Respiratory acidosis results from hypoventilation and subsequent hypercapnia. Both pulmonary and extrapulmonary disorders can cause hypoventilation.
Acute respiratory acidosis is associated with only a modest increase in bicarbonate since serum bicarbonate is an ineffective buffer because of impaired elimination of carbon dioxide. 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. In acute respiratory acidosis, HCO3– increases by 1 mEq/L for every 10 mm Hg increase in PCO2.
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. In this situation, HCO3– increases by 3 mEq/L for every 10 mm Hg increase in PCO2.
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 seizures may be seen.
Arterial pH is low and PCO2 is increased. Serum HCO3– is elevated but does not fully correct the pH. Respiratory etiologies of respiratory acidosis usually have a wide A-a difference; a relatively normal A-a difference in the presence of respiratory acidosis is highly suggestive of global hypoventilation.
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). Noninvasive or mechanical ventilation may be necessary.
et al. Alkali therapy for respiratory acidosis: a medical controversy. Am J Kidney Dis. 2020;75:265.