FIGURE 6 Relaxation pressure-volume curves of lungs (l), chest wall (w), and total respiratory system (rs). Arrows on diagrams by RV, FRC, and TLC indicate magnitude and direction of lung and chest wall elastic forces, and numbers indicate pressures. Prs equals the sum of Pl and Pcw, which are equal and opposite at FRC. Lung minimal volume (MV) cannot be measured in the intact respiratory system. (After Rahn et al, Am J Physiol 1946;146:161.)
increase much more even without the constraints of the chest wall.
Pulmonary disease frequently affects lung compliance without affecting the chest wall; this explains the particular changes in lung volume associated with different diseases. Emphysema increases lung compliance by destroying elastic tissue in the lungs. The disease disrupts the normal balance between elastases in the lung (e.g., from neutrophils) and endogenous elastase inhibitors. For example, emphysema occurs in individuals with a genetic deficiency for a ¡-antitrypsin. The normal elastase activity of trypsin destroys lung tissue when it is not inhibited by endogenous a1-antitrypsin, as is the case in normal subjects. Smoking also contributes to emphysema by inhibiting a1-antitrypsin. FRC increases in emphysema because the lung has less elastic recoil to balance chest wall expansion, so FRC moves toward the equilibrium position of the chest wall at a higher volume.
Interstitial pulmonary fibrosis, a so-called restrictive disease, can have the opposite effect. Fibroblasts lay down thick bundles of collagen in the alveolar walls, and this decreases lung compliance and volumes. FRC is a useful diagnostic measurement because it is a static volume that merely requires a person to relax after a normal exhalation. However, changes in airway resistance and the distribution of ventilation are the most important mechanical factors in lung disease.
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