Coagulopathy implications using a multiscale model of traumatic bleeding matching macro- and microcirculation

Quantifying the relationship between vascular injury and the dynamic bleeding rate requires a multiscale model that accounts for changing and coupled hemodynamics between the global and microvascular levels. A lumped, global hemodynamic model of the human cardiovascular system with baroreflex control was coupled to a local 24-level bifurcating vascular network that spanned diameters from the muscular artery scale (0.1-1.3 mm) to capillaries (5-10 μm) via conservation of momentum and conservation of mass boundary conditions. For defined injuries of severing all vessels at each th-level, the changing pressures and flowrates were calculated using prescribed shear-dependent hemostatic clot growth rates (normal or coagulopathic). Key results were as follows: ) the upstream vascular network rapidly depressurizes to reduce blood loss; ) wall shear rates at the hemorrhaging wound exit are sufficiently high (~10,000 s ) to drive von Willebrand factor unfolding; ) full coagulopathy results in >2-liter blood loss in 2 h for severing all vessels of 0.13- to 0.005-mm diameter within the bifurcating network, whereas full hemostasis limits blood loss to