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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.

Injury to the thorax is the predominant cause of fatalities in crash-involved automobile occupants over the age of 65, and many elderly-occupant automobile fatalities occur in crashes below compliance or consumer information test speeds. As the average age of the automotive population increases, thoracic injury prevention in lower severity crashes will play an increasingly important role in automobile safety. This study presents the results of a series of sled tests to investigate the thoracic deformation, kinematic, and injury responses of belted post-mortem human surrogates (PMHS, average age 44 years) and frontal anthropomorphic test devices (ATDs) in low-speed frontal crashes. Nine 29 km/h (three PMHS, three Hybrid III 50th% male ATD, three THOR-NT ATD) and three 38 km/h (one PMHS, two Hybrid III) frontal sled tests were performed to simulate an occupant seated in the right front passenger seat of a mid-sized sedan restrained with a standard (not force-limited) 3-point seatbelt.