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Original article
Moderate concentrations of supplemental oxygen worsen hypercapnia in obesity hypoventilation syndrome: a randomised crossover study
  1. Carly Ann Hollier1,2,
  2. Alison Rosemary Harmer2,
  3. Lyndal Jane Maxwell3,
  4. Collette Menadue1,
  5. Grant Neville Willson4,
  6. Gunnar Unger5,
  7. Daniel Flunt1,
  8. Deborah Ann Black2,
  9. Amanda Jane Piper1,5
  1. 1Department of Respiratory and Sleep Medicine, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia
  2. 2Faculty of Health Sciences, University of Sydney, Lidcombe, New South Wales, Australia
  3. 3Faculty of Health Sciences, Australian Catholic University, North Sydney, New South Wales, Australia
  4. 4Faculty of Health, University of Canberra, Bruce, Australian Capital Territory, Australia
  5. 5Woolcock Institute of Medical Research, University of Sydney, Glebe, New South Wales, Australia
  1. Correspondence to Carly Ann Hollier, Department of Respiratory and Sleep Medicine, Royal Prince Alfred Hospital, Sleep Unit, Level 11, Building 75, Royal Prince Alfred Hospital, Missenden Rd, Camperdown, NSW 2050, Australia; carly.hollier{at}sswahs.nsw.gov.au

Abstract

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 (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 (FiO2) 0.28 and 0.50, each for 20 min, separated by a 45 min washout period. Arterialised-venous PCO2 (PavCO2) 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 PCO2 6.7±0.5 kPa; arterial oxygen 8.9±1.4 kPa) FiO2 0.28 and 0.50 maintained oxygen saturation 98–100%. After 20 min of FiO2 0.28, PavCO2 change (ΔPavCO2) 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). FiO2 0.50 increased PavCO2 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 ΔPavCO2 (r=−0.60, p=0.024) suggested that ventilatory responses were the key determinant of PavCO2 rises. Among controls, FiO2 0.28 and 0.50 did not change PavCO2 or pH, but FiO2 0.50 significantly increased VE and VD/VT.

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.

  • Lung Physiology
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