A three-dimensional computational analysis of blood flow and fluid-structure interactions in the human aorta during traumatic rupture conditions

Traumatic aortic rupture (TAR) accounts for a significant mortality in automobile crashes. Conditions corresponding to aortic rupture are difficult to reproduce experimentally in simulated collisions involving cadaveric models due to complex mechanical interactions between the blood and the extensible aortic wall. Consequently, in situ observations of the dynamics of the flow inside the aorta, and of the dynamics of the aorta structure itself under traumatic loading conditions are virtually non-existent. 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. The result of parametric study reveals that the maximum level of 280 kPa pressure alone might cause TAR near the ascending aorta region, but that a characteristic deformation pattern, termed "dynamic self-pinch", occurs in the presence of superimposed chest deceleration, chest compression, and blood pressure. Considering combined impact loading, the model indicates that an aortic rupture initiates from the inner wall (intima) at the classical site, the isthmus. Traumatic rupture conditions of the aorta are determined as high acceleration over 50 g and large chest compression over 45 mm at the aortic root in combination with high intravascular pressure at a level of 280 kPa. In agreement with clinical findings, the tear predicted by the model is oriented transversely as a result of extremely high shear flow in the blood, coinciding with a stress concentration in the aortic wall near that region. The combined effect of chest deceleration, chest compression, and blood pressure appears to generate an aortic deformation and failure pattern that captures all the salient characteristics of clinically observed TAR.