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Rupture of the thoracic aorta is a leading cause of rapid fatality in automobile crashes, but the mechanism of this injury remains unknown. One commonly postulated mechanism is a differential motion of the aortic arch relative to the heart and its neighboring vessels caused by high-magnitude acceleration of the thorax. Recent Indy car crash data show, however, that humans can withstand accelerations exceeding 100 g with no injury to the thoracic vasculature. This paper presents a method to investigate the efficacy of acceleration as an aortic injury mechanism using high-acceleration, low chest deflection sled tests. The repeatability and predictability of the test method was evaluated using two Hybrid III tests and two tests with cadaver subjects. The cadaver tests resulted in sustained mid-spine accelerations of up to 80 g for 20 ms with peak mid-spine accelerations of up to 175 g, and maximum chest deflections lower than 11% of the total chest depth.

The objective of the current study was to provide a comprehensive characterization of human biomechanical response to whole-body, lateral impact. Three approximately 50th-percentile adult male PMHS were subjected to right-side pure lateral impacts at 4.3 ± 0.1 m/s using a rigid wall mounted to a rail-mounted sled. Each subject was positioned on a rigid seat and held stationary by a system of tethers until immediately prior to being impacted by the moving wall with 100 mm pelvic offset. Displacement data were obtained using an optoelectronic stereophotogrammetric system that was used to track the 3D motions of the impacting wall sled; seat sled, and reflective targets secured to the head, spine, extremities, ribcage, and shoulder complex of each subject. Kinematic data were also recorded using 3-axis accelerometer cubes secured to the head, pelvis, and spine at the levels of T1, T6, T11, and L3. Chest deformation in the transverse plane was recorded using a single chestband.