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Correspondence
Authors' response: hyperoxia in acute asthma
  1. Kyle Perrin,
  2. Meme Wijesinghe,
  3. Mark Weatherall,
  4. Richard Beasley
  1. Medical Research Institute of New Zealand, Capital and Coast District Health Board, Wellington, New Zealand and Department of Medicine, University of Otago Wellington, Wellington, New Zealand
  1. Correspondence to Dr Kyle Perrin, Medical Research Institute of New Zealand and Capital and Coast District Health Board, Level 7, CSB building, Wellington Hospital, Riddiford Street, Wellington 6021, New Zealand; kyle.perrin{at}mrinz.ac.nz

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We appreciate the comments by Snelson and Tunnicliffe1 regarding our study of the effects of high concentration oxygen therapy in acute exacerbations of asthma.2 We concur with the view that the effect of high concentration oxygen therapy on arterial carbon dioxide pressure (PaCO2) is not clinically relevant in all patients presenting to the emergency department (ED) with acute severe asthma. However, we consider that the 3.9-fold greater risk of patients developing an increase in transcutaneous partial pressure of carbon dioxide (PtCO2) ≥8 mm Hg (22% vs 6% in the high concentration vs titrated oxygen groups, respectively) is likely to be of clinical relevance in life-threatening asthma. Even in our study, which excluded patients who were unable to speak or perform spirometry due to breathlessness, all 10 patients who had a final PtCO2 ≥45 mm Hg had received high concentration oxygen therapy. These findings suggest that the routine administration of high concentration oxygen therapy in the ED setting is a determinant of respiratory failure, a recognised marker of near fatal asthma. This probably also applies to the routine use of high concentration oxygen therapy during ambulance transfer in patients with severe asthma, as has been noted in chronic obstructive pulmonary disease,3 but this was not assessed in our study.

While permissive hypercapnia is an approach to the management of mechanical ventilation for severe asthma, this relates to intubated patients, in whom the purpose is to reduce the risk of complications associated with hyperinflation.4 It certainly does not apply to prehospital or ED care.

We agree that there are many potential risks associated with hyperoxia, including but not limited to reductions in coronary and cerebral blood flow, decreased cardiac output, increased oxidative stress, delay in recognising a clinical deterioration and rebound hypoxaemia if oxygen therapy is abruptly stopped. However, in respiratory disorders such as severe asthma where there is significant ventilation/perfusion (V/Q) mismatch, hypercapnia represents another potential risk of high concentration oxygen therapy that needs to be recognised in clinical practice.

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Footnotes

  • Competing interests None.

  • Provenance and peer review Commissioned; internally peer reviewed.

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  • PostScript
    Catherine Snelson Bill Tunnicliffe