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      Quantifying the ventilatory control contribution to sleep apnoea using polysomnography.

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          Abstract

          Elevated loop gain, consequent to hypersensitive ventilatory control, is a primary nonanatomical cause of obstructive sleep apnoea (OSA) but it is not possible to quantify this in the clinic. Here we provide a novel method to estimate loop gain in OSA patients using routine clinical polysomnography alone. We use the concept that spontaneous ventilatory fluctuations due to apnoeas/hypopnoeas (disturbance) result in opposing changes in ventilatory drive (response) as determined by loop gain (response/disturbance). Fitting a simple ventilatory control model (including chemical and arousal contributions to ventilatory drive) to the ventilatory pattern of OSA reveals the underlying loop gain. Following mathematical-model validation, we critically tested our method in patients with OSA by comparison with a standard (continuous positive airway pressure (CPAP) drop method), and by assessing its ability to detect the known reduction in loop gain with oxygen and acetazolamide. Our method quantified loop gain from baseline polysomnography (correlation versus CPAP-estimated loop gain: n=28; r=0.63, p<0.001), detected the known reduction in loop gain with oxygen (n=11; mean±sem change in loop gain (ΔLG) -0.23±0.08, p=0.02) and acetazolamide (n=11; ΔLG -0.20±0.06, p=0.005), and predicted the OSA response to loop gain-lowering therapy. We validated a means to quantify the ventilatory control contribution to OSA pathogenesis using clinical polysomnography, enabling identification of likely responders to therapies targeting ventilatory control.

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          Author and article information

          Journal
          Eur. Respir. J.
          The European respiratory journal
          1399-3003
          0903-1936
          Feb 2015
          : 45
          : 2
          Affiliations
          [1 ] Division of Sleep Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA School of Information Technology and Electrical Engineering, The University of Queensland, Brisbane, Australia.
          [2 ] Division of Sleep Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
          [3 ] Division of Sleep Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA Neuroscience Research Australia and the School of Medical Sciences, University of New South Wales, Sydney, Australia.
          [4 ] Division of Sleep Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA Division of Pulmonary and Critical Care, University of Southern California San Diego, La Jolla, CA, USA.
          [5 ] Division of Sleep Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA Central Clinical School, The Alfred and Monash University, Melbourne, Australia sasands@partners.org.
          Article
          09031936.00062914 NIHMS664839
          10.1183/09031936.00062914
          4348093
          25323235
          Copyright ©ERS 2015.

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