Acute COPD exacerbation — the controlled oxygen and the NIV

The danger of the high-flow oxygen: in the chronic carbon-dioxide-retaining COPD patient, the excess oxygen raises the carbon dioxide through three mechanisms — the Haldane effect (the oxygen displaces the carbon dioxide from the haemoglobin, raising the dissolved blood carbon dioxide), the blunted hypoxic drive (the excess oxygen reduces the ventilatory drive the chronic retainer partly depends on), and the ventilation-perfusion mismatch (the oxygen relaxes the vasoconstriction in the poorly-ventilated units and worsens the matching). The result is the carbon dioxide narcosis and the respiratory acidosis. Hence the controlled oxygen target 88 to 92 per cent.^[4]

The role and the timing of the NIV: the non-invasive ventilation (the BiPAP) is the first-line ventilatory support for the decompensated acute hypercapnic respiratory acidosis — the pH below 7.35 with the raised carbon dioxide, despite the medical therapy (the controlled oxygen, the bronchodilators, the steroids). The BiPAP reduces the mortality, the intubation rate, and the length of stay. The start the NIV for the pH between 7.25 and 7.35; the intensive care and the intubation for the pH below 7.25 or the NIV failure, but the NIV often still the first. The high-flow nasal cannula was not non-inferior to the NIV as initial support (higher treatment failure), so the NIV remains the standard for the hypercapnic failure.^[4][3]

The principles: the controlled oxygen, the medical therapy, the NIV for the acidosis, and the intubation as the back-up. The arterial blood gas guides the escalation.^[3]