How changes in venous capacitance modulate cardiac output

Tyberg, John V.

doi:10.1007/s00424-002-0922-x

Cited by 85 publications

(71 citation statements)

References 39 publications

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“…1,[14][15][16] The concept of sympathetically mediated venous fluid volume redistribution principally from the splanchnic venous reservoir through changes in venous capacitance as a mechanism for the precipitation of acute (on chronic) HF events is comprehensively discussed by Tyberg 17 and Fallick et al 18 The concept of fluid redistribution suggests that multiple confounding factors (eg,…”

Section: Contribution Of Intravascular Fluid Redistribution To Hemodymentioning

confidence: 99%

Fluid Volume Overload and Congestion in Heart Failure

Miller

2016

Circ: Heart Failure

210

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Abstract-Volume regulation, assessment, and management remain basic issues in patients with heart failure. The discussion presented here is directed at opening a reassessment of the pathophysiology of congestion in congestive heart failure and the methods by which we determine volume overload status. Peer-reviewed historical and contemporary literatures are reviewed. Volume overload and fluid congestion remain primary issues for patients with chronic heart failure. The pathophysiology is complex, and the simple concept of intravascular fluid accumulation is not adequate. The dynamics of interstitial and intravascular fluid compartment interactions and fluid redistribution from venous splanchnic beds to central pulmonary circulation need to be taken into account in strategies of volume management. Clinical bedside evaluations and right heart hemodynamic assessments can alert clinicians of changes in volume status, but only the quantitative measurement of total blood volume can help identify the heterogeneity in plasma volume and red blood cell mass that are features of volume overload in patients with chronic heart failure and help guide individualized, appropriate therapy-not all volume overload is the same. (Circ Heart Fail. 2016;9:e002922.

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Section: Contribution Of Intravascular Fluid Redistribution To Hemodymentioning

confidence: 99%

Fluid Volume Overload and Congestion in Heart Failure

Miller

2016

Circ: Heart Failure

210

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“…Brengelmann (3), Levy (20), and Tyberg (33) argued that as CO increases, the venous reservoir is depleted (i.e., blood is translocated from the veins to the arteries), and, therefore, venous pressure (i.e., atrial pressure) decreases. In the heart, atrial pressure determines CO according to the Frank-Starling mechanism.…”

Section: Comparison With Previous Studies Of Cardiovascular Modelingmentioning

confidence: 99%

A novel framework of circulatory equilibrium

Uemura

Sugimachi

Kawada

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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A novel framework of circulatory equilibrium was developed by extending Guyton's original concept. In this framework, venous return (CO V) for a given stressed volume (V) was characterized by a flat surface as a function of right atrial pressure (P RA) and left atrial pressure (PLA) as follows: COV ϭ V/W Ϫ G SPRA Ϫ GPPLA, where W, GS, and GP denote linear parameters. In seven dogs under total heart bypass, CO V, PRA, PLA, and V were varied to determine the three parameters in each animal with use of multivariate analysis. The coefficient of determination (r 2 ϭ 0.92-0.99) indicated the flatness of the venous return surface. The averaged surface was CO V ϭ V/0.129 Ϫ 19.61PRA Ϫ 3.49PLA. To examine the invariability of the surface parameters among animals, we predicted the circulatory equilibrium in response to changes in stressed volume in another 12 dogs under normal and heart failure conditions. This was achieved by equating the standard surface with the individually measured cardiac output (CO) curve. In this way, we could predict CO [y ϭ 0.90x ϩ 5.6, r 2 ϭ 0.95, standard error of the estimate (SEE) ϭ 8.7 ml ⅐ min Ϫ1 ⅐ kg Ϫ1 ], PRA (y ϭ 0.96x, r 2 ϭ 0.98, SEE ϭ 0.2 mmHg), and P LA (y ϭ 0.89x ϩ 0.5, r 2 ϭ 0.98, SEE ϭ 0.8 mmHg) reasonably well. We conclude that the venous return surface accurately represents the venous return properties of the systemic and pulmonary circulations. The characteristics of the venous return surface are invariable enough among animals, making it possible to predict circulatory equilibrium, even if those characteristics are unknown in individual animals. venous return; cardiac output; hemodynamics THE FRAMEWORK FOR CIRCULATORY EQUILIBRIUM was pioneered by Guyton and associates in the 1950s (14 -17). They characterized the venous return properties of the systemic vein by the venous return curve and the apparent pumping ability of the cardiothoracic compartment by the cardiac output (CO) curve (Fig. 1A). The intersection of the two curves determines equilibrium CO and right atrial pressure (P RA ) (14). This concept clearly defined the circulatory equilibrium under rather simple pathophysiological conditions, such as hemorrhage and exercise, and deepened our understanding of control mechanisms of CO. However, because the original framework lumped various subsystem components, such as the right ventricle, pulmonary vascular system, and left ventricle, into a single cardiothoracic compartment, the lack of consideration of the venous return properties of the pulmonary circulation and the pumping ability of the individual ventricles makes it difficult to define the circulatory equilibrium under more complex conditions such as unilateral ventricular failures, which are often seen in clinical settings (2). In other words, redistribution of blood between the systemic and pulmonary circulations cannot be defined by their original framework.To deal with the blood redistribution, Guyton et al. (15) modified the original framework and developed a two-compartment model. However, the analysis of hem...

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“…Control of venous capacitance is important in the maintenance of cardiovascular homeostasis and cardiac output (35). Modulation of venous capacitance by sympathetic outflow has been demonstrated with studies during electrical stimulation, including splanchnic and hepatic nerves (5,7), changes in carotid artery pressure (31), and pharmacological manipulation of sympathetic activity (23).…”

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confidence: 99%

Systemic vascular effects of acute electrical baroreflex stimulation

Burgoyne

Georgakopoulos

Belenkie

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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Burgoyne S, Georgakopoulos D, Belenkie I, Tyberg JV. Systemic vascular effects of acute electrical baroreflex stimulation. Am J Physiol Heart Circ Physiol 307: H236 -H241, 2014. First published May 9, 2014; doi:10.1152/ajpheart.00422.2013.-We intended to determine if acute baroreflex activation therapy (BAT) increases venous capacitance and aortic conductance. BAT is effective in resistant hypertension, but its effect on the systemic vasculature is poorly understood. Left ventricular (LV) and aortic pressures and subdiaphragmatic aortic and caval flows (ultrasonic) were measured in six anesthetized dogs. Changes in abdominal blood volume (V abdominal) were estimated as the integrated difference in abdominal aortic inflow and caval outflow. An electrode was implanted on the right carotid sinus. Data were measured during control and BAT. Next, sodium nitroprusside (SNP) was infused and BAT was subsequently added. Finally, angiotensin II (ANG II) was infused, and three increased BAT currents were added. We found that BAT decreased mean aortic pressure (P Ao) by 22.5 Ϯ 1.3 mmHg (P Ͻ 0.001) and increased aortic conductance by 16.2 Ϯ 4.9% (P Ͻ 0.01) and V abdominal at a rate of 2.2 Ϯ 0.6 ml·kg Ϫ1 ·min Ϫ1 (P Ͻ 0.01). SNP decreased PAo by 17.4 Ϯ 0.7 mmHg (P Ͻ 0.001) and increased V abdominal at a rate of 2.2 Ϯ 0.7 ml·kg Ϫ1 ·min Ϫ1 (P Ͻ 0.05). During the SNP infusion, BAT decreased P Ao further, by 26.0 Ϯ 2.1 mmHg (P Ͻ 0.001). ANG II increased PAo by 40.4 Ϯ 3.5 mmHg (P ϭ 0.001). When an increased BAT current was added, P Ao decreased to baseline (P Ͻ 0.01) while aortic conductance increased from 62.3 Ϯ 5.2% to 80.2 Ϯ 3.3% (P Ͻ 0.05) of control. V abdominal increased at a rate of 1.8 Ϯ 0.9 ml·kg Ϫ1 ·min Ϫ1(P Ͻ 0.01), reversing the ANG II effects. In conclusion, BAT increases arterial conductance, decreases P Ao, and increases venous capacitance even in the presence of powerful vasoactive drugs. Increasing venous capacitance may be an important effect of BAT in hypertension.baroreceptors; venous capacitance; aortic conductance ELECTRICAL BARORECEPTOR activation therapy (BAT) can be achieved with an implantable medical device (CVRx Inc.) and has been used to treat resistant hypertension (27). There is also potential for this approach to be useful in heart failure (11). While the effects of BAT on cardiac function (i.e., heart rate, contractility, and cardiac output) have been established (11), the effects on the peripheral circulation (i.e., arterial conductance and venous capacitance) have not been defined. Control of venous capacitance is important in the maintenance of cardiovascular homeostasis and cardiac output (35). Modulation of venous capacitance by sympathetic outflow has been demonstrated with studies during electrical stimulation, including splanchnic and hepatic nerves (5, 7), changes in carotid artery pressure (31), and pharmacological manipulation of sympathetic activity (23). The control of vascular capacitance by the carotid baroreflex has been well-investigated and demonstrated (30). While the effects of ...

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How changes in venous capacitance modulate cardiac output

Cited by 85 publications

References 39 publications

Fluid Volume Overload and Congestion in Heart Failure

Fluid Volume Overload and Congestion in Heart Failure

A novel framework of circulatory equilibrium

Systemic vascular effects of acute electrical baroreflex stimulation

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