panel B). Increased systemic vascular resistance
decreases the slope while keeping the same
mean circulatory filling pressure. Therefore, at
a given cardiac output, a decrease in systemic
vascular resistance increases right atrial pres-
sure, whereas an increase in systemic vascu-
lar resistance decreases right atrial pressure.
These changes can be difficult to conceptual-
ize, but the following explanation might help
to clarify. When small resistance vessels dilate
at a constant cardiac output, the rate of blood
flow from the arteries into the capillaries and
veins increases. This causes a transient imbal-
ance between the rate of flow into the arterial
system (cardiac output) and the rate of flow
out of the arterial system (more blood leaves
than enters the arterial system per unit time).
The increase in venous volume causes venous
pressure and right atrial pressure to increase.
This reduces the pressure gradient for venous
return from the capillaries and will lead to a
new steady state where there is once again a
balance between the flow that enters and leaves
the arteries. This steady state will be character-
ized by increased venous volume and pressure,
and decreased arterial volume and pressure.
If the heart were suddenly stopped, the mean
appreciably different from before the systemic
vascular resistance was reduced because the
decrease in arterial diameter (which increases
arterial compliance) has little affect on overall
vascular compliance, which is overwhelmingly
determined by venous compliance.
Cardiac Function Curves
According to the Frank—Starling relationship,
an increase in right atrial pressure increases car-
diac output. This relationship can be depicted
using the same axis as used in systemic func-
tion curves in which cardiac output (depend-
ent variable) is plotted against right atrial
pressure (independent variable) (Fig. 5.20).
These curves are similar to the Frank—Starling
curves shown in Figure 4.21. There is no sin-
gle cardiac function curve, but rather a family
of curves that depends on the inotropic state
and afterload (see Chapter 4). Changes in
heart rate also shift the cardiac function curve
■ FIGURE 5.20 Cardiac function curves. Cardiac
output is plotted as a function of right atrial pres-
sure (PRA); normal
(solid black),
depressed curves
are shown. Cardiac perfor-
mance, measured as cardiac output, is enhanced
(curves shift up and to the left) by an increase in
heart rate and inotropy and a decrease in afterload.
r a
because cardiac output, not stroke volume
as in Figure 4.21, is the dependent variable.
With a “normal” function curve, the cardiac
output is about 5 L/min at a right atrial pres-
sure of about 0 mm Hg. If cardiac performance
is enhanced by increasing heart rate or inot-
ropy or by decreasing afterload, it shifts the
cardiac function curve up and to the left. At
the same right atrial pressure of 0 mm Hg,
the cardiac output will increase. Conversely,
a depressed cardiac function curve, as occurs
with decreased heart rate or inotropy or with
increased afterload, will decrease the cardiac
output at any given right atrial pressure. How-
the magnitude by which cardiac output
changes when cardiac performance is altered is
determined in large part by the state of systemic
vascular function
. Therefore, it is necessary
to examine both cardiac and system vascular
function at the same time.
Interactions between Cardiac
and Systemic Vascular
Function Curves
By themselves, systemic vascular function and
cardiac function curves provide an incomplete
picture of overall cardiovascular dynamics;
however, when coupled together, these curves
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