2,999 research outputs found

    A reaction-diffusion heart model for the closed-loop evaluation of heart-pacemaker interaction

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    The purpose of this manuscript is to develop a reaction-diffusion heart model for closed-loop evaluation of heart-pacemaker interaction, and to provide a hardware setup for the implementation of the closed-loop system. The heart model, implemented on a workstation, is based on the cardiac monodomain formulation and a phenomenological model of cardiac cells, which we fitted to the electrophysiological properties of the different cardiac tissues. We modelled the pacemaker as a timed automaton, deployed on an Arduino 2 board. The Arduino and the workstation communicate through a PCI acquisition board. Additionally, we developed a graphical user interface for easy handling of the framework. The myocyte model resembles the electrophysiological properties of atrial and ventricular tissue. The heart model reproduces healthy activation sequence and proved to be computationally efficient (i.e., 1 s simulation requires about 5 s). Furthermore, we successfully simulated the interaction between heart and pacemaker models in three well-known pathological contexts. Our results showed that the PDE formulation is appropriate for the simulation in closed-loop. While computationally more expensive, a PDE model is more flexible and allows to represent more complex scenarios than timed or hybrid automata. Furthermore, users can interact more easily with the framework thanks to the graphical representation of the spatiotemporal evolution of the membrane potentials. By representing the heart as a reaction-diffusion model, the proposed closed-loop system provides a novel and promising framework for the assessment of cardiac pacemakers

    Study of cardiovascular function using a coupled left ventricle and systemic circulation model

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    To gain insight into cardio-arterial interactions, a coupled left ventricle-systemic artery (LV–SA) model is developed that incorporates a three-dimensional finite-strain left ventricle (LV), and a physiologically-based one-dimensional model for the systemic arteries (SA). The coupling of the LV model and the SA model is achieved by matching the pressure and the flow rate at the aortic root, i.e. the SA model feeds back the pressure as a boundary condition to the LV model, and the aortic flow rate from the LV model is used as the input for the SA model. The governing equations of the coupled system are solved using a combined immersed-boundary finite-element (IB/FE) method and a Lax–Wendroff scheme. A baseline case using physiological measurements of healthy subjects, and four exemplar cases based on different physiological and pathological scenarios are studied using the LV–SA model. The results of the baseline case agree well with published experimental data. The four exemplar cases predict varied pathological responses of the cardiovascular system, which are also supported by clinical observations. The new model can be used to gain insight into cardio-arterial interactions across a range of clinical applications

    A graphical simulation software for instruction in cardiovascular mechanics physiology

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    <p>Abstract</p> <p>Background</p> <p>Computer supported, interactive e-learning systems are widely used in the teaching of physiology. However, the currently available complimentary software tools in the field of the physiology of cardiovascular mechanics have not yet been adapted to the latest systems software. Therefore, a simple-to-use replacement for undergraduate and graduate students' education was needed, including an up-to-date graphical software that is validated and field-tested.</p> <p>Methods</p> <p>Software compatible to Windows, based on modified versions of existing mathematical algorithms, has been newly developed. Testing was performed during a full term of physiological lecturing to medical and biology students.</p> <p>Results</p> <p>The newly developed CLabUZH software models a reduced human cardiovascular loop containing all basic compartments: an isolated heart including an artificial electrical stimulator, main vessels and the peripheral resistive components. Students can alter several physiological parameters interactively. The resulting output variables are printed in x-y diagrams and in addition shown in an animated, graphical model. CLabUZH offers insight into the relations of volume, pressure and time dependency in the circulation and their correlation to the electrocardiogram (ECG). Established mechanisms such as the Frank-Starling Law or the Windkessel Effect are considered in this model. The CLabUZH software is self-contained with no extra installation required and runs on most of today's personal computer systems.</p> <p>Conclusions</p> <p>CLabUZH is a user-friendly interactive computer programme that has proved to be useful in teaching the basic physiological principles of heart mechanics.</p

    Mathematical model of the mitral valve and the cardiovascular system, application for studying, monitoring and in the diagnosis of valvular pathologies

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    peer reviewedA cardiovascular and circulatory system (CVS) model has been validated in silico, and in several animal model studies. It accounts for valve dynamics using Heaviside functions to simulate a physiological accurate “open on pressure, close on flow” law. Thus, it does not consider the real time scale of the valve aperture dynamics and thus doesn’t fully capture valve dysfunction particularly where the dysfunction involves partial closure. This research describes a new closed-loop CVS model including a model describing the progressive aperture of the mitral valve and valid over the full cardiac cycle. This new model is solved for a healthy and diseased mitral valve

    Using a human cardiovascular-respiratory model to characterize cardiac tamponade and pulsus paradoxus

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    <p>Abstract</p> <p>Background</p> <p>Cardiac tamponade is a condition whereby fluid accumulation in the pericardial sac surrounding the heart causes elevation and equilibration of pericardial and cardiac chamber pressures, reduced cardiac output, changes in hemodynamics, partial chamber collapse, pulsus paradoxus, and arterio-venous acid-base disparity. Our large-scale model of the human cardiovascular-respiratory system (H-CRS) is employed to study mechanisms underlying cardiac tamponade and pulsus paradoxus. The model integrates hemodynamics, whole-body gas exchange, and autonomic nervous system control to simulate pressure, volume, and blood flow.</p> <p>Methods</p> <p>We integrate a new pericardial model into our previously developed H-CRS model based on a fit to patient pressure data. Virtual experiments are designed to simulate pericardial effusion and study mechanisms of pulsus paradoxus, focusing particularly on the role of the interventricular septum. Model differential equations programmed in C are solved using a 5<sup>th</sup>-order Runge-Kutta numerical integration scheme. MATLAB is employed for waveform analysis.</p> <p>Results</p> <p>The H-CRS model simulates hemodynamic and respiratory changes associated with tamponade clinically. Our model predicts effects of effusion-generated pericardial constraint on chamber and septal mechanics, such as altered right atrial filling, delayed leftward septal motion, and prolonged left ventricular pre-ejection period, causing atrioventricular interaction and ventricular desynchronization. We demonstrate pericardial constraint to markedly accentuate normal ventricular interactions associated with respiratory effort, which we show to be the distinct mechanisms of pulsus paradoxus, namely, series and parallel ventricular interaction. Series ventricular interaction represents respiratory variation in right ventricular stroke volume carried over to the left ventricle via the pulmonary vasculature, whereas parallel interaction (via the septum and pericardium) is a result of competition for fixed filling space. We find that simulating active septal contraction is important in modeling ventricular interaction. The model predicts increased arterio-venous CO<sub>2 </sub>due to hypoperfusion, and we explore implications of respiratory pattern in tamponade.</p> <p>Conclusion</p> <p>Our modeling study of cardiac tamponade dissects the roles played by septal motion, atrioventricular and right-left ventricular interactions, pulmonary blood pooling, and the depth of respiration. The study fully describes the physiological basis of pulsus paradoxus. Our detailed analysis provides biophysically-based insights helpful for future experimental and clinical study of cardiac tamponade and related pericardial diseases.</p

    Quantitative assessment of myocardial oxygen supply and demand using a dynamic model of the cardiovascular system

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    A quantitative understanding of the changes in coronary, pulmonary and systemic hemodynamic variables and their effect on myocardial supply and demand is important to the better management of anesthetic care of patients with impaired cardiac function. Animal studies have identified those hemodynamic factors that play an important role in determining the balance between oxygen supply and demand for the myocardium. These include myocardial contractility, left ventricular end-diastolic volume, systemic arterial pressure, systemic vascular resistance, and heart rate. The interactions of these factors are complex and their combined effects on myocardial oxygen supply and demand are difficult to predict a priori. The objective of this work was to construct a mathematical model of the cardiovascular system which will allow us to simulate the effects of changes in one or more of those hemodynamic parameters on myocardial supply and demand. The model used is a combination of several models which have been reported in the literature, along with our own modifications. The important feature of the model is that it is dynamic in nature and thus it is helpful in real time analysis. The model is also useful to conceptualize the problem and test relationships, helping researchers frame hypothesis and design experiments

    Computational Modeling for Cardiac Resynchronization Therapy

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    Mathematical multi-scale model of the cardiovascular system including mitral valve dynamics. Application to ischemic mitral insufficiency

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    Valve dysfunction is a common cardiovascular pathology. Despite significant clinical research, there is little formal study of how valve dysfunction affects overall circulatory dynamics. Validated models would offer the ability to better understand these dynamics and thus optimize diagnosis, as well as surgical and other interventions. A cardiovascular and circulatory system (CVS) model has already been validated in silico, and in several animal model studies. It accounts for valve dynamics using Heaviside functions to simulate a physiologically accurate “open on pressure, close on flow” law. However, it does not consider real-time valve opening dynamics and therefore does not fully capture valve dysfunction, particularly where the dysfunction involves partial closure. This research describes an updated version of this previous closed-loop CVS model that includes the progressive opening of the mitral valve, and is defined over the full cardiac cycle. Simulations of the cardiovascular system with healthy mitral valve are performed, and, the global hemodynamic behaviour is studied compared with previously validated results. The error between resulting pressure-volume (PV) loops of already validated CVS model and the new CVS model that includes the progressive opening of the mitral valve is assessed and remains within typical measurement error and variability. Simulations of ischemic mitral insufficiency are also performed. Pressure-Volume loops, transmitral flow evolution and mitral valve aperture area evolution follow reported measurements in shape, amplitude and trends. The resulting cardiovascular system model including mitral valve dynamics provides a foundation for clinical validation and the study of valvular dysfunction in vivo. The overall models and results could readily be generalised to other cardiac valves
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