Cardiovascular Physiology
377
20
This force reduction is evidenced by the reduced rate of
blood ejection during the last part of systole.
21
The volume in the aorta, and therefore the pressure,
falls as the rate of blood ejection from the ventricles
becomes slower than the rate at which blood drains out
of the arteries into the tissues.
Early Diastole
The phase of diastole begins as the ventricular muscle relaxes,
and ejection comes to an end.
22
Recall that the T wave of ECG corresponds to the end
of the plateau phase of ventricular action potentials–
that is, to the onset of ventricular repolarization.
23
As the ventricles relax, the ventricular pressure falls
below aortic pressure, which remains signifi cantly
elevated due to the volume of blood that just entered.
24
This change in the pressure gradient forces the
aortic valve to close, and the AV valve also remains
closed because the ventricular pressure is still higher
than atrial pressure. For a brief time, then, all valves
are again closed during this phase of isovolumetric
ventricular relaxation.
25
This phase ends as the rapidly decreasing ventricular
pressure falls below atrial pressure.
26
This change in pressure gradient results in the opening
of the AV valve.
27
Venous blood that had accumulated in the atrium since
the AV valve closed, fl ows rapidly into the ventricles.
28
The rate of blood fl ow is enhanced during this initial
fi lling phase by a rapid drop of ventricular pressure.
This occurs because the ventricle’s previous contraction
compressed the elastic elements of the chamber in such
a way that the ventricle actually tends to recoil outward
once systole is over. This expansion, in turn, lowers
ventricular pressure more rapidly than would otherwise
occur and may even create a negative (subatmospheric)
pressure. Thus, some energy is stored within the
myocardium during contraction, and its release during
the subsequent relaxation aids fi lling.
The fact that most of ventricular fi lling is completed
during early diastole is of great importance. It ensures that
fi lling is not seriously impaired during periods when the
heart is beating very rapidly, and the duration of diastole and
therefore total fi lling time are reduced. However, when rates
of approximately 200 beats/min or more are reached, fi lling
time becomes inadequate, and the volume of blood pumped
during each beat decreases. The clinical signifi cance of this
will be described in Section E.
Early ventricular fi lling also explains why the conduction
defects that eliminate the atria as effective pumps do not seri-
ously impair ventricular fi lling, at least in otherwise normal
individuals at rest. This is true, for example, of
atrial fi
bril-
lation,
a state in which the cells of the atria contract in a com-
pletely uncoordinated manner and so fail to serve as effective
pumps. Thus, the atria may be conveniently viewed as little
more than continuations of the large veins.
Pulmonary Circulation Pressures
The pressure changes in the right ventricle and pulmonary arteries
(
Figure 12–20
) are qualitatively similar to those just described
for the left ventricle and aorta. There are striking quantitative
differences, however. Typical pulmonary artery systolic and dia-
stolic pressures are 25 and 10 mmHg, respectively, compared
to systemic arterial pressures of 120 and 80 mmHg. Thus, the
pulmonary circulation is a low-pressure system, for reasons to
be described later. This difference is clearly refl ected in the ven-
tricular architecture—the right ventricular wall is much thin-
ner than the left. Despite its lower pressure during contraction,
however, the stroke volumes of the two ventricles are identical.
Heart Sounds
Two
heart sounds
resulting from cardiac contraction are nor-
mally heard through a stethoscope placed on the chest wall.
The fi rst sound, a soft low-pitched
lub,
is associated with clo-
sure of the AV valves; the second sound, a louder
dup,
is asso-
ciated with closure of the pulmonary and aortic valves. Note
in Figure 12–19 that the
lub
marks the onset of systole while
the
dup
occurs at the onset of diastole. These sounds, which
result from vibrations caused by the closing valves, are per-
fectly normal, but other sounds, known as
heart murmurs,
can be a sign of heart disease.
Murmurs can be produced by heart defects that cause
blood fl
ow to be turbulent. Normally, blood fl ow through
valves and vessels is
laminar
—that is, it fl ows in smooth con-
centric layers (
Figure 12–21
). Turbulent fl ow can be caused
by blood fl owing rapidly in the usual direction through an
abnormally narrowed valve
(
stenosis
),
by blood fl owing
backward through a damaged, leaky valve
(
insuffi
ciency
),
or by blood fl owing between the two atria or two ventricles
through a small hole in the wall separating them (called a
septal defect
).
The exact timing and location of the murmur provide
the physician with a powerful diagnostic clue. For example, a
1 = Ventricular filling
2 = Isovolumetric ventricular contraction
3 = Ventricular ejection
4 = Isovolumetric ventricular relaxation
50
0
Pressure
(mmHg)
Time
Right ventricular
pressure
4
3
12
1
Pulmonary artery
pressure
Figure 12–20
Pressures in the right ventricle and pulmonary artery during the
cardiac cycle. Note that the absolute pressures are lower than in the
left ventricle and aorta.
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