64
CARDIOVASCULAR PHYSIOLOGY CONCEPTS
is low, because most of the ventricular filling
occurs before the atria contract. Therefore,
ventricular
filling
is
mostly
passive
and
depends on the venous return. However, at
high heart rates (e.g., during exercise), the
period of diastolic filling is shortened con-
siderably (because overall cycle length is
decreased), and the amount of blood that
enters
the
ventricle
by passive
filling is
reduced. Under these conditions, the relative
contribution of atrial contraction to ventricu-
lar filling increases greatly and may account
for up to 40% of ventricular filling. In addi-
tion, atrial contribution to ventricular fill-
ing is enhanced by an increase in the force
of atrial contraction caused by sympathetic
nerve activation. Enhanced ventricular filling
owing to increased atrial contraction is some-
times referred to as the “atrial kick.” During
atrial fibrillation (see Chapter 2), the con-
tribution of atrial contraction to ventricular
filling is lost. This leads to inadequate ven-
tricular filling, particularly when ventricular
rates increase during physical activity.
After atrial contraction is complete, the atrial
pressure begins to fall, which causes a slight
pressure gradient reversal across the AV valves.
This fall in atrial pressure following the peak
of the a-wave is termed the “x descent.” As the
pressures within the atria fall, the AV valves
float upward (preposition) before closure.
At the end of this phase, which represents
the end of diastole, the ventricles are filled to
their end-diastolic volume (EDV). The left
ventricular EDV (typically about 120 mL)
is associated with end-diastolic pressures
of about 8 mm Hg. The right ventricular
end-diastolic
pressure
is
typically
about
4 mm Hg.
A heart sound is sometimes heard dur-
ing atrial contraction (Fourth Heart Sound,
S4). The sound is caused by vibration of the
ventricular wall as blood rapidly enters the
ventricle during atrial contraction. This sound
generally is noted when the ventricle com-
pliance is reduced (i.e., “stiff” ventricle), as
occurs in ventricular hypertrophy (described
later in this chapter). The sound is com-
monly present in older individuals because of
changes in ventricular compliance.
Phase 2. Isovolumetric
Contraction: All Valves Closed
This phase of the cardiac cycle, which is the
beginning of systole, is initiated by the QRS
complex of the ECG, which represents ven-
tricular depolarization. As the ventricles depo-
larize, myocyte contraction leads to a rapid
increase
in
intraventricular
pressure.
The
abrupt rise in pressure causes the AV valves to
close as the intraventricular pressure exceeds
atrial pressure. Contraction of the papillary
muscles with their attached chordae tendineae
prevents the AV valve leaflets from bulging
back or prolapsing into the atria and becom-
ing incompetent (i.e., “leaky”). Closure of the
AV valves results in the First Heart Sound
(S1). This heart sound is generated when sud-
den closure of the AV valves results in oscil-
lation of the blood, which causes vibrations
(i.e., sound waves) that can be heard with
a stethoscope overlying the heart. The first
heart sound is normally split (~0.04 second)
because mitral valve closure precedes tricus-
pid closure; however, because this very short
time interval normally cannot be perceived
through a stethoscope, only a single sound is
heard.
During the time between the closure of the
AV valves and the opening of the aortic and
pulmonic semilunar valves, ventricular pres-
sures rise rapidly without a change in ventric-
ular volumes (i.e., no ejection of blood into
the aorta or pulmonary artery occurs). Ven-
tricular contraction, therefore, is said to be
“isovolumic” or “isovolumetric” during this
phase. During this phase, some individual fib-
ers shorten when they contract, whereas oth-
ers generate force without shortening or can be
mechanically stretched as they are contracting
because of nearby contracting cells. Ventricu-
lar chamber geometry changes considerably
as the heart becomes more spheroid in shape,
although the volume does not change. Early
in this phase, the rate of pressure develop-
ment becomes maximal. The maximal rate
of pressure development, abbreviated “dP/dt
max,” is the maximal slope of the ventricular
pressure tracing plotted against time during
isovolumetric contraction.
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