Oxygen-induced hypercapnia in a COPD exacerbation

This is an acute, oxygen-induced exacerbation of type 2 respiratory failure in a patient with chronic obstructive pulmonary disease. The uncontrolled high-flow oxygen raised his saturation to 97 per cent but precipitated a sharp rise in carbon dioxide to 9.5 kPa with an acidaemia (pH 7.24). The elevated baseline bicarbonate of 32 indicates chronic carbon-dioxide retention with renal compensation, so this is an acute-on-chronic respiratory acidosis. The mechanism of the hypercapnia is predominantly ventilation-perfusion mismatch from relief of hypoxic vasoconstriction, with a contribution from the Haldane effect and a small loss of hypoxic drive.^[1]

The immediate management is to reduce the inspired oxygen and target 88 to 92 per cent, using a controlled-oxygen device — a Venturi mask at 24 or 28 per cent — rather than the uncontrolled simple mask. The oxygen is not withdrawn abruptly, because the patient still requires correction of hypoxaemia; it is controlled.^[2]

Because he has a respiratory acidosis (pH below 7.35) with a high carbon dioxide, the standard of care for the hypercapnic COPD exacerbation is non-invasive ventilation (bi-level positive airway pressure), started promptly, with controlled oxygen entrained to the same target. Bronchodilators, steroids and antibiotics for the infective exacerbation run in parallel. A repeat blood gas after an hour of therapy confirms whether the carbon dioxide is falling and the pH recovering. If the patient deteriorates despite non-invasive ventilation — worsening acidosis, falling conscious level, exhaustion — he is intubated and ventilated.^[2]