Figure 3.10 Effects of changes in (A) preload, (B) afterload, and (C) contractility on the ventricular pressure–volume loop.

b.  2 → 3 (ventricular ejection). The aortic valve opens at point 2 when pressure in the left

ventricle exceeds pressure in the aorta. Blood is ejected into the aorta, and ventricular volume decreases. The volume that is ejected in this phase is the stroke volume. Thus, stroke volume can be measured graphically by the width of the pressure–volume loop.

The volume remaining in the left ventricle at point 3 is end-systolic volume.

c.  3 → 4 (isovolumetric relaxation). At point 3, the ventricle relaxes. When ventricular pressure decreases to less than aortic pressure, the aortic valve closes. Because all of the valves are closed again, ventricular volume is constant (isovolumetric) during this phase.

d.  4 → 1 (ventricular filling). Once left ventricular pressure decreases to less than left atrial pressure, the mitral valve opens and filling of the ventricle begins. During this phase, ventricular volume increases to about 140 mL (the end-diastolic volume).

2.  Changes in the ventricular pressure–volume loop are caused by several factors (Figure 3.10). a.  Increased preload (see Figure 3.10A)

■refers to an increase in end-diastolic volume and is the result of increased venous return (e.g., increased blood volume or decreased venous capacitance)

■causes an increase in stroke volume based on the Frank-Starling relationship.

■The increase in stroke volume is reflected in increased width of the pressure–volume loop.

b.  Increased afterload (see Figure 3.10B)

■refers to an increase in aortic pressure.

■The ventricle must eject blood against a higher pressure, resulting in a decrease in stroke volume.

■The decrease in stroke volume is reflected in decreased width of the pressure–­ volume loop.

■The decrease in stroke volume results in an increase in end-systolic volume.

c.  Increased contractility (see Figure 3.10C)

■The ventricle develops greater tension than usual during systole, causing an increase in stroke volume.

■The increase in stroke volume results in a decrease in end-systolic volume.

F. Cardiac and vascular function curves (Figure 3.11)

■are simultaneous plots of cardiac output and venous return as a function of right atrial pressure or end-diastolic volume.

1.  The cardiac function (cardiac output) curve

■depicts the Frank-Starling relationship for the ventricle.

■shows that cardiac output is a function of end-diastolic volume.

Figure 3.11 Simultaneous plots of the cardiac and vascular function curves. The curves cross at the equilibrium point for the cardiovascular system.

2.  The vascular function (venous return) curve

■depicts the relationship between blood flow through the vascular system (or venous return) and right atrial pressure.

a.  Mean systemic pressure

■is the point at which the vascular function curve intersects the x-axis.

■equals right atrial pressure when there is “no flow” in the cardiovascular system.

■is measured when the heart is stopped experimentally. Under these conditions, ­cardiac output and venous return are zero, and pressure is equal throughout the cardiovascular system.

(1)  Mean systemic pressure is increased by an increase in blood volume or by a decrease in venous capacitance (where blood is shifted from the veins to the arteries). An increase in mean systemic pressure is reflected in a shift of the vascular function

curve to the right (Figure 3.12).

Figure 3.12 Effect of increased blood volume on the mean systemic pressure, vascular function curve, cardiac output, and right atrial pressure.

Figure 3.13 Effect of increased total peripheral resistance (TPR) on the cardiac and vascular function curves and on cardiac output.

(2)  Mean systemic pressure is decreased by a decrease in blood volume or by an increase in venous capacitance (where blood is shifted from the arteries to the veins). A decrease in mean systemic pressure is reflected in a shift of the vascular function curve to the left.

b.  Slope of the venous return curve

■ is determined by the resistance of the arterioles.

(1)  A clockwise rotation (not illustrated) of the venous return curve indicates a decrease in total peripheral resistance (TPR). When TPR is decreased for a given right atrial

pressure, there is an increase in venous return (i.e., vasodilation of the arterioles “allows” more blood to flow from the arteries to the veins and back to the heart).

(2)  A counterclockwise rotation of the venous return curve indicates an increase in TPR (Figure 3.13). When TPR is increased for a given right atrial pressure, there is a decrease in venous return to the heart (i.e., vasoconstriction of the arterioles decreases blood flow from the arteries to the veins and back to the heart).

3.  Combining cardiac output and venous return curves

■When cardiac output and venous return are simultaneously plotted as a function of right atrial pressure, they intersect at a single value of right atrial pressure.

■The point at which the two curves intersect is the equilibrium, or steady-state, point (see Figure 3.11). Equilibrium occurs when cardiac output equals venous return.

■Cardiac output can be changed by altering the cardiac output curve, the venous return curve, or both curves simultaneously.

■The superimposed curves can be used to predict the direction and magnitude of changes in cardiac output and the corresponding values of right atrial pressure.

a.  Inotropic agents change the cardiac output curve.

(1)  Positive inotropic agents (e.g., cardiac glycosides) produce increased contractility and increased cardiac output (Figure 3.14).

■The equilibrium, or intersection, point shifts to a higher cardiac output and a correspondingly lower right atrial pressure.

■Right atrial pressure decreases because more blood is ejected from the heart on

each beat (increased stroke volume).

Figure 3.14 Effect of a positive inotropic agent on the cardiac function curve, cardiac output, and right atrial pressure.

(2)  Negative inotropic agents produce decreased contractility and decreased cardiac output (not illustrated).

b.  Changes in blood volume or venous capacitance change the venous return curve.

(1)  Increases in blood volume or decreases in venous capacitance increase mean systemic pressure, shifting the venous return curve to the right in a parallel fashion

(see Figure 3.12). A new equilibrium, or intersection, point is established at which both cardiac output and right atrial pressure are increased.

(2)  Decreases in blood volume (e.g., hemorrhage) or increases in venous capacitance have the opposite effect—decreased mean systemic pressure and a shift of the venous

return curve to the left in a parallel fashion. A new equilibrium point is established at which both cardiac output and right atrial pressure are decreased (not illustrated).

c.  Changes in TPR change both the cardiac output and the venous return curves.

■Changes in TPR alter both curves simultaneously; therefore, the responses are more complicated than those noted in the previous examples.

(1)  Increasing TPR causes a decrease in both cardiac output and venous return (see Figure 3.13).

(a)A counterclockwise rotation of the venous return curve occurs. Increased TPR results in decreased venous return as blood is retained on the arterial side.

(b)A downward shift of the cardiac output curve is caused by the increased aortic pressure (increased afterload) as the heart pumps against a higher pressure.

(c)As a result of these simultaneous changes, a new equilibrium point is established at which both cardiac output and venous return are decreased, but right atrial pressure is unchanged.

(2)  Decreasing TPR causes an increase in both cardiac output and venous return (not illustrated).

(a)A clockwise rotation of the venous return curve occurs. Decreased TPR results in increased venous return as more blood is allowed to flow back to the heart from the arterial side.

(b)An upward shift of the cardiac output curve is caused by the decreased aortic pressure (decreased afterload) as the heart pumps against a lower pressure.

(c)As a result of these simultaneous changes, a new equilibrium point is established at which both cardiac output and venous return are increased, but right

atrial pressure is unchanged.