Respiratory acidosis is characterized by an increase in Paco2 and a decrease in pH. Respiratory acidosis results from disorders that restrict ventilation or increase CO2 production, airway and pulmonary abnormalities, neuromuscular abnormalities, or mechanical ventilator problems.

Early compensatory response to acute respiratory acidosis is chemical buffering. If prolonged (>1224 hours), proximal tubular HCO3 − reabsorption, ammoniagenesis, and distal tubular H+ secretion are enhanced, resulting in an increase in serum HCO3− concentration that raises pH to normal.


• Neuromuscular symptoms include altered mental status, abnormal behavior, seizures, stupor, and coma. Hypercapnia can mimic a stroke or CNS tumor by producing headache, papilledema, focal paresis, and abnormal reflexes. CNS symptoms are caused by increased cerebral blood flow and are variable, depending in part on the acuity of onset.


• Provide adequate ventilation if CO2 excretion is acutely and severely impaired (Paco2>80 mmHg [>10.6 kPa]) or if life-threatening hypoxia is present . Ventilation can include maintaining a patent airway (eg, emergency tracheostomy, bronchoscopy, or intubation), clearing excessive secretions, administering oxygen, and providing mechanical ventilation.

• Treat underlying cause aggressively (eg, administration of bronchodilators for bronchospasm or discontinuation of respiratory depressants such as narcotics and benzodiazepines). Bicarbonate administration is rarely necessary and is potentially harmful.

• Chronic respiratory acidosis (eg, chronic obstructive pulmonary disease [COPD]) is treated essentially the same as acute respiratory acidosis with a few important exceptions. Oxygen therapy should be initiated carefully and only if the Pao2 is less than 50 mm Hg, because the drive to breathe depends on hypoxemia rather than hypercarbia.