Pressure-Volume Curves in Smokers: Comparison with Alpha-1-Antitrypsin Deficiency

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Abstract
The diagnosis of emphysema has been associated with changes in the appearance of the pressure-volume (P-V) curve: reduced maximal recoil pressure, increased lung volume, and a shift in the position of the curve to the left. In our clinical practice, we have observed that patients with chronic obstructive lung disease (COPD) commonly had P-V curves with reduced maximal elastic recoil that are difficult to classify according to the classic description of the P-V curve in emphysema. In order to study the variability of P-V curves, we studied 39 cigarette smokers attending a pulmonary clinic (age, 61 .+-. 1 yr; smoking history, 45 .+-. 3 pack-years; mean .+-. SEM) and compared them with 20 patients with alpha-1-antitrypsin deficiency (AATD) (age, 41 .+-. 2 yr; 13 smokers with a smoking history of 17 .+-. 2 pack-years, and seven nonsmokers). Subjects underwent spirometry, lung volume, and diffusing capacity measurements as well as static deflation P-V curves. To characterize the P-V curves, we used transpulmonary pressure at 90% of TLC (PL90) as a measure of overall recoil and specific compliance (Csp) as a measure of the slope of the initial part of the P-V curve. The curves of non-AATD smokers were classified into three groups: 13 had PL90 .gtoreq. 80% predicted (Group I), 13 had PL90 < 80% predicted and Csp .gtoreq. 0.08 (Group II), and 13 had PL90 < 80% predicted and Csp < 0.08 (Group III). Group II curves resembled those typically associated with emphysema. Group III curves showed more hyperinflation and were flatter. AATD curves resembled those of Group II, but showed greater changes in compliance and PL90. The spirometry and lung volumes of Group III, in contrast, resembled those of the AATD smokers. For the same changes in elastic recoil. Group III had more abnormal flows and volumes. There appear to exist different patterns of mechanical abnormalities among smokers with loss of elastic recoil; these differences in mechanical properties may reflect differences in underlying lung disorders and, thus, in the pathogenesis of lung destruction.