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局部狹窄股動脈中脈動流的流動特性數(shù)值模擬及試驗研究

發(fā)布時間:2018-09-10 19:54
【摘要】:隨著社會生活水平的提高以及人口老齡化問題日趨嚴(yán)峻,各種誘發(fā)因素,比如高血脂、高血壓、肥胖等,都會引起血管發(fā)生硬化,導(dǎo)致血管狹窄,由此引發(fā)的各類心血管疾病威脅著人們的生命健康。開展病灶部位血流動力學(xué)的研究,對于研究其發(fā)病機理及臨床醫(yī)生手術(shù)方案的確定具有重要的實際意義。本文搭建了可模擬生理條件下的動脈血流動力學(xué)環(huán)境、參數(shù)可控的體外試驗臺,利用高精度的壓力傳感器監(jiān)測正常股動脈及病變股動脈內(nèi)的血液壓力。作為試驗研究的補充,以股動脈血管為原型,建立血管壁/血液耦合模型,對正常血管、孤立性、節(jié)段性和彌漫性病變血管四種情況進(jìn)行數(shù)值模擬,分析血管壁的壁面剪切力分布和變形情況,以及管壁對內(nèi)部血液流場的影響。具體展開以下工作:(1)研究并確定了血液非定常流動的雙向流固耦合分析方法。血液在流動過程中,由于黏性的影響,會對血管壁產(chǎn)生較大的切應(yīng)力,可將血液視為黏性流體。在血流動力學(xué)研究中,牛頓流體與非牛頓流體對所得結(jié)果影響并不大,誤差不到2%,故本文數(shù)值模擬所用的流體為牛頓流體,試驗流體用水和甘油的混合溶液(牛頓流體)代替血液。試驗是在壓強和溫度變化較小的情況下進(jìn)行的,所以可將流體視為不可壓縮流體。運用雷諾數(shù)公式,計算得出在體股動脈的最大雷諾數(shù)約為1474~1942,均小于2300,故本文選用Laminar模型。血管為薄壁、各向同性、無滲透、無滑移(no slip)的線彈性直圓管。(2)搭建了管內(nèi)脈動壓力測量試驗臺,該試驗臺由電腦、電源、伺服電機、驅(qū)動器、PLC控制器、滾珠絲桿、注射器、微型壓力傳感器和數(shù)據(jù)采集器組成。PLC和驅(qū)動器通過上機程序控制伺服電機的運行。注射器固定安裝在滾珠絲桿滑塊上,伺服電機連接滾珠絲桿,從而控制注射器桿的進(jìn)給速度。利用綜合精度為±0.2%的微型壓力傳感器測量血管內(nèi)脈動壓力值,并用數(shù)據(jù)采集器獲取數(shù)據(jù)。基于狹窄股動脈簡化模型參數(shù)要求,將人體真實血管模型幾何尺寸放大3.2倍,制備了血管試驗樣件。通過血管狹窄率公式,制作出孤立性、節(jié)段性、彌漫性血管和狹窄率為40%、60%、80%的病變血管模型。采用拉伸試驗機測量血管的彈性模量,其值為1.62×106Pa。通過試驗對比分析正常及病變股動脈兩監(jiān)測點處的壓力差可以看出,股動脈的壓力隨時間的變化范圍和趨勢與入口速度變化趨勢存在緊密的聯(lián)系。隨著速度的增大,脈沖壓力達(dá)到峰值的數(shù)值變小。狹窄段區(qū)域越長,狹窄段前后的壓力差幅值變化越大。狹窄度不同,病變血管壓力差達(dá)到的幅值也不同,狹窄度為80%的血管脈動壓力幅值最大。狹窄區(qū)域后端壓力差的增大,導(dǎo)致血管內(nèi)壁損傷,易引起其它未發(fā)病部位的病變。(3)應(yīng)用Solidworks軟件構(gòu)建血管的三維CAD模型,采用ICEM對固體和流體域劃分網(wǎng)格。應(yīng)用ANSYS軟件,模擬分析了人工血管監(jiān)測點處壓力差的大小,并與試驗結(jié)果做了對比,發(fā)現(xiàn)狹窄段前后端的試驗結(jié)果幅值比模擬結(jié)果稍大且達(dá)到峰值的時刻稍微滯后,但基本變化一致,確定了數(shù)值模擬計算方法的可行性。因此,本文所采取的流固耦合數(shù)值模擬方法可用來模擬分析人體正常股動脈和病變股動脈內(nèi)的血流動力學(xué)特性。(4)對比分析正常及病變股動脈壓力、速度、壁面切應(yīng)力、血管形變、速度流線等參數(shù)可以看出,正常血管的壓力和速度呈均勻性變化,股動脈狹窄造成狹窄處速度增大。狹窄后區(qū)域有渦流形成,對管壁造成損傷,加速了其它未發(fā)病部位的病變。在整個心動周期內(nèi),病變血管的狹窄處壁面切應(yīng)力值較大,剝離內(nèi)皮細(xì)胞,導(dǎo)致脂質(zhì)等大分子物質(zhì)沉附、累積在細(xì)胞損傷處。血管狹窄后區(qū)域管壁變形最大,管壁出現(xiàn)疲勞效應(yīng),易導(dǎo)致血管破裂。
[Abstract]:With the improvement of social living standards and the increasing severity of population aging problem, all kinds of inducing factors, such as hyperlipidemia, hypertension, obesity, will cause vascular sclerosis, resulting in vascular stenosis, resulting in a variety of cardiovascular diseases threatening people's lives and health. It is of great practical significance to study the pathogenesis and determine the operation plan of clinicians.In this paper, an in vitro test-bed with controllable parameters and simulated hemodynamic environment of arteries under physiological conditions was set up to monitor the blood pressure in normal femoral artery and diseased femoral artery with high precision pressure sensor. In order to analyze the distribution and deformation of wall shear force and the influence of wall on the internal blood flow field, the following work was carried out: (1) To study and determine the effect of wall on the internal blood flow field. A bi-directional fluid-solid coupling method for the analysis of unsteady blood flow is presented.During the process of blood flow, due to the influence of viscosity, a large shear stress will occur on the wall of the blood vessel and the blood can be regarded as a viscous fluid.In the study of hemodynamics, Newtonian and non-Newtonian fluids have little influence on the results, and the error is less than 2%. The fluid to be used is a Newtonian fluid. The mixed solution of water and glycerol (Newtonian fluid) is used to replace the blood. The experiment is carried out under the condition of small pressure and temperature change, so the fluid can be regarded as incompressible fluid. The maximum Reynolds number of the femoral artery in vivo is calculated by using Reynolds number formula, which is about 1474-1942, and is less than that of the femoral artery in vivo. In this paper, the Laminar model is used. The blood vessels are thin-walled, isotropic, impermeable and no-slip linear elastic straight circular tubes. (2) A test-bed for measuring the fluctuating pressure in tubes is built. The test-bed consists of a computer, a power supply, a servo motor, a driver, a PLC controller, a ball screw, a syringe, a micro-pressure sensor and a data collector. The actuator controls the operation of the servo motor by a program on the computer.The syringe is fixed on the ball screw slider and the servo motor is connected to the ball screw to control the feed speed of the syringe rod.The pulsating pressure in the blood vessel is measured by a micro-pressure sensor with a comprehensive accuracy of (+0.2%) and the data is obtained by a data collector. The parameters of the simplified model of narrow femoral artery were enlarged by 3.2 times the geometric size of the real blood vessel model, and the vascular test sample was prepared. The pressure difference between normal and diseased femoral arteries was compared and analyzed. It was found that the range and trend of femoral arterial pressure with time were closely related to the trend of inlet velocity. The greater the amplitude of pressure difference is, the different the degree of stenosis is, the greater the amplitude of pressure difference is. The amplitude of pressure difference is 80% of the stenosis. ICEM was used to mesh the solid and fluid domains. ANSYS software was used to simulate and analyze the pressure difference at the monitoring point of artificial blood vessel. The results were compared with the experimental results. It was found that the amplitude of the experimental results at the front and back of the narrow segment was slightly larger than that of the simulation results and the time lagged slightly when the peak value was reached, but the basic changes were consistent. Therefore, the fluid-solid coupling numerical simulation method adopted in this paper can be used to simulate and analyze the hemodynamic characteristics of normal and diseased femoral arteries. (4) Comparing and analyzing the normal and diseased femoral arteries pressure, velocity, wall shear stress, vascular deformation, velocity streamline and other parameters can be seen, normal blood vessels. The stenosis of the femoral artery results in an increase in the velocity of the stenosis. Eddies form in the stenosis area, causing damage to the wall of the vessel and accelerating the pathological changes of other non-pathogenic sites. After vascular stenosis, the wall deformation is the greatest, and fatigue effect appears on the wall, which is easy to lead to vascular rupture.
【學(xué)位授予單位】:吉林大學(xué)
【學(xué)位級別】:碩士
【學(xué)位授予年份】:2017
【分類號】:R54

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