• Am. J. Respir. Crit. Care Med. · Jan 2019

    Randomized Controlled Trial

    Effect of Supplemental Oxygen on Blood Pressure in Obstructive Sleep Apnea (SOX): A Randomised, CPAP Withdrawal Trial.

    • Chris D Turnbull, Dushendree Sen, Malcolm Kohler, Nayia Petousi, and John R Stradling.
    • 1 National Institute for Health Research Oxford Biomedical Research Centre, University of Oxford, Oxford, United Kingdom.
    • Am. J. Respir. Crit. Care Med. 2019 Jan 15; 199 (2): 211219211-219.

    RationaleObstructive sleep apnea (OSA) is associated with systemic hypertension. Either overnight intermittent hypoxia, or the recurrent arousals that occur in OSA, could cause the daytime increases in blood pressure (BP).ObjectivesTo establish the role of intermittent hypoxia in the increased morning BP in patients with OSA.MethodsRandomized, double-blinded, crossover trial assessing the effects of overnight supplemental oxygen versus air (sham) on morning BP, after continuous positive airway pressure (CPAP) withdrawal in patients with moderate to severe OSA. The primary outcome was the change in home morning BP after CPAP withdrawal for 14 nights, oxygen versus air. Secondary outcomes included oxygen desaturation index (ODI), apnea-hypopnea index (AHI), subjective sleepiness (Epworth Sleepiness Scale score), and objective sleepiness (Oxford Sleep Resistance Test).Measurements And Main ResultsSupplemental oxygen virtually abolished the BP rise after CPAP withdrawal and, compared with air, significantly reduced the rise in mean systolic BP (-6.6 mm Hg; 95% confidence interval [CI], -11.3 to -1.9; P = 0.008), mean diastolic BP (-4.6 mm Hg; 95% CI, -7.8 to -1.5; P = 0.006), and median ODI (-23.8/h; interquartile range, -31.0 to -16.3; P < 0.001) after CPAP withdrawal. There was no significant difference, oxygen versus air, in AHI, subjective sleepiness, or objective sleepiness.ConclusionsSupplemental oxygen virtually abolished the rise in morning BP during CPAP withdrawal. Supplemental oxygen substantially reduced intermittent hypoxia, but had a minimal effect on markers of arousal (including AHI), subjective sleepiness, or objective sleepiness. Therefore intermittent hypoxia, and not recurrent arousals, appears to be the dominant cause of daytime increases in BP in OSA.

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