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We read with interest the recent article ‘Randomised controlled trial of high concentration versus titrated oxygen therapy in severe exacerbations of asthma’ by Perrin et al1 and the accompanying editorial. We note that data presented in the online supplement suggest, unsurprisingly, response to treatment at 60 min in terms of respiratory rate and forced expiratory volume in one second, probably explaining the rise in transcutaneous partial pressure of carbon dioxide (PtCO2) in this population. Therefore, it cannot be assumed that the PtCO2 levels would have continued to rise after 60 min as the authors suggest.
We are unconvinced by the implication that the levels of normocarbia and hypercarbia (up to 50 mm Hg) demonstrated in this study are deleterious in acute asthma. Life-threatening respiratory failure in asthma is multifactorial, with ventilation–perfusion mismatch, lung hyperinflation and an increased work of breathing leading to respiratory muscle fatigue all being contributory factors.2 A degree of ‘permissive hypercapnea’ is now regarded as best practice and a safe approach in the management of mechanical ventilation for respiratory failure in critical care, including the management of severe asthma. Conversely, hyperoxia is known to cause excess reactive oxygen species causing oxidative stress and free radical damage in exposed tissues,3 and has been implicated in worsening myocardial and cerebral ischaemia.4 Maintaining hyperoxia may also result in delays in recognising clinical deterioration.
We are in full agreement with current guidelines that therapy should target physiological levels of oxygen,5 but would argue that hyperoxia per se may be more harmful than the predominant normocarbia found in this study population of acute exacerbations of asthma.
Competing interests None.
Provenance and peer review Not commissioned; internally peer reviewed.