Abstract
The paper presents a numerical investigation of non-Newtonian modeling effects on unsteady periodic flows in a two-dimensional (2D) constricted channel with moving wall using finite volume method. The governing Navier-Stokes equations have been modified using the Cartesian curvilinear coordinates to handle complex geometries, such as, arterial stenosis. The physiological pulsatile flow has been used at the inlet position as an inlet velocity. The flow is characterized by the Reynolds numbers 300, 500, and 750 that are appropriate for large arteries. The investigations have been carried out to characterize four different non-Newtonian constitutive equations of blood, namely, the (i) Carreau, (ii) Cross, (iii) Modified-Casson, and (iv) Quemada. In these four models, blood viscosity is a nonlinear function of shear rates. The Newtonian model has been investigated to study the physics of fluid and the results are compared with the non-Newtonian viscosity models. The numerical results are presented in terms of streamwise velocity, wall shear stress, pressure distribution as well as the vorticity, streamlines, and vector plots indicating recirculation zones at the poststenotic region. Comparison has also been illustrated in terms of wall pressure and wall shear stress for the Cross model considering different amplitudes of wall oscillation.
Highlights
Atherosclerosis is known as a major arterial disease
The precise mechanisms responsible for the initiation of this phenomenon are not apparently known, it has been established that once a mild stenosis is developed, the resulting flow disorder plays a significant function in the further development of the disease that eventually changes the regional blood rheology as well [2, 3]
In the following parts of the discussion, we have studied the hemodynamic parameters, that is, streamlines, wall pressure and wall shear stress, vorticity, and so forth, for two different Reynolds numbers; that is, Re = 300 and Re = 500 considering various rheological models
Summary
Atherosclerosis is known as a major arterial disease. In atherosclerosis, localized deposits and accumulation of cholesterol and lipid compounds as well as proliferation of connective tissues originate a partial decline in the arterial cross-sectional area which, in particular, is called stenosis. Tu and Deville [5] implemented Galerkin finite-element method simulations for physiological pulsatile flow through a severe stenosis They treated blood as nonNewtonian fluid employing a Herschel-Bulkley model which roughly behaves like blood. They illustrated results for steady and pulsatile flow conditions in terms of velocity profile, formation of vortex in separate regions, pressure drop across the stenosis, wall shear stress, and the vorticity contours. The power-law model demonstrated higher deviations in terms of velocity and wall shear stress compared to Newtonian and six other non-Newtonian viscosity models in their investigation They found that increasing stenosis intensity causes more disturbed flow patterns in the downstream of the stenosis and WSS develops remarkably at the stenosis throat. Sriram et al [9] reveal the importance of incorporating non-Newtonian blood properties into estimates of WSS in microvessels
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