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Review

Oxygen therapy in acute exacerbations of chronic obstructive pulmonary disease

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Abstract

During the last decade, there have been major advances in knowledge of the effects of oxygen therapy in patients with acute exacerbations of chronic obstructive pulmonary disease. This includes a randomised controlled trial of oxygen therapy in the pre-hospital setting, which showed that high concentration oxygen therapy leads to a 2.4-fold increased risk of mortality compared with titrated oxygen therapy to maintain oxygen saturations (SpO2) within a target range of 88–92%. Professional guidelines now recommend the use of supplementary oxygen in acute exacerbations of chronic obstructive pulmonary disease only if the SpO2 is less than 88%, with titration to achieve an SpO2 of 88–92%, and the delivery of bronchodilators by air-driven nebulisation or metered dose inhaler with a spacer. The aim of this review is to provide an overview of the evidence base that underpins these recommendations. We suggest that their implementation will require important changes to current clinical practice in which there is an entrenched culture of the use of high concentration oxygen therapy.

Financial & competing interests disclosure

The Medical Research Institute of New Zealand has received research funding from Fisher & Paykel Healthcare (<$NZ 50,000). J Pilcher is a Health Research Council of New Zealand Clinical Training Fellow. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

Key issues
  • There is Level 1b evidence that acute exacerbations of chronic obstructive pulmonary disease (COPD) should be treated with titrated oxygen therapy to achieve an oxygen saturation target of 88–92%, thereby avoiding the potential risks of both hypoxaemia and hyperoxaemia.

  • In acute exacerbations of COPD, there is a 2.4-fold increase in the risk of death if patients receive high concentration oxygen therapy, compared with titrated oxygen therapy.

  • The increased mortality is likely due to increased partial pressure of carbon dioxide; however, other mechanisms may include hyperoxaemia causing reduced coronary blood flow or myocardial reperfusion injury, or rebound hypoxia if oxygen therapy is abruptly stopped.

  • Further research is needed to determine if the 88–92% target saturation range for oxygen therapy is optimal (e.g., compared with 85–90% or 90–95% ranges).

  • Exposure to high concentration oxygen therapy is avoided by delivering bronchodilators by air-driven nebuliser or metered-dose inhaler with a spacer rather than an oxygen-driven nebuliser.

  • If there is diagnostic uncertainty with acute severe asthma, it is preferable to administer oxygen therapy as if the patient is having an acute exacerbation of COPD and therefore may be at risk of oxygen-induced hypercapnia.

  • High concentration oxygen therapy may also lead to an increase in partial pressure of carbon dioxide in a number of other acute and chronic respiratory disorders, including severe asthma, community-acquired pneumonia, obesity–hypoventilation syndrome, and acute lung injury.

  • Appropriate use of oxygen therapy requires a practice change by health professionals who administer this potentially life-saving but also life-threatening therapy.

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