The pulmonary capillary hemorrhage (PCH) bioeffect by ultrasound was recognized as a lung ultrasound (LUS) risk in 2012 when PCH was found in rats for LUS with a 7.6-MHz linear array at a peak rarefactional pressure (PRP) amplitude threshold of 1.0 MPa. The physical mechanism could be acoustical radiation pressure at the lung blood–air interface, but the detailed injurious process is not understood. An intravital microscopy study of the sonicated lung surface was initiated to observe the development of PCH that involved anesthesia, surgery for the chest wall window, spontaneous breathing or ventilation at 15–20 cm H2O, and LUS, with heated stage, physiological monitoring and fluid infusion. At least six rats had acceptable exposure and observational conditions, but no PCH was induced for 9 MHz LUS with 1.25 cm focal depth, at the maximum 4.4 MPa. This result was puzzling, especially given the lack of chest wall attenuation. Recent tests of human LUS have also had mixed results (Wolfram et al. ILUS 2025). LUS PCH has also been found to vary with physiological conditions such as shock or fraction of inspired oxygen. Physiological patient conditions are entangled with the physical ultrasound exposure conditions to determine the risk of LUS PCH.
Miller et al. (Wed,) studied this question.