80
CARDIOVASCULAR PHYSIOLOGY CONCEPTS
FIGURE 4.18 Effects of changes In afterload
(aortic pressure) on steady-state left ventricular
C
LV)
pressure-volume loops. Increased aortic
pressure (TPAo; solid red loop) decreases stroke
volume (width of loop) and increases end-systolic
volume
(ESV),
whereas decreased aortic pressure
(J-PAo; dashed red loop) increases stroke volume
and decreases end-systolic volume. Preload and
inotropy are held constant in this illustration.
will have the opposite effects—increased SV
and decreased ESV As described later in this
chapter, changes in afterload in a normal,
healthy heart do not affect SV as dramatically
as shown in Figure 4.18 because of compen-
satory changes in preload (EDV).
EFFECTS OF INOTROPY
ON STROKE VOLUME
Effects of Inotropy on Length-
Tension Relationship
Ventricular SV is altered not only by changes
in preload and afterload, hut also by changes
in ventricular inotropy (sometimes referred
to as contractility).
Changes in inotropy are
caused by cellular mechanisms that regulate
CASE 4-2
A 67-year-old male patient is diagnosed with left ventricular failure 4 months following
an acute myocardial infarction. One of the drugs he is given for treatment acts as a
systemic arterial vasodilator. Using Frank-Starling curves and left ventricular pressure-
volume loops, explain how decreasing afterload will improve left ventricular EF.
the interaction between actin and myosin inde-
pendent of changes in sarcomere length
(see
Chapter 3). Therefore, an increase in ino-
tropy augments the force of myocyte contrac-
tion independent of changes in either preload
or afterload, although changes in inotropy
may result in secondary changes in preload
and afterload. For example, if isolated car-
diac muscle is exposed to norepinephrine,
it increases active tension development at
any initial preload length as shown by the
length-tension relationship (Fig. 4.19). This
occurs because the norepinephrine binds to
(31
-adrenoceptors, increasing calcium entry
into the cell and calcium release by the sar-
coplasmic reticulum during contraction (see
Chapter 3). Because the increase in active ten-
sion occurs at a given preload length, the ino-
tropic response exhibits length-independent
activation.
Length
FIGURE 4.19 Effects of increased inotropy on
the length-tension relationship for cardiac muscle.
Increasing inotropy (e.g., by stimulating the cardiac
muscle with norepinephrine) shifts the total tension
curve upward, which increases active tension devel-
opment
(vertical arrows)
at any given preload length.
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