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At least 145 records · Page 8Linked to original sources
PubMedDate not supplied

Identification algorithm for systemic arterial parameters with application to total artificial heart control.

A new algorithm for estimating systemic arterial parameters from systolic pressure and flow measurements at the root of the aorta is developed and tested through a systems identification approach. The resulting procedure has direct application to a total artificial heart (TAH) control system currently under development. Identification models, representing the systemic arterial system, are developed from existing work in the area of cardiovascular modeling. The resistive and compliance components of these models are physically significant, representing overall hydraulic properties of the systemic arterial system. A unique method of parameterizing the identification models is designed which operates on the basis of aortic pressure and flow measurements taken exclusively during systole. The estimator is a modified recursive least squares algorithm which utilizes covariance modification to track time-varying parameters and a dead-zone to improve the robustness. Performance of the estimation algorithm was tested on data generated by a higher-order distributed model of the systemic arterial bed using normal canine parameters. Results from model-to-model experiments verify the consistency of the estimates and the ability of the estimator to converge quickly and track dynamically varying parameters.

Adaptation, Physiological↗
PubMed2001

Introduction of computational models to PhysioNet.

PhysioNet is a national research resource that provides experimental data sets and open-source software for their analysis. Computational modeling can complement studies of these experimental data sets so as to facilitate the advancement of physiologic research. Thus, in order to introduce computational models to PhysioNet, we have developed and posted a cardiovascular model designed for research that generates reasonable human pulsatile hemodynamic waveforms, cardiac output and venous return curves, and beat-to-beat variability. Some of the key features of the software include: 1) compatibility with PhysioNet's open-source data analysis software; 2) online viewing and parameter updating as the data are being calculated; 3) off-line viewing after completion of the simulation; 4) pre-compiled Linux binaries; 5) open-source code that may be compiled on other platforms; and 6) an extensive user's manual and software guide.

Cardiac Output↗
PubMed1998

Estimation of cardiac function from computer analysis of the arterial pressure waveform.

This paper presents a method for estimating parameters of a cardiovascular model, including the left-ventricular function, using the sequential quadratic programming (SQP) and the least minimum square (LMS) algorithms. In a first stage, a radial arterial-pressure waveform with corresponding cardiac output are used to automatically seek the set of parameters of the diastolic model. Computer simulation of the model using these parameters generate a pressure waveform and a cardiac output very close to those used for the estimation. In a second stage, the estimated arterial load parameters are used to select the best left-ventricular model function, from four different possibilities, and to estimate its optimum parameter values. The method has been tested numerically and applied to real cases, using data obtained from cardiovascular patients. It has also been subjected to preliminary validation using data obtained from laboratory dogs, in which cardiovascular function was artificially altered.

Algorithms↗
PubMed2005

Design and initial testing of a mock human circulatory loop for left ventricular assist device performance testing.

A mock circulatory loop, which simulates the human circulatory system, is needed to bench test the various versions of continuous flow (CF) left ventricular assist devices (LVADs). This article describes the design and initial testing of such a loop. The loop consists of: (1) pulsatile left and right cardiac simulators; (2) air/water tanks to model the venous and arterial compliances; (3) tygon tubes to model the venous, arterial, and other system flow resistances; and (4) a tuning clamp to model the variation in system resistance characteristics under different cardiac pressure/flow conditions. Several loop measurements were carried out without an LVAD to verify the cardiovascular modeling of a healthy person in sleep, rest, and physical activity, and in different pathological states, and compared to the data found in the literature to validate the loop performance prior to LVAD testing.

Blood Circulation↗
PubMed1994

Venous collapse and the respiratory variability in systemic venous return.

OBJECTIVE: Venous collapse limits systemic venous return, but its effects on beat to beat respiratory venous return variations are less well known. The aim of this study was to investigate the effects of venous collapse on respiratory variations in venous return. METHODS: A model of venous collapse which included both an increase in haemodynamic resistance to flow and an increase in vessel compliance was incorporated in a previously described cardiovascular model. Respiration was simulated by 5 mm Hg swings of intrathoracic pressure (PTH) at different mean pressures such that the abdominal vena cava and jugular vein were either fully collapsed (mean PTH -11 mm Hg), in the transition zone between collapse and distension (mean PTH -6 mm Hg), or fully distended (mean PTH 9 mm Hg). The mean and standard deviations over each respiratory cycle of the venous return volume (flow integral over heart cycle) and the abdominal vena caval volume were recorded. RESULTS: Different venous return volume variabilities in the three operating zones of the vena cava were identified: (1) reduced variability in the collapsed zone associated with the increased haemodynamic resistance [venous return 93(SD 6) ml, abdominal vena caval volume 30(3) ml. absolute right atrial pressure -6.3(1.1) mm Hg]; (2) increased variability in the transition zone [venous return 86(24) ml, abdominal vena caval volume 81(15) ml, right atrial pressure -2.2(0.8) mm Hg]; (3) low variability in the distended zone [venous return 42(11) ml, abdominal vena caval volume 120(2) ml, right atrial pressure 10.1(1.1) mm Hg]. The greater the change in compliance with collapse the greater the increase in flow variability in the transition zone; with no change in compliance there was no increased flow variability in the transition zone. CONCLUSIONS: The results suggest that venous collapse increases the respiratory variations in venous return in the transition zone. As venous return variations contribute to arterial pressure variations, the collapsible nature of the great veins may influence respiratory variations in systemic arterial pressure.

Blood Circulation↗
PubMed1999

[Computer simulation of cardiovascular response to lower body negative pressure].

OBJECTIVE: To simulate the cardiovascular response to lower body negative pressure (LBNP). METHOD: A computer model was developed. It had 7 subparts: the redistribution of blood, the filling of left ventricle, left ventricle, peripheral circulation, control of heart rate, control of peripheral resistance and control of venous tone. The heart rate and venous tone were controlled by high-pressure receptor baroreflex, while the peripheral resistance was controlled by high- and low-pressure receptor baroreflexes. RESULT: With the help of the model, cardiovascular response to LBNP up to -10.64 kPa (-80 mmHg) were simulated, including the changes of systolic blood pressure, mean blood pressure, heart rate and cardiac output. The time-dependent response to a LBNP profile was also simulated. The simulation results coincided well with human experiments. CONCLUSION: The model is valid and can accurately reproduce the short-term hemodynamic response to LBNP.

Aerospace Medicine↗
PubMed1989

Characteristics of Doppler blood-velocity waveforms in a cardiovascular in vitro model. II. The influence of peripheral resistance, perfusion pressure and blood flow.

A cardiovascular in vitro model was used to examine the influence of peripheral resistance on the Doppler blood-velocity waveforms. In the study the velocity indices were determined as a function of peripheral resistance either with the flow kept constant (the perfusion pressure varied) or with the pressure constant (the flow varied). The peak velocity (Vpeak) is normally accepted as a simple expression of the stroke volume. However, in this study Vpeak did increase with resistance when the stroke volume was constant. Rising slope (RS) is said to correlate with heart contractility, but in this study such a relation was not found. Pulsatility index (PI) and A/B ratio (A/B) are normally considered to reflect peripheral resistance. PI was found to be a flow- and pressure-independent proportional expression of peripheral resistance. A/B also increased with resistance but this relationship is more uncertain. The results of this in vitro study support the clinical use of PI as a flow- and pressure-independent estimate of peripheral resistance. The relation of RS and Vpeak to heart contractility and stroke volume, respectively, is found to be dependent also on resistance, blood flow, and pressure.

Blood Flow Velocity↗
PubMedDate not supplied

Numeric modeling of the cardiovascular system with a left ventricular assist device.

A numeric model consisting of a lump-parameter cardiovascular system (CVS) model and a model for the Cleveland Clinic Implantable Ventricular Assist System (IVAS), a nonpulsatile rotary pump designed to augment the failing left ventricle, are described in this paper. The purposes of this study were to 1) observe the hemodynamic interactions between CVS and IVAS under various physiologic and pathophysiologic conditions running at different speeds; and 2) allow testing and optimization of various IVAS control algorithms. An existing numeric model of CVS (24 coupled differential equations, representing all cardiac chambers and systemic and pulmonary vasculature) was modified to add the IVAS pump as an auxiliary chamber between the left ventricle and aorta with pressure-flow-speed characteristics derived from in vitro testing. Simulations were conducted for ventricles with normal and abnormal systolic and diastolic dysfunction at different exercise levels with the pump running at various speeds. Computer simulations show that 1) numeric modeling is useful for predicting hemodynamic response of CVS to IVAS in various circumstances; 2) IVAS results in normalization of cardiac output, especially in failing hearts, although with reduced pulse pressure; and 3) various control algorithms allowing adaptation of IVAS to physiologic demands of CVS could be developed based on the simulation study.

Blood Pressure↗
PubMed2000

Bifurcation in a simple model of the cardiovascular system.

A simple nonlinear beat-to-beat model of the human cardiovascular system has been studied. The model, introduced by DeBoer et al. was a simplified linearized version. We present a modified model which allows to investigate the nonlinear dynamics of the cardiovascular system. We found that an increase in the alpha-sympathetic gain, via a Hopf bifurcation, leads to sustained oscillations both in heart rate and blood pressure variables at about 0.1 Hz (Mayer waves). Similar oscillations were observed when increasing the beta-sympathetic gain or decreasing the vagal gain. Further changes of the gains, even beyond reasonable physiological values, did not reveal another bifurcation. The dynamics observed were thus either fixed point or limit cycle. Introducing respiration into the model showed entrainment between the respiration frequency and the Mayer waves.

Blood Pressure↗
PubMed2004

Introducing a baroreflex model for studying cardiovascular effects of mental workload.

A quantitative baroreflex control model is presented aimed at estimating differences in autonomic activation due to mental task performance. The model, which builds on earlier work of Wesseling and colleagues, is strongly supported by well-established knowledge of physiological control processes. Spectral measures of heart rate and blood pressure variability provide the information to estimate autonomic gain and tone parameters. The article gives a detailed model description as well as an evaluation in terms of spectral variability distributions, respiratory sinus arrhythmia, and vagal control mechanisms. The estimation procedure is outlined while presenting two studies that describe the effects of mental workload and vagal blockade, respectively. It is concluded that, using the model approach, cardiovascular effects of mental task performance can be interpreted in terms of specific changes in autonomic state. The model is implemented in a Matlab/Simulink environment and is available for other researchers in the field.

Adult↗
PubMed1991

Flow estimation using ultrasound imaging (color M-mode) and computer postprocessing.

We have developed a method to calculate flow noninvasively in blood vessels using color Motion-mode (M-mode) and computer postprocessing. The velocity of each point in the cross-sectional area of the vessel was found from the color M-mode recording by correcting for angle both distances and velocities and by assuming a symmetrical circular velocity field. Volume flow was then found by integrating the velocity field at 5-ms intervals through the cardiac cycle. In a cardiovascular hydromechanical model, a correlation of 0.99 and p value of less than 0.001 were found between estimated and measured flow in the model (n = 8). In 20 healthy individuals, we made 31 investigations in the common carotid (CCA), internal carotid (ICA), and external carotid (ECA) artery, comparing flow in the CCA with the added flow in the ICA and ECA. The values (CCA versus ICA + ECA) correlated with r = 0.91 and p less than 0.01. Repeated investigations (n = 8) in one individual gave flow estimates of 495 +/- 50 ml/min in the CCA, 304 +/- 45 ml/min in the ICA, and 165 +/- 37 ml/min in the ECA (means +/- SD). This article shows that this system can make accurate estimation of blood flow to the brain noninvasively.

Blood Flow Velocity↗
PubMed2002

Simulation study of the cardiovascular functional status in hypertensive situation.

An extended cardiovascular model was established based on our previous work to study the consequences of physiological or pathological changes to the homeostatic functions of the cardiovascular system. To study hemodynamic changes in hypertensive situations, the impacts of cardiovascular parameter variations (peripheral vascular resistance, arterial vessel wall stiffness and baroreflex gain) upon hemodynamics and the short-term regulation of the cardiovascular system were investigated. For the purpose of analyzing baroregulation function, the short-term regulation of arterial pressure in response to moderate dynamic exercise for normotensive and hypertensive cases was studied through computer simulation and clinical experiments. The simulation results agree well with clinical data. The results of this work suggest that the model presented in this paper provides a useful tool to investigate the functional status of cardiovascular system in normal or pathological conditions.

Blood Pressure↗
PubMed1994

The mouse as a model for human cardiovascular disease and hyperlipidemia.

The mouse has been used as an experimental model for atherosclerosis research for only a short time; however, the sophisticated genetics of this species has resulted in a number of innovative approaches that are not possible with other models. The availability of inbred, congenic, recombinant inbred, and mutant strains has resulted in the discovery of a number of genes affecting atherosclerosis susceptibility. More importantly, the newer genetic technologies such as quantitative trait-loci mapping, transgenic mice, and gene-targeted mice are producing important insights into atherosclerosis. This review, focusing on murine models of cardiovascular disease and hyperlipidemia, will be divided into two parts: naturally occurring models and genetically engineered models.

Animals↗
PubMed2006

A new multi-scale simulation model of the circulation: from cells to system.

We developed a comprehensive cell model that simulates the sequential cellular events from membrane excitation to contraction in the human ventricle. By combining this ventricular cell model with a lumped circulation model, we examined how blood pressure dynamics in the ventricle and aorta are related to the cellular processes. To convert cell contraction into ventricular pressure using Laplace's law, we introduced a simple geometric model of a ventricle: one shaped like a thin-walled hemisphere. The force of contraction of a single cell induces tension in the hemispheric ventricular wall, which generates the ventricular and aortic pressures in the lumped circulation model. The time courses of the hemodynamic properties, as well as the volume-pressure trajectory of the left ventricle, were well reproduced. Our multi-scale cardiovascular model, which covers from cardiac cells to the circulatory system, simulates the typical characteristics of heart mechanics, such as the pressure-volume relationship, stroke volume and the effect of the increased maximum free calcium concentration on cardiovascular hemodynamics. To test the cell-circulation coupling characteristics of the model, we simulated the effects of a decrease in L-type calcium channel conductance (cell level) on left ventricular pressure (system level). The variation due to different pacing frequencies for myocyte excitation was also investigated to assess the effects of heart rate on cardiac cells and the circulatory system.

Action Potentials↗
PubMed1993

A comparison of overall mathematical models of the cardiovascular system for simulating response to orthostatic stresses.

Although numerous mathematical models of the cardiovascular system (CVS) have appeared in the literature only a few of them are models of the entire system with detailed representation of the heart, the vasculature, and the control elements. Like all models of biological systems, these models vary in complexity, and most of them are stimulus- specific. Their ability to simulate with acceptable accuracy either responses over a wide range of the stimulus or responses to stimuli of similar kind has not been reported. In this paper, three mathematical models of the CVS are examined in terms of their response to different orthostatic stresses, namely, lower body negative pressure (LBNP), head-up tilt, and blood loss. The short-term orthostatic responses of the models are compared to available experimental data. The models are: (i) Croston and Fitzjerrell's for study of LBNP and head-up tilt response, (ii) Jaron et al.'s for study of +Gz response, and (iii) Pullen's for simulation of response to blood loss. We will henceforth refer to these models by the letters C, J, and P, respectively.

Hemorrhage↗