Parameter estimation to study the immediate impact of aortic cross-clamping using reduced order models.

Aortic cross-clamping is a common strategy during vascular surgery, however, its instantaneous impact on hemodynamics is unknown. We, therefore, developed two numerical models to estimate the immediate impact of aortic clamping on the vascular properties. To assess the validity of the models, we recorded continuous invasive pressure signals during abdominal aneurysm repair surgery, immediately before and after clamping. The first model is a zero-dimensional (0D) three-element Windkessel model, which we coupled to a gradient-based parameter estimation algorithm to identify patient-specific parameters such as vascular resistance and compliance. We found a 10% increase in the total resistance and a 20% decrease in the total compliance after clamping. The second model is a nine-artery network corresponding to an average human body in which we solved the one-dimensional (1D) blood flow equations. With a similar parameter estimation method and using the results from the 0D model, we identified the resistance boundary conditions of the 1D network. Determining the patient-specific total resistance and the distribution of peripheral resistances through the parameter estimation process was sufficient for the 1D model to accurately reproduce the impact of clamping on the pressure waveform. Both models gave an accurate description of the pressure wave and had a high correlation (R2 > .95) with experimental blood pressure data.

Effects of Cross-Clamping on Vascular Mechanics: Comparing Waveform Analysis With a Numerical Model.

BACKGROUND: Immediate changes in vascular mechanics during aortic cross-clamping remain widely unknown. By using a numerical model of the arterial network, vascular compliance and resistance can be estimated and the time constant of pressure waves can be calculated and compared with results from the classic arterial waveform analysis. METHODS: Experimental data were registered from continuous invasive radial artery pressure measurements from 11 patients undergoing vascular surgery. A stable set of beats were chosen immediately before and after each clamping event. Through the arterial waveform analysis, the time constant was calculated for each individual beat and for a mean beat of each condition as to compare with numerical simulations. Overall proportional changes in resistance and compliance during clamping and unclamping were calculated using the numerical model. RESULTS: Arterial waveform analysis of individual beats indicated a significant 10% median reduction in the time constant after clamping, and a significant 17% median increase in the time constant after unclamping. There was a positive correlation between waveform analysis and numerical values of the time constant, which was moderate (ρ = 0.51; P = 0.01486) during clamping and strong (ρ = 0.77; P ≤ 0.0001) during unclamping. After clamping, there was a significant 16% increase in the mean resistance and a significant 23% decrease in the mean compliance. After unclamping, there was a significant 19% decrease in the mean resistance and a significant 56% increase in the mean compliance. CONCLUSIONS: There are significant hemodynamic changes in vascular compliance and resistance during aortic clamping and unclamping. Numerical computer models can add information on the mechanisms of injury due to aortic clamping.

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.

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 sheep's 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 Young's 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 Young's 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.

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.