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This paper presents an analysis of the displacement measurement of the Hybrid III 50th percentile male dummy chest in quasistatic and dynamic loading environments. In this dummy, the sternal chest deformation is typically characterized using a sliding chest potentiometer, originally designed to measure inward deflection in the central axis of the dummy chest. Loading environments that include other modes of deformation, such as lateral translations or rotations, can create a displacement vector that is not aligned with this sensitive axis. To demonstrate this, the dummy chest was loaded quasistatically and dynamically in a series of tests. A string potentiometer array, with the capability to monitor additional deflection modes, was used to supplement the measurement of the chest slider.

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.

This study evaluated the response of restrained post-mortem human subjects (PMHS) in 40 km/h frontal sled tests. Eight male PMHS were restrained on a rigid planar seat by a custom 3-point shoulder and lap belt. A video motion tracking system measured three-dimensional trajectories of multiple skeletal sites on the torso allowing quantification of ribcage deformation. Anterior and superior displacement of the lower ribcage may have contributed to sternal fractures occurring early in the event, at displacement levels below those typically considered injurious, suggesting that fracture risk is not fully described by traditional definitions of chest deformation. The methodology presented here produced novel kinematic data that will be useful in developing biofidelic human models.

Traumatic aortic rupture (TAR) accounts for a significant mortality in automobile crashes. A numerical method by means of a mesh-based code coupling is employed to elucidate the injury mechanism of TAR. The aorta is modeled as a single-layered thick wall composed of two families of collagen fibers using an anisotropic strain energy function with consideration of viscoelasticity. A set of constitutive parameters is identified from experimental data of the human aorta, providing strict local convexity. An in vitro aorta model reconstructed from the Visible Human dataset is applied to the pulsatile blood flow to establish the references of mechanical quantities for physiological conditions. A series of simulations is performed using the parameterized impact pulses obtained from frontal sled tests.

Very little experimental research has focused on the kinematics, dynamics, and injuries of rear-seated occupants. This study seeks to develop a baseline response for rear-seated post mortem human surrogates (PMHS) in frontal crashes. Three PMHS sled tests were performed in a sled buck designed to represent the interior rear-seat compartment of a contemporary midsized sedan. All occupants were positioned in the right-rear passenger seat and subjected to simulated frontal crashes with an impact speed of 48 km/h. The subjects were restrained by a standard, rear seat, 3-point seat belt. The response of each subject was evaluated in terms of whole-body kinematics, dynamics, and injury. All the PMHS experienced excessive forward translation of the pelvis resulting in a backward rotation of the torso at the time of maximum forward excursion.

Rear seat adult occupant protection is receiving increased attention from the automotive safety community. Recent anthropomorphic test device (ATD) studies have suggested that it may be possible to improve kinematics and reduce injuries to rear seat occupants in frontal collisions by incorporating shoulder-belt force-limiting and pretensioning (FL+PT) technologies into rear seat 3-point belt restraints. This study seeks to further investigate the feasibility and potential kinematic benefits of a FL+PT rear seat, 3-point belt restraint system in a series of 48 kmh frontal impact sled tests (20 g, 80 ms sled acceleration pulse) performed with post mortem human surrogates (PMHS). Three PMHS were tested with a 3-point belt restraint with a progressive (two-stage) force limiting and pretensioning retractor in a sled buck representing the rear seat occupant environment of a 2004 mid-sized sedan.

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.

Thoracic trauma is the principle causative factor in 30% of road traffic deaths. Researchers have developed force-deflection corridors of the thorax for various loading conditions in order to elucidate injury mechanisms and to validate the mechanical response of ATDs and numerical human models. A corridor, rather than a single response characteristic, results from the variability inherent in biological experimentation. This response variability is caused by both intrinsic and extrinsic factors. The intrinsic factors are associated with individual differences among human subjects, e.g., the differences in material properties and in body geometry. The extrinsic sources of variability include fluctuations in the loading and supporting conditions in experimental tests.