Respiratory Acidosis

Primary respiratory acidosis develops as a result of ineffective alveolar ventilation and is suggested by an arterial PCO 2 >45 mm Hg (6.0 kPa). However, an arterial PCO 2 <45 mm Hg (6.0 kPa) may indicate respiratory acidosis in a patient with primary metabolic acidosis that is not adequately compensated by alveolar ventilation. This condition must be differentiated from primary respiratory acidosis (see Table 1). Respiratory acidosis is caused by a primary increase in arterial PCO 2, which accumulates when ventilation is inadequate. Hypoventilation can result from neurologic disorders (eg, stroke) or medications (eg, opiates) that affect the central nervous system respiratory center, respiratory muscle weakness (eg, myasthenia gravis, Guillain-Barré syndrome) or chest wall deformity (eg, severe kyphoscoliosis), obstruction of airways (eg, COPD), or ventilation–perfusion mismatch (eg, pulmonary embolism). Respiratory acidosis may manifest as hypercapnic encephalopathy, a clinical syndrome that initially can present as irritability, headache, mental cloudiness, apathy, confusion, anxiety, and restlessness and can progress to asterixis, transient psychosis, delirium, somnolence, and coma. Severe hypercapnia may cause decreased myocardial contractility, arrhythmias, and peripheral vasodilatation, particularly when the serum pH decreases to <7.1. Patients with acute respiratory acidosis are primarily at risk for hypoxemia rather than hypercapnia or acidemia. Therefore, initial therapy should focus on establishing and maintaining a patent airway and improving ventilation to provide adequate oxygenation. Excessive oxygen may worsen hypoventilation in patients with chronic respiratory acidosis and should be used with caution in this population. The expected acute and chronic compensation for respiratory acidosis is indicated in Table 2.