Small-bubble transport and splitting dynamics in a symmetric bifurcation.

Simulations of small bubbles traveling through symmetric bifurcations are conducted to garner information pertinent to gas embolotherapy, a potential cancer treatment. Gas embolotherapy procedures use intra-arterial bubbles to occlude tumor blood supply. As bubbles pass through bifurcations in the blood stream nonhomogeneous splitting and undesirable bioeffects may occur. To aid development of gas embolotherapy techniques, a volume of fluid method is used to model the splitting process of gas bubbles passing through artery and arteriole bifurcations. The model reproduces the variety of splitting behaviors observed experimentally, including the bubble reversal phenomenon. Splitting homogeneity and maximum shear stress along the vessel walls is predicted over a variety of physical parameters. Small bubbles, having initial length less than twice the vessel diameter, were found unlikely to split in the presence of gravitational asymmetry. Maximum shear stresses were found to decrease exponentially with increasing Reynolds number. Vortex-induced shearing near the bifurcation is identified as a possible mechanism for endothelial cell damage.

Microbubble transport through a bifurcating vessel network with pulsatile flow.

Motivated by two-phase microfluidics and by the clinical applications of air embolism and a developmental gas embolotherapy technique, experimental and theoretical models of microbubble transport in pulsatile flow are presented. The one-dimensional time-dependent theoretical model is developed from an unsteady Bernoulli equation that has been modified to include viscous and unsteady effects. Results of both experiments and theory show that roll angle (the angle the plane of the bifurcating network makes with the horizontal) is an important contributor to bubble splitting ratio at each bifurcation within the bifurcating network. When compared to corresponding constant flow, pulsatile flow was shown to produce insignificant changes to the overall splitting ratio of the bubble despite the order one Womersley numbers, suggesting that bubble splitting through the vasculature could be modeled adequately with a more modest constant flow model. However, bubble lodging was affected by the flow pulsatility, and the effects of pulsatile flow were evident in the dependence of splitting ratio of bubble length. The ability of bubbles to remain lodged after reaching a steady state in the bifurcations is promising for the effectiveness of gas embolotherapy to occlude blood flow to tumors, and indicates the importance of understanding where lodging will occur in air embolism. The ability to accurately predict the bubble dynamics in unsteady flow within a bifurcating network is demonstrated and suggests the potential for bubbles in microfluidics devices to encode information in both steady and unsteady aspects of their dynamics.

Tear size and location impacts false lumen pressure in an ex vivo model of chronic type B aortic dissection.

BACKGROUND: Follow-up mortality is high in patients with type B aortic dissection (TB-AD) approaching one in four patients at 3 years. A predictor of increased mortality is partial thrombosis of the false lumen which may occlude distal tears. The hemodynamic consequences of differing tear size, location, and patency within the false lumen is largely unknown. We examined the impact of intimal tear size, tear number, and location on false lumen pressure. METHODS: In an ex-vivo model of chronic type B aortic dissection connected to a pulsatile pump, simultaneous pressures were measured within the true and false lumen. Experiments were performed in different dissection models with tear sizes of 6.4 mm and 3.2 mm in the following configurations; model A: proximal and distal tear simulating the most common hemodynamic state in patients with TB-AD; model B: proximal tear only simulating patients with partial thrombosis and occlusion of distal tear; and model C: distal tear only simulating patients sealed proximally via a stent graft with persistent distal communication. To compare false lumen diastolic pressure between models, a false lumen pressure index (FPI%) was calculated for all simulations as FPI% = (false lumen diastolic pressure/true lumen diastolic pressure) x 100. RESULTS: In model A, the systolic pressure was slightly lower in the false lumen compared with the true lumen while the diastolic pressure (DP) was slightly higher in the false lumen (DP 66.45 +/- 0.16 mm Hg vs 66.20 +/- 0.12 mm Hg, P < .001, FPI% = 100.4%). In the absence of a distal tear (model B), diastolic pressure was elevated within the false lumen compared with the true lumen (58.95 +/- 0.10 vs 54.66 +/- 0.17, P < .001, FPI% = 107.9%). The absence of a proximal tear in the presence of a distal tear (model C) diastolic pressure was also elevated within the false lumen versus the true lumen (58.72 +/- 0.24 vs 56.15 +/- 0.16, P < .001, FPI% 104.6%). The difference in diastolic pressure was greatest with a smaller tear (3.2 mm) in model B. In model B, DBP increased by 13.9% (P < .001, R(2) 0.69) per 10 beat per minute increase in heart rate (P < .001) independent of systolic pressure. CONCLUSIONS: In this model of chronic type B aortic dissection, diastolic false lumen pressure was the highest in the setting of smaller proximal tear size and the lack of a distal tear. These determinants of inflow and outflow may impact false lumen expansion and rupture during the follow-up period.