Arthur Ghigo

The dicrotic notch analyzed by a numerical model

Divergent concepts on the origin of the dicrotic notch are widespread in medical literature and education. Since most medical textbooks explain the origin of the dicrotic notch as caused by the aortic valve closure itself, this is commonly transmitted in medical physiology courses. We present clinical data and numerical simulations to demonstrate that reflected pressure waves could participate as one of the causes of the dicrotic notch. Our experimental data from continuous arterial pressure measurements from adult patients undergoing vascular surgery suggest that isolated changes in peripheral vascular resistance using an intravenous bolus of phenylephrine (a selective alpha 1-receptor agonist and thus a potent vasoconstrictor) modify the dicrotic notch. We then explore the mechanisms behind this phenomenon by using a numerical model based on integrated axisymmetric Navier-Stokes equations to compute the hemodynamic flow. Our model illustrates clearly how modifications in peripheral artery resistance may result in changes in the amplitude of the dicrotic notch by modifying reflected pressure waves. We believe that this could be a useful tool in teaching medical physiology courses.

Fluid friction and wall viscosity of the 1D blood flow model

We study the behavior of the pulse waves of water into a flexible tube for application to blood flow simulations. In pulse waves both fluid friction and wall viscosity are damping factors, and difficult to evaluate separately. In this paper, the coefficients of fluid friction and wall viscosity are estimated by fitting a nonlinear 1D flow model to experimental data. In the experimental setup, a distensible tube is connected to a piston pump at one end and closed at another end. The pressure and wall displacements are measured simultaneously. A good agreement between model predictions and experiments was achieved. For amplitude decrease, the effect of wall viscosity on the pulse wave has been shown as important as that of fluid viscosity.

Linear and nonlinear viscoelastic arterial wall models: application on animals

This work deals with the viscoelasticity of the arterial wall and its influence on the pulse waves. We describe the viscoelasticity by a nonlinear Kelvin-Voigt model in which the coefficients are fitted using experimental time series of pressure and radius measured on a sheeps arterial network. We obtained a good agreement between the results of the nonlinear Kelvin-Voigt model and the experimental measurements. We found that the viscoelastic relaxation time-defined by the ratio between the viscoelastic coefficient and the Youngs modulus-is nearly constant throughout the network. Therefore, as it is well known that smaller arteries are stiffer, the viscoelastic coefficient rises when approaching the peripheral sites to compensate the rise of the Youngs modulus, resulting in a higher damping effect. We incorporated the fitted viscoelastic coefficients in a nonlinear 1D fluid model to compute the pulse waves in the network. The damping effect of viscoelasticity on the high-frequency waves is clear especially at the peripheral sites.

Numerical simulations of a bypass repair of an iliac artery obliteration.

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A Novel Interpretation for Arterial Pulse Pressure Amplification in Health and Disease

Arterial pressure waves have been described in one dimension using several approaches, such as lumped (Windkessel) or distributed (using Navier-Stokes equations) models. An alternative approach consists of modeling blood pressure waves using a Korteweg-de Vries (KdV) equation and representing pressure waves as combinations of solitons. This model captures many key features of wave propagation in the systemic network and, in particular, pulse pressure amplification (PPA), which is a mechanical biomarker of cardiovascular risk. The main objective of this work is to compare the propagation dynamics described by a KdV equation in a human-like arterial tree using acquired pressure waves. Furthermore, we analyzed the ability of our model to reproduce induced elastic changes in PPA due to different pathological conditions. To this end, numerical simulations were performed using acquired central pressure signals from different subject groups (young, adults, and hypertensive) as input and then comparing the output of the model with measured radial artery pressure waveforms. Pathological conditions were modeled as changes in arterial elasticity (E). Numerical results showed that the model was able to propagate acquired pressure waveforms and to reproduce PPA variations as a consequence of elastic changes. Calculated elasticity for each group was in accordance with the existing literature.