Evaluation of the acoustic boundary conditions at the pleural surface that causes ultrasound-induced lung hemorrhage

Abstract

In a previous study [J. Acoust. Soc. Am. 108, 1290 (2000)], the acoustic impedance difference between intercostal tissue and lung was evaluated as a possible explanation for the enhanced lung damage with increased hydrostatic pressure, but the hydrostatic-pressure-dependent impedance difference alone could not explain the enhanced occurrence of hemorrhage. A hypothesis was suggested that the animal’s breathing pattern might be altered as a function of hydrostatic pressure, which in turn might affect the volume of air inspired and expired. The acoustic impedance difference between intercostal tissue and lung would be affected with altered lung inflation, thus altering the acoustic boundary conditions. In this study, the rat’s respiratory system was inhibited, a ventilator was used to control lung volume, and superthreshold ultrasound exposures of the lungs were conducted (3.14-MHz, 1000-Hz PRF, 1.3-μm pulse duration, 10-s exposure duration, 16.9-MPa in situ peak rarefactional pressure, MI of 5.8). Deflated lung was more easily damaged than inflated lung. The acoustic impedance difference between intercostal tissue and lung is much less for the deflated lung condition, suggesting that the extent of lung damage is related to the amount of acoustic energy that is propagated across the pleural surface boundary. [Work supported by NIH Grant No. HL58218.]