• Amany F Elbehairy, Katherine A Webb, Pierantonio Laveneziana, Nicolle J Domnik, J Alberto Neder, Denis E O'Donnell, and Canadian Respiratory Research Network (CRRN).
• Department of Medicine, Queen's University and Kingston Health Sciences Centre, Kingston, ON, Canada; Department of Chest Diseases, Faculty of Medicine, Alexandria University, Alexandria, Egypt; National Heart and Lung Institute, Faculty of Medicine, Imperial College London, UK.
• Respir Physiol Neurobiol. 2018 Jun 1; 252-253: 64-71.

AbstractThis randomized, double-blind, crossover study aimed to determine if acute treatment with inhaled bronchodilators, by improving regional lung hyperinflation and ventilation distribution, would reduce dead space-to-tidal volume ratio (VD/VT); thus contributing to improved exertional dyspnea in COPD. Twenty COPD patients (FEV1 = 50 ± 15% predicted; mean ± SD) performed pulmonary function tests and symptom-limited constant-work rate exercise at 75% peak-work rate (with arterialized capillary blood gases) after nebulized bronchodilator (BD; ipratropium 0.5mg + salbutamol 2.5 mg) or placebo (PL; normal saline). After BD versus PL: Functional residual capacity decreased by 0.4L (p = .0001). Isotime during exercise after BD versus PL (p < .05): dyspnea decreased: 1.2 ± 1.9 Borg-units; minute ventilation increased: 3.8 ± 5.5 L/min; IC increased: 0.24 ± 0.28 L and VT increased 0.19 ± 0.16 L. There was no significant difference in arterial CO2 tension or VD/VT, but alveolar ventilation increased by 3.8 ± 5.5 L/min (p = .02). Post-BD improvements in respiratory mechanics explained 51% of dyspnea reduction at a standardized exercise time. Bronchodilator-induced improvements in respiratory mechanics were not associated with reduced wasted ventilation - a residual contributory factor to exertional dyspnea during exercise in COPD.Copyright © 2018 Elsevier B.V. All rights reserved.

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