CHAPTER 4 ■
CARDIAC FUNCTION
75
FIGURE 4.11 Effects of increasing venous
return on left ventricular
(LV)
pressure-vol-
ume loops. This diagram shows the acute
response to an increase in venous return. It
assumes no cardiac or systemic compensation
and that aortic pressure remains unchanged.
Increased venous return increases end-dias-
tolic volume (
EDV
), but it normally does not
change ESV; therefore, stroke volume (SI/) is
increased.
ESPVR,
end-systolic pressure-volume
relationship.
curves, however, do not show how changes
in venous return affect end-diastolic and
end-systolic volumes. These changes in ven-
tricular volumes are hest illustrated by using
pressure-volume diagrams.
When venous return is increased, increased
filling of the ventricle occurs along its pas-
sive filling curve (Fig. 4.11). This leads to
an increase in
EDV
If the ventricle now con-
tracts at this increased preload, and the aortic
pressure is held constant, the ventricle will
empty to the same
ESy
and therefore,
SV
will
be increased. This is shown as an increase in
the width of the pressure-volume loop. The
ventricle ejects to the same
ESV
because, as
shown in Figure 4.8, increasing preload leads
to a more rapid fiber shortening, and the fiber
shortens to the same minimal length at the end
of contraction. The normal ventricle, there-
fore, is capable of increasing its
SV
to match an
increase in venous return. The increase in the
area within the pressure-volume loop, which
represents the ventricular stroke work, will also
be increased.
PROBLEM 4-2
If the left ventricular output is 60 mL/
beat and the right ventricular SV is only
0.1% greater, by how much would the
pulmonary blood volume increase over
1 hour if the heart rate is 75 beats/min?
Factors Determining Ventricular
Preload
Ventricular filling, and therefore preload of
the right ventricle, is altered by several factors
(Fig. 4.12).
1. Venous Pressure. An increase in venous
blood pressure outside of the right atrium
increases right ventricular preload. This
venous pressure is determined by venous
blood
volume
and
compliance
(see
Chapter 5). For example, reduced venous
compliance brought about by contraction
of the venous smooth muscle increases
venous pressure. Venous blood volume,
particularly in the thoracic (central) com-
partment, is influenced by the total blood
volume (regulated by the kidneys) and
the rate of venous return into the thoracic
compartment.
2. Ventricular Compliance. The compliance
of the ventricle determines the EDV for
any given intraventricular filling pressure.
Therefore, the greater the compliance, the
greater the ventricular filling at a given
filling pressure.
3. Heart Rate. Through its influence on filling
time, heart rate and ventricular filling are
inversely related.
4. Atrial Contraction. At resting heart rates,
atrial contraction normally has only a
small influence on ventricular preload
because most of ventricular filling occurs
passively. An increase in the force of atrial
contraction caused by sympathetic activa-
tion, for example, can significantly enhance
ventricular filling. This becomes especially
important for maintaining preload at high
heart rates when there is less time for dias-
tolic filling of the right ventricle.
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