Siegel John H, Yang King H, Smith Joyce A, Siddiqi Shabana Q, Shah Chirag, Maddali Muralikrishna, Hardy Warren
Department of Cell Biology and Molecular Medicine, New Jersey Medical School, NJ 07631, USA.
J Trauma. 2006 May;60(5):1072-82. doi: 10.1097/01.ta.0000203542.38532.02.
Can aortic isthmus disruption occurring in a lateral motor vehicle crash (LMVC) be explained by the Archimedes Lever Hypothesis, where the intrathoracic aorta, super-pressurized by the thoracic impact force, functions as a rigid lever system? The long arm of this lever system is the proximal aorta-aortic arch, the short arm is the aortic isthmus fixed distally at the descending aorta, and the fulcrum is at the great vessels, especially the left subclavian artery.
The theory was tested by a simulation technique using a computer-based finite element numerical model system. This simulation model included the dynamics of the crashed vehicles, the direction of force impact, and the structure of the thorax and intrathoracic viscera, including the entire intrathoracic aorta. The specific patient whose data were entered into the model was chosen from a study of 34 LMCV aortic injuries (AIs). The model was constrained by patient and vehicle data from this surviving case.
Three sequential lateral thoracic levels impacted by the vehicle side structures were selected. At each level, the maximum mean intra-aortic pressure was 50 to 100 ms after impact, the structure dynamics of the actual crash and the resultant vehicle deformation were simulated; only when the lateral impact was induced in a transverse plane including the first 4 ribs at the level of the aortic arch/isthmus system, with intra-aortic pressures from 200 to 500 mm Hg, were AI-compatible stresses and deformations in the aortic wall achieved at the isthmus.
In LMVC AI, the simulation suggests that the aorta functions as an Archimedes Lever System in which the magnified force mediated by the long lever arm produces sufficient strain on the short lever arm to rupture the aorta at the isthmus.
在侧面机动车碰撞(LMVC)中发生的主动脉峡部破裂能否用阿基米德杠杆假说解释,即胸内主动脉在胸冲击力作用下超压,作为一个刚性杠杆系统发挥作用?该杠杆系统的长臂是近端主动脉-主动脉弓,短臂是在降主动脉远端固定的主动脉峡部,支点位于大血管处,尤其是左锁骨下动脉。
通过使用基于计算机的有限元数值模型系统的模拟技术对该理论进行测试。该模拟模型包括碰撞车辆的动力学、力的冲击方向以及胸部和胸内脏器的结构,包括整个胸内主动脉。输入模型数据的特定患者选自一项对34例LMVC主动脉损伤(AI)的研究。该模型受此存活病例的患者和车辆数据约束。
选择车辆侧面结构撞击的三个连续胸段水平。在每个水平,撞击后最大平均主动脉内压力出现在50至100毫秒,模拟了实际碰撞的结构动力学和由此产生的车辆变形;只有当在包括主动脉弓/峡部系统水平的前4根肋骨的横向平面内诱导横向撞击,主动脉内压力为200至500毫米汞柱时,才在峡部实现与AI兼容的主动脉壁应力和变形。
在LMVC AI中,模拟表明主动脉作为一个阿基米德杠杆系统发挥作用,其中由长杠杆臂介导的放大力在短杠杆臂上产生足够的应变,导致主动脉峡部破裂。