Manipulating Cardiac Output and Venous Return Curves

A Practical Guide

Robert W. Baer, Ph.D.

Department of Physiology

Kirksville College of Osteopathic Medicine

            The purpose of this guide is to describe the manipulation of cardiac output curves and venous return curves to simultaneously solve for the two dependent variables: cardiac output and right atrial pressure.  The cardiac output curve relates cardiac output to right atrial pressure.  For this curve right atrial pressure is a measure of end diastolic fiber stretch and the curve may be thought of as a graphical expression of Starling's Law of the Heart.  Please note that "cardiac output" is not the same thing as the "cardiac output curve".  The venous return curve relates the rate of venous flow back to the heart (i.e., venous return) to the right atrial pressure.  For this curve right atrial pressure is the downstream end of the pressure gradient that drives venous return.  Note that right atrial pressure has a dual role and plays an important but different role for the two curves.  It takes knowledge of both curves (two equations) to figure out what will happen to the 2 unknowns (cardiac output and right atrial pressure). Neither curve alone gives enough information to solve for either of the variables (cardiac output and right atrial pressure).  Clinically, the "cardiac output curve" is often referred to as the "Starling Curve" and is drawn without a corresponding "venous return curve".  When this happens you should consider mentally constructing the missing venous return curve.

The Normal Cardiac Output Curve and Venous Return Curve Intersection.

            At any given point in time there is an operational cardiac output curve and an operational venous return curve, but we are operating at one and only one point on each curve.  The graphical solution of these two curves is for "steady‑ state" which by definition implies that cardiac output equals venous return.  If cardiac output did not equal venous return then volume would be collecting in one part of the circulation or another.  In considering the effect of an intervention it is extremely useful to draw "normal" curves first for use as a frame of reference.  To draw a set of "normal" curves we need to have in mind three normal values:  normal cardiac output is 5 L/min; normal right atrial pressure is 0 mmHg; and normal mean systemic filling pressure (Pms) is 7 mmHg.  The axes of these curves are such that the y‑axis is cardiac output and the x‑ axis is right atrial pressure. 

            Drawing a normal cardiac output curve is straightforward.  The curve starts at a slightly negative right atrial pressure (remember that negative pressure just means subatmospheric) and projects upward and to the right.  Its exact position for use in qualitative analysis is not critical. 

            The normal venous return curve is only slightly more difficult to draw.  The mean systemic filling pressure is the pressure at which the venous return curve intersects the right atrial pressure axis and cardiac output is zero.  Therefore, the normal venous return curve must intersect the right atrial pressure axis at a right atrial pressure of 7 mmHg.  This intersection point acts as a "hinge" on which the venous return curve rotates clockwise (decreased resistance to venous return) or counter‑clockwise (increased resistance to venous return).  The "normal" venous return curve starts at mean systemic pressure of 7 mmHg and is drawn with a slope which causes it to intersect with the cardiac output curve at a right atrial pressure of 0 mmHg and a cardiac output of 5 L/min.  The slope of this curve is a reflection of "normal" resistance to venous return (RVR).  A "normal" set composed of the normal cardiac output curve and the normal venous return curve is shown below (figure 1).  Note the dotted lines projecting to the cardiac output and right atrial pressure axes.  This is how a graphical "solution" is read from the graph because this is the one point at which the cardiac output curve intersects the venous return curve.

FIGURE 1

The Effect of Interventions

            The manipulation of the curves depends on systematically figuring out: first, how an intervention will affect the cardiac output curve, and then how it will affect the venous return curve.  Figuring out how an intervention affects the cardiac output curve involves answering only a single question as discussed below.  Figuring out how an intervention will affect the venous return curve involves figuring out: first, how it will affect the mean systemic filling pressure (Pms); and second, how it will affect the resistance to venous return (RVR).  Thus, 2 questions must be answered to figure out how a venous return curve moves.  Each of these inputs to the cardiac output curve and venous return curve equations (independent variables) should be systematically considered in the following order:

            1) Cardiac Output Curve.  Does the intervention cause the heart to become hypereffective or hypoeffective, or does the intervention have no effect?

            2) Venous Return Curve.  Does the intervention cause the mean systemic filling pressure to increase or decrease, or does the intervention have no effect?

            3) Venous Return Curve.  Does the intervention cause the resistance to venous return to increase or decrease or does the intervention have no effect?

            In asking and answering these three questions about an intervention, students most frequently have trouble when the answer with regard to one of the questions is "no effect".  With this problem in mind we will attempt to describe a very limited set of conditions that alter each of the 3 inputs (independent variables) listed above.  If the intervention under consideration is not on a given input's list, then the student should conclude that there is no effect on that input.   This approach produces right answers in the vast majority of cases.  By taking this simplistic approach we may miss an occasional "zebra" in our "herd of horses", but the gain in terms of having a workable tool is well worth the potential sacrifice of simplifying.

            The effect of an intervention is systematically drawn on the same graph as the normal curves.  First, any change in the cardiac output curve is drawn.  Then any change in the venous return curve is drawn by determining whether the mean systemic pressure (the hinge) moves, and whether the resistance to venous return is altered (the slope projecting from the hinge).  If heart function does not change the cardiac output curve superimposes on its previous position.  If the mean systemic pressure does not change, the "hinge" remains in the same place.  If resistance to venous return does not change, the venous return curve is parallel to its previous position.  If neither mean systemic pressure nor resistance to venous return change, the venous return curve does not move.

Cardiac Output Curve Changes
 
Remember that the "cardiac output curve" is something quite different than "cardiac output".  Cardiac output curves are sometimes called "Starling curves".  When cardiac function improves, the Starling Curve shifts up and to the left, and we say that we have a "hypereffective heart" (Figure 2).  When cardiac function deteriorates, the curve shifts down and to the right and we say that we have a hypoeffective heart (Figure 2).

FIGURE 2

 

            We will consider only 4 things that can change the slope of the cardiac output curve:

            1) A Change in Sympathetic Tone.  An increase in sympathetic tone will make the heart hypereffective and will shift the cardiac output curve up and to the left.  A decrease in sympathetic tone will make the heart hypoeffective and will shift the curve down and to the right.

            2) Administration of an Inotropic Agent.  A positive inotropic agent will increase contractility, make the heart hypereffective, and will shift the cardiac output curve up and to the left.  A negative inotropic agent will decrease contractility, will make the heart hypoeffective, and will shift the cardiac output curve down and to the right.  Note that some inotropic agents (eg. epinephrine) may also have vascular effects.  These effects will move the venous return curve, and these effects should be considered separately as described below.  Pure inotropic agents will affect only the cardiac output curve.

            3) A Myocardial Infarct.  A myocardial infarct makes the heart hypoeffective and shifts the cardiac output curve down and to the right.

            4) Other primary heart problems such as cardiomyopathies or valvular heart disease.  These make the heart hypoeffective and shift the cardiac output curve down and to the right.

            If an intervention is not one of the four items listed above, it does not move the cardiac output curve.  Once again, this does not mean that it does not change cardiac output; it only means that it does not change the position of the cardiac output curve.  Cardiac output may still change if we move to a new position on the original cardiac output curve by moving to a new venous return curve.

Mean Systemic Filling Pressure

            The second thing that must be determined is whether the intervention changes mean systemic filling pressure.  From a physiological point of view this boils down to the question of what happens to blood volume in relationship to the vascular (primarily venous) container size.  When blood volume increases relative to vascular container size, the mean systemic filling pressure increases. 

            From a graphical point of view we are asking where the "hinge" is. When Pms increases, the hinge point moves to the right (figure 2a).  When Pms decreases, the hinge point moves to the left (figure 2b).  When Pms does not change the hinge point does not move.  Note that the slope of the venous return curve may change even if the hinge does not move (for example see 3a and 3b).

FIGURE 3

Two things will change mean systemic filling pressure:

            1) A Change in Blood Volume.  An increase in blood volume increases mean systemic filling pressure and shifts the hinge point to the right.  A decrease in blood volume decreases mean systemic filling pressure and shifts the hinge point to the left.  Anything that causes volume retention increases mean systemic filling pressure, despite the fact that there is some passive distension of the container.  Examples of things that increase blood volume include transfusion and fluid retention by renal mechanisms (ADH, renin‑angiotensin, and aldosterone).  Examples of things that decrease blood volume are hemorrhage and dehydration.

            2) A Change in Vascular Container Size.  An increase in sympathetic tone constricts the veins, increases mean systemic pressure, and moves the hinge to the right.  A decrease in sympathetic tone increases the venous container size, decreases mean systemic pressure, and moves the hinge to the left.  Circulating catecholamines act the same as an increase in sympathetic tone. Increased skeletal muscle tone and abdominal compression also decrease venous container size, increase the mean systemic filling pressure, and move the hinge point to the right.

If an intervention does not alter blood volume or vascular capacity it does not change mean systemic filling pressure.  If mean systemic pressure is unchanged, the new venous return curve is drawn beginning from the same hinge point as the old venous return curve. 

Resistance to Venous Return

            The resistance to venous return determines the slope of the venous return curve.  After an intervention the new mean systemic filling pressure point acts as the hinge on which the venous return curve rotates.  One may picture this point as the center‑post of a clock about which the venous return curve rotates either clockwise or counter‑clockwise.  Any intervention which decreases resistance to venous return causes the venous return curve to rotate clockwise (figure 4A).  Some students like to say, "the resistance goes down so the curve goes up; that is, more parallel to the flow axis."  Any intervention which increases the resistance to venous return causes the venous return curve to rotate counter‑clockwise (figure 4B).  Some students like to say, "resistance goes up so the curve rotates down; that is, more parallel to the pressure axis." 

            If an intervention does not affect resistance to venous return, then the venous return curve lies parallel to the old venous return curve but is drawn starting at the new mean systemic filling pressure (figures 4C and 4D).  If both mean systemic filling pressure and resistance to venous return change the venous return curve is both shifted (new hinge as determined above) and rotated (figures 4E and 4F).  If neither mean systemic filling pressure nor resistance to venous return have changed, then the new venous return curve superimposes the old venous return curve.

FIGURE 4

            Resistance to venous return only changes when an intervention affects the total peripheral resistance.  When total peripheral resistance increases the resistance to venous return increases.  When total peripheral resistance decreases, the resistance to venous return decreases.  Basically, only three things change resistance to venous return:

            1) Changes in vasomotor tone.  Any intervention which causes vasoconstriction increases the resistance to venous return and rotates the venous return curve counter‑clockwise.    Any intervention which causes vasodilation decreases resistance to venous return and causes the venous return curve to rotate clockwise.    Changes in vasomotor tone occur with changes in sympathetic tone (increased tone causing increased resistance to venous return) or local metabolic vasodilation (decreased tone causing decreased resistance to venous return). 

            2) Changes in Viscosity.  Anemia decreases viscosity and decreases resistance to venous return so that the venous return curve rotates clockwise about mean systemic pressure.  Polycythemia increases viscosity and increases resistance to venous return so that the venous return curve rotates counter‑clockwise about mean systemic pressure.

            3) Formation of new low resistance pathways in parallel.  When an AV fistula (arterial‑venous) connects an artery directly to a vein, resistance to venous return decreases.  The venous return curve rotates clockwise about mean systemic filling pressure.

            Exercise is a special case where local vasodilation exceeds the generalized sympathetic vasoconstriction so that total peripheral resistance and resistance to venous return decrease.  Therefore, the venous return curve rotates clockwise about the new mean systemic filling pressure in exercise.  However, the effects of increased sympathetic tone will still be apparent on the cardiac output curve and at the mean systemic filling pressure "hinge" point.

Some Final Considerations

            We have ignored the effect of afterload changes on the cardiac output curve.  While this is not strictly correct it simplifies the analysis, and the curves still generally yield the right answers. 

            There are a number of instances where vasodilation and fluid retention occur together.  Fluid retention almost always predominates so blood volume rises in relation to container size.  The result is an increase in mean systemic filling pressure and a decrease in resistance to venous return.

            When an intervention causes the heart to become hypereffective at the same time that mean systemic filling pressure increases (increased sympathetic tone), the effect on right atrial pressure is indeterminate.  Likewise, when an intervention causes the heart to become hypoeffective at the same time that mean systemic filling pressure decreases (spinal anesthesia) the effect on right atrial pressure is indeterminate.  In these instances one may usually safely predict little change in right atrial pressure.  Note however that the effect on cardiac output is clear in both cases: increasing when the heart becomes hypereffective and mean systemic pressure increases; decreasing when the heart becomes hypoeffective and mean systemic pressure decreases.

            When an intervention causes an increase or decrease in both mean systemic filling pressure and resistance to venous return, the effect on cardiac output is indeterminate.  Such conflicts generally resolve themselves such that the change in mean systemic filling pressure predominates.  The effect of the intervention may therefore be determined by shifting the venous return curve in a parallel fashion in an appropriate direction.  For example, an increase in sympathetic tone increases mean systemic pressure and resistance to venous return.  The overall effect on cardiac output will depend on the relative magnitude of the increase in mean systemic pressure versus the increase in resistance to venous return.  Using our rule and parallel shifting the venous return curve to the right we would predict an increase in cardiac output, which is indeed what happens.

            The manipulation of cardiac output and venous return curves is quite difficult for most students.  However, with a little practice it can even become fun.  The tool is a powerful one that has many potential applications in understanding cardiovascular pathophysiology.  Cardiac output and right atrial pressure are variables that are often used clinically to assess cardiovascular function.  An understanding of the cardiac output curve and the venous return curve can be valuable in interpreting these clinically measured variables.