Bronchodilators increase airway instability in cystic fibrosis.

Abstract

Supramaximal flow transients of partial expiratory flow-volume curves are caused by a rapidly emptying compartment. By superimposing a maximal and a series of partial expiratory flow-volume curves, the volume of the flow transient equivalent for the maximal curve was estimated (volume of airway contribution = VACMEFV). This flow transient equivalent is caused by an extra dead space, created in the large airways by a full inspiration. In 18 children with cystic fibrosis (CF), routine pulmonary functions and VACMEFV were measured before and after bronchodilator medication. Baseline VACMEFV correlated directly with the curvilinearity of the flow-volume curve and inversely with the clinical and radiologic score. Significantly, bronchodilator medication improved FVC, FEV1, FEF25-75, VC, PEF, Raw, and also VACMEFV. In 6 children, VEmax25 increased as a result of apparent peripheral bronchodilation. In 3 others, end-expiratory flow increased slightly but the expanded VACMEFV included the measuring point invalidating the measurement. In the remaining 9 patients, VEmax25 decreased after bronchodilator. As an apparent discrepancy, FEV1, FVC, PEF, VC, FEF25-75 increased, and Raw decreased in 4 to 9 patients. The volumes and flow rates measured early in forced expiration and the end-expiratory flow behaved differently because VACMEFV expanded beyond the measuring points of early expiratory and mid-expiratory flow rates. As the bronchodilator rendered the compliant large airways still more distensible, the amount of air emptied from the dead space in early forced expiration increased. Simultaneously, end-expiratory flow decreased because of enhanced airway compression.(ABSTRACT TRUNCATED AT 250 WORDS)