Skip Navigation LinksHome > April 2008 - Volume 108 - Issue 4 > Venous Function and Central Venous Pressure: A Physiologic S...
Anesthesiology:
doi: 10.1097/ALN.0b013e3181672607
Review Article

Venous Function and Central Venous Pressure: A Physiologic Story

Gelman, Simon M.D., Ph.D.*
Section Editor(s): Warner, David S. M.D.; Warner, Mark A. M.D., Editors

Free Access
Article Outline
Collapse Box

Author Information

Collapse Box

Abstract

The veins contain approximately 70% of total blood volume and are 30 times more compliant than arteries; therefore, changes in blood volume within the veins are associated with relatively small changes in venous pressure. The terms venous capacity, compliance, and stressed and unstressed volumes are defined. Decreases in flow into a vein are associated with decreases in intravenous pressure and volume, and vice versa. Changes in resistance in the small arteries and arterioles may affect venous return in opposite directions; this is explained by a two-compartment model: compliant (mainly splanchnic veins) and noncompliant (nonsplanchnic veins). Effects of intrathoracic and intraabdominal pressures on venous return and central venous pressure as well as the value of central venous pressure as a diagnostic variable are discussed.
IN the era of genetic revolution and exciting discoveries in molecular mechanisms of diseases, the systems’ physiology is often forgotten and poorly understood by many, including anesthesiologists. This review intends to cover one of many gaps in the understanding of cardiovascular physiology. The main goal of this article is to describe the functions of the venous system as an important part of the overall cardiovascular physiology. Understanding of these functions would help to prevent many mistakes in the interpretation of one or another variable, particularly values of central venous pressure (CVP), in clinical settings.
Schematically we can look at the cardiovascular system as a heart and a circuit. This article is focused on one part of the circuit, namely the venous system. The function of the heart and the arterial system will be mentioned only in light of their effects on the venous system and the effects of the venous system on the function of the heart. Moreover, the focus of this article is on the gross physiologic relation within the venous system rather than on molecular and biochemical mechanisms of smooth muscle contraction and relaxation of the venous walls. Finally, the article will address the question of usefulness (or lack of it) of the CVP as a clinical guide for physiologic diagnoses and therapeutic interventions.
Back to Top | Article Outline

Function of the Venous System

The main functions of the venous system are to return blood to the heart from the periphery and to serve as a capacitance to maintain filling of the heart. Veins contain approximately 70% of total blood volume compared with 18% in arteries and only 3% in terminal arteries and arterioles; veins are 30 times more compliant than the arteries.1,2 The compliance of the arteries, being much lower than compliance of the veins, may increase under certain conditions, e.g., arterial compliance significantly increases during pregnancy3 and during certain pharmacologic interventions such as nitroglycerin administration.4,5 The splanchnic system receives approximately 25% of cardiac output (CO) and contains approximately 20% of total blood volume. Because of high compliance of the veins, changes in blood volume are associated with relatively small changes in venous transmural pressure.2 Veins are the most compliant vasculature in the human body and are easily able to accommodate changes in the blood volume. Therefore, they are called capacitance vessels and serve as a reservoir of blood that easily and immediately changes volume in it to maintain filling pressure in the right heart. Splanchnic and cutaneous veins are the most compliant and represent the largest blood volume reservoirs in the human body. Veins of the extremities are less compliant than splanchnic veins, and therefore, their role as blood volume reservoir is relatively minimal. Splanchnic and cutaneous veins have a high population of α1- and α2-adrenergic receptors and therefore are highly sensitive to adrenergic stimulation, contrary to skeletal muscle veins, which have relatively insignificant sympathetic innervation.6 This pattern of innervation of the veins and the fact that cutaneous circulation is controlled mainly by the temperature suggest that venoconstriction and mobilization of blood volume is mainly limited to the splanchnic veins.7,8
Back to Top | Article Outline

Definitions and Basic Concepts

Venous Capacity and Compliance
There is some confusion in the literature regarding the relevant terminology. The definitions described in this article are used by the majority of authors and clearly summarized by the authority in the field.1,9
Venous capacity is a blood volume contained in a vein at a specific distending pressure.6,9–11
Venous compliance is a change in volume (ΔV) of blood within a vein (or venous system) associated with a change in intravenous distending pressure (ΔP).
Fig. 1
Fig. 1
Image Tools
Therefore, capacity is a point of volume at a certain pressure while compliance is a slope of change in volume associated with a change in pressure. A decrease in volume within a vein (or venous system) can be achieved by a decrease in capacity (position of the curve) or by a change in compliance (slope of the curve) or both (fig. 1). Venoconstrictors, α-adrenergic agonists, decrease venous capacity without changing compliance.12
It is important to distinguish intraluminal (intramural) venous pressure, which is the pressure within a vessel (which can be measured directly via an inserted catheter), regardless of the pressure surrounding the vessel. Transmural pressure or distending pressure refers to a difference between the pressure within the vessel and outside the vessel.
Back to Top | Article Outline
Stressed and Unstressed Volume
The intersection of the line of compliance with the y-axis reflects an unstressed volume (Vu; fig. 1), which is a volume of blood in a vein at transmural pressure equal to zero. Stressed volume is a volume of blood within a vein under transmural pressure above zero (Vs; fig. 1). The sum of stressed (approximately 30% of total volume) and unstressed (approximately 70% of total volume) volumes is the total blood volume within the venous system.
Fig. 2
Fig. 2
Image Tools
An analog with a tub is helpful to understand the relation between Vu and Vs13–15 (fig. 2). Both volumes are important: Vs determines mean circulatory filling pressure (MCFP; see Mean Circulatory Filling Pressure section) and directly affects venous return (VR) and CO, whereas Vu is a reserve of blood that can be mobilized into circulation when needed.
Back to Top | Article Outline
Flow–Pressure–Volume Relation
Equation 1
Equation 1
Image Tools
Fig. 3
Fig. 3
Image Tools
This relation is an important homeostatic mechanism in the body,8,16 (fig. 3). The described relation between flow, pressure, and volume within the veins occurs in very compliant (splanchnic) veins and represents a passive distribution of volume between veins (mainly the splanchnic system) and the heart, which is associated with changes in venous capacity without change in compliance (fig. 1, black lines).
A decrease in flow through the splanchnic arteries, being associated with a decrease in volume in the splanchnic veins and the liver and transfer of this volume into the systemic circulation, plays an important role not only in compensation of hypovolemia but also in compensation of cardiac failure. If CO is decreasing, a simultaneous decrease in flow through splanchnic arteries is associated with a shift of blood volume from splanchnic veins to the heart recruiting Frank-Starling mechanism (an increase in preload leading to an increase in contractility). Reduction in CO by 27% was associated with 9.2 ml/kg of blood recruitment from the splanchnic system when reflexes were intact.17 Similar reduction in CO in conditions of ganglioblockade with hexamethonium led to recruitment of blood volume of 6.8 ml/kg. In a 75-kg human, this would mean a shift of blood volume of approximately 700 versus 500 ml of blood into systemic circulation with and without reflexes intact, respectively. Therefore, the active constriction of veins would transfer only approximately 25% of total transferred blood.17 Thus, passive mechanisms due to change in flow followed by change in pressure and volume are more important in maintaining VR and CO than active venoconstricting mechanisms (fig. 3).8,17
Passive change in blood volume within the splanchnic system is more important within the intestines, whereas the active constriction of the vasculature is more prominent within the liver.9,17–19 The distribution of blood flow governs the distribution of blood volume within the body.17,20 These flow–pressure–volume relations adequately explain many physiologic and clinical conditions. More than 70 yr ago, an enlargement of cardiac dimensions was observed during cross clamping of the thoracic aorta.21 The authors attributed this to an increased afterload. They also observed that the cross clamping increased “systemic flow” (CO). They attributed (but did not prove) this increase to “blood transference” from the lower to the upper part of the body. Many other studies confirmed these observations.22 We observed a twofold increase in blood flow through the upper part of the body during aortic cross clamping at the diaphragmatic level.23–25 Finally, our experiments using whole body scintigraphy with technetium 99m–labeled plasma albumin have demonstrated that aortic cross clamping at the diaphragmatic level is associated with a significant increase in blood volume in the organs and tissues proximal to the level of occlusion.26 This is a direct unequivocal illustration of the shift of blood volume from the organs distal to the aortic cross clamp (from the compliant splanchnic veins) to the proximal, upper part of the body. Therefore, aortic cross clamping proximal to celiac artery leads to a drastic decrease in splanchnic flow, followed by a decrease in volume within the splanchnic veins and a shift of the volume to the upper part of the body with an increase in VR and CO.22
Back to Top | Article Outline
Mean Circulatory Filling Pressure
Let us imagine the heart is stopped for a relatively short period of time. Blood will not be flowing from the heart and toward the heart, and pressure will be the same in all parts of the circulatory system. Such a pressure is called mean circulatory filling pressure.27,28 When the heart starts pumping the blood, pressure within the arterial system is increasing and pushes the blood through the arteries, then through the capillaries into the venous system. The pressure in the small veins becomes higher than in the large veins and right atrium—CVP. Blood flow from the veins into the heart is determined by the gradient between peripheral and central venous pressures. According to Guyton, the main driving force for VR is MCFP, and
Equation (Uncited)
Equation (Uncited)
Image Tools
During cardiac arrest, the pressure within the venulae and small veins is not changing and remains the same as it was before cardiac arrest. Therefore, this pressure is considered the “pivoting pressure” for the whole circulatory system.9
The heart cannot pump more blood into circulation than it receives. Therefore, in physiologic conditions, CO is determined entirely by VR, and VR can be increased only by an increase in MCFP and/or a decrease in CVP because venous resistance is usually not changing much and relatively small. A normal heart itself can increase VR mainly by decreasing CVP, and only to a limited extent by increasing MCFP because of high resistance across arterial (resistance) vessels: The main pressure gradient within the circulatory system occurs at the level of arterial resistance.
The main factor determining the MCFP is Vs; others include venomotor tone, the vascular pump, the effects of ventricular contraction and relaxation, and the function of the venous valves and skeletal muscle. In dogs and presumably in humans, MCFP is approximately between 7 and 12 mmHg, whereas CVP is approximately 2–3 mmHg.15,27–31 Thus, the gradient for VR is somewhere between 5 and 10 mmHg, and therefore, the change in CVP just by a few millimeters of mercury can have considerable effect on VR.15,32
An interesting question is why in the normally functioning heart an increase in CVP (e.g., secondary to an infusion of volume) increases CO despite the increased downstream pressure. The tempting answer to this question is because myocardial contractility is increased. But this would not be enough because an increased contractility can increase the ejection fraction and would solve the problem of the heart but would not solve the problem of the circuit. The problem is solved by an increase in MCFP secondary to an increase in Vs. Because an increase in MCFP is at least equal or usually larger than an increase in CVP, even larger increases in pressure gradient to VR would be achieved at a higher level of both pressures, MCFP and CVP, with subsequent increases in VR and CO.
Back to Top | Article Outline
Venous Resistance
Fig. 4
Fig. 4
Image Tools
Constriction of the veins decreases their capacity and expels blood from them into the systemic circulation. However, venoconstriction may increase venous resistance and subsequently decrease VR and CO. How is the body recruiting the blood volume without an increase in resistance to VR? The constriction of splanchnic veins is not associated with an increase in resistance to VR because the splanchnic system is outside of the mainstream of blood flow to the heart through the caval veins1,15,33 (fig. 4, inside).
Venous return is increased by an increase in MCFP secondary to an increase in Vs, which can be achieved by an infusion of additional volume and/or by a decrease in venous capacity by venoconstrictors. The latter decreases Vu and increases Vs without change in the elastic properties of the venous wall, i.e., without change in venous compliance (fig. 1). In the analog with the tub, the outlet hole in the tub is moved down by venoconstriction: increasing the volume above the outlet hole and decreasing the volume below it (fig. 2).
This understanding of physiology and governing variables explains why patients at the beginning of bleeding, (up to 10–12% of blood volume loss) maintain their systemic hemodynamics well without changes in heart rate, blood pressure, or CVP, yet later, hemodynamics quickly deteriorate. The period of compensation reflects successful mobilization of Vu into Vs. Then, when the entire Vu has been mobilized, decompensation occurs suddenly. Similarly, when mobilization of Vu is secondary to an increase in sympathetic tone, an intervention associated with venodilation (general or regional anesthesia, opioids, sedatives), may cause rapid decompensation without additional blood loss because venodilation would be associated with a shift of volume from Vs back to Vu, resulting in a decrease in MCFP.
There is another interesting mechanism: Venous capacitance vessels are much more sensitive to sympathetic stimulation than arterial resistance vessels. Sympathetic stimulation of only 1 Hz results in a capacity response of almost 50% of maximal response observed during 20-Hz stimulation. On the other hand, the resistance response to 1 Hz stimulation is only 10% of maximum.2,34 Clinical implications of this and other observations are that a response to a moderate increase in sympathetic tone (or a small dose of vasoconstrictors) is a constriction of capacitance (splanchnic) vessels which would expel blood from the splanchnic vasculature into the systemic circulation without a significant increase in systemic arterial resistance. On the other hand, the response to larger doses of vasoconstrictors would be associated with both decrease in venous capacity with recruitment of blood volume from splanchnic vasculature and an increase in arterial tone and blood pressure.
There is another important component in this picture: resistance within the splanchnic venous system. The main place of resistance to the venous flow out of the splanchnic vasculature is located within the hepatic veins15,35–37 or within the liver itself.37 One way or the other, an increase in resistance within the distal part of the splanchnic venous system would impede the outflow of blood from splanchnic organs, sequestering blood within the liver and more proximal parts of the splanchnic veins. Profound arterial hypotension during septic shock in piglets was not associated with a decreased MCFP but rather with a drastic increase in venous resistance within the distal part of the splanchnic vasculature.38 A similar picture was observed in a porcine model of endotoxic shock.39
A decrease in resistance to venous flow within the liver and/or hepatic veins would facilitate the blood flow and volume shift from splanchnic vasculature to the inferior caval vein and right atrium, thereby increasing VR. Resistance within the liver and hepatic veins is mainly regulated by adrenergic receptors: Activation of α-adrenergic receptors increases resistance,15,40 whereas activation of β2-adrenergic receptors decreases it, resulting in volume shift from the splanchnic vasculature into the systemic circulation.15,35 Thus, the administration of pure α-adrenergic agonists could result in a decrease in venous capacity and an increase in Vs and MCFP, thereby increasing VR.40–54 However, activation of α-adrenergic receptors also could be associated with an increase in resistance within the liver and hepatic veins, which would impede the blood flow and shift of blood volume from the splanchnic system into systemic circulation.46,53–58 In conditions of normovolemia and a relatively small degree of α-adrenergic receptor activation, a decrease in venous capacity probably plays a more prominent role than an increase in resistance to the blood flow and volume shift from splanchnic vasculature. However, in conditions of hypovolemia (when further mobilization of Vu is decreased) and/or a high degree of α-adrenergic receptor activation, sequestration of blood volume within the liver and further decrease in VR and CO may occur.53,54 The combination of α- and β2-adrenergic agonists may facilitate the shift of blood volume from the splanchnic system into the systemic circulation more effectively than α-adrenergic agonists alone: Such a combination would lead to a decrease in venous capacity, recruitment of Vu into Vs, and a decrease in resistance to venous outflow from the splanchnic system. Obviously, in conditions of severe hypovolemia, such shifts of blood volume would not be possible simply because of absence of Vu to be recruited; an increase in arterial pressure, if observed, would result mainly from α receptor–mediated arterial constriction.53 An increase in venous capacity by an α-adrenergic agonist may also result from an activation of baroreceptors in the carotid sinuses secondary to an increase in arterial blood pressure.59,60
Back to Top | Article Outline
Two-compartment Model of the Venous System
Another important mechanism regulating the VR is resistance within the splanchnic arterial vasculature. Almost a century ago, the concept of a two-compartment model within the venous system was introduced61; one is very compliant and slow (splanchnic vasculature) and another is noncompliant and fast (nonsplanchnic venous vasculature; fig. 4, inside). This model has been used to explain many physiologic observations. It has also been periodically challenged.62 However, as the reader will see, this theoretical model can logically and convincingly explain many observations regarding the behavior of venous system during one or another insult to cardiovascular function. The model can be described as follows: An increase in resistance in arteries and arterioles feeding compliant splanchnic veins decreases flow, pressure, and volume within splanchnic veins, shifting blood volume from the splanchnic veins into the systemic circulation, and vice versa, a dilation of these arteries leads to blood pooling within the splanchnic veins (fig. 3 and fig. 4, outside). Such shift of blood volume is reflected in a rapid increase in flow from the splanchnic vasculature into the systemic circulation. Such an increase in flow is transient and the resulting blood volume redistribution would remain until the altered resistance in these arteries is maintained. When the change in resistance is reversed, the opposite shift of blood volume would occur.
Nonsplanchnic, less compliant veins behave differently. Dilation of small arteries and arteriolae in the nonsplanchnic vasculature, if associated with a relatively minor or no decrease in arterial pressure, would increase VR (fig. 4, outside). Such an increase may be attributed to a few different mechanisms, including translocation of arterial blood centrally through the venous system as well as direct or more often indirect (via activation of the sympathetic nervous system and/or angiotensin system) constriction of veins leading to translocation of venous blood toward the heart; a simultaneous decrease in venous resistance within the distal part of the splanchnic venous vasculature may also play a role in such observations.63,64 Finally and most importantly, a decrease in arterial resistance in the nonsplanchnic compartment, if associated with only a minor decrease in arterial pressure, leads to a significant increase in MCFP resulting from a decrease in the gradient between arterial and peripheral venous pressures increasing the MCFP and VR. This relation can be illustrated by an opening of a large arteriovenous fistula.28 However, if a decrease in arterial resistance is associated with a significant decrease in arterial pressure, it could be associated with a decrease in MCFP and VR.
Hemodynamic response to exercise is a beautiful illustration of how the different vascular beds respond in opposite directions to fulfill the changing requirements of the body for blood volume and oxygen delivery redistribution. During exercise, splanchnic blood flow can reduce from 1,500 ml/min to 350 ml/min. Splanchnic oxygen consumption is preserved by an increase in arteriovenous oxygen difference in this region from 4 to 17 ml of oxygen/100 ml of blood.65 On the other hand, total muscle blood flow can increase from approximately 1,000 ml/min at rest to almost 22,000 ml/min with an increase in CO to 25 l/min and oxygen uptake of almost 4 l/min. Arteriovenous oxygen difference in the muscle increases to 18 ml of oxygen/100 ml of blood, which represents approximately 90% oxygen extraction.66 The mechanisms responsible for such hemodynamic adjustments involve different responses of the arteries and arteriolae in the muscles versus the splanchnic system. An increase in sympathetic discharge during exercise leads to splanchnic arterial vasoconstriction leading to a decrease in flow, pressure, and volume within the splanchnic veins and an increase in VR and CO (fig. 3 and fig. 4, outside). The vasodilation within the exercising muscle, resulting to a minor extent from β2-adrenergic receptor activation but mainly from a local accumulation of vasodilating metabolites (lactate, adenosine, and other compounds), leads to a decrease in arteriovenous pressure gradient in the muscle and a significant increase in MCFP, VR, and CO. Simultaneous increase in sympathetic discharge constricts vasculature in nonexercising muscle and other tissues, helping to increase arterial pressure and MCFP, also increasing VR and CO. Additional mechanisms include “muscle pump” (during exercise contraction of muscles squeezes blood out of the muscles towards the heart), increase in heart rate and myocardial contractility, and many others.66
The effect of different vasodilators on VR and CO can depend on blood flow distribution between the two compartments, splanchnic and nonsplanchnic vasculature. For example, we and others observed that sodium nitroprusside decreases splanchnic blood flow.67,68 Decrease in splanchnic flow should be associated with a decrease in pressure and volume within the splanchnic veins (fig. 3 and fig. 4, outside). However, it does not happen69,70: In another study, during similar degrees of arterial hypotension, vascular capacity was increased during sodium nitroprusside and to a greater extent during nitroglycerin-induced hypotension, whereas it was not changed during adenosine triphosphate administration.68 That is, adenosine triphosphate and, to a lesser extent, sodium nitroprusside dilated nonsplanchnic arterial vasculature, leading to an increase in MCFP (due to a decrease in the pressure gradient between arteries and veins) and in VR. On the other hand, nitroglycerin dilated arterial vasculature within the splanchnic system, increasing flow, pressure, and splanchnic vascular volume and decreasing VR and CO (fig. 3 and fig. 4, outside). Active dilation of the splanchnic veins, in addition to the passive distention due to an increase in transmural pressure and volume, reinforces the accumulation of blood volume within the splanchnic venous system. Clinical observations support the notion that both sodium nitroprusside and nitroglycerin decrease arterial resistance and increase venous capacity.71 However, it seems that sodium nitroprusside affects arterial resistance to a greater extent than venous capacity, whereas nitroglycerin increases venous capacity to a greater extent than decreases arterial resistance.71
Experiments using right heart bypass preparation, where blood flow and CVP were independently controlled and blood was drained separately from splanchnic and nonsplanchnic vasculature, demonstrated different effects of four vasodilators on splanchnic and nonsplanchnic arterial resistance.72 The authors studied captopril, nifedipine, hydralazine, and prazosin in three doses that decreased arterial blood pressure to similar degrees. Captopril decreased arterial resistance, increased flow and volume within splanchnic vasculature, and decreased central blood volume; in the absence of bypass, it would lead to a decrease in VR and CO. Nifedipine did not affect arterial resistance within the splanchnic system but did significantly decrease it within the nonsplanchnic system. This was associated with a decrease in the pressure gradient between arterial and venous pressures within the nonsplanchnic system, and increased MCFP and central blood volume, which in the absence of bypass would increase VR and CO. The differences in the effects of two remaining vasodilators were less drastic than the effects of nifedipine and captopril.72
The direct effects of vasodilators may be modified by indirect effects of mediators released during the administration of a drug in question. For example, isoproterenol administration is associated with an increase in norepinephrine release,73–77 and that effect is mediated specifically via β2- but not β1-adrenergic receptors.78 Isoproterenol also increases release of angiotensin.79 As a result of such complexity, isoproterenol administration is associated with a drastic decrease in splanchnic and intrahepatic volume despite a significant increase in splanchnic blood flow.80 According to the basic concepts of the relation between flow, pressure, and volume within the splanchnic vasculature (fig. 3), an increase in splanchnic flow should be associated with sequestration of blood volume within the splanchnic vasculature. In reality, this does not occur, and splanchnic volume significantly decreases.35,80 Therefore, an increase in VR by blood volume shift from the splanchnic system results from a decrease in resistance within the liver and hepatic veins (mediated via β2-adrenergic receptors), and venoconstriction, elicited by release of norepinephrine and/or angiotensin. Epinephrine increases VR mainly through activation of β2-adrenergic receptors.59 The role of an increased myocardial contractility (mediated via β1-adrenergic receptors) in an increase in CO in a normal heart is probably minimal.53,59,78
Back to Top | Article Outline
Intrathoracic Pressure
An increase in intrathoracic pressure (ThorP) during controlled positive-pressure ventilation increases intramural CVP. This would decrease the pressure gradient for VR, VR itself, and blood volume in the right heart at diastole. On the other hand, every lung inflation moves the diaphragm downward, increasing intraabdominal pressure. The latter squeezes blood out of the veins within the abdominal cavity, increasing MCFP and VR, thereby helping to maintain the MCFP–CVP gradient and minimizing the effect of an increase in ThorP on VR.81
Reflexes and neurohumoral factors that increase MCFP also minimize the effects of increased ThorP on VR by an increase in arterial resistance within the splanchnic vasculature (leading to an increase in passive elastic recoil of splanchnic veins) and active venoconstriction; both result in a shift of blood volume from the splanchnic system into systemic circulation, increasing Vs and maintaining VR and CO. This shift is reinforced by an increase in intravascular volume secondary to antidiuresis (release of antidiuretic hormones).82–88 An activation of the renin–angiotensin–aldosterone system during positive-pressure ventilation contributes to both mechanisms, namely an increase in MCFP by venoconstriction and an increase in blood volume by water and sodium retention. An increase in intramural CVP during such a situation might be misinterpreted as hypervolemia and/or cardiac failure.
Finally, right ventricular filling pressure (defined as a gradient between CVP and pericardial pressure81) does not change during changes in ThorP because the right atrium, right ventricle, and pericardium are within the thorax, and an increase in ThorP is associated with equal increases in both right atrial and pericardial pressures. Therefore, absence of change in transmural right ventricular pressure during diastole further minimizes the effects of an increase in ThorP on VR. However, overinflation of the lung, introduction of positive end-expiratory pressure, and/or hypovolemia, present before introduction of controlled ventilation, might have exhausted the compensatory mechanisms and lead to a decrease in VR and CO.89 An additional infusion of fluid and/or venoconstrictor might be needed to increase MCFP in order to maintain the necessary pressure gradient for VR.
During spontaneous inspiration, ThorP decreases, leading to a decrease in intramural CVP and a subsequent increase in gradient between MCFP and CVP, facilitating VR. However, an increase in VR secondary to a decrease in CVP works only when CVP is equal to or above atmospheric pressure because negative pressure in intrathoracic veins leads to their collapse, preventing a significant increase in VR. Also, pericardial pressure limits the overdistension of the right ventricle (see Pericardial Pressure section). If these mechanisms did not exist, forceful inspirations could lead to overextension of the right ventricle and its failure.31,81,90–93
Back to Top | Article Outline
Systolic Blood Pressure and Pulse Pressure Variations.
During inspiration of positive-pressure ventilation, left ventricular stroke volume initially increases secondary to (1) temporary increase in left ventricular end-diastolic volume resulting from a compression of pulmonary veins, (2) decrease in afterload resulting from a decrease in left ventricular transmural pressure (i.e., an increase in lung volume compresses the left ventricle and helps the left ventricular ejection), and (3) diminished right ventricular volume secondary to compression of the heart by inflated lungs. These factors lead to a temporary increase in left ventricular stroke volume, pulse pressure, and systolic blood pressure, compared with end of expiration (baseline). This deflection of blood pressure is called delta-up and usually is around 2–4 mmHg.94–96 On the other hand, such inflation of the lung and an increase in ThorP decreases the pressure gradient for VR with subsequent decrease in VR. This in a few beats ends up with a decrease in left heart filling, in stroke volume of left ventricle and systolic pressure. This decrease in systolic pressure is called delta-down94,95 and usually is around 5–6 mmHg. Total variation, delta-up/delta-down, thus is approximately 8–10 mmHg. If this variation is larger than that, it may reflect hypovolemia and predict a positive response (an increase in CO) to additional fluid load. Systolic blood pressure variation not exceeding approximately 10 mmHg would reflect adequacy of ventricular preload15,94–99 and may reflect the status of preload better than CVP.98
Back to Top | Article Outline
Intraabdominal Pressure
Every inspiration, spontaneous or during positive-pressure breathing, moves the diaphragm downward, increases intraabdominal pressure, and shifts blood volume from the splanchnic system into the systemic circulation. At the same time, venous flow from the lower extremities along the inferior caval vein decreases. During expiration, the diaphragm shifts upward, decreases blood flow from the splanchnic system, and increases blood flow from the lower extremities. These cyclic events overall do not drastically affect VR and CO. However, a longer-lasting increase in intraabdominal pressure to any level lower than pressure within inferior caval vein may lead to a simultaneous increase in VR due to shift of blood volume from the compliant splanchnic venous system toward the right atrium; on the other hand, such an increase in intraabdominal pressure may decrease VR secondary to an increase in venous resistance within the inferior caval vein and to a shift of the diaphragm upward, an increase in ThorP with concomitant increase in intramural CVP.100–105 Such an increase in CVP does not reflect the volume status of a patient106 and may be associated with a decrease in VR100,101,107 resulting from a decrease in the gradient between MCFP and CVP. This effect can be modified by an increase in Vs, which in turn can be achieved by an infusion of additional fluid and/or an administration of a venoconstrictor.108 Such intervention is not always needed because of the activation of sympathetic and renin–angiotensin systems; this is associated with an increase of MCFP and maintenance of the needed MCFP–CVP gradient to preserve VR and CO.103,109,110 Anesthetics, sedatives, and other interventions might minimize such a homeostatic response.105,111–114
Back to Top | Article Outline
Positions (Tilts)
Different positions, e.g., head up versus head down, affect systemic hemodynamics including function of the venous system. A head-up position (e.g., standing up) could be associated with a gravity-induced shift of blood volume from the upper to the lower part of the body. In healthy, awake patients, head-up or head-down positions do not affect blood pressure, CO, or CVP105 because of immediate activation of sympathically mediated reflexes as well as the renin–angiotensin system and release of other vasoconstricting mediators115 prevent such a drastic shift of blood volume. However, during anesthesia, the head-up position is practically always associated with a decrease in CVP, CO, and blood pressure100,105,107,116 because the reflexes are blunted as the depth of anesthesia increases.105
The head-down (Trendelenburg) position is always associated with an increase in CVP. However, CO and blood pressure may be maintained37,100,107,115 or decreased.105,116 Left ventricular end-diastolic area (reflecting volume) and intrathoracic blood volume are increased.37 After change from a head-down to a horizontal position in an anesthetized patient, a decrease in blood pressure and CO may occur.37 It might be due to a failure to increase afterload or to hypovolemia which may have been misinterpreted as normovolemia or hypervolemia secondary to high CVP with the head-down position.105
Back to Top | Article Outline
Pericardial Pressure
Any significant increase in VR (e.g., during spontaneous inspiration) could lead to overloading of the right heart.117–121 The limited rigid space of pericardium prevents overexpansion of the right heart.121 In animals and humans, pericardectomy is associated with higher values of stroke volume and CO during exercise compared with similar exercises before pericardiectomy.122 Other mechanisms limiting overloading of the right heart include an increase in ThorP during controlled ventilation and, to a certain extent, during spontaneous expiration, as well as so-called ventricular interdependence121–125: An increase in right ventricular volume shifts the intraventricular septum leftward, leading to a decrease in left ventricular compliance, which decreases left ventricular filling, resulting a few beats later in a decrease in right ventricular preload.81
Back to Top | Article Outline
Role of Reflexes
Many different pathophysiologic insults, e.g., blood loss, the upright position,126 initiation of positive pressure breathing, particularly with positive end-expiratory pressure, are associated with immediate increase in sympathetic discharge, which leads to an increase in arterial resistance, heart rate, and myocardial contractility and a decrease in venous capacity. The latter is particularly important: Capacitance vessels respond to hemorrhage much earlier than resistance vessels; both of these responses, arterial and venous, are mediated via the sympathetic nervous system. When the carotid sinus receptors sense low blood pressure, the sympathetic tone increases, splanchnic veins constrict, Vs and MCFP increase, and vice versa.2,10,19,127–133 Pretreatment with the α-adrenergic antagonist phentolamine decreased such response by 72%, whereas pretreatment with the β-adrenergic antagonist propranolol decreased such response by 35%. Combination of both decreased response by 73%. Therefore, α-adrenergic mechanisms contribute more significantly to active changes in systemic venous capacity than the β-adrenergic system.134 The responses to high or low arterial blood pressure are mediated not only through the carotid sinus but also through the aortic baroreceptors. Their role in maintaining blood pressure is smaller than the role of the carotid sinuses.132
There are other types of reflexes, e.g., an increase in intravenous volume and associated distension of the vein increases arterial resistance (upstream of the affected veins) via the so-called local sympathetic axon reflex or venoarterial reflex.135 Teleologically speaking, this reflex helps to modify the degree of venous distention: Less blood inflow into a vein leads to a decrease in intramural pressure and volume (fig. 3).
Back to Top | Article Outline

Is Central Venous Pressure a Useful or a Misleading Variable?

Values of CVP, intramural or even transmural, as well as values of pulmonary artery occluded pressure, do not correlate with the values of measured circulating blood volume or with responsiveness to fluid challenge (an increase in CO after infusion of fluid).99,136–143 Moreover, attempts to assess the differences between the changes in CVP and changes in circulating blood volume also failed to find any significant correlation.144 A sophisticated approach of measuring separately total blood volume and circulating blood volume, using a dye dilution technique, also did not demonstrate any correlation between values of CVP and blood volume, total or circulating (possibly total and stressed volumes).145 Dramatic changes in systemic hemodynamics may not be associated with any significant changes in CVP, e.g., significant decrease in mean arterial pressure and CO during high thoracocervical epidural and general anesthesia,146 or drastic changes in arterial pressure, vascular resistance and venous capacity induced by changes in pressure within the carotid sinuses,147 or a significant decrease in arterial resistance and an increase in CO induced by an infusion of prostaglandin E1148 were not associated with any significant changes in CVP.
Fig. 5
Fig. 5
Image Tools
The main reason for lack of correlation between values of CVP and blood volume is that the body does everything possible to maintain homeostasis; an adequate transmural CVP is a must for cardiovascular function. The most accurate measurement of “volume status” would be the MCFP, which cannot be measured in a clinical setting.15 Values of CVP depend on the relation between cardiac pump function and VR (determined by MCFP, Vs, venous resistance, and other factors) (fig. 5).139,149–154 The pulmonary artery occluded pressure is an even worse indicator of volume status than CVP because it is far removed from the action of MCFP.15 The pulmonary artery occluded pressure is a better indicator of left ventricular function than of volume status.15
Thus, considering the importance of maintaining the CVP adequate for cardiovascular function, it is not surprising that values of CVP remain unchanged, despite serious stresses and changes in other cardiovascular variables. The correlation between CVP and circulating blood volume has never been found simply because it does not exist. To tease out when CVP may be useful or misleading, let us consider factors that affect CVP (fig. 5).
Back to Top | Article Outline
Factors That Decrease Central Venous Pressure
The main variable that tends to decrease intramural and transmural CVP is a decrease in Vs that can result from hypovolemia, which would initially lead to a decrease in Vu and shift of blood volume from Vu to Vs; when such shifts of volume exhaust the reservoir of blood volume, the Vu, Vs starts to decrease, eventually leading to a decrease in CVP. The second reason for a decrease in Vs is venodilation or, in other words, an increase in Vu; in this situation, blood volume shifts from Vs to Vu. A considerable decrease in Vs, whether it is due to hypovolemia or venodilation, leads to a decrease in CVP secondary to a decrease in VR. Such a decrease initially would play a compensatory role because it would increase the pressure gradient between MCFP and CVP, mitigating the decrease in VR.
An isolated increase in venous resistance also may decrease intramural and transmural CVP secondary to a decrease in VR.155,156 A decrease in ThorP (e.g., during forceful inspiration) temporarily decreases intramural CVP resulting from negative pressure created within the thorax. This effect is not very powerful and is limited: During forceful inspiration, intrathoracic pressure decreases below zero, leading to collapse of large veins entering the thorax (waterfall phenomenon) and limiting the possible change in VR.
Nonetheless, if one observes a clearly noticeable decrease in CVP, it most probably reflects hypovolemia which exceeds 10–12% of blood volume loss, or venodilation associated with a shift of blood volume from Vs to Vu, i.e., sequestration of blood within the splanchnic veins. Decreased CVP might also indicate an attempt by the heart to compensate for relatively mild hypovolemia: The heart would try to decrease CVP to increase gradient between peripheral and central venous pressures and to facilitate VR; therefore, the degree of hypovolemia might not correlate with the degree of a decrease in CVP. Clinically, it might be difficult to distinguish absolute hypovolemia from venodilation, which is hypovolemia relative to increased venous capacity. Overall analysis of the clinical course and appreciation of the difference between intramural and transmural pressures usually are helpful in such a differential diagnosis. Additional information such as stroke volume and CO can be crucially important in diagnosis of the pathophysiologic hemodynamic condition of a patient.
Back to Top | Article Outline
Factors That Increase Central Venous Pressure
The main factor that increases intramural and transmural CVP is a decrease in cardiac pump function, secondary to a decrease in contractility, valvular disease, dysrhythmias, etc. An increase in ThorP during ventilation, particularly with positive end-expiratory pressure, increases intramural (not transmural) CVP. Also, controlled ventilation increases pulmonary arterial resistance, which may increase intramural and transmural CVP. An increase in pulmonary arterial resistance can be caused by other reasons, including hypoxic pulmonary vasoconstriction, e.g., secondary to a decrease in inspired fraction of oxygen, an increase in ventilation–perfusion abnormalities within the lung, an increase in pericardial pressure and/or in intraabdominal pressure, which might lead to an increase in intramural CVP through an increase in ThorP.
Venoconstriction (a shift of blood volume from Vu to Vs) induced by an increase in sympathetic discharge and/or activation of the renin–angiotensin system, as well as use of venoconstrictors, also tends to increase intramural and transmural CVP. An increase in Vs, secondary to venoconstriction, or arterial/arteriolar constriction of splanchnic vasculature, or infusion of additional fluid, if associated with a decrease in cardiac pump function relative to an increased demand, would lead to an increase in intramural and transmural CVP. A high CVP, and CVP increasing during fluid load, indicates a heart problem rather than a circuit problem.
In clinical settings, intramural CVP often increases as a result of an increase in ThorP during controlled ventilation, particularly with positive end-expiratory pressure; transmural CVP may be close to normal. Some other physiologic insults may increase intramural and transmural CVP without heart problems; the Trendelenburg position, which increases CVP, is rarely harmful because of a concomitant increase in MCFP. The potential problem is that high CVP may lead to misdiagnosis of a patient’s condition.
Back to Top | Article Outline
Potential Misinterpretations of Normal Central Venous Pressure
Correct interpretation of CVP values and changes in these values demand correct positioning of the transducer at the level of zero pressure all the time; periodic rezeroing of the transducer is also needed. Normal CVP per se does not necessarily reflect normovolemia. The body can mobilize (and pool) blood volume from (or in) compliant splanchnic veins. Loss of 10–12% of blood volume does not decrease CVP. Normal CVP may reflect normovolemia or compensated hypovolemia (up to 600–700 ml of blood loss) or compensated hypervolemia: An excessive infusion of fluid may be compensated by accumulation of blood in the splanchnic veins without any change in central hemodynamics including CVP. Combination of factors that have a tendency to decrease and increase CVP may lead to a normal value of CVP despite serious hemodynamic derangements, e.g., the combination of heart failure and hypovolemia, or hypovolemia in the Trendelenburg position. Drastic increases in MCFP and CO during exercise without any changes in CVP are well known.157,158
Therefore, considering the complexity of the physiologic feedback and clinical picture, robust reflexes, and homeostatic mechanisms (fig. 5), only at the extremes may CVP be a useful indicator of the hemodynamic state of a patient. An attempt to create a certain scoring system that takes into account almost all clinically available hemodynamic variables failed to identify CVP as a useful indicator.159 The authors concluded that only extreme values of CVP may have clinical significance.
Back to Top | Article Outline
Dynamic Variables That Reflect Volume Status
Respiratory variations in CVP (namely a decrease in CVP during spontaneous inspiration) were relatively acceptable predictors of the CO response to fluid challenge.154,160,161 Other dynamic variables, such as systolic pressure variations, pulse pressure variations,139 respiratory variations in pulse oximetry plethysmographic waveform amplitude,143 and just a CVP and/or CO response to fluid challenge, are better indicators of volume status151 than static hemodynamic variables including CVP. Critical analysis of the literature suggests a similar conclusion, that the inspiratory decrease in CVP (a dynamic variable) exceeding 1 mmHg is a much better predictor of responsiveness of CO to fluid challenge than CVP per se.138
A force applied to the abdomen with relaxed abdominal muscles is usually associated with a temporary increase in CVP resulting from blood volume shift from compressed splanchnic veins into the systemic circulation. This increase under normal situations is temporary because a normal heart responds to an increase in preload with an increase in contractility and temporary increase in CO. This increase in CVP lasts a few seconds, usually less than 10 s.162 This is called hepatojugular reflux. Absence of such an increase in CVP might mean that splanchnic venous vasculature is relatively empty and there is no temporary increase in preload. If an increase in CVP lasts much longer than 10 s, it probably attests to some right or left ventricular insufficiency or both.162 Passive leg raising can predict fluid responsiveness (an increase in pulse pressure) with 97% sensitivity and 94% specificity.163 The Trendelenburg position is probably less telling than passive leg raising because the latter compresses the abdomen, squeezing the splanchnic vasculature and transferring blood into the systemic circulation. Many observers believe that these dynamic variables are more useful in identifying hemodynamic problems, particularly hypovolemia, than CVP.
Understanding the complexity of the function of the cardiovascular system in general and the venous system specifically, and an appreciation of the limitation of one or another hemodynamic variable including CVP, would help to properly diagnose the pathophysiologic condition of a patient and help to plan and execute appropriate therapeutic intervention.
The author thanks George Topulos, M.D. (Associate Professor of Anaesthesia, Harvard Medical School, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women’s Hospital, Boston, Massachusetts), for his criticisms and advice; James Bell, B.A. (Graphic Designer, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women’s Hospitals), for preparation of the illustrations; and Nancy Axelrod, B.S. (Administrative Assistant, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women’s Hospital), for the preparation of the manuscript.
Back to Top | Article Outline

References

1. Rothe CF: Reflex control of veins and vascular capacitance. Physiol Rev 1983; 63:1281–342

2. Hainsworth R: The importance of vascular capacitance in cardiovascular control. News Physiol Sci 1990; 5:250–4

3. Edouard DA, Pannier BM, London GM, Cuche JL, Safar ME: Venous and arterial behavior during normal pregnancy. Am J Physiol 1998; 274:1605–12

4. McGregor M: Pathogenesis of angina pectoris and role of nitrates in relief of myocardial ischemia. Am J Med 1983; 74:21–7

5. Kelly RP, Gibbs HH, O’Rourke MF, Daley JE, Mang K, Morgan JJ, Avolio AP: Nitroglycerin has more favourable effects on left ventricular afterload than apparent from measurement of pressure in a peripheral artery. Eur Heart J 1990; 11:138–44

6. Rowell LB: Human Cardiovascular Control. New York, Oxford University Press, 1993, pp 37–96

7. Hainsworth R: Vascular capacitance: Its control and importance. Rev Physiol Biochem Pharmacol 1986; 105:101–73

8. Rowell LB: Human Cardiovascular Control. New York, Oxford University Press, 1993, pp 204–35

9. Rothe CF: Mean circulatory filling pressure: Its meaning and measurement. J Appl Physiol 1993; 74:499–509

10. Shoukas AA, Sagawa K: Control of total systemic vascular capacity by the carotid sinus baroreceptor reflex. Circ Res 1973; 33:22–33

11. Trippodo NC: Total circulatory capacity in the rat: Effects of epinephrine and vasopressin on compliance and unstressed volume. Circ Res 1981; 49:923–31

12. Caldini P, Permutt S, Waddell JA, Riley RL: Effect of epinephrine on pressure, flow, and volume relationships in the systemic circulation of dogs. Circ Res 1974; 34:606–23

13. Magder S: Heart-lung interactions in sepsis, Cardiopulmonary Critical Care. Edited by Dantzker DR, Scharf SM. Philadelphia, WB Saunders, 1998, pp 435–48

14. Magder S, De Varennes B: Clinical death and the measurement of stressed vascular volume. Crit Care Med 1998; 26:1061–4

15. Magder S, Scharf SM: Venous return, Respiratory-Circulatory Interactions in Health and Disease. Edited by Scharf SM, Pinsky MR, Magder S. New York, Marcel Dekker, 2001, pp 93–112

16. Rothe CF: Reflex control of the veins in cardiovascular function. Physiologist 1979; 22:28–35

17. Rothe CF, Gaddis ML: Autoregulation of cardiac output by passive elastic characteristics of the vascular capacitance system. Circulation 1990; 81:360–8

18. Rowell LB: Reflex control of regional circulations in humans. J Auton Nerv Syst 1984; 11:101–14

19. Noble BJ, Drinkhill MJ, Myers DS, Hainsworth R: Blood mobilization from the liver of the anaesthetized dog. Exp Physiol 1998; 83:513–22

20. De Jager S: Experiments and considerations on haemodynamics. J Physiol (Lond) 1886; 7:130–215

21. Barcroft H, Samaan A: The explanation of the increase in systemic flow caused by occluding the descending thoracic aorta. J Physiol 1935; 85:47–61

22. Gelman S: The pathophysiology of aortic cross-clamping and unclamping. Anesthesiology 1995; 82:1026–60

23. Gelman S, Rabbani S, Bradley EL Jr: Inferior and superior vena caval blood flows during crossclamping of the thoracic aorta in pigs. J Thorac Cardiovasc Surg 1988; 96:387–92

24. Gregoretti S, Gelman S, Henderson T, Bradley EL: Hemodynamics and oxygen uptake below and above aortic occlusion during crossclamping of the thoracic aortic and sodium nitroprusside infusion. J Thorac Cardiovasc Surg 1990; 100:830–6

25. Gregoretti S, Henderson T, Parks DA, Gelman S: Haemodynamic changes and oxygen uptake during crossclamping of the thoracic aorta in dexmedetomidine pretreated dogs. Can J Anaesth 1992; 39:731–41

26. Gelman S, Khazaeli MB, Orr R, Henderson T: Blood volume redistribution during crossclamping of the descending aorta. Anesth Analg 1994; 78:219–24

27. Guyton AC: Determination of cardiac output by equating venous return curves with cardiac response curves. Physiol Rev 1955; 35:123–9

28. Guyton AC, Jones CE, Coleman TG: Circulatory Physiology: Cardiac Output and Its Regulation, 2nd edition. Philadelphia, WB Saunders, 1973, pp 205–20

29. Fessler HE, Brower RG, Wise RA, Permutt S: Effects of positive end-expiratory pressure on the canine venous return curve. Am Rev Respir Dis 1992; 146:4–10

30. Nanas S, Magder S: Adaptations of the peripheral circulation to PEEP. Am Rev Respir Dis 1992; 146:688–93

31. Tarasiuk A, Scharf SM: Effects of periodic obstructive apneas on venous return in closed-chest dogs. Am Rev Respir Dis 1993; 148:323–9

32. Fessler HE, Brower RG, Wise RA, Permutt S: Effects of positive end-expiratory pressure on the gradient for venous return. Am Rev Respir Dis 1991; 143:19–24

33. Deschamps A, Magder S: Effects of heat stress on vascular capacitance. Am J Physiol 1994; 266:H2122–9

34. Karim F, Hainsworth R: Responses to abdominal vascular capacitance to stimulation of splanchnic nerves. Am J Physiol 1976; 231:434–40

35. Green JF: Mechanism of action of isoproterenol on venous return. Am J Physiol 1977; 232:H152–6

36. Deschamps A, Magder S: Baroreflex control of regional capacitance and blood flow distribution with or without alpha adrenergic blockade. J Appl Physiol 1992; 263:H1755–63

37. Reuter DA, Felbinger TW, Schmidt C, Moerstedt K, Kilger E, Lamm P, Goetz AE: Trendelenburg positioning after cardiac surgery: Effects on intrathoracic blood volume index and cardiac performance. Eur J Anaesth 2003; 20:17–20

38. Bressack MA, Morton NS, Hortop J: Group B streptococcal sepsis in the piglet: Effects of fluid therapy on venous return, organ edema, and organ blood flow. Circ Res 1987; 61:659–69

39. Ayuse T, Brienza N, Revelly JP, O’Donnell CP, Boitnott JK, Robotham JL: Alterations in liver hemodynamics in an intact porcine model of endotoxin shock. Am J Physiol 1995; 268:H1106–14

40. Appleton C, Olajos M, Morkin E, Goldman S: Alpha-1 adrenergic control of the venous circulation in intact dogs. J Pharmacol Exp Ther 1985; 233:729–34

41. Kaiser GA, Ross J Jr, Braunwald E: Alpha and beta adrenergic receptor mechanisms in the systemic venous bed. J Pharmacol Exp Ther 1964; 144:156–62

42. Marino RJ, Romagnoli A, Keats AS: Selective venoconstriction by dopamine in comparison with isoproterenol and phenylephrine. Anesthesiology 1975; 43:570–2

43. Yamazaki R, Tsuchida K, Aihara H: Effects of α-adrenoceptor agonists on cardiac output and blood pressure in spinally anesthetized ganglion-blocked dogs. Arch Int Pharmacodyn 1988; 295:80–93

44. Bell L, Hennecken J, Zaret BL, Rutlen DL: Alpha-adrenergic regulation of splanchnic volume and cardiac output in the dog. Acta Physiol Scand 1990; 138:321–9

45. Muller-Ruchholtz ER, Losch HM, Grund E, Lochner W: Effect of alpha adrenergic receptor stimulation on integrated systemic venous bed. Pflugers Arch Eur J Physiol 1977; 370:241–6

46. Imai Y, Satoh K, Taira N: Role of the peripheral vasculature in changes in venous return caused by isoproterenol, norepinephrine, and methoxamine in anesthetized dogs. Circ Res 1978; 43:553–61

47. Stokland O, Thorvaldson J, Ilebekk A, Kiil F: Factors contributing to blood pressure elevation during norepinephrine and phenylephrine infusions in dogs. Acta Physiol Scand 1983; 117:481–9

48. Zandberg P, Timmermans PB, van Zwieten PA: Hemodynamic profiles of methoxamine and B-HT 933 in spinalized ganglion-blocked dogs. J Cardiovasc Pharmacol 1984; 6:256–62

49. Hiley CR, Thomas GR: Effects of alpha-adrenoceptor agonists on cardiac output and its regional distribution in the pithed rat. Br J Pharmacol 1987; 90:61–70

50. Richer C, Lefevre-Borg F, Lechaire J, Gomeni C, Gomeni R, Giudicelli JF, Cavero I: Systemic and regional hemodynamic characterization of alpha-1 and alpha-2 adrenoceptor agonists in pithed rats. J Pharmacol Exp Ther 1987; 240:944–53

51. MacLean MR, Hiley CR: Effects of enalapril on changes in cardiac output and organ vascular resistances induced by alpha1- and alpha 2-adrenoceptor agonists in pithed normotensive rats. Br J Pharmacol 1988; 94:449–62

52. Supple EW, Graham RM, Powell WJ Jr: Direct effects of α2-adrenergic receptor stimulation on intravascular systemic capacity in the dog. Hypertension 1988; 11:352–9

53. Gelman S, Mushlin PS: Catecholamine-induced changes in the splanchnic circulation affecting systemic hemodynamics. Anesthesiology 2004; 100:434–9

54. Gelman S, Mushlin PS: Do alpha agonists increase venous return? Anesthesiology 2004; 101:1038–9

55. Lewis CM, Weil MH: Hemodynamic spectrum of vasopressor and vasodilator drugs. JAMA 1969; 208:1391–8

56. Rutlen DL, Supple EW, Powell WJ Jr: The role of the liver in the adrenergic regulation of blood flow from the splanchnic to the central circulation. Yale J Biol Med 1979; 52:99–106

57. Rothe CF, Maass-Moreno R: Hepatic venular resistance responses to norepinephrine, isoproterenol, adenosine, histamine, and ACh in rabbits. Am J Physiol 1998; 274:H777–85

58. Rothe CF, Maass-Moreno R: Active and passive liver microvascular responses from angiotensin, endothelin, norepinephrine, and vasopressin. Am J Physiol Heart Circ Physiol 2000; 279:H1147–56

59. Leenen FH, Chan YK, Smith DL, Reeves RA: Epinephrine and left ventricular function in humans: Effects of beta-1 versus nonselective beta-blockade. Clin Pharmacol Ther 1988; 43:519–28

60. Brooker RF, Butterworth JF IV, Kitzman DW, Berman JM, Kashtan HI, McKinley AC: Treatment of hypotension after hyperbaric tetracaine spinal anesthesia: A randomized, double-blind, cross-over comparison of phenylephrine and epinephrine. Anesthesiology 1997; 86:797–805

61. Krogh A: The regulation of the supply of blood to the right heart. Scand Arch Physiol 1912; 27:227–48

62. Brunner MJ, Shoukas AA, MacAnespie CL: The effect of the carotid sinus baroreceptor reflex on blood flow and volume redistribution in the total systemic vascular bed of the dog. Circ Res 1981; 48:274–85

63. Emerson TE Jr: Changes of venous return and other hemodynamic parameters during bradykinin infusion. Am J Physiol 1967; 212:1455–60

64. Emerson TE Jr, Jelks GW, Daugherty RM Jr, Hodgman RE: Effects of prostaglandin E1 and F on venous return and other parameters in the dog. Am J Physiol 1971; 220:243–9

65. Rowell LB: Human Cardiovascular Control. New York, Oxford University Press, 1993, pp 205–19

66. Rowell LB: Human Cardiovascular Control. New York, Oxford University Press, 1993, pp 255–88

67. Gelman S, Ernst EA: Hepatic circulation during sodium nitroprusside infusion in the dog. Anesthesiology 1978; 49:182–7

68. Hoka S, Siker D, Bosnjak ZJ, Kampine JP: Alteration of blood flow distribution and vascular capacitance during induced hypotension in deafferented dogs. Anesthesiology 1987; 66:647–52

69. Pouleur H, Covell JW, Ross J Jr: Effects of nitroprusside on venous return and central blood volume in the absence and presence of acute heart failure. Circulation 1980; 61:328–37

70. Smiseth OA, Manyari DE, Lima JA, Scott-Douglas NW, Kingma I, Smith ER, Tyberg JV: Modulation of vascular capacitance by angiotensin and nitroprusside: A mechanism of changes in pericardial pressure. Circulation 1987; 76:875–83

71. Gall WE, Clarke WR, Doty DB: Vasomotor dynamics associated with cardiac operations: I. Venous tone and the effects of vasodilators. J Thorac Cardiovasc Surg 1982; 83:724–31

72. Ogilvie RI: Comparative effects of vasodilator drugs on flow distribution and venous return. Can J Physiol Pharmacol 1985; 63:1345–55

73. Adler-Graschinsky E, Langer SZ: Possible role of a beta-adrenoceptor in the regulation of noradrenaline release by nerve stimulation through a positive feed-back mechanism. Br J Pharmacol 1975; 53:43–50

74. Stjärne L, Brundin J: Β2-adrenoceptors facilitating noradrenaline secretion from human vasoconstrictor nerves. Acta Physiol Scand 1976; 97:88–93

75. Stjärne L, Brundin J: Affinity of Noradrenaline and dopamine for neural alpha-receptors mediating negative feedback control of noradrenaline secretion in human vasoconstrictor nerves. Acta Physiol Scand 1975; 95:89–94

76. Yamaguchi N, de Champlain J, Nadeau RA: Regulation of norepinephrine release from cardiac sympathetic fibers in the dog by presynaptic alpha and beta receptors. Circ Res 1977; 41:108–17

77. Langer SZ: Presynaptic regulation of the release of catecholamines. Pharmacol Rev 1981; 32:337–62

78. Chang PI, Rutlen DL: Effect of beta-adrenergic agonists on splanchnic vascular volume and cardiac output. Am J Physiol 1991; 261:H1499–507

79. Winer N, Chokshi DS, Walkenhorst WG: Effects of cyclic AMP, sympathomimetic amines, and adrenergic receptor antagonists on renin secretion. Circ Res 1971; 29:239–48

80. Greenway CV: Effects of sodium nitroprusside, isosorbide dinitrate, isoproterenol, phentolamine and prazosin on hepatic venous responses to sympathetic nerve stimulation in the cat. J Pharmacol Exp Ther 1979; 209:56–61

81. Pinsky MR: Hemodynamic effects of ventilation and ventilatory maneuvers, Respiratory-Circulatory Interactions in Health and Disease. Edited by Scharf SM, Pinsky MR, Magder S. New York, Marcel Dekker, 2001, pp 183–218. Lung Biology in Health and Disease, vol. 157. Edited by Lenfant C

82. Henry JP, Gauer OH, Reeves JL: Evidence of the atrial location of receptors influencing urine flow. Circ Res 1956; 4:85–90

83. Baisset A, Montestruc P: Polyurie par distention auricularire chez le chien: Role de l’hormone antidiuretique. J Physiol (Paris) 1957; 49:33–6

84. Sladen A, Laven MB, Pontoppidan H: Pulmonary complications and water retention in prolonged mechanical ventilation. N Engl J Med 1968; 279:448–53

85. Baratz RA, Philbim DM, Patterson RW: Plasma ADH and urinary output during continuous positive pressure breathing in the dog. Anesthesiology 1971; 34:510–3

86. Bark H, LeRoith D, Nyska M, Glick SM: Elevations in plasma ADH levels during PEEP ventilation in the dog: Mechanisms involved. Am J Physiol 1980; 239:E474–81

87. Meehan JP: Cardiovascular receptors and fluid volume control. Aviat Space Environ Med 1986; 57:267–75

88. Said SI: Neurohumoral aspects of respiratory-cardiovascular interactions, Respiratory-Circulatory Interactions in Health and Disease. Edited by Scharf SM, Pinsky MR, Magder S. New York, Marcel Dekker, 2001, pp 427–45. Lung Biology in Health and Disease, vol. 157. Edited by Lenfant C

89. Brienza N, Revelly J-P, Ayuse T, Robotham JL: Effects of PEEP on liver arterial and venous blood flows. Am J Resp Crit Care Med 1995; 152:504–10

90. Guyton AC, Lindsey AW, Abernathy B, Richardson T: Venous return at various right atrial pressures and the normal venous return curve. Am J Physiol 1957; 189:609–15

91. Stalcup SA, Mellins RB: Mechanical forces producing pulmonary edema in acute asthma. N Engl J Med 1977; 297:592–6

92. Lores ME, Keagy BA, Vassiliades T, Henry GW, Lucas CL, Wilcox BR: Cardiovascular effects of positive end-expiratory pressure (PEEP) after pneumonectomy in dogs. Ann Thorac Surg 1985; 40:464–8

93. Scharf S, Tow DE, Miller MJ, Brown R, McIntyre K, Dilts C: Influence of posture and abdominal pressure on the hemodynamic effects of Mueller’s maneuver. J Crit Care 1989; 4:26–34

94. Perel A, Pizov R, Cotev S: Systolic blood pressure variation is a sensitive indicator of hypovolemia in ventilated dogs subjected to graded hemorrhage. Anesthesiology 1987; 67:498–502

95. Rooke GA, Schwid HA, Shapira Y: The effect of graded hemorrhage and intravascular volume replacement on systolic pressure variation in humans during mechanical and spontaneous ventilation. Anesth Analg 1995; 80:925–32

96. Perel A: Assessing fluid responsiveness by the systolic pressure variation in mechanically ventilated patients. Anesthesiology 1998; 89:1310–2

97. Coriat P, Vrillon M, Perel A, Baron JF, LeBret F, Saada M, Vlars P: A comparison of systolic blood pressure variations and echocardiographic estimates of end-diastolic left ventricular size in patients after aortic surgery. Anesth Analg 1994; 78:46–53

98. Ornstein E, Eidelman LA, Drenger B, Elami A, Pizov R: Systolic pressure variation predicts the response to acute blood loss. J Clin Anesth 1998; 10:137–40

99. Wiesenack C, Flegl C, Keyser A, Prasser C, Keyl C: Assessment of fluid responsiveness in mechanically ventilated cardiac surgical patients. Eur J Anaesth 2005; 22:658–65

100. Joris JL, Didier PN, Legrand MJ, Jacquet NJ, Lamy ML: Hemodynamic changes during laparoscopic cholecystectomy. Anesth Analg 1993; 76:1067–71

101. McLaughlin J, Scheeres D, Dean R, Bonnell B: The adverse hemodynamic effects of laparoscopic cholecystectomy. Surg Endosc 1995; 9:121–4

102. Koivusalo AM, Kellokumpu I, Scheinin M, Tikkanen I, Mäkisalo H, Lindgren L: A comparison of gasless mechanical and conventional carbon dioxide pneumoperitoneum methods for laparoscopic cholecystectomy. Anesth Analg 1998; 86:153–8

103. Koivusalo AM, Lindgren L: Effects of carbon dioxide pneumoperitoneum for laparoscopic cholecystectomy. Acta Anaesth Scand 2000; 44:834–41

104. Mann C, Boccara G, Pouzeratte Y, Eliet J, Serradeil-LeGal C, Vergnes C, Bichet DG, Guillon G, Fabre JM, Colson P: The relationship among carbon dioxide pneumoperitoneum, vasopressin release, and hemodynamic changes. Anesth Analg 1999; 89:278–83

105. Hofer CK, Zalunardo MP, Klaghofer R, Spahr T, Pasch T, Zollinger A: Changes in intrathoracic blood volume associated with pneumoperitoneum and positioning. Acta Anesth Scand 2002; 46:303–8

106. Andersson L, Wallin CJ, Sollevi A, Odeberg-Wennerman S: Pneumoperitoneum in healthy humans is not associated with increased central blood volume. Acta Anaesth Scand 1999; 43:809–14

107. Odeberg S, Ljugqvist O, Svenberg T, Gannedahl P, Bäckdahl M, von Rosen A, Sollevi A: Haemodynamic effects of pneumoperitoneum and the influence of posture during anaesthesia for laparoscopic surgery. Acta Anaesth Scand 1994; 38:276–83

108. Goldberg P: Abdominal-circulatory interactions, Respiratory-Circulatory Interactions in Health and Disease. Edited by Scharf SM, Pinsky MR, Magder S. New York, Marcel Dekker, 2001, pp 883–903. Lung Biology in Health and Disease, vol. 157. Edited by Lenfant C

109. Mikami O, Kawakita S, Fujise K, Shingu K, Takahashi H, Matsuda T: Catecholamine release caused by carbon dioxide insufflation during laparoscopic surgery. J Urol 1996; 155:1368–71

110. Bäcklund M, Kellokumpu I, Scheinin T, von Smitten K, Tikkanen I, Lindgren L: Effect of temperature of insufflated cardiac output2 during and after prolonged laparoscopic surgery. Surg Endosc 1998; 12:1126–30

111. Stekiel Ta Ozono K, McCallum JB, Bosnjak ZJ, Stekiel WJ, Kampine JP: The inhibitory action of halothane on reflex constriction in mesenteric capacitance veins. Anesthesiology 1990; 73:1169–78

112. McCallum JB, Stekiel TA, Bosnjak ZJ, Kampine JP: Does isoflurane alter mesenteric venous capacitance in the intact rabbit? Anesth Analg 1993; 76:1095–105

113. Hogan QH, Stadnicka A, Bosnjak ZJ, Kampine JP: Effects of lidocaine and bupivacaine on isolated rabbit mesenteric capacitance veins. Reg Anesth Pain Med 1998; 23:409–17

114. Thorlacius K, Bodelsson M: Sevoflurane promotes endothelium-dependent smooth muscle relaxation in isolated human omental arteries and veins. Anesth Analg 2004; 99:423–8

115. Moller S, Norgaard A, Henriksen JH, Frandsen E, Bendtsen F: Effects of tilting on central hemodynamics and homeostatic mechanisms in cirrhosis. Hepatology 2004; 40:811–9

116. Hirovonen EA, Nuutinen LS, Vuolteenaho O: Hormonal responses and cardiac filling pressures in head-up or head-down position and pneumoperitoneum in patients undergoing operative laparoscopy. Br J Anaesth 1997; 78:128–33

117. Olsen CO, Tyson GS, Maier GW, Davis JW, Rankin JS: Diminished stroke volume during inspiration: A reverse thoracic pump. Circulation 1985; 72:668–79

118. Robotham JL: Hemodynamic consequences of mechanical ventilation. Acta Anaesth Scand 1987; 36:7–52

119. Takata M, Wise R, Robotham JL: Effects of abdominal pressure on venous return: Abdominal vascular zone conditions. J Appl Physiol 1990; 69:1961–72

120. Takata M, Robotham JL: Effects of inspiratory diaphragmatic descent on inferior vena caval venous return. J Appl Physiol 1992; 72:597–607

121. Takata M, Robotham JL: Mechanical heart-pericardium-lung interactions, Respiratory-Circulatory Interactions in Health and Disease. Edited by Scharf SM, Pinsky MR, Magder S. New York, Marcel Dekker, 2001, pp 257–78. Lung Biology in Health and Disease, vol. 157. Edited by Lenfant C

122. Rowell LB: Human Cardiovascular Control. New York, Oxford University Press, 1993, pp 39–74, 195–9

123. Brinker JA, Weiss JL, Lappe DL, Rabson JL, Summer WR, Permutt S, Weisfeldt ML: Leftward septal displacement during right ventricular loading in man. Circulation 1980; 61:623–33

124. Cassidy SS, Wead WB, Seibert GB, Ramanathan M: Changes in left ventricular geometry during spontaneous breathing. J Appl Physiol 1987; 63:803–11

125. Peters J, Fraser C, Stuart RS, Baumgartner W, Robotham JL: Negative intrathoracic pressure independently decreases both left ventricular inflow and outflow. Am J Physiol 1989; 257:H120–31

126. Rowell LB: Human Cardiovascular Control. New York, Oxford University Press, 1993, pp 39–74

127. Rashkind WJ, Lewis DH, Henderson LB, Heiman DF, Dietrick RB: Venous return as affected by cardiac output and total peripheral resistance. Am J Physiol 1953; 175:415–23

128. Ross J, Frahm CJ, Braunwald E: Influence of carotid baroreceptors and vasoactive drugs on systemic vascular volume and venous distensibility. Circ Res 1961; 9:75–82

129. Browse NL, Conald DE, Shepherd JT: Role of the veins in the carotid sinus reflex. Am J Physiol 1966; 210:1424–34

130. Drees JA, Rothe CF: Reflex venoconstriction and capacity vessel pressure-volume relationships in dogs. Circ Res 1974; 34:360–73

131. Karim F, Hainsworth R, Pandey RP: Reflex responses of abdominal vascular capacitance from aortic baroreceptors in dogs. Am J Physiol 1978; 235:H488–93

132. Carneiro JJ, Donald DE: Change in liver blood flow and blood content in dogs during direct and reflex alteration of hepatic sympathetic nerve activity. Circ Res 1977; 40:150–8

133. Brunner MJ, Greene AS, Frankle AE, Shoukas AA: Carotid sinus baroreceptor control of splanchnic resistance and capacity. Am J Physiol 1988; 255:H1305–10

134. Shigemi K, Brunner MJ, Shoukas AA: Alpha and beta adrenergic mechanisms in the control of vascular capacitance by the carotid sinus baroreflex system. Am J Physiol 1994; 267:H201–10

135. Henriksen O: Local sympathetic reflex mechanism in regulation of blood flow in human subcutaneous adipose tissue. Acta Physiol Scand Suppl 1977; 450:1–48

136. Cohn JN: Central venous pressure as a guide to volume expansion. Ann Int Med 1967; 66:1283–7

137. Baek S-M, Makabali GG, Bryan-Brown CW, Kusek JM, Shoemaker WC: Plasma expansion in surgical patients with high central venous pressure (CVP): The relationship of blood volume to hematocrit, CVP, pulmonary wedge pressure, and cardiorespiratory changes. Surgery 1975; 78:304–15

138. Michard F, Teboul J-L: Predicting fluid responsiveness in ICU patients: A critical analysis of the evidence. Chest 2002; 121:2000–8

139. Bendjelid K, Romand JA: Fluid responsiveness in mechanically ventilated patients: A review of indices used in intensive care. Intensive Care Med 2003; 29:352–60

140. Rex S, Brose S, Metzelder S, Huneke R, Schalte G, Autschbach R, Rossaint R, Buhre W: Prediction of fluid responsiveness in patients during cardiac surgery. Br J Anaesth 2004; 93:782–8

141. Michard F: Changes in arterial pressure during mechanical ventilation. Anesthesiology 2005; 103:419–28

142. Pinsky MR, Teboul JL: Assessment of indices of preload and volume responsiveness. Curr Opin Crit Care 2005; 11:235–9

143. Cannesson M, Atof Y, Rosamel P, Desebbe O, Joseph P, Metton O, Bastien O, Lehot J-J: Respiratory variations in pulse oximetry plethysmographic waveform amplitude to predict fluid responsiveness in the operating room. Anesthesiology 2007; 106:1105–11

144. Oohashi S, Endoh H: Does central venous pressure or pulmonary capillary wedge pressure reflect the status of circulating blood volume in patients after extended transthoracic esophagectomy? J Anesth 2005; 19:21–5

145. Hoeft A, Schorn B, Weyland A, Scholz M, Buhre W, Stepanek E, Allen SJ, Sonntag H: Bedside assessment of intravascular volume status in patients undergoing coronary bypass surgery. Anesthesiology 1994; 81:76–86

146. Funayama T, Aida S, Matsukawa T, Okada K, Kumazawa T: Systemic, but not pulmonary, hemodynamics are depressed during combined high thoraco-cervical epidural and general anesthesia in dogs. Can J Anesth 2003; 50:454–9

147. Shoukas AA, Brunner MC: Epinephrine and the carotid sinus baroreceptor reflex. Influence on capacitive and resistive properties of the total systemic vascular bed of the dog. Circ Res 1980; 47:249–57

148. Sato H, Okuda Y: Prostaglandin E1 has the same vasodilatory as sympathetic block and increases cardiac output to maintain blood pressure in anesthetized dogs. Dokkyo J Med Sci 2001; 28:535–8

149. Calvin JE, Driedger AA, Sibbald WJ: The hemodynamic effect of rapid fluid infusion in critically ill patients. Surgery 1981; 90:61–76

150. Reuse C, Vincent JL, Pinsky MR: Measurements of right ventricular volumes during fluid challenge. Chest 1990; 98:1450–4

151. Wagner JG, Leatherman JW: Right ventricular end-diastolic volume as a predictor of the hemodynamic response to a fluid challenge. Chest 1998; 113:1048–54

152. Michard F, Boussat S, Chemla D, Anguel N, Mercat A, Lecarpentier Y, Richard C, Pinsky MR, Teboul JL: Relation between respiratory changes in arterial pulse pressure and fluid responsiveness in septic patients with acute circulatory failure. Am J Respir Crit Care Med 2000; 162:134–8

153. Kumar A, Anel R, Bunnell E, Habet K, Zanotti S, Marshall S, Neumann A, Ali A, Cheang M, Kavinsky C, Parrillo JE: Pulmonary artery occlusion pressure and central venous pressure fail to predict ventricular filling volume, cardiac performance, or the response to volume infusion in normal subjects. Crit Care Med 2004; 32:691–9

154. Coudray A, Romand J-A, Treggiari M, Bendjelid K: Fluid responsiveness in spontaneously breathing patients: A review of indexes used in intensive care. Crit Care Med 2005; 33:2757–62

155. Guyton AC: Venous return, Handbook of Physiology. Edited by Hamilton WF. Circulation. Washington, DC, American Physiological Society, 1963, sect. 2, chap. 32, pp 1099–133

156. Sagawa K: Baroreflex control of systemic arterial pressure and vascular bed, Handbook of Physiology: Section 2: The Cardiovascular System, vol. 3, Peripheral Circulation and Organ Blood Flow, part 2. By Shepherd JT, Abboud FM. Bethesda, Maryland, American Physiological Society, 1983, pp 453–96

157. Rowell LB: Human Cardiovascular Control. New York, Oxford University Press, 1993, pp 180–99

158. Tyberg JV: How changes in venous capacitance modulate cardiac output. Eur J Physiol 2002; 445:10–7

159. Stéphan F, Flahault A, Dieudonné N, Hollande J, Paillard F, Bonnet F: Clinical evaluation of circulating blood volume in critically ill patients: Contribution of a clinical scoring system. Br J Anaesth 2001; 86:754–62

160. Magder S, Georgiadis G, Cheong T: Respiratory variations in right atrial pressure predict the response to fluid challenge. J Crit Care 1992; 7:76–85

161. Magder S, Lagonidis D: Effectiveness of albumin versus normal saline as a test of volume responsiveness in post-cardiac surgery patients. J Crit Care 1999; 14:164–71

162. Magder S: Diagnostic information from the respiratory variations in central hemodynamics pressures, Respiratory-Circulatory Interactions in Health and Disease. Edited by Scharf SM, Pinsky MR, Magder S. New York, Marcel Dekker, 2001, pp 861–82. Lung Biology in Health and Disease, vol. 157. Edited by Lenfant C

163. Monnet X, Rienzo M, Osman D, Anguel N, Richard C, Pinsky MR, Teboul J-L: Passive leg raising predicts fluid responsiveness in the critically ill. Crit Care Med 2006; 34:1402–7

† Modified from references 27 and 28.

Cited By:

This article has been cited 35 time(s).

International Journal of Medical Sciences
Is Stroke Volume Variation a Useful Preload Index in Liver Transplant Recipients? A Retrospective Analysis
Kim, SH; Hwang, GS; Kim, SO; Kim, YK
International Journal of Medical Sciences, 10(6): 751-757.
10.7150/ijms.6074
CrossRef
Journal of the American College of Cardiology
Timing of Hemoconcentration During Treatment of Acute Decompensated Heart Failure and Subsequent Survival Importance of Sustained Decongestion
Testani, JM; Brisco, MA; Chen, J; McCauley, BD; Parikh, CR; Tang, WHW
Journal of the American College of Cardiology, 62(6): 516-524.
10.1016/j.jacc.2013.05.027
CrossRef
World Journal of Surgery
Assessment of Liver Stiffness Measurement: Novel Intraoperative Blood Loss Predictor?
Kim, MS; Lee, JR
World Journal of Surgery, 37(1): 185-191.
10.1007/s00268-012-1774-y
CrossRef
Journal of Clinical Monitoring and Computing
Outcome impact of goal directed fluid therapy during high risk abdominal surgery in low to moderate risk patients: a randomized controlled trial
Ramsingh, DS; Sanghvi, C; Gamboa, J; Cannesson, M; Applegate, RL
Journal of Clinical Monitoring and Computing, 27(3): 249-257.
10.1007/s10877-012-9422-5
CrossRef
Journal of Maternal-Fetal & Neonatal Medicine
Physiological implications of arteriovenous anastomoses and venous hemodynamic dysfunction in early gestational uterine circulation: a review
Gyselaers, W; Peeters, L
Journal of Maternal-Fetal & Neonatal Medicine, 26(9): 841-846.
10.3109/14767058.2013.766705
CrossRef
Artificial Organs
Hypovolemia in Extracorporeal Life Support Can Lead to Arterial Gaseous Microemboli
Simons, AP; Ganushchak, YM; Teerenstra, S; Bergmans, DC; Maessen, JG; Weerwind, PW
Artificial Organs, 37(3): 276-282.
10.1111/j.1525-1594.2012.01560.x
CrossRef
Interactive Cardiovascular and Thoracic Surgery
Short-term independent mortality risk factors in patients with cirrhosis undergoing cardiac surgery
Lopez-Delgado, JC; Esteve, F; Javierre, C; Perez, X; Torrado, H; Carrio, ML; Rodriguez-Castro, D; Farrero, E; Ventura, JL
Interactive Cardiovascular and Thoracic Surgery, 16(3): 332-338.
10.1093/icvts/ivs501
CrossRef
Anesthesia and Analgesia
Stroke Volume Variation During Acute Normovolemic Hemodilution
Kungys, G; Rose, DD; Fleming, NW
Anesthesia and Analgesia, 109(6): 1823-1830.
10.1213/ANE.0b013e3181ba41af
CrossRef
Journal of Veterinary Emergency and Critical Care
A technique for central venous pressure measurement in normal horses
Wilsterman, S; Hackett, ES; Rao, S; Hackett, TB
Journal of Veterinary Emergency and Critical Care, 19(3): 241-246.
10.1111/j.1476-4431.2009.00420.x
CrossRef
Hypertension
Sympathetic Activity, Vascular Capacitance, and Long-Term Regulation of Arterial Pressure
Fink, GD
Hypertension, 53(2): 307-312.
10.1161/HYPERTENSIONAHA.108.119990
CrossRef
British Journal of Anaesthesia
Hypotension in obstetric spinal anaesthesia: a lesson from pre-eclampsia
Sharwood-Smith, G; Drummond, GB
British Journal of Anaesthesia, 102(3): 291-294.
10.1093/bja/aep003
CrossRef
Journal of the American College of Cardiology
Venous Congestion and Worsening Renal Function
Testani, J; Sutton, MS; Kirkpatrick, J
Journal of the American College of Cardiology, 54(7): 661.
10.1016/j.jacc.2009.03.074
CrossRef
European Journal of Applied Physiology
Identification of the human electrical impedance indifferent point: a surrogate for the volume indifferent point?
Jarvis, SS; Pawelczyk, JA
European Journal of Applied Physiology, 107(4): 473-480.
10.1007/s00421-009-1148-9
CrossRef
American Journal of Physiology-Heart and Circulatory Physiology
Venous response to orthostatic stress
Krabbendam, I; Jacobs, LCA; Lotgering, FK; Spaanderman, MEA
American Journal of Physiology-Heart and Circulatory Physiology, 295(4): H1587-H1593.
10.1152/ajpheart.00571.2008
CrossRef
Acta Anaesthesiologica Scandinavica
Association between central venous pressure and blood loss during hepatic resection in 984 living donors
Kim, YK; Chin, JH; Kang, SJ; Jun, IG; Song, JG; Jeong, SM; Park, JY; Hwang, GS
Acta Anaesthesiologica Scandinavica, 53(5): 601-606.
10.1111/j.1399-6576.2009.01920.x
CrossRef
Anaesthesia
The obligatory role of the kidney in long-term arterial blood pressure control: extending Guyton's model of the circulation
Dorrington, KL; Pandit, JJ
Anaesthesia, 64(): 1218-1228.
10.1111/j.1365-2044.2009.06052.x
CrossRef
Journal of Cardiothoracic and Vascular Anesthesia
CASE 1-2010 Pulmonary Thrombectomy in an Adult With Fontan Circulation
Gaitan, BD; Ramakrishna, H; DiNardo, JA; Cannesson, M
Journal of Cardiothoracic and Vascular Anesthesia, 24(1): 173-182.
10.1053/j.jvca.2009.11.003
CrossRef
British Journal of Anaesthesia
NICE and warm
Harper, CM; Andrzejowski, JC; Alexander, R
British Journal of Anaesthesia, 101(3): 293-295.
10.1093/bja/aen233
CrossRef
Perfusion-Uk
Reserve-driven flow control for extracorporeal life support: proof of principle
Simons, AP; Reesink, KD; Lance, MD; van der Nagel, T; van der Veen, FH; Weerwind, PW; Maessen, JG
Perfusion-Uk, 25(1): 25-29.
10.1177/0267659109360284
CrossRef
Anaesthesist
Volume status and central venous pressure
Janssens, U; Graf, J
Anaesthesist, 58(5): 513-519.
10.1007/s00101-009-1531-2
CrossRef
Cardiology
The Effects of Intra-Aortic Balloon Pump Support on Macrocirculation and Tissue Microcirculation in Patients with Cardiogenic Shock
den Uil, CA; Lagrand, WK; van der Ent, M; Jewbali, LSD; Brugts, JJ; Spronk, PE; Simoons, ML
Cardiology, 114(1): 42-46.
10.1159/000212060
CrossRef
Obesity Surgery
Stroke Volume Variation as a Guide to Fluid Administration in Morbidly Obese Patients Undergoing Laparoscopic Bariatric Surgery
Jain, AK; Dutta, A
Obesity Surgery, 20(6): 709-715.
10.1007/s11695-009-0070-x
CrossRef
Acta Anaesthesiologica Scandinavica
Do we really need a low central venous pressure in elective liver resection
Mansour, N; Lentschener, C; Ozier, Y
Acta Anaesthesiologica Scandinavica, 52(9): 1306-1307.
10.1111/j.1399-6576.2008.01750.x
CrossRef
European Journal of Heart Failure
Fluid loss, venous congestion, and worsening renal function in acute decompensated heart failure
Aronson, D; Abassi, Z; Allon, E; Burger, AJ
European Journal of Heart Failure, 15(6): 637-643.
10.1093/eurjhf/hft036
CrossRef
Intensive Care Medicine
The impact of early goal-directed fluid management on survival in an experimental model of severe acute pancreatitis
Trepte, CJC; Bachmann, KA; Stork, JH; Friedheim, TJ; Hinsch, A; Goepfert, MS; Mann, O; Izbicki, JR; Goetz, AE; Reuter, DA
Intensive Care Medicine, 39(4): 717-726.
10.1007/s00134-012-2775-x
CrossRef
Chinese Medical Journal
Responsiveness of stroke volume variation and central venous pressure during acute normovolemic and hypervolemic hemodilution
Ji, FH; Li, WJ; Li, J; Peng, K; Yang, JP; Liu, H
Chinese Medical Journal, 126(): 1838-1843.
10.3760/cma.j.issn.0366-6999.20122525
CrossRef
Anesthesiology
Inspiratory Increases in Systolic Blood Pressure (“Delta-up”) and Pulse Pressure Are Not Equivalent
Tavernier, B; Robin, E; Granet, F
Anesthesiology, 109(5): 934-935.
10.1097/ALN.0b013e3181895de1
PDF (735) | CrossRef
Current Opinion in Critical Care
Bedside assessment of mean systemic filling pressure
Jansen, JR; Maas, JJ; Pinsky, MR
Current Opinion in Critical Care, 16(3): 231-236.
10.1097/MCC.0b013e3283378185
PDF (288) | CrossRef
ASAIO Journal
Tissue Doppler Measurements Correlate With Central Venous Pressure in Pediatric Patients After Cardiac Surgery
Learn, C; Yates, A; Nicholson, L; Milton, K; Lloyd, E; Cua, C
ASAIO Journal, 56(4): 377-382.
10.1097/MAT.0b013e3181e5d543
PDF (323) | CrossRef
Transplantation
Effects of Phlebotomy and Phenylephrine Infusion on Portal Venous Pressure and Systemic Hemodynamics During Liver Transplantation
Karakiewicz, P; Massicotte, L; Perrault, M; Denault, A; Klinck, J; Beaulieu, D; Roy, J; Thibeault, L; Roy, A; McCormack, M
Transplantation, 89(8): 920-927.
10.1097/TP.0b013e3181d7c40c
PDF (418) | CrossRef
Anesthesiology
Venous Function and Pressure: What Is Their Role in the Management of Spinal Cord Ischemia after Thoracoabdominal Aortic Aneurysm Repair?
Augoustides, JG
Anesthesiology, 109(5): 933.
10.1097/ALN.0b013e3181895d7f
PDF (735) | CrossRef
Anesthesiology
Arterial and Plethysmographic Waveform Analysis in Anesthetized Patients with Hypovolemia
Pizov, R; Eden, A; Bystritski, D; Kalina, E; Tamir, A; Gelman, S
Anesthesiology, 113(1): 83-91.
10.1097/ALN.0b013e3181da839f
PDF (1494) | CrossRef
Critical Care Medicine
Physiology of the circulation—An old–new vocabulary*
Bar-Yosef, S
Critical Care Medicine, 37(3): 1143-1144.
10.1097/CCM.0b013e318196fd37
PDF (2138) | CrossRef
Anesthesiology
Inspiratory Increases in Systolic Blood Pressure (“Delta-up”) and Pulse Pressure Are Not Equivalent
Gelman, S
Anesthesiology, 109(5): 935-936.
10.1097/ALN.0b013e3181897dcd
PDF (735) | CrossRef
Anesthesiology
What Is Simple Is Perhaps Not Always the Truth
Jayant, A
Anesthesiology, 109(5): 933-934.
10.1097/ALN.0b013e3181895dd0
PDF (735) | CrossRef
Back to Top | Article Outline

© 2008 American Society of Anesthesiologists, Inc.

Publication of an advertisement in Anesthesiology Online does not constitute endorsement by the American Society of Anesthesiologists, Inc. or Lippincott Williams & Wilkins, Inc. of the product or service being advertised.
Login

Article Tools

Images

Share