LV-arterial coupling: interactive model to predict effect of wave reflections on LV energetics

1991 ◽  
Vol 261 (4) ◽  
pp. H1026-H1033 ◽  
Author(s):  
D. H. Fitchett

The interaction between the left ventricle (LV) and the arterial system was simulated using sequential convolution of the flow output generated by a time-varying elastance model of the LV with an impulse response calculated from a 128-element model of the arterial system. The model illustrates the effect of independent changes of components of the arterial load on LV performance and energetics. This report studies the response of the model LV to an increase in arterial resistance, a decrease in arterial compliance, and an increase in discrete vascular reflections. Although arterial resistance exerts the greatest effect on ventricular stroke output, a reduction of arterial compliance or an increase in early reflections resulted in less optimal coupling of the heart to the arteries and less efficient energy utilization by the LV. In addition, the earlier the reflections return, the greater the disturbance of ventricular arterial coupling.

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Payman Zamani ◽  
Prasad Konda ◽  
Scott Akers ◽  
Neetha Vadde ◽  
Anjaneyulu Dunde ◽  
...  

Background: In aortic stenosis (AS), the valve imparts an additional hemodynamic burden on the LV in proportion to the degree of valve narrowing. Yet the relative contributions of valve stenosis and arterial load on LV fiber stress are unknown. Furthermore, it has recently been shown that end-systolic measurements of wall stress are unrepresentative of the time-resolved wall stress patterns. Yet, time-resolved LV fiber stress has never been assessed in AS. Hypothesis: Arterial load is an important determinant of time-resolved wall stress in AS. Methods: We assessed time-resolved LV geometry (using SSFP cine MRI), aortic flow (using phase-contrast MRI) and central aortic pressure (using carotid tonometry) among 40 patients with AS (16 mild, 20 moderate, and 4 severe AS). Arterial load parameters were determined using pressure-flow analyses, including systemic vascular resistance, characteristic impedance of the aorta (Zc), total arterial compliance (pulse-pressure method, TAC), and the amplitudes of the backward (Pb) and forward (Pf) waves. We computed time-resolved ejection-phase myocardial fiber stress using the Arts method. Results: Peak fiber stress occurred at 94.4 msec into systole and was significantly greater than end-systolic fiber stress (847±265 vs. 361±149 kdynes/cm2, P<0.0001). After adjusting for cardiac output, AVA, and end-diastolic mass and volume, Pb, TAC, and SVR were all associated with peak and end-systolic fiber stress (Table). Interestingly, while AVA was associated with peak stress, it was not associated with end-systolic stress in any model. Conclusion: Peak fiber stress occurs early in systole in AS, demonstrating the importance of time-resolved fiber stress assessments. Our findings demonstrate important contributions from the arterial system to LV fiber stress in AS, including resistive load and various measured of pulsatile arterial load.


1992 ◽  
Vol 263 (4) ◽  
pp. H1054-H1063 ◽  
Author(s):  
G. M. Drzewiecki ◽  
E. Karam ◽  
J. K. Li ◽  
A. Noordergraaf

In the past, the dynamics of the left ventricle were studied by its response to altered venous and arterial load for a given heart. This led researchers to propose the concept of an arterioventricular match or optimal point of function. The model of this paper reverses that idea by fixing preload and afterload while computing cardiac function due to altered left ventricular size or shape, resulting from modification of the number of parallel and series sarcounits. A mathematical model of physiological hypertrophy is introduced. Series and parallel arrangements of sarcounits constitute a cylindrical model of the left ventricle. Filling occurs from a venous reservoir with constant pressure through a valve, while ejection takes place into a three-element model of the systemic arterial system through another valve. It is found that the dynamics of the myofibrils can be matched to those of the left ventricle by choosing a ventricular shape that results in a minimum in myocardial O2 consumption (MVO2) for any constant ventricular load. A unique solution for the size of the ventricle results if the rate of MVO2 is specified. The model is able to predict correctly hypertrophy due to hypoxia and due to pressure (concentric) and volume (eccentric) overloads.


2021 ◽  
Vol 1717 ◽  
pp. 012034
Author(s):  
N. Padmapriya ◽  
S. Vinothini ◽  
S. Yuvasri

1976 ◽  
Vol 40 (3) ◽  
pp. 425-433 ◽  
Author(s):  
M. G. Bottomley ◽  
G. W. Mainwood

A device was designed to provide a “square” pulse of blood flow into the arterial system. Pulses were injected into the carotid artery of the rabbit during transient cardiac arrest. Analysis of pressure response curves generated by the flow provides information as to the state of the arterial tree. With certain assumptions it is possible to estimate from these curves lumped values of peripheral resistance, critical closing pressure, and arterial compliance. In a series of 12 rabbits the mean value of peripheral resistance was found to be 0.21 +/- 0.7 mmHg-ml-1-min and critical closing pressure was estimated to be 23.6 +/- 3.8 mmHg. This method gives two possible values for arterial compliance 0.036 +/- 0.010 and 0.055 +/- 0.010 ml-mm-1 based, respectively, on the rise and decay curves of the pressure response. The theory and limitations of the method are discussed. The use of the method is illustrated in following the response to increased PCO2 and hemorrhage.


Energy Policy ◽  
2011 ◽  
Vol 39 (6) ◽  
pp. 3630-3637 ◽  
Author(s):  
Héctor Campbell ◽  
Gisela Montero ◽  
Carlos Pérez ◽  
Alejandro Lambert

Endocrinology ◽  
2004 ◽  
Vol 145 (7) ◽  
pp. 3289-3296 ◽  
Author(s):  
Kirk P. Conrad ◽  
Dan O. Debrah ◽  
Jackie Novak ◽  
Lee A. Danielson ◽  
Sanjeev G. Shroff

Abstract Relaxin emanates from the corpus luteum of the ovary and circulates during pregnancy. Because the hormone is a potent renal vasodilator and mediates the renal vasodilation and hyperfiltration of pregnancy in conscious rats, we reasoned that it might also contribute to the broader cardiovascular changes of pregnancy. We began investigating this concept by testing whether relaxin can modify systemic arterial hemodynamics and load when chronically administered to nonpregnant rats. The major objectives of the present work were to determine whether relaxin administration to nonpregnant rats 1) modifies cardiac output (CO), systemic vascular resistance, and global arterial compliance (AC), and 2) regulates the passive mechanics of isolated arteries. To accomplish the first objective, we developed a conscious rat model for assessment of global AC. Passive mechanics of small renal arteries were assessed using a pressure arteriograph. Chronic administration of recombinant human relaxin by sc osmotic minipump to conscious, female, nonpregnant rats reduced the steady arterial load by decreasing systemic vascular resistance, increased CO, and reduced the pulsatile arterial load by increasing global AC as quantified by two indices—AC estimated from the diastolic decay of aortic pressure and CO and AC estimated by the ratio of stroke volume-to-pulse pressure. In another group of rats, relaxin administration also regulated the passive mechanics of small renal arteries, indicating that, in addition to reduction in vascular smooth muscle tone, modification of the vascular structure (e.g. extracellular matrix) contributes to the increase in global AC. These findings suggest a role for relaxin in the systemic hemodynamic changes of pregnancy, as well as novel therapeutic potential for relaxin in modifying arterial stiffness and cardiac afterload.


Sign in / Sign up

Export Citation Format

Share Document