Function of arteries and veins in conditions of simulated cardiac arrest

Abstract

Introduction: The study examined the behavior of vasculature in conditions of eliminated cardiac function using mathematical modeling. In addition, we addressed the question of whether the stretch-recoil capability of veins, at least in part accounts for the slower response to simulated cardiac arrest. Methods: In the first set of computational experiments, blood flow and pressure patterns in veins and arteries during the first few seconds after cardiac arrest were assessed via a validated multi-scale mathematical model of the whole cardiovascular system, comprising cardiac dynamics, arterial and venous blood flow dynamics, and microcirculation. In the second set of experiments, the effects of stretch-recoil zones of venous vessels with different diameters and velocities on blood velocity and dynamic pressure analyzed using computational fluid dynamics (CFD) modeling. Results: In the first set of experiments, measurement of changes in velocity, dynamic pressure, and fluid flow revealed that the venous system responded to cardiac arrest more slowly compared to the arteries. This disparity might be due to the intrinsic characteristics of the venous system, including stretch-recoil and elastic fiber composition. In the second set of experiments, we attempted to determine the role of the stretch-recoil capability of veins in the slower response to cardiac arrest. During the second set of experiments, we found that this recoil behavior increased dynamic pressure, velocity, and blood flow. The enhancement in dynamic pressure through combining the results from both experiments yielded a 15-40% increase in maximum dynamic pressure due to stretch-recoil, depending on vein diameter under normal conditions. Conclusion: In the situation of cardiac arrest, the vein geometry changes continue, promoting smooth responses of the venous system. Moreover, the importance of such vein behavior in blood displacement may grow as the pressure on the venous side gradually decreases with time. Our experiments suggest that the driving force for venous return is the pressure difference that remains within the venous system after the energy coming from every ventricular systole spent to overcome the resistance created by arterial and capillary systems.

What drives venous return?

“…Following complete elimination of cardiac function in this model, the arterial flow stopped almost immediately whereas venous flow continued for 10–13 s. During this short period of time the venous flow was gradually and markedly decreasing but was maintained at a very low level during the 10 to 13 s. The main underlying mechanism of this effect could be the stretch–recoil phenomenon of the veins. Such phenomena have been observed 13 . Temporary accumulation of blood in the proximal part of the veins was followed by venous wall recoil, effectively squeezing blood out of that segment into the next segment of the vein.…”

“…The next steps for research in this area would be establishing the role of cardiac output in regulation of venous return not only in a mathematical model but also in laboratory experiments in vivo and then in the clinical setting. It is hoped that studies, such as ours 13 might shed further light on ‘What drives venous return?’.…”

“…The alternative theory states that through cardiac activity, every systole, maintains venous flow using the energy remaining within circulatory system after the larger part of it is spent to overcome the resistance of arterial and capillary vascular beds, blood viscosity and other factors. Quite a few observations provided support for either of these two theories 3–13 . Thus, the question remains, ‘What drives venous return, cardiac output or MCFP?’…”

“…In a recent publication, 13 we used distal avatar software and a computational fluid dynamic approach. This model allowed us to simulate a condition of absence of cardiac activity and observe only vascular (including venous) events.…”

How to end the ‘venous return’ controversy

“…As to the ‘stretch-recoil’ effect that Gelman and colleagues described in their computational study, 4 it cannot be the driver of steady-state flow for the reasons described above. Interestingly, the presence and relevance of any sort of ‘peristaltic’ vasomotion at the level of the peripheral veins has appealed to proponents of the Guytonian model, 6 presumably as a mechanistic explanation or evidence for something like a heart-independent venous flow.…”