Moderate concentrations of supplemental oxygen worsen hypercapnia in obesity hypoventilation syndrome: A randomised crossover study

Introduction In people with obesity hypoventilation syndrome (OHS), breathing 100% oxygen increases carbon dioxide (PCO ₂), but its effect on pH is unknown. This study investigated the effects of moderate concentrations of supplemental oxygen on PCO ₂, pH, minute ventilation (VE) and physiological dead space to tidal volume ratio (VD/VT) among people with stable untreated OHS, with comparison to healthy controls. Methods In a double-blind randomised crossover study, participants breathed oxygen concentrations (F _iO ₂) 0.28 and 0.50, each for 20 min, separated by a 45 min washout period. Arterialised-venous PCO ₂ (PavCO ₂) and pH, VE and VD/VT 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 PCO ₂ 6.7±0.5 kPa; arterial oxygen 8.9±1.4 kPa) F _iO ₂ 0.28 and 0.50 maintained oxygen saturation 98-100%. After 20 min of F _iO ₂ 0.28, PavCO ₂ change (ΔPavCO ₂) was 0.3±0.2 kPa (p=0.013), with minimal change in VE and rises in VD/VT of 1±5% (p=0.012). F _iO ₂ 0.50 increased PavCO ₂ by 0.5±0.4 kPa (p=0.012), induced acidaemia and increased VD/VT by 3±3% ( p=0.012). VE fell by 1.2±2.1 L/min within 5 min then recovered individually to varying degrees. A negative correlation between ΔVE and ΔPavCO ₂ (r=-0.60, p=0.024) suggested that ventilatory responses were the key determinant of PavCO ₂ rises. Among controls, F _iO ₂ 0.28 and 0.50 did not change PavCO ₂ or pH, but F _iO ₂ 0.50 significantly increased VE and VD/VT. Conclusion Commonly used oxygen concentrations caused hypoventilation, PavCO ₂ rises and acidaemia among people with stable OHS. This highlights the potential dangers of this common intervention in this group.