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 (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 i O 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, 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 PCO 2 6.7±0.5 kPa; arterial oxygen 8.9±1.4 kPa) F i O 2 0.28 and 0.50 maintained oxygen saturation 98–100%. After 20 min of F i O 2 0.28, PavCO 2 change (ΔPavCO 2 ) 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 i O 2 0.50 increased PavCO 2 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 ΔPavCO 2 (r=−0.60, p=0.024) suggested that ventilatory responses were the key determinant of PavCO 2 rises. Among controls, F i O 2 0.28 and 0.50 did not change PavCO 2 or pH, but F i O 2 0.50 significantly increased V E and V D /V T . 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.