Christy K. Holl
Diagnostic Radiology, Yale Univ. School of Medicine, 333 Cedar St., New Haven, CT 06510
Advanced Technology Labs., Bothell, WA 98041-3003
Yale Univ., New Haven, CT 06520
Advanced Technology Labs., Bothell, WA
Ronald A. Roy
Univ. of Washington, Seattle, WA 98105-6698
Extravasation of blood cells has been observed in the lungs of mice and monkeys exposed to pulsed ultrasound conditions comparable to diagnostic levels [Child et al., Ultrasound Med. Biol. 16, 817--825 (1990) and A. F. Tarantal and D. R. Canfield, Ultrasound Med. Biol. (in press)]. In order to understand the ultrasound exposure conditions under which damage occurs, lung was modeled as a simple interface from water to air. The acoustic pressure output of an Advanced Technology Laboratories Ultramark 9 High Definition Imaging[sup (registered)] system with a 5-MHz linear array transducer in pulsed Doppler mode (4 MHz) was interrogated near the pressure release surface ((less than or equal to)3 mm) with a Marconi 0.5-mm bilaminar membrane-type PVDF hydrophone. For the nonlinear waveforms produced, peak negative pressures of 2.0 MPa measured in free filed were increased to 4.5 MPa due to constructive interference near the interface. The behavior of the pressure release surface was also simulated computationally as a low-pass filter with a 180(degrees) phase shift. The impulse response of the interface was constructed using experimentally measured spectra of the incoming and reflected waves. The pressure waveform was calculated as a function of position by superimposing the incoming and reflected waves and was compared to the hydrophone measurements. The implications of these observations on in situ acoustic exposure near lung will be discussed.