download Section PDF Listen +++ ++ 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 Download Section PDF Listen +++ ++ 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