382
Chapter 12
Afterload
An increased arterial pressure tends to reduce stroke volume.
This is because, in analogy to the situation in skeletal muscle,
the arterial pressure constitutes the “load” (technically termed
the
afterload
) for contracting ventricular muscle. The greater
this load, the less the contracting muscle fi bers can shorten at
a given contractility. This factor will not be dealt with further,
because in the normal heart, several inherent adjustments
minimize the overall infl
uence of arterial pressure on stroke
volume. However, in the sections on high blood pressure and
heart failure, we will see that alterations in vascular resistance
and long-term elevations of arterial pressure can weaken the
heart and thereby infl uence stroke volume.
In summary, the two most important physiologic con-
trollers of stroke volume are the Frank-Starling mechanism,
which depends on changes in end-diastolic volume, and ven-
tricular contractility, which is infl uenced by cardiac sympa-
thetic nerves and circulating epinephrine. The contribution of
each of these two mechanisms in specifi c physiological situa-
tions is described in later sections.
Figure 12–28
integrates the factors that determine
stroke volume and heart rate into a summary of the control of
cardiac output.
Measurement of Cardiac Function
Human cardiac output can be measured by a variety of meth-
ods. Moreover, two- and three-dimensional images of the
heart can be obtained throughout the entire cardiac cycle. For
example, in
echocardiography,
ultrasonic waves are beamed
at the heart, and returning echoes are electronically plotted
by computer to produce continuous images of the heart. This
technique can detect the abnormal functioning of cardiac
valves or contractions of the cardiac walls, and can also be
used to measure ejection fraction.
Echocardiography is a noninvasive technique because
everything used remains external to the body. Other visual-
ization techniques are invasive. One,
cardiac angiography,
requires the temporary threading of a thin, fl exible tube called
a catheter through an artery or vein into the heart. A dye is
then injected through the catheter during high-speed x-ray
videography. This technique is useful not only for evaluating
cardiac function, but also for identifying narrowed coronary
arteries.
Cardiac outpu
tH
e
art rate
x
=
Stroke volume
Cardiac muscle
Stroke volume
SA node
Heart rate
Cardiac output
Activity of
parasympathetic
nerves to heart
Plasma
epinephrine
Activity of sympathetic
nerves to heart
End-diastolic
ventricular volume
Begin
Figure 12–28
Major factors determining cardiac output. Reversal of all arrows in
the boxes would illustrate how cardiac output is decreased.
Hypertrophic Cardiomyopathy
Hypertrophic cardiomyopathy
is one of the most common
genetically transmitted cardiac diseases, occurring in one
out of 500 people. As the name implies, it is characterized
by an increase in thickness of the heart muscle, in particular
the interventricular septum and the wall of the left ventricle.
In conjunction with wall thickening, there is a disruption
of the orderly array of myocytes and conducting cells within
the walls. The thickening of the septum interferes with
the ejection of blood through the aortic valve, particularly
during exercise, which can prevent cardiac output from rising
suffi ciently to meet tissue needs. The heart itself is commonly
a victim of this reduction in blood fl ow, and one symptom
that can be an early warning sign is the associated chest pain
(
angina pectoris
).
Moreover, disruption of the conduction
ADDITIONAL CLINICAL EXAMPLES
pathway can lead to dangerous, sometimes fatal arrhythmias.
Many people with this disease have no symptoms, though,
and thus it can go undetected until it has progressed
to an advanced stage. For these reasons, hypertrophic
cardiomyopathy is the leading cause of sudden cardiac death
in young athletes. If it progresses without treatment, it
can lead to
heart failure
(further discussed in Section E).
Although the mechanisms by which this disease process
develops are not completely understood, all of the genetic
mutations that have been found to cause it involve proteins
of the contractile system, including troponin, tropomyosin,
and myosin. Depending on the severity of the condition when
it is discovered, treatments include administering drugs that
prevent arrhythmias, surgical repair of the septum and valve,
or even heart transplantation.
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