A patient with chronic obstructive pulmonary disease and a PaO2 of 52 mmHg receives high-flow oxygen, after which PaCO2 rises from 58 to 72 mmHg. The MOST important physiological mechanism contributing to this CO2 retention is:
- A Suppression of the hypoxic ventilatory drive
- B Haldane effect: oxygenation of hemoglobin releases CO2 from blood ✓
- C Increased dead space ventilation from oxygen-induced bronchoconstriction
- D Reduced diaphragmatic contractility caused by hyperoxia
Explanation
Contemporary evidence shows that the Haldane effect accounts for approximately two-thirds of the CO2 rise when COPD patients breathe supplemental oxygen. Oxygenated hemoglobin is a less effective CO2 carrier than deoxyhemoglobin; when PaO2 rises, hemoglobin releases CO2 into plasma, raising PaCO2. Concomitant reversal of hypoxic pulmonary vasoconstriction increases perfusion to poorly ventilated regions (V/Q mismatch worsening). While suppression of hypoxic drive (option A) was the historical explanation, it accounts for only about one-third of the CO2 rise and is no longer considered the primary mechanism.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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