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Clinical Features - Reviews

Pathophysiology of dyspnea in COPD

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Pages 366-374 | Received 30 Nov 2016, Accepted 27 Feb 2017, Published online: 17 Mar 2017
 

ABSTRACT

Dyspnea refers to the sensation of breathlessness, shortness of breath, or difficulty breathing that is commonly observed in patients with respiratory and cardiac disease. In the United States alone, dyspnea is reported in up to 4 million all-cause emergency room visits annually. Dyspnea can be a symptom of several different underlying physical conditions, typically involving the lung and heart. Indeed, it is an important symptom in chronic obstructive pulmonary disease (COPD), where it is associated with limited physical activity, increased anxiety and depression, decreased health-related quality of life (HRQoL), and reduced survival. Currently there is no single physiological correlate that will accurately predict dyspnea, particularly because the mechanisms that contribute to respiratory discomfort can vary between diseases and between individuals experiencing breathlessness who have been diagnosed with the same disease. Therefore, various subjective clinical and psychophysical scales and questionnaires are typically used to measure or predict dyspnea. It is the goal of this review to discuss the pathophysiological mechanisms leading to dyspnea, particularly those associated with COPD, the physical and psychological impact on patients, assessment approaches, and modalities currently used to treat it.

Acknowledgments

The authors thank Beverly E. Barton, PhD, Dan Rigotti, PhD, Devin Gary, PhD, and Stella Chow, PhD of Scientific Connexions, an Ashfield Company, who provided writing and editorial assistance funded by AstraZeneca.

Declaration of interest

M Miravitlles has received speaker fees from Almirall, AstraZeneca, Boehringer Ingelheim, Chiesi, GlaxoSmithKline, Grifols, Menarini, Novartis, and Teva, and consulting fees from Almirall, Bayer Schering, Boehringer Ingelheim, Cipla, CLS Behring, Gebro Pharma, GlaxoSmithKline, Grifols, MedImmune, Novartis, Takeda, and Teva. A Anzueto has received speaker fees from AstraZeneca, Bayer Pharma, Boehringer Ingelheim, GlaxoSmithKline, Grifols, Novartis, and Pfizer, and consulting fees from AstraZeneca, Bayer Pharma, Boehringer Ingelheim, Novartis, and Sunovion Pharmaceutical. Writing and editorial assistance was provided by Scientific Connexions, an Ashfield Company, and funded by AstraZeneca. 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.

Additional information

Funding

This paper was funded by AstraZeneca LP.

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