A Method for the Experimental Investigation of Acceleration as a Mechanism of Aortic Injury

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. Transient increases in intra-aortic pressure up to 177 kPa were measured. No macroscopic injuries to the thoracic aorta resulted from these tests. The method employed proved consistent and repeatable. This method may be appropriate for future investigation of the efficacy of acceleration as a predictor of aortic injury.