Department of Respiratory and Sleep Medicine, Royal Prince Alfred Hospital, , Camperdown, New South Wales, Australia.
Thorax. 2014 Apr;69(4):346-53. doi: 10.1136/thoraxjnl-2013-204389. Epub 2013 Nov 19.
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.
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.
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.
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.
在肥胖低通气综合征（OHS）患者中，呼吸 100%的氧气会增加二氧化碳分压（PCO2），但目前尚不清楚其对 pH 值的影响。本研究旨在探讨在稳定的未治疗 OHS 患者中，中浓度补充氧气对 PCO2、pH 值、分钟通气量（VE）和生理死腔与潮气量比（VD/VT）的影响，并与健康对照组进行比较。
在一项双盲随机交叉研究中，参与者分别呼吸氧浓度（FiO2）0.28 和 0.50，各持续 20 分钟，间隔 45 分钟洗脱期。在基线时以及之后每 5 分钟测量动脉化静脉 PCO2（PavCO2）和 pH 值、VE 和 VD/VT。使用一般线性模型分析数据。
共招募了 28 名参与者（14 名 OHS 患者，14 名对照组）。在 OHS 患者中（平均动脉 PCO2 6.7 ± 0.5 kPa；动脉氧 8.9 ± 1.4 kPa），FiO2 0.28 和 0.50 维持氧饱和度在 98-100%之间。在 FiO2 0.28 20 分钟后，PavCO2 变化（ΔPavCO2）为 0.3 ± 0.2 kPa（p = 0.013），VE 仅有微小变化，VD/VT 增加 1 ± 5%（p = 0.012）。FiO2 0.50 增加了 0.5 ± 0.4 kPa 的 PavCO2（p = 0.012），导致酸中毒，并使 VD/VT 增加 3 ± 3%（p = 0.012）。VE 在 5 分钟内下降了 1.2 ± 2.1 L/min，然后各自恢复到不同程度。ΔVE 和 ΔPavCO2 之间呈负相关（r = -0.60，p = 0.024），表明通气反应是 PavCO2 升高的关键决定因素。在对照组中，FiO2 0.28 和 0.50 并未改变 PavCO2 或 pH 值，但 FiO2 0.50 显著增加了 VE 和 VD/VT。
在稳定的 OHS 患者中，常用的氧气浓度会导致通气不足、PavCO2 升高和酸中毒。这凸显了这种常见干预措施在该人群中的潜在危险。
