The Physics of Stroke

B. Okeahialam, Anil I. Sirisena
{"title":"The Physics of Stroke","authors":"B. Okeahialam, Anil I. Sirisena","doi":"10.1177/25166085231174796","DOIUrl":null,"url":null,"abstract":"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.","PeriodicalId":93323,"journal":{"name":"Journal of stroke medicine","volume":"56 1","pages":"7 - 10"},"PeriodicalIF":0.0000,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of stroke medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1177/25166085231174796","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

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.
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
中风的物理学
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。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
A Study of the Correlation of Pulsatility Index by Transcranial Doppler in the Clinical Outcome of Patients with Cerebral Venous Sinus 
Thrombosis Acute Ischaemic Stroke in a Young Adult in Sub-Saharan Africa: A Case Report of Post-strangulation Carotid Artery Dissection The Effect of Biological Sex on a County Pre-hospital Stroke Initiative COVID and Vaccine-related Cerebral Venous Thrombosis Expert Consensus on Improving Stroke Care Ecosystem in India
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1