Unsuspected Pseudophysiologic Emphysema in Chronic Persistent Asthma

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Abstract
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 6 15 yr (mean 6 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 asth- matics, 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. Hyperin- flation was present at residual volume (RV), FRC, and TLC in all subjects. Diffusing capacity was normal or elevated and lung com- puted 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 com- pletely 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. Airway structural studies in chronic asthma have emphasized morphologic alterations of injury associated with an ongoing inflammatory process. The structural changes, leading to fi- brosis, include denuding of epithelium, deposition of collagen in subepithelial layers, smooth muscle thickening, bronchovas- cular permeability, edema, goblet cell hyperplasia, and sub- mucosal gland hypertrophy (1-5). These changes are referred to collectively as airway remodeling (1-5), potentially leading to irreversible airway obstruction (3, 5-14). In a prospective 10-yr follow-up study, Ulrik and Backer (14) reported that a subgroup of treated asthmatics may expe- rience irreversible, very steep rates of decline in FEV 1 despite persistent normal TLC and diffusing capacity. They suggested emphysema did not develop. The present physiologic study evaluated patients with mod- erate to severe, chronic persistent asthma who have seemingly irreversible lung function despite aggressive treatment, to de- termine the mechanisms of airflow limitation. We attempted to explore the contribution of intrinsic airway obstruction, ab- normal lung elastic recoil, or both in limiting expiratory air- flow. Of 18 patients studied, 15 had marked loss of static lung elastic recoil pressure. This loss was responsible for a 35% to 55% reduction in maximal expiratory airflow. Physiologic consequences of loss of lung elastic recoil in chronic persistent asthma include hyperinflation, premature airway closure, and abnormal expiratory airflow. The mecha- nism remains elusive.