La modélisation de la pression intracrânienne est un sujet de thèse pluridisciplinaire faisant intervenir aussi bien des connaissances en mathématiques appliquées, utiles pour résoudre les équations de la mécanique des fluides et des interactions fluide-structure, qu'en anatomie ou en physiologie, afin de modéliser correctement le système cérébrospinal. L'objectif de ce travail est de déterminer de manière non invasive la pression intracrânienne. Différentes méthodes numériques, utilisant la méthode des éléments finis, sont présentées puis validées avant d'être appliquées à nos modèles numériques. Le premier modèle, faisant intervenir uniquement la composante fluide du système cérébrospinal, est une bifurcation prenant en compte les trois compartiments principaux de liquide cérébrospinal. Le second modèle, prenant maintenant en compte les structures présentes dans le système cérébrospinal, est une représentation simplifiée de ce système en interaction fluide-structure. Parallèlement à cette étude numérique, une étude sur des données expérimentales, de flux et de pression, est réalisée afin d'alimenter nos modèles numériques, de comparer nos résultats de simulation, et de mieux appréhender le comportement du système cérébrospinal in vivo / Intracranial pressure modeling is a multidisciplinary PhD thesis subject involving both applied mathematics knowledge, useful to solve the fluid mechanics equations and fluid-structure interactions problems, and in anatomy or physiology, to correctly model the cerebrospinal system. The goal of this work is to determine non-invasively the intracranial pressure. Different numerical methods, using the finite element method, are presented and validated before being applied to our numerical models. The first model, involving fluid component of the cerebrospinal system only, is a bifurcation taking into account the three main cerebrospinal fluid compartments. The second model, now taking into account structure in the cerebrospinal system, is a simplified representation of this system in fluid-structure interaction. Along with the numerical study, a study on experimental data, flow and pressure, is conducted to serve our numerical models, to compare our simulation results, and to better understand the cerebrospinal system behavior in vivo

Despite improved life expectancy compared to medical management alone, Ventricular Assist Device (VAD) recipients show survival rates of 80% at 12 months and 70% at 24 months. A large portion of VAD-associated mortality results from increased risk of stroke with an event frequency reported between 14-47%. Recent concerns have been raised about unprecedented increases of thrombus formation in VAD recipients with subsequent reports pointing towards implantation techniques as a critical contributor to these events. Thus, the overall prognosis with mechanical support can improve by advancing the surgeon’s approach to VAD implantation. Previous studies using Computational Fluid Dynamics (CFD) were aimed at reducing stroke rates by tailoring the VAD outflow graft (VAD-OG) angle to direct any circulating emboli away from the cerebral vessels. In-vitro, or benchtop, models are often developed as computational counterparts. In order to accurately model the hemodynamics in the cardiovascular system, pulsatile flow must be mimicked. This is achieved in the computational domain by what is called a Windkessel model. This project seeks to develop a physical analogy to the Windkessel model for use in the benchtop experiments.

Arterial pulse pressure is critically important to a number of diseases such as isolated systolic hypertension, coronary artery disease and heart failure. Determining the cause of increased pulse pressure has been hampered for two reasons. First, pulse pressure results from contraction of the heart and the load formed by the complex arterial tree. Pressure pulses travel from the heart to the peripheral arteries. As they reach a bifurcation or change in arterial wall properties, some of the pulses get reflected and propagate retrograde towards the heart. Second, two different modeling approaches (0-D and 1-D) describe the arterial system. The Windkessel model ascribed changes in pulse pressure to changes in total arterial compliance (Ctot) and total arterial resistance, whereas the transmission model ascribed them to changes in the magnitude, timing and sites of reflection. Our investigation has addressed both these limitations by finding that a complex arterial system degenerates into a simple 2-element Windkessel model when wavelength of the propagated pulse increases. This theoretical development has yielded three practical results. First, isolated systolic hypertension can be viewed as a manifestation of a system that has degenerated into a Windkessel, and thus increased pulse pressure is due to decreased Ctot. Second, the well-discussed Augmentation Index does not truly describe augmentation of pulse pressure by pulse reflection. Third, the simple 2-element Windkessel can be used to characterize the interaction among heart, arterial system and axial-flow left ventricular assist device analytically. The fact that arterial systems degenerate into Windkessels explains why it becomes much easier to estimate total arterial compliance in hypertension?total arterial compliance is the dominant determinant of pulsatile pressure.

Arterial pulse pressure is critically important to a number of diseases such as isolated systolic hypertension, coronary artery disease and heart failure. Determining the cause of increased pulse pressure has been hampered for two reasons. First, pulse pressure results from contraction of the heart and the load formed by the complex arterial tree. Pressure pulses travel from the heart to the peripheral arteries. As they reach a bifurcation or change in arterial wall properties, some of the pulses get reflected and propagate retrograde towards the heart. Second, two different modeling approaches (0-D and 1-D) describe the arterial system. The Windkessel model ascribed changes in pulse pressure to changes in total arterial compliance (Ctot) and total arterial resistance, whereas the transmission model ascribed them to changes in the magnitude, timing and sites of reflection. Our investigation has addressed both these limitations by finding that a complex arterial system degenerates into a simple 2-element Windkessel model when wavelength of the propagated pulse increases. This theoretical development has yielded three practical results. First, isolated systolic hypertension can be viewed as a manifestation of a system that has degenerated into a Windkessel, and thus increased pulse pressure is due to decreased Ctot. Second, the well-discussed Augmentation Index does not truly describe augmentation of pulse pressure by pulse reflection. Third, the simple 2-element Windkessel can be used to characterize the interaction among heart, arterial system and axial-flow left ventricular assist device analytically. The fact that arterial systems degenerate into Windkessels explains why it becomes much easier to estimate total arterial compliance in hypertension?total arterial compliance is the dominant determinant of pulsatile pressure.

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Au cours des examens d'Imagerie par Résonance Magnétique du cœur, l'ÉlectroCardioGramme recueilli pour la synchronisation est fortement perturbé par plusieurs artéfacts gênant la bonne détection du cycle cardiaque. Une des sources contaminantes est l'artéfact MagnétoHydroDynamique, dû aux mouvements des particules chargées du sang dans le champ magnétique. Dans ce travail, une méthode fiable pour la double synchronisation sur le rythme cardiaque et respiratoire est élaborée, permettant l'amélioration des IRM cardiaques haute résolution. Les altérations temporelles et fréquentielles des signaux ECG provoquées par l'effet MHD sont examinées. Et, dans le but de prédire le niveau de contamination dû à cet artéfact, différents modèles d'écoulements sanguins dans un champ magnétique sont étudiés. Les effets du champ sur l'écoulement sont mis en évidence, et des potentiels surfaciques susceptibles de se superposer à l'ECG sont estimés.

The number of patients that are waiting for heart transplants far exceed the number of available donor hearts. Left Ventricular Assist Devices are mechanical alternatives that can help and are helping several patients. They work by taking blood from the left ventricle and ejecting that blood into the aorta. In the University of Louisville they are developing a similar device that will take the blood from the aorta instead of the ventricle. This new device is called an Artificial Vasculature Device. In this thesis the arterial system and AVD are modeled and a simple control algorithm for the AVD proposed. The arteries are modeled as a tube with linear resistance and inertia followed by a chamber with linear compliance and last a tube with linear resistance. The model is identical to the 4-element Windkessel model. The values for the resistances, inertia and compliance are identified using pressure and flow measurements from the ventricle and aortic root from a healthy patient. In addition to the Windkessel model the aortic valve is also modeled. The valve is modeled as a drum that closes the aorta and the parameters identified like before. The measurements are also used to model the left ventricle by assuming it has a constant compliance profile. The AVD is modeled using common modeling structures for servo motors and simple structures for tubes and pistons. The values for the AVD could not be measured and identified so they are fetched from preliminary motor and part specifications. The control algorithm for the AVD uses a wanted load to create a reference aortic flow. This wanted aortic flow is then achieved by using a PI controller. With these models and controller the interaction between the arterial system and AVD is investigated. With this preliminary understanding of the interaction further research can be made in the future to improve the understanding and improve the AVD itself.

<p>The number of patients that are waiting for heart transplants far exceed the number of available donor hearts. Left Ventricular Assist Devices are mechanical alternatives that can help and are helping several patients. They work by taking blood from the left ventricle and ejecting that blood into the aorta. In the University of Louisville they are developing a similar device that will take the blood from the aorta instead of the ventricle. This new device is called an Artificial Vasculature Device. In this thesis the arterial system and AVD are modeled and a simple control algorithm for the AVD proposed. </p><p>The arteries are modeled as a tube with linear resistance and inertia followed by a chamber with linear compliance and last a tube with linear resistance. The model is identical to the 4-element Windkessel model. The values for the resistances, inertia and compliance are identified using pressure and flow measurements from the ventricle and aortic root from a healthy patient. In addition to the Windkessel model the aortic valve is also modeled. The valve is modeled as a drum that closes the aorta and the parameters identified like before. The measurements are also used to model the left ventricle by assuming it has a constant compliance profile. </p><p>The AVD is modeled using common modeling structures for servo motors and simple structures for tubes and pistons. The values for the AVD could not be measured and identified so they are fetched from preliminary motor and part specifications. </p><p>The control algorithm for the AVD uses a wanted load to create a reference aortic flow. This wanted aortic flow is then achieved by using a PI controller. With these models and controller the interaction between the arterial system and AVD is investigated. </p><p>With this preliminary understanding of the interaction further research can be made in the future to improve the understanding and improve the AVD itself.</p>