Impact of Respiratory Fluctuation on Hemodynamics in Human Cardiovascular System: A 0-1D Multiscale Model

To explore hemodynamic interaction between the human respiratory system (RS) and cardiovascular system (CVS), here we propose an integrated computational model to predict the CVS hemodynamics with consideration of the respiratory fluctuation (RF). A submodule of the intrathoracic pressure (ITP) adjustment is developed and incorporated in a 0-1D multiscale hemodynamic model of the CVS specified for infant, adolescent, and adult individuals. The model is verified to enable reasonable estimation of the blood pressure waveforms accounting for the RF-induced pressure fluctuations in comparison with clinical data. The results show that the negative ITP caused by respiration increases the blood flow rates in superior and inferior vena cavae; the deep breathing improves the venous return in adolescents but has less influence on infants. It is found that a marked reduction in ITP under pathological conditions can excessively increase the flow rates in cavae independent of the individual ages, which may cause the hemodynamic instability and hence increase the risk of heart failure. Our results indicate that the present 0-1D multiscale CVS model incorporated with the RF effect is capable of providing a useful and effective tool to explore the physiological and pathological mechanisms in association with cardiopulmonary interactions and their clinical applications.

Cortical Depth-Dependent Modeling of Visual Hemodynamic Responses

A physiologically based three-dimensional (3D) hemodynamic model is used to predict the experimentally observed blood oxygen level dependent (BOLD) responses versus the cortical depth induced by visual stimuli. Prior 2D approximations are relaxed in order to analyze 3D blood flow dynamics as a function of cortical depth. Comparison of the predictions with experimental data for typical stimuli demonstrates that the full 3D model matches at least as well as previous approaches while requiring significantly fewer assumptions and model parameters.

Dynamic Fractioning of the Gravitational Hydrostatic Pressure: A hemodynamic model for the venous pressure control by the valvo-muscular pump

Dynamic Fractioning of the Gravitational Hydrostatic Pressure (DFGHSP) is a pillar of a hemodynamic model of the venous pathophysiology. It describes how the valvo-muscular pump varies the distal venous pressure in the lower limbs. It results from an inductive reasoning based on clinical signs and instrumental data at rest and during the action of the valvo-muscular pump of the calf. It does not claim to be the final truth, but a new "as if" model that improved the diagnosis and the treatment of the venous insufficiency (CHIVA, French acronym for Cure Conservatrice et Hémodynamique de l’Insuffisance Veineuse en Ambulatoire) according to several randomized studies and meta-analyses. That approach overturns the classic diagnosis and treatment of venous insufficiency because it is conservative and opposes the widely spread destructive based view. It needs a minimal study of basic fluid mechanics which can explain venous hemodynamics, the core of venous pathophysiology. The proposed DFGHSP fluid mechanics model is compared with the hemodynamic clinical and instrumental data in order to assess its pathophysiologic relevance.

Generation of a Simplified Brain Geometry for the Calculation of Local Cerebral Temperature using a 1D Hemodynamic Model

In Western countries, stroke is the third-most cause of death; 35- 55% of the survivors experience permanent disability. Mild therapeutic hypothermia (TH) showed neuroprotective effect in patients returning from cardiac arrest and is therefore assumed to decrease stroke induced cerebral damage. Recently, an intracarotid cooling sheath was developed to induce local TH in the penumbra using the cooling effect of cerebral blood flow via collaterals. Computational modeling provides unique opportunities to predict the resulting cerebral temperature without invasive procedures. In this work, we generated a simplified brain model to establish a cerebral temperature calculation using Pennes’ bio-heat equation and a 1D hemodynamics model of the cranial artery tree. In this context, we performed an extensive literature research to assign the terminal segments of the latter to the corresponding perfused tissue. Using the intracarotid cooling method, we simulated the treatment with TH for different degrees of stenosis in the middle cerebral artery (MCA) and analyzed the resulting temperature spatialtemporal distributions of the brain and the systemic body considering the influence of the collaterals on the effect of cooling.

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 nth-level, the changing pressures and flowrates were calculated using prescribed shear-dependent hemostatic clot growth rates (normal or coagulopathic). Key results were as follows: 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−1) to drive von Willebrand factor unfolding; 3) 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 <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-to-diameter ratio and branching exponent demonstrated that bleeding was strongly dependent on these tissue-dependent network parameters. This is the first bleeding model that prescribes the geometry of the injury to calculate the rate of pressure-driven blood loss and local wall shear rate in the presence or absence of coagulopathic blood. NEW & NOTEWORTHY We developed a multiscale model that couples a lumped, global hemodynamic model of a patient to resolved, single-vessel wounds ranging from the small artery to capillary scale. The model is able to quantify wall shear rates, seal rates, and blood loss rates in the presence and absence of baroreflex control and hemodilution.