CHAPTER 4 • CARDIAC FUNCTION
73
Resting
Length
A
Increased
Preload
I
D L
B
Time
■ FIGURE 4.8 Effects of increased initial muscle length (increased preload) on muscle shortening
(isotonic contractions). The le ft panel shows a muscle lifting a load (afterload) at tw o different preload
lengths (A and
B).
The rig ht panel shows how increasing the preload leads to increased shortening (DL)
and increased velocity of shortening (dL/dt; change in length w ith respect to time). The muscle shortens
to the same minimal length when preload is increased.
isolated muscles, can be applied to the whole
heart. By substituting ventricular volume for
length and ventricular pressure for tension,
the length-tension relationship becomes a
pressure-volume relationship for the ven-
tricle. This can be done because a quantita-
tive relationship exists between tension and
pressure and between length and volume
that is determined by the geometry of the
ventricle. Figure 4.9 shows that as ventricu-
lar EDV increases, an increase in isovolumet-
■ FIGURE 4.9 Effects of increasing ventricular
volume (preload) on ventricular pressure develop-
ment. Increasing ventricular volume from
a
to
c
and then stim ulating the ventricle to contract
isovolumetrically increases the developed pressure
and the peak-systolic pressure.
ric ventricular pressure development occurs
during
ventricular
contraction,
analogous
to what is observed with a single papillary
muscle (see Fig. 4.7). This can be observed
experimentally in the ventricle by occluding
the aorta during ventricular contraction at
different ventricular volumes and measuring
the peak systolic pressure generated by the
ventricle under this isovolumetric condition.
The peak systolic pressure curve is analogous
to the ESPVR shown in Figure 4.4 because
this is the maximal pressure that can be gen-
erated by the ventricle at a given ventricular
volume.
What
mechanisms
are
responsible
for the increase in force generation with
increased preload in the heart? In the past,
it was thought that changes in active ten-
sion caused by altered preload could be
explained by the overlap of actin and myo-
sin and therefore by a change in the number
of actin and myosin cross bridges formed
(see Chapter 3). However, unlike skeletal
muscle that can operate under a very wide
range of sarcomere lengths (1.3 to 3.5 pm),
the intact heart under physiologic condi-
tions operates within a narrow range of
previous page 86 Cardiovascular Physiology Concepts  2nd Edition read online next page 88 Cardiovascular Physiology Concepts  2nd Edition read online Home Toggle text on/off