中风的物理学

B. Okeahialam, Anil I. Sirisena
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摘要

流体在管道中的流动遵循物理的自然规律。它取决于推进力、通道长度、通道口径和流过的流体粘度。在人类中,流向大脑的血液遵循这些规律。当受到疾病的干扰时,血流和氧气输送受到损害,导致脑血管疾病或中风。流向人脑的流量取决于心脏产生的力、血液的粘度、血管的长度和血管通道的直径及其可变性。在正常情况下,脑血管可以自动调节自身,保证充足的脑灌注。脑血管粥样硬化性心血管疾病,血流动力学紊乱,结果就是中风。动脉粥样硬化性心血管疾病使血管僵硬,从而增加腔内压力。这会损害内层,内皮细胞,并为斑块的形成做好准备。斑块使血管口径变窄,狭窄处的血流压力增大,但在此点以外的血流压力减小。气流不再是层流而变成湍流。当斑块在狭窄处被高压破裂时,凝血级联被激活,血液粘度上升。这些易形成血栓。血管变薄,失去了血管壁的弹性,血管壁很容易随着血压突然升高而破裂。在这种状态下,血管失去了改变直径以缓冲这些影响的固有能力。血液流动变得不稳定。超过这些点的脑组织遭受缺血,实际上可能有血液流入这些点。新陈代谢受损,大脑高级功能受损,导致脑血管疾病或中风。了解疾病如何改变血流动力学将使临床医生更好地掌握对抗导致中风的动脉粥样硬化性心血管疾病发展所需的知识。
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The Physics of Stroke
Flow of fluids in channels obey the natural law of Physics. It is dependent on force of propulsion, length of channel, caliber of channel and viscosity of fluid flowing through. In humans, blood flow to the brain obeys these laws. When perturbed by disease, flow and oxygen delivery are compromised resulting in cerebrovascular disease or stroke. Flow to the human brain depends on the force generated by the heart, viscosity of blood, length of the vessels, and diameter of the vascular channels with their variability. In normal situation, the cerebrovascular vessels can automatically regulate itself to ensure adequate cerebral perfusion. With Atherosclerotic Cardiovascular disease in the cerebral vasculature, flow dynamics is deranged and the result is the disease called stroke. Atherosclerotic cardiovascular diseases make the vessels stiff thus increasing intraluminal pressure. This damages the inner lining, the endothelium, and prepares grounds for the development of plaques. Plaques narrow vascular caliber increasing flow pressure at the narrow point but decreasing it beyond that point. The flow ceases to be laminar and becomes turbulent. When the plaques are ruptured by the high pressure at the points of narrowing, the blood coagulation cascade is activated and blood viscosity rises. These predispose to thrombus formation. The vessels thin out having lost elasticity of the walls rupturing easily with sudden blood pressure surges. In this state, the vessels lose their intrinsic ability to vary their diameters to cushion these effects. Blood flow becomes precarious. Cerebral tissue beyond such points suffer from ischemia and may actually have blood egress into them. Metabolism is impaired and higher cerebral function suffers resulting in cerebrovascular disease or stroke. Understanding how disease alters flow dynamics will equip clinicians better with the knowledge required to counter development of atherosclerotic cardiovascular diseases that result in stroke.
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