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Veno-arterial extracorporeal membrane oxygenation (V-A ECMO) is a life saving therapy for critically ill patients experiencing a heart and lung failure. During this therapy, a common complication is limb ischemia in the leg where the return cannula reintroduces the oxygenated blood to the patient. The hemodynamics leading to limb ischemia during V-A ECMO therapy is not yet understood. This work uses computational fluid dynamics to model the interacting blood flows from the V-A ECMO return cannula and the native cardiac output in the abdominal aorta and iliac bifurcation. A two-element Windkessel (WK) model is used to model the downstream vasculature. In total, five simulations of four cardiac cycles are conducted, where either one WK model parameter or the aorta inflow boundary condition (BC) is altered. Results suggest that the outflow distribution between the iliac arteries is dependent on the WK model parameters, but it is independent of the inflow BC imposed at the aorta inlet. Increasing the resistance value of the WK model leads to an increase of pressure in the domain relative to the 0.8 L/min baseline case and increases the outflow through the non-cannulated iliac artery. The opposite effect is reached when decreasing the resistive value or increasing the compliance value. The velocity field close to the aortic bifurcation, where the return cannula flow is redirected, shows large variations and complex, three-dimensional flow structures. At the aorta inlet, the velocity field is sensitive to the aorta inflow BC. In the XY -plane, areas of high sensitivity are located in areas with high unsteady flow motion. The sensitivity analysis of the velocity field in the XY -plane seems to be independent of the BCs. The pressure field is sensitive to the BC since the pressure in the domain is dependent on the WK model parameters. This work can be a starting point to further investigate the influence of a change in BCs on the flow structures and the outflow distribution between the iliac arteries. Those results can develop a framework stating the factors with an increased patient’s risk for developing limb ischemia. Veno-arteriell extrakorporeal membranoxygenering (V-A ECMO) är en behandling som kan rädda liv på patienter med kraftigt nedsatt hjärt- och lungfunktion. En vanlig komplikation under behandlingen är ischemi i benet där kanylen återför oxygenerat blod till patienten. Hemodynamiken bakom ischemi under V-A ECMO är illa förstådd idagsläget. I det här arbetet används beräkningsströmningsdynamik för att modellera interaktionen mellan blodflödet från returkanylen och blodflödet från patientens hjärta i bukaortan bifurkation med iliak artärerna. En Windkesselmodell (WK) med två element används för att modellera kärlen nedströms från illiakartärerna. Sammanlagt utförs fem simulationer av fyra hjärtcykler, vari antingen en av WK-parametrarna eller randvillkoret för aortans inflöde ändras. Resultatet tyder på att utflödet distribueras mellan iliak artärer beroende på WK parametrarna, men oberoende av randvillkoret för aortans inflöde. Med ett flöde på 0.8 L{min vid ursprungsläget ökas trycket i området och utflödet genom iliak artären utan kanyl om resistansen i WK-modellen ökas, och motsatt effekt nås genom att sänka resistansen eller genom att öka modellens värde för artärernas följsamhet. Hastighetsfältet kring aortabifurkation, där återflödet byter riktning, visar starka och komplexa tre-dimensionella variationer. Hastighetsfältet i ingången till aortan är känsligt för randvillkoret för aortans inflöde. I XY -planet finns områden med hög känslighet där flödet är högostadigt. Hastighetsfältets känslighet i XY -planet verkar vara oberoende av randvillkoren. Tryckfältet är känsligt för randvillkoren då trycket i området beror på WK-modellens parametrar. Det här arbetet kan vara en utgångspunkt för framtida studier i randvillkorens effekt på flödesstrukturer och utflödesdistribution mellan iliak artärer. Resultaten från sådana studier kan användas för att bygga upp en förståelse för hur olika faktorer påverkar en patients risk för ischemi under V-A ECMO behandling.

Background: Many detailed features of the cochlear anatomy have not been included in existing 3D cochlear models, including the microstructures inside the modiolar bone, which in turn determines the path of auditory nerve fibers (ANFs). Method: We captured the intricate modiolar microstructures in a 3D human cochlea model reconstructed from μCT scans. A new algorithm was developed to reconstruct ANFs running through the microstructures within the model. Using the finite element method, we calculated the electrical potential as well as its first and second spatial derivatives along each ANF elicited by the cochlear implant electrodes. Simulation results of electrical potential was validated against intracochlear potential measurements. Comparison was then made with a simplified model without the microstructures within the cochlea. Results: When the stimulus was delivered from an electrode located deeper in the apex, the extent of the auditory nerve influenced by a higher electric potential grew larger; at the same time, the maximal potential value at the auditory nerve also became larger. The electric potential decayed at a faster rate toward the base of the cochlea than toward the apex. Compared to the cochlear model incorporating the modiolar microstructures, the simplified version resulted in relatively small differences in electric potential. However, in terms of the first and second derivatives of electric potential along the fibers, which are relevant for the initiation of action potentials, the two models exhibited large differences: maxima in both derivatives with the detailed model were larger by a factor of 1.5 (first derivative) and 2 (second derivative) in the exemplary fibers. More importantly, these maxima occurred at different locations, and opposite signs were found for the values of second derivatives between the two models at parts along the fibers. Hence, while one model predicts depolarization and spike initiation at a given location, the other may instead predict a hyperpolarization. Conclusions: Although a cochlear model with fewer details seems sufficient for analysing the current spread in the cochlear ducts, a detailed-segmented cochlear model is required for the reconstruction of ANF trajectories through the modiolus, as well as the prediction of firing thresholds and spike initiation sites.