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FIGURE 3 Volume versus pressure (compliance curves) for an animal lung filled and emptied with air or saline. Surface tension decreases compliance (AV/AP) in the air-filled lung compared to the saline-filled lung. Compliance would be even lower in an air-filled lung without surfactant (not shown). (After Clements, Physiologist 1968;5:11.)

Pressure (cm H2O)

FIGURE 3 Volume versus pressure (compliance curves) for an animal lung filled and emptied with air or saline. Surface tension decreases compliance (AV/AP) in the air-filled lung compared to the saline-filled lung. Compliance would be even lower in an air-filled lung without surfactant (not shown). (After Clements, Physiologist 1968;5:11.)

pressure is not observed in lungs inflated with saline, indicating that surface tension contributes to this behavior (see later discussion). After the critical opening pressure is reached, large increases in lung volume occur with relatively small increases in pressure. Eventually, compliance decreases as the lung becomes fully distended and cannot stretch anymore. The lung has reached its elastic limits, set by the biomechanical properties of cartilage in conducting airways and a network of connective tissue in the alveolar walls. This network has rubber-like elastin bands that can stretch to a point at which the twine-like collagen fibers are fully extended and can stretch no further.

Deflation of air-filled lungs also shows changes in compliance with volume (Fig. 3). Lung volume decreases relatively little for a given drop in pressure near maximum volumes, but then compliance increases at lower lung volumes. At the end of deflation, there is no distending pressure but some volume remains in the lungs. This is airway closure, or trapping of gas in terminal spaces distal to collapsed airways. Airway closure is at its worst with lung compliance changes caused by aging or disease (see later discussion).

Inflating and deflating the lungs with saline eliminates hysteresis between the inflation and deflation curves (Fig. 3). This indicates that the interface between a gas phase and the wet alveolar surface contributes to hysteresis. The consequences of this for lung mechanics are considered next.

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