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Oxygen-induced hypercapnia in COPD — SCE Respiratory MCQ

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HardRespiratory PhysiologyOxygen-induced hypercapnia in COPDSCE Respiratory

A 68-year-old man with severe COPD is admitted with an acute exacerbation. Before oxygen therapy, arterial blood gases show pH 7.34, PaCO2 7.0 kPa and PaO2 6.7 kPa. He inadvertently receives high-concentration oxygen through a correctly configured reservoir mask for 20 minutes. The reservoir remains inflated throughout. Repeat arterial blood gases show pH 7.22, PaCO2 10.5 kPa and PaO2 24.0 kPa. Simultaneous respiratory measurements show that minute ventilation changes from 12.0 to 11.7 L/min, carbon dioxide production is unchanged, and physiological dead-space fraction increases from 0.46 to 0.68. There is no sedative exposure, and chest radiography shows no new lobar or dependent collapse. Which physiological change most directly accounts for the predominant rise in PaCO2?

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Reveal the answer and explanation

Correct answer: B — Reversal of hypoxic pulmonary vasoconstriction causing worsening ventilation–perfusion matching

Explanation lettering: E = shown as B · D = shown as C · B = shown as D · C = shown as E

The dominant mechanism is reversal of hypoxic pulmonary vasoconstriction. High inspired oxygen raises alveolar PO2 in poorly ventilated units, restoring perfusion to regions that retain a high alveolar PCO2. Perfusion is also redistributed away from better-ventilated units, increasing wasted ventilation. Here, total minute ventilation is nearly unchanged, but effective alveolar ventilation falls markedly because VD/VT rises from 0.46 to 0.68; unchanged carbon dioxide production therefore produces a substantial PaCO2 increase. A is attractive because relief of hypoxaemia can reduce ventilatory drive, but the measured minute ventilation falls by only 2.5%, insufficient to explain this response. Moreover, carotid-body discharge is already largely attenuated once PaO2 exceeds approximately 13 kPa. B contributes to oxygen-induced hypercapnia by reducing haemoglobin carbon dioxide buffering, but does not best explain the large increase in wasted ventilation. C can occur at high FiO2, particularly distal to obstructed airways, but the absence of new collapse and the dead-space pattern rather than a dominant shunt pattern argue against it. D would require inspired carbon dioxide from a faulty or inadequately flowing circuit; the correctly configured, continuously inflated reservoir and absence of additional external dead space make this unlikely.

Reference: BTS guideline for oxygen use in adults in healthcare and emergency settings (2017) — https://www.brit-thoracic.org.uk/document-library/guidelines/emergency-oxygen/bts-guideline-for-oxygen-use-in-adults-in-healthcare-and-emergency-settings/