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Original Research: COPD |

Parasternal Muscle Activity Decreases in Severe COPD With Salmeterol-Fluticasone Propionate

Paul A. Easton, MD, PhD, FCCP; Harvey G. Hawes, MSc, MD; Christopher J. Doig, MD, MSc; Malcolm W. Johnson, PhD; Masanori Yokoba, MD; Eric R. Wilde, MD
Author and Funding Information

From the Department of Critical Care Medicine (Drs Easton, Hawes, Doig, and Wilde), University of Calgary, Calgary, AB, Canada; Kitasato University (Dr Yokoba), Sagamihara, Japan; and GlaxoSmithKline Research and Development (Dr Johnson), Uxbridge, England.

Correspondence to: Paul Easton, MD, PhD, Department of Critical Care Medicine, Room 223 Heritage Bldg, University of Calgary, 3330 Hospital Dr NW, Calgary, AB, Canada T2N 4N1; e-mail: peaston@ucalgary.ca


Funding/Support: This study was funded by the Canadian Institutes of Health Research and GlaxoSmithKline Research and Development, UK.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestpubs.org/site/misc/reprints.xhtml).


© 2010 American College of Chest Physicians


Chest. 2010;137(3):558-565. doi:10.1378/chest.09-0197
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Background:  The effect of the long acting β2-agonist/corticosteroid combination salmeterol-fluticasone propionate (SFC) on respiratory muscles and ventilation in severe COPD is unknown. As COPD hyperinflation worsens, diaphragm efficiency decreases, and a compensatory increase in chest wall inspiratory muscle activity occurs. If a bronchodilator successfully alleviates hyperinflation and improves diaphragm efficiency in severe COPD, then the extraordinary activation of the chest wall may be relieved. We examined directly the effect on the parasternal intercostal respiratory chest wall muscle and ventilation of four puffs of salmeterol 25 μg and fluticasone propionate 125 μg via the metered dose combination inhaler in 12 patients with severe Global Initiative on Obstructive Lung Disease stage III-IV COPD, mean FEV1 = 0.91 L (32% predicted).

Methods:  We measured parasternal intercostal electromyogram (EMG) recorded from implanted fine-wire electrodes, ventilation, and breathing pattern, during resting and CO2-stimulated breathing. Full pulmonary function tests were recorded at the beginning and end of the study.

Results:  In this patient group, severe airflow obstruction and hyperinflation were poorly reversible after SFC: FEV1 increased 4.2%, functional residual capacity decreased 1.4%, and inspiratory capacity increased 5.9%. However, with SFC there was a significant increase in minute ventilation, tidal volume, and mean inspiratory flow. There was a very large decrease in directly recorded parasternal EMG, with parasternal EMG disappearing completely in some patients after SFC.

Conclusions:  In severe COPD, with minimal change in hyperinflation or pulmonary mechanics, salmeterol-fluticasone induced a significant decrease in activity of the chest wall parasternal inspiratory muscle. This may be of practical benefit to reverse the extensive use of the chest wall muscles and alleviate dyspnea in severe COPD.

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