High-Resolution Measurements of Leakage Flow Inside the Hinge of a Large-scale Bileaflet Mechanical Heart Valve Hinge Model.

PURPOSE: It is believed that non-physiological leakage flow through hinge gaps during diastole contributes to thrombus formation in Bileaflet Mechanical Heart Valves (BMHVs). Because of the small scale and difficulty of experimental access, fluid dynamics inside the hinge cavity has not yet been characterised in detail. The objective is to investigate small-scale structure inside the hinge experimentally, and gain insight into its role in stimulating cellular responses. METHODS: An optically accessible scaled-up model of a BMHV hinge was designed and built, preserving dynamic similarity to a clinical BMHV. Particle Image Velocimetry (PIV) was used to visualize and quantify the flow fields inside the hinge at physiological Reynolds number and dimensionless pressure drop. The flow was measured at in-plane and out-of-plane spatial resolution of 32 and 86 µm, respectively, and temporal resolution of [Formula: see text] RESULTS: Likely flow separation on the ventricular surface of the cavity has been observed for the first time, and is a source of unsteadiness and perhaps turbulence. The shear stress found in all planes exceeds the threshold of platelet activation, ranging up to 168 Pa. CONCLUSIONS: The scale-up approach provided new insight into the nature of the hinge flow and enhanced understanding of its complexity. This study revealed flow features that may induce blood element damage.

Analysis of Shear-Induced Platelet Aggregation and Breakup.

To better understand the mechanisms leading to the formation of thrombi of hazardous sizes in the bulk of the blood, we have developed a kinetic model of shear-induced platelet aggregation (SIPA). In our model, shear rate regulates a mass-conservative population balance equation which computes the aggregation and disaggregation of platelets in a cluster mass distribution. Aggregation is modeled by the Smoluchowski coagulation equation, and disaggregation is incorporated using the aggregate breakup model of Pandya and Spielman. Previous experimental data for SIPA have been correlated with a special case of this model where only the two-body collision of free platelets was considered. However, the two-body collision theory is oblivious to the steady-state condition, and it required the use of a shear-dependent aggregation efficiency parameter to fit it to experimental data. Our method not only predicts steady states but also correlates with literature data without employing a shear-dependent aggregation efficiency.

High-Resolution Measurements of Velocity and Shear Stress in Leakage Jets From Bileaflet Mechanical Heart Valve Hinge Models.

In flow through cardiovascular implants, hemolysis, and thrombosis may be initiated by nonphysiological shear stress on blood elements. To enhance understanding of the small-scale flow structures that stimulate cellular responses, and ultimately to design devices for reduced blood damage, it is necessary to study the flow-field at high spatial and temporal resolution. In this work, we investigate flow in the reverse leakage jet from the hinge of a bileaflet mechanical heart valve (BMHV). Scaled-up model hinges are employed, enabling measurement of the flow-field at effective spatial resolution of 167 µm and temporal resolution of 594 µs using two-component particle image velocimetry (PIV). High-velocity jets were observed at the hinge outflow, with time-average velocity up to 5.7 m/s, higher than reported in previous literature. Mean viscous shear stress is up to 60 Pa. For the first time, strongly unsteady flow has been observed in the leakage jet. Peak instantaneous shear stress is up to 120 Pa, twice as high as the average value. These high-resolution measurements identify the hinge leakage jet as a region of very high fluctuating shear stress which is likely to be thrombogenic and should be an important target for future design improvement.

High-resolution measurement of the unsteady velocity field to evaluate blood damage induced by a mechanical heart valve.

We investigate the potential of prosthetic heart valves to generate abnormal flow and stress patterns, which can contribute to platelet activation and lysis according to blood damage accumulation mechanisms. High-resolution velocity measurements of the unsteady flow field, obtained with a standard particle image velocimetry system and a scaled-up model valve, are used to estimate the shear stresses arising downstream of the valve, accounting for flow features at scales less than one order of magnitude larger than blood cells. Velocity data at effective spatial and temporal resolution of 60 µm and 1.75 kHz, respectively, enabled accurate extraction of Lagrangian trajectories and loading histories experienced by blood cells. Non-physiological stresses up to 10 Pa were detected, while the development of vortex flow in the wake of the valve was observed to significantly increase the exposure time, favouring platelet activation. The loading histories, combined with empirical models for blood damage, reveal that platelet activation and lysis are promoted at different stages of the heart cycle. Shear stress and blood damage estimates are shown to be sensitive to measurement resolution.

Effect of eddy length scale on mechanical loading of blood cells in turbulent flow.

Non-physiological turbulent blood flow is known to occur in and near implanted cardiovascular devices, but its effects on blood are poorly understood. The objective of this work is to investigate the effect of turbulent eddy length scale on blood cell damage, and in particular to test the hypothesis that only eddies similar in size to blood cells can cause damage. The microscale flow near a red blood cell (RBC) in an idealized turbulent eddy is modeled computationally using an immersed boundary method. The model is validated for the special case of a tank-treading RBC. In comparisons between turbulent flow fields, based on Kolmogorov theory, the model predicts that damage due to the smallest eddies is almost independent of the Kolmogorov length scale. The model predicts that within a given flow field, however, eddies of sub-cellular scale are less damaging than larger eddies. Eddy decay time and the turbulent energy spectral density are highlighted as important factors. The results suggest that Kolmogorov scale is not an adequate predictor of flow-induced blood trauma, and highlights the need for deeper understanding of the microscale structure of turbulent blood flow.

Fluid dynamics of gas exchange in high-frequency oscillatory ventilation: in vitro investigations in idealized and anatomically realistic airway bifurcation models.

The objective of this work is to develop understanding of the local fluid dynamic mechanisms that underpin gas exchange in high-frequency oscillatory ventilation (HFOV). The flow field during HFOV was investigated experimentally using particle image velocimetry in idealized and realistic models of a single bifurcation. Results show that inspiratory and expiratory fluid streams coexist in the airway at flow reversal, and mixing between them is enhanced by secondary flow and by vortices associated with shear layers. Unsteady flow separation and recirculation occurs in both geometries. The magnitude of secondary flow is greater in the realistic model than in the idealized model, and the structure of secondary flow is quite different. However, other flow structures are qualitatively similar.

Models of flow-induced loading on blood cells in laminar and turbulent flow, with application to cardiovascular device flow.

Viscous shear stress and Reynolds stress are often used to predict hemolysis and thrombosis due to flow-induced stress on blood elements in cardiovascular devices. These macroscopic stresses are distinct from the true stress on an individual cell, which is determined by the local microscale flow field. In this paper the flow-induced stress on blood cells is calculated for laminar and turbulent flow, using simplified models for cells and for turbulent eddies. The model is applied to estimate shear stress on red blood cells in flow through a prosthetic heart valve, using the energy spectral density measured by Liu et al. [J. Biomech. Eng. 122:118-124, 2000]. Results show that in laminar flow, the maximum stress on a cell is approximately equal to the macroscopic viscous shear stress. In turbulent flow through a prosthetic heart valve, the estimated root mean square of flow-induced stress on a cell is at least an order of magnitude less than the Reynolds stress. The results support the hypothesis that smaller turbulent eddies cause higher stress on cells. However, the stress due to an eddy depends on the velocity scale of the eddy as well as its length scale. For the heart valve flow investigated, turbulence contributes to flow-induced stress on cells almost equally across a broad range of the frequency spectrum. The model suggests that Reynolds stress alone is not an adequate predictor of cell damage in turbulent flow, and highlights the importance of the energy spectral density.