The in vivo implantation of a mechanical device contributes to hemodynamic disturbances, which are responsible for damage to the membranes of red blood cells that in turn can lead to their rupture (hemolysis). It is important to ascertain at the design stage of such mechanical devices that they are innocuous to blood. Because there is no in vivo hemolysis index, we concentrated our efforts on the in vitro hemolysis index of the American Society for Testing and Material (ASTM) standard. We present in this work a framework for minimizing medical device-induced hemolysis by the development of a numerical method for predicting hemolysis similar to that used in in vitro experiments. The method is based on a novel interpretation of the Giersiepen-Wurzinger blood damage correlation that replaces the computation of blood damage along the streamline by a volume integration of a damage function over the computational domain. We assess the behavior and accuracy of this methodology with 3D examples.

No abstract

In a previous communication, we have proposed a numerical framework for the prediction of in vitro hemolysis indices in the preselection and optimization of medical devices. This numerical methodology is based on a novel interpretation of Giersiepen-Wurzinger blood damage correlation as a volume integration of a damage function over the computational domain. We now propose an improvement of this approach based on a hyperbolic equation of blood damage that is asymptotically consistent. Consequently, while the proposed correction has yet to be proven experimentally, it has the potential to numerically predict more realistic red blood cell destruction in the case of in vitro experiments. We also investigate the appropriate computation of the shear stress scalar of the damage fraction model. Finally, we assess the validity of this consistent approach with an analytical example and with some 3D examples.

The flow through a smooth axisymmetric constriction (a stenosis in medical applications) of 75% restriction in area is measured using stereoscopic and time-resolved particle image velocimetry (PIV) in the Reynolds number range Re ~ 100–1100. At low Reynolds numbers, steady flow results reveal an asymmetry of the flow downstream of the constriction. The jet emanating from the throat of the nozzle is deflected towards the wall causing the formation of a one-sided recirculation region. The asymmetry results from a Coanda-type wall attachment already observed in symmetric planar sudden expansion flows. When the Reynolds number is increased above the critical value of 400, the separation surface cannot remain attached and an unsteady flow regime begins. Low-frequency axial oscillations of the reattachment point are observed along with a slow swirling motion of the jet. The phenomenon is linked to a periodic discharge of the unstable recirculation region inducing alternating laminar and turbulent flow phases. The resulting flow is highly non-stationary and intermittent. Discrete wavelet transforms are used to discriminate between the large-scale motions of the mean flow and the vortical and turbulent fluctuations. Continuous wavelet transforms reveal the spectral structure of flow disturbances. Temporal measurements of the three velocity components in cross-sections are used with the Taylor hypothesis to qualitatively reconstruct the three-dimensional velocity vector fields, which are validated by comparing with two-dimensional PIV measurements in meridional planes. Visualizations of isosurfaces of the swirling strength criterion allow the identification of the topology of the vortices and highlight the formation and evolution of hairpin-like vortex structures in the flow. Finally, with further increase of the Reynolds number, the flow exhibits less intermittency and becomes stationary for Re ~ 900. Linear stochastic estimation identifies the predominance of vortex rings downstream of the stenosis before breakdown to turbulence.

No abstract