研究生: |
何正陽 Cheng-yang Ho |
---|---|
論文名稱: |
動脈硬化對心臟血管主動脈弓動態流場結構與衍化的影響:質點軌跡視流法與PIV量測技術的開發與應用 Influence of Atherosclerosis on Pulsatiles Flows in Human Aortic Arch:Flow Diagnostics using Particle Image Velocimetry |
指導教授: |
黃榮芳
Rong-fung Huang |
口試委員: |
劉昌煥
Chang-huan Yeh 楊騰芳 Ten-fang Yang |
學位類別: |
碩士 Master |
系所名稱: |
工程學院 - 機械工程系 Department of Mechanical Engineering |
論文出版年: | 2006 |
畢業學年度: | 94 |
語文別: | 中文 |
論文頁數: | 191 |
中文關鍵詞: | 脈動流 、壁面定律 、壁函數 、主動脈弓 、心臟血管 、質點軌跡視流法 、動脈硬化 、PIV量測技術 |
外文關鍵詞: | wall function, normal stress, aortic arch, pulsatiles flow, shear stress, PTFV, PIV, law of wall |
相關次數: | 點閱:231 下載:2 |
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本研究利用質點軌跡流場觀察法(PTFV)與質點影像速度儀(PIV),針對主動脈弓彎管模型進行流場診測,探討動脈粥狀硬化斑所造成的管路窄縮對主動脈弓血流的影響。三種不同主動脈弓模型的窄縮率分別為0%、25%及50%,使用血液脈動泵輸出心臟脈動波搭配兩種不同的脈動頻率,分別為f = 0.5Hz與f = 1.2Hz,Womersley number為9.02 與13.97。觀察管內流場之結構衍化以及量測速度、壁面剪應力和壁面垂直應力的分佈。並利用壁面定律(law of wall)驗證此套PIV後處理軟體,在徑向速度很小的情況下,靠近壁面的計算規則符合此定律。在實驗中可觀察到,在心搏脈動波中,隨著脈動頻率的增加,流場衍化結構會發生時間延後的現象。在心搏脈動波收縮行程中,當管路拱型區窄縮率越高時,管路的紊流臨界雷諾數就越低,流體經過硬化物發生分離現象的特徵時間會提前,分離點位置會延後。分離區從拱型區延伸至降胸主動脈內側壁面,分離區內的流場型態包含二次流、螺旋狀上升流以及渦漩逸放、渦漩拉伸的流場結構。在正常主動脈弓中,拱型區域中心截面內側壁面所受到的壁面剪應力最小,加上二次流往內側壁面的衝擊,造成脂肪斑塊容易在此區聚集產生動脈硬化脂肪塊,使得管路窄縮。在上升主動脈及降胸主動脈的內外側壁面剪應力較大。在管路即將轉彎處的外側壁面,承受較大的動量垂直分量衝擊,當血管組織發生病變彈性降低時,較容易產生動脈瘤。隨管路窄縮率升高,而窄縮區的剪應力也會劇烈的增加,此時強大的剪應力會作用在硬化物纖維狀的脂肪斑,與膠原蓋,破壞其組織。一旦組織被破壞,血小板將匯聚在此處並凝結形成血栓,導致血液中的氧氣與養分無法運送到器官造成器官機能衰竭、壞死。
flow characteristics and evolution processes in aortic arch models with atherosclerosis are diagnosed by using the particle tracking flow visualization method (PTFV) and the particle image velocimeter (PIV) over various experimental models and pulsating frequencies. These aortic arch models are made of transparent plexiglas U-tubes. The pulsating frequencies are set at 0.5 Hz and 1.2 Hz. Quantitative flow properties, e.g., the velocity vector maps, streamline patterns, axial velocity, wall shear-stress, and wall normal stress, are obtained by analyzing the measured PIV data. It is found that the flows evolve complicatedly into three dimensional structures during the processes of acceleration, deceleration, and reversing. During systole stroke, the boundary layer on the inner wall separates from the area near the turning arch to the descending thoracic aorta and three dimensional secondary flows are observed. These characteristic flow structures induce reverse and low speed flows and therefore would increase the probability of plaque deposition around the inner wall of the arch. When the stenosis increases, the separation point would be deferred a little to the downstream area and the timing for separation would be advanced. During the systole stroke, the normal impulse component developed in the flow in the regions around the up- and downstream turning arches of the outer tube-wall are relatively high. During the diastolic process, strong reversed flow is produced along the inner walls of curvature. In the aortic arch model without the atherosclerosis, the maximum wall shear stress appears on the inner and outer walls of the ascending aorta, which implies that the aortic dissection would be occurring there most likely. In the aortic arch model with the atherosclerotic, the maximum wall shear stress appears on the inner wall of the arch might crack fibrolipid plaque and collagenous cap of atherosclerotic plaque and therefore would induce rapid assembling of platelets on the exposed connective tissues, form the thrombosis, and therefore diminish the transport of oxygen and metabolites to the organs.
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