Respiratory acidosis results from hypoventilation and subsequent hypercapnia. Pulmonary and extrapulmonary disorders can cause hypoventilation.
Acute respiratory failure is 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 is 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 the kidneys excrete the excess bicarbonate over 2–3 days.
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 pseudotumor cerebri may be seen.
Arterial pH is low and PCO2 is increased. 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.
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 38-14). In all forms of respiratory acidosis, treatment is directed at the underlying disorder to improve ventilation.
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