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The effect of 50% oxygen on PtCO(2) in patients with stable COPD, bronchiectasis, and neuromuscular disease or kyphoscoliosis: randomised cross-over trials
BACKGROUND: High-concentration oxygen therapy causes increased arterial partial pressure of carbon dioxide (PaCO(2)) in patients with COPD, asthma, pneumonia, obesity and acute lung injury. The objective of these studies was to investigate whether this physiological response to oxygen therapy occurs...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7203892/ https://www.ncbi.nlm.nih.gov/pubmed/32380988 http://dx.doi.org/10.1186/s12890-020-1132-z |
Sumario: | BACKGROUND: High-concentration oxygen therapy causes increased arterial partial pressure of carbon dioxide (PaCO(2)) in patients with COPD, asthma, pneumonia, obesity and acute lung injury. The objective of these studies was to investigate whether this physiological response to oxygen therapy occurs in stable patients with neuromuscular disease or kyphoscoliosis, and bronchiectasis. METHODS: Three randomised cross-over trials recruited stable patients with neuromuscular disease or kyphoscoliosis (n = 20), bronchiectasis (n = 24), and COPD (n = 24). Participants were randomised to receive 50% oxygen and 21% oxygen (air), each for 30 min, in randomly assigned order. The primary outcome was transcutaneous partial pressure of carbon dioxide (PtCO(2)) at 30 min. The primary analysis was a mixed linear model. RESULTS: Sixty six of the 68 participants had baseline PtCO(2) values < 45 mmHg. The intervention baseline adjusted PtCO(2) difference (95% CI) between oxygen and room air after 30 min was 0.2 mmHg (− 0.4 to 0.9), P = 0.40; 0.5 mmHg (− 0.2 to 1.2), P = 0.18; and 1.3 mmHg (0.7 to 1.8), P < 0.001, in the neuromuscular/kyphoscoliosis, bronchiectasis and COPD participants respectively. CONCLUSIONS: The small increase in PtCO(2) in the stable COPD patients with high-concentration oxygen therapy contrasts with the marked increases in PaCO(2) seen in the setting of acute exacerbations of COPD. This suggests that the model of studying the effects of high-concentration oxygen therapy in patients with stable respiratory disease is not generalisable to the use of oxygen therapy in the acute clinical setting. Appropriate studies of high-concentration compared to titrated oxygen in acute clinical settings are needed to determine if there is a risk of oxygen-induced hypercapnia in patients with neuromuscular disease, kyphoscoliosis or bronchiectasis. TRIAL REGISTRATION: Australian New Zealand Clinical Trials Registry ACTRN12615000970549 Registered 16/9/15, ACTRN12615000971538 Registered 16/9/15 and ACTRN12615001056583 Registered 7/10/15. |
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