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• W2010866295 abstract "Author's reply Sir—S Ramsay and colleagues note the lack of control data to support the views of Plant and colleagues. I tried to balance the different strands of evidence suggesting that suppression of hypoxic drive to breathing was an important mechanism in these patients, although I think that the work by Robinson and colleagues1Robinson TD Freiberg DB Regnis JA Young IH The role of hypoventilation and ventilation-perfusion redistribution in oxygen-induced hypercapnia during acute exacerbations of chronic obstructive pulmonary disease.Am J Respir Crit Care Med. 2000; 161: 1524-1529Crossref PubMed Scopus (136) Google Scholar suggests that this mechanism is a factor in some people. Ramsay is incorrect in suggesting that uncontrolled oxygen was used in the study reported by Campbell. He gave a detailed account of the treatment approach in his lecture, and it is clear that patients were initially managed on 24·5% oxygen. The physiological principles outlined 33 years ago remain just as relevant today and the need for close monitoring of these patients and avoidance of unnecessary carbon dioxide retention and acidosis are still relevant. This point is emphasised by a review of practice in our University Teaching Hospital.2Hawkins S Lipscombe S Wilkinson M Babores M Angus RM Deficiencies in the use of oxygen therapy in the management of acute exacerbations of COPD.Thorax. 2000; 55: A17Crossref Google Scholar Poor management of acute chronic respiratory failure due to chronic obstructive pulmonary disease is still occurring. Worryingly, patients who develop oxygen-induced hypercapnia seem to have worse mortality, despite similar previous pulmonary function, than those in whom this complication has been avoided. This review falls short of a controlled clinical trial, but the ethics of such investigations and the need to obtain informed consent makes data of this type particularly difficult to obtain. L Cohen correctly reminds me that the Cornell group were pioneers in this field. However Campbell and colleagues published the first systematic observations about the effects of oxygen therapy in this area, and I defend my choice of reference. Campbell has pointed out that I inaccurately equated his data with lowflow controlled oxygen therapy. He used a high-airflow oxygen entrainment system that achieves controlled oxygen administration in a different way to current controlled oxygen masks. I am delighted to have this opportunity to put the record straight. Treatment of oxygeninduced hypercapniaP M A Calverley, in his Nov 4 commentary,1 describes the conventional treatment for patients with oxygen-induced hypercapnia, but clinical data to support this approach are lacking. Although respiratory acidosis and narcosis are important complications in patients with chronic obstructive pulmonary disease, the belief that they arise because of abolition of hypoxic respiratory drive is not well established. Full-Text PDF Treatment of oxygeninduced hypercapniaP M A Calverley1 expresses more truth than he realises about the necessity for each generation to repeat the errors of its predecessors. Although he claims that McNichol and Campbell2 were the first to appreciate the risk of oxygen in severe hypercapnia in 1965, he is probably unaware that this phenomenon was well known in the Bellevue Hospital Chest Service, New York City, USA, at least as early at the late 1950s. Full-Text PDF" @default.
• W2010866295 created "2016-06-24" @default.
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• W2010866295 date "2001-03-01" @default.
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• W2010866295 title "Treatment of oxygeninduced hypercapnia" @default.
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