Cardiac Output & Vascular Function Curves
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Vascular and Cardiac Function Curves
VASCULAR FUNCTION (VENOUS RETURN) CURVE
Plots the relationship between venous return and right atrial pressure.
Venous return is the blood flow returned to the heart (ie, "cardiac input").
Demonstrates an inverse relationship between venous return and right atrial pressure:
Increases in right atrial pressure (RAP) lower the driving pressure for blood flow, which, in turn, reduces venous return (VR);recall that driving pressure, the pressure gradient between two points, largely determines blood flow.
As we read the graph from right to left, venous return increases as right atrial pressure decreases. However, when right atrial pressure reaches roughly -2 to 1 mmHg, the venous return curve plateaus. This is because at such low right atrial pressure, the large veins collapse, which limits venous return at approximately 7 L/min.
Mean systemic filling pressure
Sometimes referred to as mean systemic pressure, it is the uniform pressure throughout the vasculature when blood flow, and, therefore, venous return, ceases (eg, after cardiac arrest).
Mean systemic filling pressure is ~7 mmHg (not zero, because of elastic recoil and vessel compliance, which we learn in detail elsewhere).
Shifts in blood volume change venous return, and, therefore, shift the vascular function curve:
An increase in blood volume (for example, from a blood transfusion) will shift the curve upwards, and mean systemic filling pressure increases.
A decrease in blood volume (for example, as result of hemorrhage) will shift the curve downwards; mean systemic filling pressure decreases.
CARDIAC FUNCTION CURVE (CARDIAC OUTPUT):
Plots the relationship of cardiac output L/min of left ventricle vs. right atrial pressure.
Demonstrates that as right atrial pressure increases, so does cardiac output, up to a point:
When right atrial pressure reaches ~ 5 mmHg, cardiac output maxes out at ~ 9 L/min; at this pressure, cardiac output can no longer keep up.
Until this point, increasing right atrial pressure increases both end-diastolic volume and cardiac muscle fiber length, which, in turn, increase cardiac output.
This is a reflection of the Frank-Starling mechanism, which refers to the intrinsic ability of the heart to adapt to changes in venous return.
The muscle fibers of the heart stretch to accommodate returning blood volume; in turn, the degree of stretch determines the amount of force used to eject that blood.
Shifts in contractility (inotropy) affect the cardiac output curve:
Contractility refers to the intrinsic ability of cardiac muscle fibers to produce force.
Increased contractility shifts the curve upward, so that cardiac output is increased at any given right atrial pressure value; remember that sympathetic stimulation and/or increases in heart rate increase contractility to ensure that body tissues receive sufficient blood flow during exercise.
Decreased contractility shifts the curve downwards, so that cardiac output is reduced at any given right atrial pressure value.
Clinical/Pharmacologic correlation: Patients with congestive heart failure, in which ventricular contractility is greatly decreased, are often given cardiac glycosides.
These drugs increase contractility (by raising intracellular calcium concentration) and, therefore, increase cardiac output.
Combined vascular and cardiac function curves:
Changes in total peripheral resistance alter the steady state:
Arteriole constriction will increase the total peripheral resistance:
Increased total peripheral resistance reduces both venous return and cardiac output; the steady state shifts to reflect these changes.
Arteriole dilation decreases total peripheral resistance:
Both venous return and cardiac output increase, and the new steady state reflects this.
Be aware that, although we've shown no change in right atrial pressure, this is not always the case; changes in right atrial pressure are less predictable, and depend on a variety of factors not discussed, here.
Recognize that right atrial pressure, cardiac output, and venous return are interdependent, so that no single variable is "driving" the others. In other words, a change in one variable can affect the others —keep this interdependence in mind when faced with clinical cases!