{"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.