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Impacting patient-centred outcomes in COPD: breathlessness and exercise tolerance

CORRESPONDENCE: D. E. O'Donnell, Division of Respiratory and Critical Care Medicine, Respiratory Investigation Unit, Dept of Medicine, Queen's University, 102 Stuart Street, Kingston, ON K7L 2V6, Canada. Fax: 1 6135491459. E-mail: odonnell{at}post.queensu.ca

The physiological hallmark of chronic obstructive pulmonary disease (COPD) is expiratory flow limitation. However, it is the resultant air trapping and associated increases in lung volume (hyperinflation) that provide a mechanistic link between the physiological impairment and the characteristic symptoms of COPD, such as dyspnoea (breathlessness), exercise intolerance and reduced health-related quality of life (HRQoL).

During exercise, the negative consequences of hyperinflation are particularly apparent. Delayed lung emptying and increased end-expiratory lung volume are aggravated, and tidal volume cannot rise to meet the increased ventilatory demands. Dyspnoea intensity rises abruptly to intolerable levels, and further increases in ventilation can only be achieved by rapid breathing. This rebounds to cause greater hyperinflation in a vicious cycle. As a result, patients with COPD often prematurely stop or avoid activity, leading to deconditioning, increased dyspnoea, worsening of disease and, ultimately, reduced HRQoL.

The Global Initiative for Chronic Obstructive Lung Disease guidelines recommend long-acting bronchodilators as first-line maintenance treatment in COPD.

Once-daily tiotropium 18 µg, a long-acting anticholinergic agent with 24-h efficacy, has been consistently shown to relieve dyspnoea and improve exercise tolerance and health status. These improvements may allow patients with chronic obstructive pulmonary disease to increase their daily activities, thereby reversing the cycle of chronic inactivity and muscle deconditioning.

KEYWORDS: Bronchodilators, chronic obstructive pulmonary disease, dyspnoea, exercise tolerance