Am. J. Respir. Crit. Care Med., Volume 162, Number 5, November 2000, 1778-1782

Unsuspected Pseudophysiologic Emphysema in Chronic Persistent Asthma

ARTHUR F. GELB and NOE ZAMEL

Pulmonary Division, Department of Medicine; Lakewood Regional Medical Center, University of California, Los Angeles, School of Medicine; and University of Toronto, Faculty of Medicine, Toronto, Ontario, Canada

The current literature emphasizes the role of airway remodeling in chronic persistent asthma and its putative effect on causing fixed expiratory airflow limitation. We studied 18 adults with chronic persistent asthma; 12 men, six women, age 59 ± 15 yr (mean ± SD) with fixed expiratory airflow obstruction. We measured lung elastic recoil and examined the mechanism of expiratory airflow limitation. Diaphragmatic strength was also measured in six asthmatics, using both sniff and partially occluded airway technique. All 18 asthmatics had markedly abnormal maximal expiratory flow-volume curves at both high and low lung volumes. Hyperinflation was present at residual volume (RV), FRC, and TLC in all subjects. Diffusing capacity was normal or elevated and lung computed tomography (CT) was normal in all 18 asthmatic subjects. There was a significant loss of lung elastic recoil in three of four asthmatics age 30 to 49, all five age 51 to 60 yr, and seven of nine age 61 to 82 yr. Maximal expiratory airflow limitation in only four elderly asthmatics and only at low lung volumes was due completely to loss of lung elastic recoil. In the others, we estimate the reduction in lung elastic recoil was responsible for 35% reduction in maximal expiratory airflow at 80% of TLC, and 55% at 70% of TLC. Despite hyperinflation, transdiaphragmatic pressures and strength were normal. The mechanisms responsible for loss of lung elastic recoil remain elusive. The high incidence of loss of lung elastic recoil in chronic persistent asthma was unexpected, and its contribution to abnormal lung function needs to be emphasized.

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