Abstract

Computational Fluid Dynamics Characterization of Pulsatile Flow in a Bidirectional Glenn Shunt Supplemented with a Modified Blalock-Taussig Shunt: Flow Vortices Augment Pulmonary Artery Wall Shear Stress and Worsen Power Loss

Background: The bidirectional Glenn shunt (BGS’S), superior vena cava (SVC) to right pulmonary artery (RPA), has become an important step in the surgical management of infants and children with single-ventricle heart disease. In some patients, however, the BGS’S is inadequate to maintain satisfactory pulmonary artery (PA) growth, in part due to a lack of pulsatile flow. In these cases, the BGS’S is often supplemented with a modified Blalock-Taussig shunt (mBTS) connected to the left pulmonary artery (LPA). Little is known about the hemodynamic consequences of combining BGS’S (low velocity passive) with mBTS (high velocity pulsatile) flow. Thus, the objective of this study is to employ simulations of cavopulmonary pathways, based on angiography, and computational fluid dynamics (CFD), using in vivo flow rates and pressures, to determine blood flow characteristics in a BGS’S supplemented with a mBTS. We focused on the flowvessel wall interaction through wall shear stress (WSS), which plays a fundamental role in PA growth, thrombus formation and power loss, critical factors involved in the management of patients awaiting Fontan completion.

Methods: We employed a CFD model of pulsatile fluid flow, using the finite volume method, in conjunction with a non-Newtonian description of viscosity, to gain insight into blood flow behavior in a BGS’S combined with a mBTS. Our approach allows quantitative assessment of pressure distribution, flow-velocity field, WSS profile and regional power loss. The computational domain included simulations of the internal jugular, subclavian and innominate veins, SVC, central RPA and LPA with first- order branches and the mBTS. Clinically relevant boundary conditions were employed in solving the Navier-Stokes equations describing the fluid’s motion. These conditions included reported sizes and flow rates of systemic veins leading to the SVC, measured pressure in the ascending aorta for the inlet to the mBTS and recorded pressures in outlets of central PA first-order branches. The hemodynamic consequences of connecting a mBTS to the PAs, or directly to the SVC, were considered.

Findings: For a planar reproduction of a BGS’S supplemented with a 4 mm mBTS connected to the LPA, the pressure in the SVC became 16.4 mmHg (peak systole), 10.2 mmHg (end diastole) and 14.5 mmHg (averaged over the cardiac cycle), consistent with the representative pressure of 12 mmHg (averaged over the cardiac cycle) at the outlets of the central PA first- order branches. The mBTS's high velocity (3-4 L/min) jet interacting with BGS’S low-velocity (0.2-0.3 L/min) flow created counter- rotating, power- depleting vortices in the cross-sectional plane of the LPA. These vortices markedly increased WSS in the LPA to 53.7 Pa (averaged over the luminal area, and the cardiac cycle), compared to ~ 0.9 Pa for the PAs with a BGS’S alone, and ~ 2 Pa in the PAs of a normal heart. Such a high WSS in the PAs can produces intimal dysfunction, which can: enhance endothelial cell expression of coagulatory molecules and initiate platelet aggregation. However, as flow advanced from the LPA to the RPA, WSS was found to dramatically decrease to 6.2 Pa as power dissipation increased, indicative of decelerating flow. This feature of the shear stress field is critically important, as recent in vitro studies have demonstrated that high WSS’s harmful effects on endothelial function are lessened when the imposed WSS possesses a negative spatial gradient, i.e, is associated with decelerating flow. The overall power efficiency (PE) for the BGS’S with a 4 mm mBTS was only ~30%, compared to 96% for the BGS’S alone. Similar results were obtained when the mBTS was attached at the origin of the branch PAs. In contrast, connecting the mBTS directly to the SVC resulted in a lower WSS burden and less flow-energy loss in the PAs.

Conclusions: BGS’S hemodynamics is greatly influenced by the addition of a mBTS. The SVC pressure becomes pulsatile and moderately increases and flow is disrupted, as anticipated. Counter- rotating vortices are established in the PAs juxtaposed to the insertion of the mBTS. These vortices can augment WSS to levels conducive to endothelial cell dysfunction, thrombus formation and worsening power loss, which are well-recognized complications with single- ventricle palliation. Nevertheless, the WSS distribution in the PAs was found to possess a spatial characteristic that has been shown to lessen flow fields’ adverse shearing effects on vessels' luminal wall.


Author(s):

Seda Aslan, Martin Guillot, Nancy Ross Ascuitto and Robert Ascuitto



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