John K-J. Li

Dynamics of the vascular system

Historical Background and Book Content Vascular Biology, Structure and Function Physical Concepts and Basic Fluid Mechanics Hemodynamics of Large Arteries Vascular Branching The Venous System The Microcirculation The Integrated Vascular System and Diseased Conditions.

A nonlinear model of the arterial system incorporating a pressure-dependent compliance

An examination is made of the consequences of incorporating a pressure dependent compliance in a modified arterial system model. This nonlinear model is evaluated under control and acute pressure-loading conditions. Results show that the nonlinear compliance model in general can more accurately predict the measured pressure waveforms during control and during acute pressure loading. The difference between the predicted waveforms is more pronounced when blood pressure is high and when the pulse pressure is large.<<ETX>>

Time Domain Resolution of Forward and Reflected Waves in the Aorta

A simple, fast time domain method for the resolution of aortic pressure and flow pulses into their forward and reflected components is presented. Accuracy of the method depends on the estimation of characteristic impedance and the frequency responses of the transducer systems.

Vessel growth and collapsible pressure-area relationship

The role that the pattern of vessel wall growth plays in determining pressure-lumen area (P-A) and pressure-compliance curves was examined. A P-A vessel model was developed that encompasses the complete range of pressure, including negative values, and accounts for size given the fixed length, nonlinear elastic wall properties, constant wall area, and collapse. Data were obtained from excised canine carotid and femoral arteries, jugular veins, and elastic tubing. The mean error of estimate was 8 mmHg for all vessels studied and 2 mmHg for blood vessels. The P-A model was employed to examine two patterns of arterial wall thickening, outward growth and remodeling (constant wall area), under the assumption of constant wall properties. The model predicted that only outward wall growth resets compliance such that it increases at a given arterial pressure, explaining previously contradictory data. In addition, it was found that outward wall growth increases the lumen area between normal and high pressures. Remodeling resulted in lumen narrowing and a decrease in compliance for positive pressures.

Concurrent compliance reduction and increased peripheral resistance in the manifestation of isolated systolic hypertension

The hemodynamic mechanisms responsible for producing isolated systolic hypertension (ISH) in the elderly are generally attributed to a decrease in arterial compliance. However, no consistent theoretical or experimental model has been proposed for the production of ISH. This problem was investigated with the use of computer simulation of the modified Windkessel model, an often-used tool in the study of arterioventricular function. Aortic pressure (Pa(t] and aortic flow (Qa(t] data were used to obtain the model parameters: peripheral resistance (Rs), arterial compliance (C) and characteristic impedance of the proximal aorta (Zo). Using Qa(t) as the input to the model, the effects of altered vascular properties on Pa(t) were studied by changing these model parameters. Graded reductions of C (25, 50 and 75%) alone increased systolic pressure (Ps), but also decreased diastolic pressure (Pd) to values below those found in ISH. On the other hand, an increase in Rs of 25% along with a 50 to 75% increase in C resulted in percent changes in Ps and Pd that would result in ISH from a normal pressure level. These results were consistent for a wide range of pressures. Decreased arterial compliance alone is not always responsible for the production of ISH. Rather, isolated systolic hypertension is usually the result of greatly reduced arterial compliance along with a smaller but significant increase in peripheral resistance.

Arterial Compliance and Its Pressure Dependence in Hypertension and Vasodilation

Arterial compliance has been recognized to be pressure-dependent. Its varia tion due to changing systolic and diastolic blood pressures in hypertension and subsequent vasodilation has not been investigated. The authors examined this aspect by combining an animal experiment and a recently established nonlinear windkessel model of the arterial system that incorporates a pressure-dependent arterial compliance, C(P). Aortic pressure and flow were simultaneously mea sured in experimental dogs during control and during methoxamine-induced hypertension and nitroprusside-induced vasodilation. A numerical procedure was implemented to compute the nonlinear compliance and account for the pressure dependence. Results show that within the cardiac cycle, C(P) reached its maximum at end-systole and increased in diastole when diastolic aortic pres sure decayed. The magnitude of C(P) and its variation within the cardiac cycle was larger at low pressures, while the reverse was found when blood pressure was high. C(P) decreased significantly in hypertension and increased during subsequent vasodilation.

Temporal relationship between left ventricular and arterial system elastances

The authors investigated the temporal relationship of arterial compliance to ventricular elastance of the left ventricle (E/sub lv/(t)) in five open-chest anesthetized dogs, where simultaneous aortic pressure and flow and left-ventricular pressure were measured. E/sub lv/(t) was derived using an elastance-resistance model of the left ventricle. The nonlinear pressure-dependent compliance (C(P)) of the arterial system was incorporated in a three-element Windkessel model and determined by accurate prediction of aortic pressure from aortic flow. The resulting arterial elastance E/sub as/(t) was computed as E/sub as/(t)=1/C(P). Results show that E/sub as/(t) reaches a minimum value at or near the start of ventricular ejection and attains its peak value at or near the time that maximum left ventricular elastance is reached, at end-systole. Numerical simulation of the model demonstrates its ability to adequately reproduce measured pressure and flow. Thus, the arterial system, in terms of elastance, is dynamically and temporally coupled to the left-ventricle during ejection.<<ETX>>

Comparative cardiac mechanics: Laplace's law

The pumping ability of the heart is determined by mechanical and geometrical factors. These latter are governed by Laplaces Law. The extent of the applicability of this law across mammalian species is examined utilizing allometric relations and dimensional analysis. Results show that Laplaces Law plays an important role in linking the anatomical design to the functional capability of mammalian hearts.

Analysis and Assessment of Cardiovascular Function

1. Cardiovascular Function.- 1. Cardiovascular Concepts in Antiquity.- 2. A New Approach to the Analysis of Cardiovascular Function: Allometry.- 2. Cardiac Muscle.- 3. Muscle Contraction Mechanics from Ultrastructural Dynamics.- 4. Crossbridge Cycling and Cooperative Recruitment Can Account for Oscillatory Dynamics of Constantly Activated Heart.- 5. Modeling Reversible Mechanical Dysfunction in the Stunned Myocardium.- 6. Computer-Based Myocardial Tissue Characterization Using Quantitative Description of Texture.- 3. Coronary Circulation.- 7. Interpretation of Coronary Vascular Perfusion.- 8. New-Age Rapid Diagnosis of Acute Myocardial Injury.- 4. Ventricular Dynamics.- 9. Modeling of the Effects of Aortic Valve Stenosis and Arterial System Afterload on Left Ventricular Hypertrophy.- 10. Ventricular Shape: Spherical or Cylindrical?.- 11. Pathophysiology of Diastole and Left Ventricular Filling in Humans: Noninvasive Evaluation.- 12. Echocardiographic Evaluation of Thrombolytic Intervention After Acute Myocardial Infarction.- 5. Arterial/Ventricular Circulation.- 13. Modeling of Noninvasive Arterial Blood Pressure Methods.- 14. Measurement and Applications of Arterial and Ventricular Pressure-Dimension Relationships in Animals and Humans.- 6. Microcirculation.- 15. Quantitative Analysis of the Lee Method for Determination of the Capillary Filtration Coefficient.- 16. Assessment of Human Microvascular Function.- 7. Venous System.- 17. Dynamic Response of the Collapsible Blood Vessel.- 8. Electrophysiology.- 18. Microvolt-Level T Wave Alternans as a Marker of Vulnerability to Cardiac Arrhythmias: Principles and Detection Methods.- 19. Quantification of Heart Rate Variability Using Methods Derived from Nonlinear Dynamics.- 20. Transesophageal Electrophysiology.- 21. Occurrence and Diagnostic Importance of Postural ST-Segment Depression in Ambulatory Holter Monitoring in Male Patients After Myocardial Infarction.

Modeling of mechanical dysfunction in regional stunned myocardium of the left ventricle

Reversible mechanical dysfunction of the myocardium after a single or multiple episode(s) of coronary artery occlusion has been observed in previous studies and is termed myocardial stunning. The hypothesis that stunning could be represented by a decrease in maximum available muscle force in the stunned region was examined by means of a mathematical model that incorporates series viscoelastic elements. A canine experimental model was also employed to demonstrate depressed contractility and a consistent delay of shortening in the stunned region. The mechanical model of the left ventricle was designed to include a normal and stunned region, for which the stunned region was allowed to have variable size. Each region consisted of a volume and time dependent force generator in parallel with a passive elastic force element. The passive elastic element was placed in series with a constant viscosity component and a series elastic component. The model was solved by means of a computer. Passive and active properties of each region could be altered independently. The typical regional measures of muscle performance such as percent shortening, percent bulge, percent thickening, delay of shortening, percent increase in end-diastolic length and other hemodynamic measures were computed. These results were similar to those observed in animal models of stunning. In addition, a nearly linear relationship with end-diastolic length and delay of shortening was predicted by the model. It was concluded that a decrease in the peak isovolumic elastance and augmentation of viscosity effect of creep during stunning can explain mechanical abnormalities of stunned myocardium.