lapse the extrathoracic trachea because of the rigidity of the trachea and stiffening of pharyngeal muscles by neurological influences. During unforced exhalation, the intraluminal airway pressure becomes positive relative to both the intrapleural and extrathoracic atmospheric pressures. With forced exhalation, however, the intrapleural pressure may exceed the intraluminal pressure and cause dynamic compression of the airway. This becomes important in interpreting the FVL, and in diagnosing the site and nature of an obstruction.

The normal expiratory FVL has two components (see Figure 2-1A). The first part is approximately the initial 20% of the FVC, comprised of the rise and the initial descent of flow rate, and is effort dependent. The remainder is effort independent, meaning that, above a moderate effort, no increase in flow is obtained by increasing muscular effort. This is related to the phenomenon of dynamic compression, in which high intrapleural pressure, caused by contraction of the diaphragm and intercostal muscles, is added to the elastic recoil of the distended alveoli to compose the intra-alveolar driving pressure. However, the same intrapleural pressure also compresses the airways, leaving alveolar elastic recoil as the sole driving pressure, irrespective of the degree of muscular effort. At high lung volume, airflow increases with effort because high intrapleural pressures cannot be developed and because elastic recoil is high. Furthermore, the so-called choke point, the point at which intraluminal pressures equal extraluminal pressures, is in the trachea, and the more proximal trachea with its cartilaginous support is resistant to collapse. This choke point moves more distally with decreasing volume to a point where the airways are susceptible to pressure and collapse.

The expiratory portion of the FVL of emphysema (Figure 2-2) has a recognizably different shape from a normal FVL. The resistance of the small airways is increased by intrinsic disease and by the loss of the tethering effect of alveoli on the airways. In addition, there is loss of alveolar elastic recoil as a result of alveolar destruction. Thus, at every lung volume, flow rates are lower than normal. In addition, the expiratory loop becomes concave downwards. The maximum flow of the inspiratory loop may be almost normal because the laxity of the airways allows them to be easily opened by negative intrapleural pressure, or the flow may be reduced when intrinsic inflammatory disease stiffens airways, producing increased resistance to flow.

Proper performance of the FVL is extremely important in interpretation (Figure 2-3). A poor initial expiratory effort may produce an apparent plateau on the expiratory loop and simulate a variable intrathoracic obstruction such as tracheomalacia. This often presents as a rounding rather than a plateau-like flat-

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