Abstract

It is known that different bronchodilator drugs are capable of alleviating dyspnea without a significant improvement in FEV1 in patients with severe COPD. It has been only in the last few years that the mechanisms underlying this effect are becoming understood. Dynamic pulmonary hyperinflation that develops as a consequence of expiratory flow limitation at rest impairs the mechanics of the respiratory system and inspiratory muscle function in these patients. Changes in the level of pulmonary hyperinflation can be evaluated using spirometry, by measuring changes in inspiratory and/or vital capacity. These parameters increase more often and to a larger extent than FEV1 with the use of bronchodilators. Unlike what happens with FEV1, the degree of hyperinflation correlates with dyspnea and exercise tolerance. Maximal exercise capacity inversely correlates with the reduction in inspiratory capacity. Bronchodilator drugs, by decreasing dynamic hyperinflation, alleviate dyspnea even without a change in FEV1. Other interventions capable of reducing dynamic pulmonary hyperinflation are: lung volume reduction surgery, oxygen administration and non-invasive mechanical ventilation. We review the mechanisms underlying the effects of these interventions