Abstract
Dyspnea and reduced exercise tolerance are common consequences of chronic obstructive pulmonary disease (COPD) and contribute importantly to poor perceived health status. While the origins of dyspnea and reduced exercise tolerance are complex and multifactorial, there is increasing evidence that lung hyperinflation is an important contributory factor that can be targeted for treatment. In this review, the authors summarize current concepts of the origin and clinical and physiological consequences of both static and dynamic lung hyperinflation in COPD. In particular, they review recent studies that have examined the role of lung hyperinflation in dyspnea causation during exacerbations and physical activity in COPD. Finally, current concepts of the mechanisms of symptom relief and improved exercise tolerance following pharmacological lung volume reduction are reviewed.
Financial & competing interests disclosure
DE O’Donnell has received research funding via Queen’s University from AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline, Merck, Novartis, Nycomed and Pfizer; and has served on speakers bureaus, consultation panels and advisory boards for AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline, Nycomed and Pfizer. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript