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Lung hyperinflation in COPD: the impact of pharmacotherapy

Division of Respiratory and Critical Care Medicine, Dept of Medicine, Queen's University, Kingston, ON, Canada.

CORRESPONDENCE: D. E. O'Donnell, 102 Stuart Street, Kingston, ON, Canada K7L 2V6. Fax: 1 6135491459. E-mail: odonnell{at}post.queensu.ca

Improvement in airway function in response to bronchodilator therapy is generally confirmed by simple spirometry. However, improvements in maximal expiratory flow rates have been shown to correlate poorly with important patient-centred outcomes, such as reduced exertional dyspnoea and improved exercise performance. Recent studies have suggested that attendant reductions in end-expiratory lung volume as a result of bronchodilator-induced improvements in lung emptying may be more closely associated with symptom relief and increased exercise capacity than traditional spirometric indices. To the extent that chronic lung hyperinflation and the superimposition of acute dynamic hyperinflation (in response to increased ventilation or expiratory flow limitation) result in excessive loading and weakening of the inspiratory muscles, then pharmacological lung volume reduction should have important mechanical and sensory benefits for the patient.

The present article will examine the mechanisms of lung deflation following short-term bronchodilator therapy. The physiological links between reduced hyperinflation, improved dyspnoea and exercise endurance will be examined, and the emerging evidence for the additive effects of combining various modern pharmacological therapies will be reviewed.

KEYWORDS: Bronchodilators, chronic obstructive pulmonary disease, dynamic hyperinflation, dyspnoea, exercise, respiratory mechanics