University of Pennsylvania, 394 Town Building, United States.
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 n-level, the changing pressures and flowrates were calculated using prescribed shear-dependent hemostatic clot growth rates (normal or coagulopathic). Key results were: (1) the upstream vascular network rapidly depressurizes to reduce blood loss, (2) wall shear rates at the hemorrhaging wound exit are sufficiently high (~10,000 s) to drive von Willebrand Factor unfolding, (3) full coagulopathy results in >2L blood loss in 2 hours for severing all vessels of 0.13 to 0.005 mm diameter within the bifurcating network, whereas full hemostasis limits blood loss to <100 mL within 2 min, and (4) hemodilution from transcapillary refill increases blood loss and could be implicated in trauma induced coagulopathy. A sensitivity analysis on length/diameter ratio and branching exponent demonstrated that bleeding was strongly dependent upon these tissue-dependent network parameters. This is the first bleeding model that prescribes the geometry of the injury in order to calculate the rate of pressure-driven blood loss and local wall shear rate in the presence or absence of coagulopathic blood.
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