  Proper heart morphogenesis requires a delicate balance between hemodynamic
forces, myocardial activity, morphogen gradients, and epigenetic signaling, all
of which are coupled with genetic regulatory networks. Recently both in vivo
and in silico studies have tried to better understand hemodynamics at varying
stages of vertebrate cardiogenesis. In particular, the intracardial
hemodynamics during the onset of trabeculation is notably complex - the
inertial and viscous fluid forces are approximately equal at this stage and
small perturbations in morphology, scale, and steadiness of the flow can lead
to significant changes in bulk flow structures, shear stress distributions, and
chemical morphogen gradients. The immersed boundary method was used to solve
the computational fluid dynamics problem involving fluid flow moving through
the trabeculated ventricles of 72, 80, and 120 hours post fertilization wild
type zebrafish embryos and ErbB2-inhibited embryos at 7 days post
fertilization. An idealized trabeculated ventricular model was explored to map
the bifurcations in flow structure that occur as a result of the unsteadiness
of flow, trabeculae height, and fluid scale ($Re$). Vortex formation occurred
in intertrabecular regions for biologically relevant parameter spaces, wherein
flow velocities increased. This indicates that trabecular morphology may alter
intracardial flow patterns and hence ventricular shear stresses and morphogen
gradients. A potential implication of this work is that the onset of vortical
(disturbed) flows can upregulate Notch1 expression in endothelial cells in
vitro and hence impacts chamber morphogensis, valvulogenesis, and the formation
of the trabeculae themselves.
