Bulletin of the American Physical Society
64th Annual Meeting of the APS Division of Fluid Dynamics
Volume 56, Number 18
Sunday–Tuesday, November 20–22, 2011; Baltimore, Maryland
Session L26: Minisymposium: Cardiac Fluid Dynamics: Translating Fundamental Insights into Clinical Practice |
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Chair: Rajat Mittal, Johns Hopkins University Room: 329 |
Monday, November 21, 2011 3:35PM - 4:01PM |
L26.00001: How the heart works when it fills: what every fluid mechanician needs to know Invited Speaker: The two principles that govern the diastolic (filling) phase of all human hearts are: ``constant volume pump'' and ``suction pump.'' The $\approx$ 850 ml volume of the pericardial sack decreases by only $\approx$ 40 ml by end systole. This requires that atrial-ventricular volumes simultaneously reciprocate and it underscores the pressure pump (systolic) and volume pump (diastolic) roles of the chambers. Of the 4 heart chambers -- ONLY the left ventricle actually serves as a systolic pressure pump. When the normal left ventricle initiates filling after mitral valve opening, it generates only a small (4mmHg) maximum atrioventricular pressure gradient (LVP$<$ LAP) while its pressure continues to decrease for about 100 msec while its volume increases (dP/dV$<$ 0). Because the chamber recoils faster than it can fill it is a suction (volume) pump. The purpose of diastole is to fill the chamber (mass transfer) in the fraction of a second available in order to maintain cardiac output. The streamlines entering through the 5cm$^2$ mitral valve initially have a blunt velocity profile and because mitral valve plane alignment is off-center relative to LV long axis, blood rapidly forms an asymmetric toroidal vortex whose formation time has been shown to depend on LV chamber parameters of stiffness, relaxation and load. Recent Lagrangian coherent structure (LCS) analysis of vortex ring growth in the LV reveals nature's elegant fluid mechanics based solution to the diastolic mass transfer problem. The intraventricular vortex also ``rinses'' the trabeculated inner surface of the heart thereby preventing formation of blood clots and facilitates mitral leaflet coaptation to minimize mitral valve regurgitation. [Preview Abstract] |
Monday, November 21, 2011 4:01PM - 4:27PM |
L26.00002: Hypertrophic Cardiomyopathy (HCM): How Flow Analysis May Drive Medical Management and Surgical Approach Invited Speaker: Hypertrophic Cardiomyopathy (HCM) is the most common inherited heart disease and occurs in 1 in 500 persons worldwide regardless of race, age and gender. It is the most common cause of sudden death in the young and also causes heart failure and cardiac arrhythmias. The primary anatomic abnormality is thickening of certain walls, or sometimes global thickening of the left or right ventricle. The patterns of thickening along with increased ventricular stiffness lead to suboptimal ventricular filling and inefficient ejection of blood from the ventricle. Treatment for HCM can be medical or surgical. The choice of therapy is driven by the presence and severity of outflow obstruction. Flow analysis could provide sophisticated information about outflow and inflow ventricular dynamics. These flow dynamics features may enable better medical choices and provide information that would allow superior surgical planning. [Preview Abstract] |
Monday, November 21, 2011 4:27PM - 4:53PM |
L26.00003: Vortices formed on the mitral valve tips aid normal left ventricular filling Invited Speaker: For the left ventricle to function as an effective pump it must be able to fill from a low left atrial pressure. However, this ability is lost in patients with heart failure. We investigated the fluid dynamics of the left ventricle filling by imaging the blood flow in patients with healthy and impaired diastolic function, using 2D phase contrast magnetic resonance imaging and we quantified the intraventricular pressure gradients and the strength and location of the formed vortices. We found that during early filling in normal subjects, prior to the opening of the mitral valve the flow moves towards the apex and subsequently at the time of the opening of the valve the rapid movement of the mitral annulus away from the left ventricle apex enhances the formation of a vortex ring at the mitral valve tips. Instead of being a passive byproduct of the process as was previously believed, this vortex ring facilitates filling by reducing convective losses and enhancing the function of the left ventricle as a suction pump. Impairment of this mechanism contributes to diastolic dysfunction, with the left ventricle filling becoming dependent on left atrial pressure, and eventually leading to heart failure. [Preview Abstract] |
Monday, November 21, 2011 4:53PM - 5:19PM |
L26.00004: Multiscale modeling and surgical planning for single ventricle heart patients Invited Speaker: Single ventricle heart patients are among the most challenging for pediatric cardiologists to treat, and typically undergo a palliative course of three open-heart surgeries starting immediately after birth. We will present recent tools for modeling blood flow in single ventricle heart patients using a multiscale approach that couples a 3D Navier-Stokes domain to a 0D closed loop lumped parameter network comprised of circuit elements. This coupling allows us to capture the effect of changes in local geometry, such as shunt sizes, on global circulatory dynamics, such as cardiac output. A semi-implicit numerical method is formulated to solve the coupled system in which flow and pressure information is passed between the two domains at the inlets and outlets of the model. A finite element method with outflow stabilization is applied in the 3D Navier-Stokes domain, and the LPN system of ordinary differential equations is solved numerically using a Runge-Kutta method. These tools are coupled via automated scripts to a derivative-free optimization method. Optimization is used to systematically explore surgical designs using clinically relevant cost functions for two stages of single ventricle repair. First, we will present results from optimization of the first stage Blalock Taussig Shunt. Second, we will present results from optimization of a new Y-graft design for the third stage of single ventricle repair called the Fontan surgery. The Y-graft is shown, in simulations, to successfully improve hepatic flow distribution, a known clinical problem. Preliminary clinical experience with the Y-graft will be discussed. [Preview Abstract] |
Monday, November 21, 2011 5:19PM - 5:45PM |
L26.00005: Cardiac Hemodynamics in the Pathogenesis of Congenital Heart Disease and Aortic Valve Calcification Invited Speaker: An improved understanding of the roles of hemodynamic forces play in cardiac development and the pathogenesis of cardiac disease will have significant scientific and clinical impact. I will focus on the role of fluid dynamics in congenital heart disease and aortic valve calcification. Congenital heart defects are the most common form of birth defect. Aortic valve calcification/stenosis is the third leading cause of adult heart disease and the most common form of acquired valvular disease in developed countries. Given the high incidence of these diseases and their associated morbidity and mortality, the potential translational impact of an improved understanding of cardiac hemodynamic forces is very large. [Preview Abstract] |
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