Respiratory Failure and Non-Invasive Ventilation — Written Clinical Reasoning

Model answer — Part A: the acidotic COPD exacerbation

Frame the problem first. This is acute-on-chronic type 2 respiratory failure with a respiratory acidosis (pH below 7.35) persisting despite one hour of maximal medical therapy on controlled oxygen — the textbook trigger for NIV. The HCO3 of 31 signals a degree of chronic retention underneath the acute decompensation ^[1].

Immediate assessment runs alongside treatment: severity (work of breathing, conscious level, haemodynamics), the driver (infective exacerbation — sputum, cultures, CXR to exclude pneumonia or pneumothorax), the contraindication screen for NIV (he is cooperative, not vomiting, haemodynamically stable — none present), and the escalation question — is he for intubation if NIV fails? I document that ceiling decision before starting ^[1].

Management: continue controlled oxygen to target SpO2 88–92%, and commence bilevel NIV now — IPAP starting at 10 cmH2O titrated up toward 20–30 as tolerated, EPAP 4–5, in a monitored setting. The evidence anchor is the Plant ward RCT (intubation halved, in-hospital mortality reduced) consolidated by the Cochrane meta-analysis showing reduced mortality and intubation in acidotic COPD exacerbations ^{[2] [3]}.

Judging success is protocolised: repeat the ABG at 1–2 hours. Success is a rising pH, falling PaCO2, falling respiratory rate and improving comfort. Failure is a static or falling pH, rising PaCO2, exhaustion, copious secretions or deteriorating conscious level — and failure in a patient for escalation means intubation without further delay, a threshold I write down at the start ^{[1] [2]}.