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Effect of acute hypoxia on QTc interval in respiratory patients undergoing fitness to fly tests
  1. J R A Skipworth1,2,3,
  2. Z Puthucheary1,2,
  3. D A Raptis3,
  4. J Rawal1,2,3,
  5. D Shrikrishna1,
  6. J Windsor2,
  7. D Cramer4,
  8. M I Polkey1,
  9. H E Montgomery2,
  10. N S Hopkinson1
  1. 1NIHR Respiratory Biomedical Research Unit at the Royal Brompton Hospital and National Heart and Lung Institute, Imperial College, London, UK
  2. 2Institute of Human Health and Performance, University College London, London, UK
  3. 3Department of Surgery and Interventional Science, University College London, London, UK
  4. 4Lung Function Department, Royal Brompton Hospital, London, UK
  1. Correspondence to James Skipworth, Respiratory Muscle Laboratory, Royal Brompton Hospital, London SW3 6NP, UK; j.skipworth{at}ucl.ac.uk

https://doi.org/10.1136/thx.2010.151712

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    Introduction

    Current UK guidelines recommend administration of in-flight supplemental oxygen to patients with chronic respiratory disease who have sea level arterial oxygen saturations <92% or partial pressure of oxygen (Pao2) <6.6 kPa (50 mm Hg) during a hypoxic challenge fitness to fly test.1 Hypoxia has been shown to prolong cardiac repolarisation, assessed by the QT interval corrected for heart rate (QTc), and this may underlie the occurrence of potentially life-threatening cardiac arrhythmias2–4; however, few data exist about the cardiac response to hypoxia in patients with respiratory disease.

    To establish whether hypoxia prolongs the QTc, potentially increasing the risk of significant arrhythmias in patients with respiratory disease, we analysed data from respiratory patients referred to our lung function department for fitness to fly testing.

    Methods

    Between …

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    Footnotes

    • JS drafted the manuscript and all authors have significantly contributed to, read and approved the final manuscript.

    • These data were orally presented in part at the British Thoracic Society Winter Meeting 2009 and have been published in abstract form in Thorax 2009;64:Supplement IV.

    • Funding This work was supported by the NIHR Respiratory Disease Biomedical Research Unit at the Royal Brompton and Harefield NHS Foundation Trust and Imperial College London.

    • Competing interests None.

    • Provenance and peer review Not commissioned; not externally peer reviewed.