Introduction In people with obesity hypoventilation syndrome (OHS), breathing 100% oxygen increases carbon dioxide (PCO₂), but its effect on pH is unknown. This study investigated the effects of moderate concentrations of supplemental oxygen on PCO₂, pH, minute ventilation (V_E) and physiological dead space to tidal volume ratio (V_D/V_T) among people with stable untreated OHS, with comparison to healthy controls.

Methods In a double-blind randomised crossover study, participants breathed oxygen concentrations (F_iO₂) 0.28 and 0.50, each for 20 min, separated by a 45 min washout period. Arterialised-venous PCO₂ (PavCO₂) and pH, V_E and V_D/V_T were measured at baseline, then every 5 min. Data were analysed using general linear model analysis.

Results 28 participants were recruited (14 OHS, 14 controls). Among OHS participants (mean±SD arterial PCO₂ 6.7±0.5 kPa; arterial oxygen 8.9±1.4 kPa) F_iO₂ 0.28 and 0.50 maintained oxygen saturation 98–100%. After 20 min of F_iO₂ 0.28, PavCO₂ change (ΔPavCO₂) was 0.3±0.2 kPa (p=0.013), with minimal change in V_E and rises in V_D/V_T of 1±5% (p=0.012). F_iO₂ 0.50 increased PavCO₂ by 0.5±0.4 kPa (p=0.012), induced acidaemia and increased V_D/V_T by 3±3% (p=0.012). V_E fell by 1.2±2.1 L/min within 5 min then recovered individually to varying degrees. A negative correlation between ΔV_E and ΔPavCO₂ (r=−0.60, p=0.024) suggested that ventilatory responses were the key determinant of PavCO₂ rises. Among controls, F_iO₂ 0.28 and 0.50 did not change PavCO₂ or pH, but F_iO₂ 0.50 significantly increased V_E and V_D/V_T.

Conclusion Commonly used oxygen concentrations caused hypoventilation, PavCO₂ rises and acidaemia among people with stable OHS. This highlights the potential dangers of this common intervention in this group.