Abstract
In anesthetized pigs (25-40 kg), we generated stress waves in the lung by rapid deflation of an esophageal balloon. The source distortion was measured by an accelerometer (1 g wt) bonded to the balloon. Stress waves were detected by three accelerometers bonded to intercostal muscle and to the skin near midchest. The distance between the source and chest receivers were measured radiographically. Cross-spectral analysis was used to calculate transit times. We measured stress wave velocities at airway pressures of 0 (functional residual capacity) and 25 cmH2O. Transpulmonary pressure (Ptp) was measured by an esophageal balloon. In vivo, stress wave velocities increased from 291 +/- 117 (SD) cm/s at 3.0 +/- 0.9 cmH2O Ptp to 573 +/- 73 cm/s at 13.8 +/- 3.5 cmH2O Ptp (n = 6). These velocities agreed with longitudinal wave velocities measured in isolated sheep lungs and predictions based on the elastic moduli of lung parenchyma. Post-mortem edema was induced by intratracheal instillation of 200 ml of saline, resulting in a wet-to-dry weight ratio of 7.7 +/- 1.4 (n = 5). At 15 cmH2O Ptp, stress wave velocities decreased from 565 +/- 155 cm/s before edema to 445 +/- 130 cm/s after edema. This decrease correlated well with predictions based on the increased lung density, as dictated by elasticity theory.
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