Respiratory Failure and Non-Invasive Ventilation

The answer first

Acute respiratory failure is a failure of gas exchange, defined on arterial blood gas — and the entire clinical game is matching the type of failure to the right respiratory support, early. Four rules carry you through almost every DWE question and every after-hours ward call ^{[1] [2]}:

1. Type 1 is oxygenation failure; type 2 is ventilation failure. Type 1 is a PaO₂ below 8 kPa with a normal or low PaCO₂ — the problem is the lung (V/Q mismatch, shunt). Type 2 adds a PaCO₂ above 6 kPa — the problem is the pump (reduced ventilatory drive, muscle weakness, or a load the muscles cannot meet) ^{[2] [20]}.
2. Oxygen is a drug with a target, not a reflex. Most acutely ill adults are targeted to 94–98%, but anyone at risk of CO₂ retention — COPD above all — gets controlled oxygen (24–28% Venturi) aiming for 88–92%, with a blood gas checked after any change ^{[3] [4]}.
3. An acidotic COPD exacerbation is an NIV emergency. pH below 7.35 with hypercapnia despite maximal medical therapy means BiPAP now — it reduces intubation and death, and the evidence is among the strongest in acute medicine. Cardiogenic pulmonary oedema, by contrast, gets CPAP ^{[2] [7] [9]}.
4. NIV is a trial with an exit, not a destination. Repeat the blood gas at 1–2 hours. Improving pH and PaCO₂ means continue; worsening acidosis, exhaustion, secretions or agitation means stop escalating and intubate — delayed intubation is the classic fatal error ^{[2] [19]}.

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References23ShowHide

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