Chest
Original ResearchCritical CareThe Effect of Supplemental Oxygen on Hypercapnia in Subjects With Obesity-Associated Hypoventilation: A Randomized, Crossover, Clinical Study
Section snippets
Subjects
Patients with newly diagnosed OAH were approached to participate in the study. To be included in the study, subjects had to be obese (BMI > 30 kg/m2) and have evidence of daytime hypercapnia (transcutaneous CO2 tension [Ptco2] ≥ 45 mm Hg). Patients were excluded if they had COPD (defined by a postbronchodilator FEV1/FVC ratio < 0.7, FEV1 < 80% predicted, and > 10 pack-year smoking history); had another disorder associated with hypercapnic respiratory failure, such as neuromuscular disease; or
Characteristics of Subjects
A total of 76 patients with obesity (mean BMI, 47.6 kg/m2) without a history of COPD were screened for evidence of daytime hypercapnia (Fig 1). Of these, 25 met the inclusion criteria, and 24 consented to take part in the study. As a result, 24 subjects were randomized; one subject did not attend for the second test. The study took place between June 2008 and May 2009.
Table 1 shows the baseline characteristics of the subjects included in the study. The 24 subjects were morbidly obese with a
Discussion
This double-blind, randomized, crossover study has demonstrated that breathing 100% oxygen causes worsening hypercapnia in subjects with OAH in a stable condition. After 20 min breathing 100% oxygen, the Ptco2 increased by a mean of 5 mm Hg, with three of 24 subjects withdrawn before completion of the study while breathing oxygen because of an increase in Ptco2 of ≥ 10 mm Hg. This finding indicates that patients with stable OAH are at risk for worsening hypercapnia with high-flow uncontrolled
Conclusions
To the best of our knowledge, this investigation is the first double-blind, randomized, controlled study of high-concentration oxygen therapy in subjects with OAH. It has demonstrated that breathing 100% oxygen leads to worsening hypercapnia in subjects with OAH and that the magnitude and speed of the effect may be striking. This physiologic response is due to a reduction in MV, resulting in alveolar hypoventilation and an associated increase in Vds/Vt. We suggest that in patients with morbid
Acknowledgments
Author contributions: Dr Wijesinghe had full access to all of the data in the study and takes full responsibility for their integrity and the accuracy of the data analysis, including any adverse effects.
Dr Wijesinghe: contributed to planning the study, conducting the testing, and preparing the manuscript.
Mr Williams: contributed to conducting the testing and preparing the manuscript.
Dr Perrin: contributed to planning the study, conducting the testing, and preparing the manuscript.
Dr Weatherall:
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Funding/Support: Dr Wijesinghe is a Wellington Hospitals and Health Foundation Research Fellow, and Dr Perrin is a Health Research Council of New Zealand Training Fellow.
Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).