Cardiovascular Physiology
379
stimulation increases the slope of the pacemaker potential by
increasing the F-type channel permeability. Because the main
current through these channels is sodium entering the cell,
faster depolarization results. This causes the SA node cells to
reach threshold more rapidly and the heart rate to increase.
Stimulation of the parasympathetics has the opposite
effect—the slope of the pacemaker potential decreases due to
a reduction in the inward current. Threshold is thus reached
more slowly, and heart rate decreases. Parasympathetic stim-
ulation also hyperpolarizes the plasma membranes of SA
node cells by increasing their permeability to potassium. The
pacemaker potential thus starts from a more negative value
(closer to the potassium equilibrium potential) and has a
reduced slope.
Factors other than the cardiac nerves can also alter heart
rate. Epinephrine, the main hormone liberated from the adrenal
medulla, speeds the heart by acting on the same beta-adrenergic
receptors in the SA node as norepinephrine released from neu-
rons. The heart rate is also sensitive to changes in body tempera-
ture, plasma electrolyte concentrations, hormones other than
epinephrine, and a metabolite—adenosine—produced by myo-
cardial cells. These factors are normally of lesser importance,
however, than the cardiac nerves.
Figure 12–23
summarizes
the major determinants of heart rate.
As stated in the previous section on innervation, sym-
pathetic and parasympathetic neurons innervate not only the
SA node but other parts of the conducting system as well.
Sympathetic stimulation increases conduction velocity through
the entire cardiac conducting system, whereas parasympathetic
stimulation decreases the rate of spread of excitation through
the atria and the AV node.
Control of Stroke Volume
The second variable that determines cardiac output is stroke
volume—the volume of blood each ventricle ejects during
each contraction. Recall that the ventricles do not completely
empty themselves during contraction. Therefore, a more force-
ful contraction can produce an increase in stroke volume by
causing greater emptying. Changes in the stroke volume can
be produced by a variety of factors, but three are dominant
under most physiological and pathophysiological conditions:
(1) changes in the end-diastolic volume (the volume of blood
in the ventricles just before contraction, sometimes referred
to as the
preload
); (2) changes in the magnitude of sympa-
thetic nervous system input to the ventricles; and (3) changes
in
afterload
(i.e., the arterial pressures against which the ven-
tricles pump).
Relationship Between Ventricular End-
Diastolic Volume and Stroke Volume:
The Frank-Starling Mechanism
The mechanical properties of cardiac muscle form the basis
for an inherent mechanism for altering stroke volume: The
ventricle contracts more forcefully during systole when it has
been fi lled to a greater degree during diastole. In other words,
all other factors being equal, the stroke volume increases as
the end-diastolic volume increases. This is illustrated graphi-
cally as a
ventricular function curve
(
Figure 12–24
). This
relationship between stroke volume and end-diastolic volume
is known as the
Frank-Starling mechanism
(also called
Starling’s law of the heart) in recognition of the two physiolo-
gists who identifi ed it.
What accounts for the Frank-Starling mechanism?
Basically it is simply a length-tension relationship, as described
for skeletal muscle in Chapter 9, because end-diastolic volume
is a major determinant of how stretched the ventricular sarco-
meres are just before contraction. Thus, the greater the end-
diastolic volume, the greater the stretch, and the more forceful
the contraction. However, a comparison of Figure 12–24 with
Figure 9–21 reveals an important difference between the
length-tension relationship in skeletal and cardiac muscle. The
normal point for cardiac muscle in a resting individual is not
at its optimal length for contraction, as it is for most resting
skeletal muscles, but is on the rising phase of the curve. For
this reason, greater fi lling causes additional stretching of the
cardiac muscle fi bers and increases the force of contraction.
SA node
Heart rate
Plasma epinephrine
Activity of
sympathetic
nerves to heart
Activity of
parasympathetic
nerves to heart
Figure 12–23
Major factors infl uencing heart rate. All effects are exerted upon the
SA node. The fi gure shows how heart rate is increased; reversal of all
the arrows in the boxes would illustrate how heart rate is decreased.
Figure 12–24
A ventricular function curve, which expresses the relationship
between end-diastolic ventricular volume and stroke volume (the
Frank-Starling mechanism). The horizontal axis could have been
labeled “sarcomere length,” and the vertical “contractile force.” In
other words, this is a length-tension curve, analogous to that for
skeletal muscle (see Figure 9–21). At very high volumes, force (and
thus stroke volume) declines as in skeletal muscle (not shown).
400
300
200
100
0
Ventricular end-diastolic volume (ml)
Normal
resting
value
Increased
stroke
volume
Increased
venous return
100
200
Stroke volume (ml)
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