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Physiology of Venous Return?

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Physiology of Venous Return? Concise Definitive Review Series Editor, Jonathan E. Sevransky, MD, MHS Deepa & Naresh CCM The Role of Venous Return in Critical Illness and CCM Shock—Part I: Physiology Critical Care Medicine Duane J. Funk, MD1,2; Eric Jacobsohn, MD1,2; Anand Kumar, MD1,3 Crit Care Med Objective: To provide a conceptual and clinical review of the phys- stressed conditions. The first part describes the basic physiology of Lippincott Williams & Wilkins iology of the venous system as it is relates to cardiac function in the venous system, and part two focuses on the role of the venous health and disease. system in different pathophysiologic states, particularly shock. Hagerstown, MD Data: An integration of venous and cardiac physiology under nor- Conclusion: An improved understanding of the role of the venous mal conditions, critical illness, and resuscitation. system in health and disease will allow intensivists to better ap- Summary: The usual teaching of cardiac physiology focuses on left preciate the complex circulatory physiology of shock and may al- 10.1097/CCM.0b013e3182772ab6 ventricular function. As a result of the wide array of shock states low for better hemodynamic management of this disorder. (Crit with which intensivists contend, an approach that takes into account Care Med 2013; 41:255–262) 204217 the function of the venous system and its interaction with the right Key Words: cardiogenic shock; cardiovascular physiology; and left heart may be more useful. This two-part review focuses on hemodynamics; hemorrhagic shock; obstructive shock; septic the function of the venous system and right heart under normal and shock n the modern era, the typical hemodynamic analysis of This two-part review discusses the role of the heart and cardiovascular function focuses on left ventricular (LV) venous system in regulating venous return (VR) and cardiac Iphysiology. The reason for this is the primacy of ischemic output (CO). The primary determinants of VR are explained heart disease (which most obviously affects LV function) as a and alterations in VR in different pathophysiologic states are cause of death in the developed world as well as the complex described. In the second part of this review, the physiology of pathophysiology of the right ventricle (RV)/venous system, VR is graphically integrated with RV physiology in the con- which results in practical difficulties in assessing RV/venous text of a variety of pathophysiologic states including shock. In performance in the critically ill. An approach that centers on LV addition, the effects of common therapies for the shock states function is appropriate for most cardiologists given their focus on (fluid administration, vasopressor and inotropic support, management of myocardial infarction and congestive heart fail- and mechanical ventilation) are examined in relation to their ure. However, intensivists deal with a broader array of cardiovas- impact on VR and CO interactions. cular perturbations including shock states in which vascular dys- function and other extracardiac perturbations may dominate the FUNCTION OF THE VENOUS SYSTEM clinical picture (e.g., septic, hypovolemic, or obstructive shock). The main functions of the systemic venous system are to act An approach to cardiovascular physiology that incorporates both as a conduit to return blood to the heart from the periphery cardiac and vascular elements may be more useful to intensiv- and to serve as a reservoir of the circulating blood volume. Al- ists than one that focuses exclusively on LV physiology. though the cardiovascular circuit is a two-compartment model comprising both a systemic and pulmonary circuit, >80% of the blood volume held in veins is in the systemic venous circu- 1 Section of Critical Care Medicine, Department of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada. lation with three fourths of that in small veins and venules (1, 2 Department of Anesthesiology and Perioperative Medicine, University of 2) (Table 1). The pulmonary veins contain only a small blood Manitoba, Winnipeg, Manitoba, Canada. volume and left atrial pressure has a relatively modest effect 3 Section of Critical Care Medicine, Cooper University Hospital, Cooper Medical School of Rowan University, Camden, NJ. on left heart function. For these reasons, the physiology of VR The authors have not disclosed any potential conflicts of interest. can be described, in practical terms, as the physiology of VR to For information regarding this article, E-mail: [email protected] the heart. Copyright © 2013 by the Society of Critical Care Medicine and Lippincott Veins have a compliance 30 times greater than arteries and Williams & Wilkins contain approximately 70% of the total blood volume com- DOI: 10.1097/CCM.0b013e3182772ab6 pared with only 18% for the arteries (3–5). Because of the Critical Care Medicine www.ccmjournal.org 255 Funk et al TABLE 1. Distribution of Blood in the Various of the venous reservoir. The concept of Pms is described more Components of the Circulatory System fully subsequently. Note that resistance to flow in both equations (SVR and vR ) Percentage of Total Blood is directly proportional to the length of the blood vessels (l), Structure Volume the viscosity of blood (η), and it is inversely proportional to the Systemic venous system 64 radius (r) of the vessels to the fourth power. Mathematically: Systemic arterial system 13 8nl R = 4 Capillaries 7 πr Pulmonary circuit 9 In most pathophysiologic analyses, the radius and length of Heart 7 the conduit are emphasized in the assessment of resistance to flow; viscosity is ignored. However, in clinical settings, liters Reprinted with permission from Milnor W: Cardiovascular Physiology. New York, NY, Oxford University Press, 1990. of low-viscosity (relative to whole blood) crystalloid or col- loids may be administered over short periods. Furthermore, priming a cardiopulmonary bypass or extracorporeal mem- high compliance of veins, large changes in blood volume are brane oxygenation circuit also involves administration of large not associated with significant changes in venous transmural amounts of low viscosity fluids. In these settings, alterations pressure. These features make the venous system an ideal blood in blood viscosity resulting from hemodilution may provide a reservoir that can maintain filling of the right heart despite significant contribution to changes in resistance (8, 9). significant variations in circulatory volume. The veins of the Although the most common theoretical construct of car- splanchnic bed alone hold approximately 20% to 33% of the diac function used by clinicians suggests that the left heart total blood volume (6, 7). plays a major role in the regulation of CO (three of the four Hagen-Poiseuille’s law is central to the understanding of determinants of left heart CO, that is, preload, heart rate, and both VR and CO. This law (analogous to Ohm’s law of electri- contractility, are intrinsically cardiac-related indices), the VR cal current flow) states that the fluid flow (Q) through a system equation suggests cardiac function plays only an indirect role (such as the cardiovascular circuit) is related to the pressure in the governance of VR. The only way that cardiac function drop across the system divided by the resistance of the system: can affect VR is by altering PRA and thereby changing the driv- ing pressure gradient. As a consequence of the normal modest • − Q = PP12 operating range of pressures in the venous circuit (8–12 mm R Hg in venules to 1–2 mm Hg in the vena cava/right atrium) where P is upstream pressure, P is downstream pressure, 1 2 (10), small changes in PRA can drive very large changes in VR. and R is resistance to flow. Given that CO and VR must be equal in a closed system, the Left heart output (i.e., CO) and flow through the sys- obvious corollary is that CO, under most physiological and temic circulation are commonly described using a variation of pathophysiological conditions, is not primarily dependent on Hagen-Poiseuille’s law. The difference between mean arterial LV cardiac function, but on VR to the right heart. pressure (MAP [P1]) and right atrial pressure (PRA [P2]) is the Further to this issue, CO/VR is, in fact, determined by pressure drop across the system and systemic vascular resis- the interaction of the heart as a whole (inclusive of the right tance (SVR) represents resistance to flow through the circuit: heart, pulmonary circuit, and left heart characteristics) with the systemic vascular circuit, not by any individual element. MAP − CO = P RA The elements contributing to cardiac function in this context SVR include the loads on and compliance of the right and left ven- tricles and the compliance and resistance of the pulmonary Because CO must equal VR, it is intuitive that VR to the circuit. For the sake of simplicity, our subsequent discussion right heart can be similarly described: often focuses on right heart function but it should be under- − VR = PPms RA stood that right heart function in this context represents an amalgam of all influences on the heart as a whole. R v To appreciate VR physiology, three related factors must be where P is the mean systemic pressure of the circula- ms appreciated: the concepts of Pms, stressed and unstressed vol- tion and R is the resistance to VR. The P is the upstream V ms umes, and venous resistance (Rv). The concept of Pms dates pressure for the venous circulation, whereas PRA is again the back to the late 1800s when Bayliss and Starling surmised downstream pressure (as it is in the equation describing sys- that if the circulation was transiently halted, arterial pressure temic blood flow). This equation represents the application of would fall and venous pressure would rise (11). They reasoned Hagen-Poiseuille’s law to the venous circulation. Note that this that the pressure in the entire system during cardiac standstill conceptual framework suggests that arterial pressure is unre- would equilibrate at what they termed Pms.
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