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

Abstract

The effect of the long acting beta(2)-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 microg and fluticasone propionate 125 microg via the metered dose combination inhaler in 12 patients with severe Global Initiative on Obstructive Lung Disease stage III-IV COPD, mean FEV(1) = 0.91 L (32% predicted). We measured parasternal intercostal electromyogram (EMG) recorded from implanted fine-wire electrodes, ventilation, and breathing pattern, during resting and CO(2)-stimulated breathing. Full pulmonary function tests were recorded at the beginning and end of the study. In this patient group, severe airflow obstruction and hyperinflation were poorly reversible after SFC: FEV(1) 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. 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.