主动脉夹层裂纹面内扩展的数值模拟

Numerical Simulation of In-Plane Crack Propagation in Aortic Dissection

目的基于界面损伤提出一种裂纹面内扩展的数值模拟方法,探究裂纹面内扩展的规律。方法基于双线性牵引分离定律表征中膜层的3种界面损伤模式,模拟剥离实验和剪切实验以标定其损伤参数。通过内聚力模型法将损伤界面引入理想化的双层圆管状主动脉模型中,模拟假腔在面内的扩展趋势。通过控制变量法建立多个计算模型,研究假腔几何参数对裂纹面内扩展方向、临界扩展压力以及界面损伤模式的影响。结果界面损伤在轴向扩展中以张开型(I型)为主,在环向扩展中以滑移型(II型)为主;随着初始假腔径向深度增加,裂纹扩展方向由环向转变为轴向,临界扩展压力降低,且轴向损伤更趋近于纯张开型;随着初始假腔环向角度和轴向长度的增加,临界压力降低,环向损伤更趋近于纯滑移型。单一型损伤比混合型损伤具有更低的临界压力。结论通过内聚力模型法可有效模拟主动脉中膜弹性层之间的界面损伤行为,适用于夹层假腔面内扩展的数值模拟。研究结果有助于理解夹层裂纹扩展的复杂病理生理过程。

Objective Based on interface damage,a numerical simulation method for in-plane propagation of false lumen(FL)was proposed to explore the regular pattern of in-plane propagation of the initial cavity.Methods Three interface damage modes were characterized by bi-linear traction separation law,and the damage parameters were calibrated by simulating peeling and shearing tests.The damage interface was introduced into the ideal double-layer cylindrical tube aortic model by means of cohesive zone model(CZM)to simulate the in-plane propagation of FL.The control variable method was used to establish several computational models to investigate the influence of cavity geometric parameters on propagation direction,critical pressure and interface damage mode.Results The interface damage was mainly opening mode(Mode I)in axial propagation and sliding mode(Mode II)in circumferential propagation.With radial depth of the initial cavity increasing,the propagation of the FL changed from circumferential direction to axial direction,the critical pressure decreased,and the axial damage tended to be pure opening mode.With circumferential angle and axial length of the initial cavity increasing,the critical pressure decreased and the circumferential damage tended to be pure sliding mode.The critical pressure of single damage was lower than that of mixed damage.Conclusions The CZM can effectively characterize interface damage behavior of elastic lamellae within the media,and it applies to numerical simulation of in-plane propagation of the FL.The results of this study are helpful to understand the complex pathophysiological process of dissection crack propagation.