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Low arterial pH, increased PCO2
Respiratory acidosis results from hypoventilation 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 a compensatory metabolic alkalosis
When chronic respiratory acidosis is corrected suddenly, posthypercapnic metabolic alkalosis may persist until kidneys excrete excess HCO3– over 2–3 days
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Low arterial pH, increased PCO2
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
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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
For all forms of respiratory acidosis, treatment must aim to improve ventilation