C h a p t e r 1 7
Control of Cardiovascular Function
387
delays impulse transmission. A further delay occurs as
the impulse travels through the transitional fibers and
into the AV bundle, also known as the
bundle of His.
This delay provides a mechanical advantage whereby
the atria can complete their ejection of blood before
ventricular contraction begins. Under normal circum-
stances, the AV node provides the only connection
between the atrial and ventricular conduction systems.
The atria and ventricles would beat independently of
each other if the transmission of impulses through the
AV node were blocked.
The
Purkinje system
, which supplies the ventricles,
has large specialized fibers that allow for rapid conduc-
tion and almost instantaneous excitation of both the
right and left ventricles. This rapid rate of conduction
is necessary for the swift and efficient ejection of blood
from the heart. Fibers of the Purkinje system originate in
the AV node and then travel downward in the AV bundle
into the ventricular septum, where they divide to form
the
right
and
left bundle branches
that lie beneath the
endocardium on the two respective sides of the ventricu-
lar septum. The main trunk of the left bundle branch
extends for approximately 1 to 2 cm before fanning out
as it enters the septal area and divides further into two
segments: the
left posterior
and
anterior fascicles.
The AV nodal fibers, when not stimulated, discharge
at an intrinsic rate of 45 to 50 times a minute, and the
Purkinje fibers discharge at 15 to 40 times per minute.
Although the AV node and Purkinje system have the abil-
ity to control the rhythm of the heart, they do not nor-
mally do so because the discharge rate of the SA node is
considerably faster. Each time the SA node discharges, its
impulses are conducted into the AV nodal and Purkinje
fibers, causing them to fire. Should the SA node fail to
discharge, the AV node can assume the pacemaker func-
tion of the heart, and the Purkinje system can assume the
pacemaker function of the ventricles should the AV junc-
tion fail to conduct impulses from the atria to the ven-
tricles. Under these circumstances, the heart rate reflects
the intrinsic firing rate of the prevailing structures.
Action Potentials
An action potential represents the sequential change in
electrical potential that occurs across a cell membrane
when excitation occurs (see Chapter 1, “Understanding
Membrane Potentials”). Action potentials can be divided
into three parts: the
resting
or
unexcited
state during
which the membrane is polarized (positive on the outside
and negative on the inside of the membrane),
depolariza-
tion
or change in the direction of polarity (positive on
the inside and negative on the outside), and
repolariza-
tion
or reestablishment of polarity of the resting mem-
brane potential. The sodium (Na
+
), potassium (K
+
), and
calcium (Ca
++
) ions are the major electrical charge carri-
ers in cardiac muscle cells. Disorders of the ion channels
along with disruption in the flow of these current-carry-
ing ions are increasingly being linked to the generation
of cardiac arrhythmias and conduction disorders.
The action potential of cardiac muscle is divided
into five phases:
phase 0
—the upstroke or rapid depo-
larization;
phase 1
—early repolarization;
phase 2
—the
plateau;
phase 3
—rapid repolarization; and
phase 4
—
the resting membrane potential (Fig. 17-12A). Cardiac
muscle has three types of membrane ion channels that
contribute to the voltage changes that occur during
these phases of the action potential. They are the (1) fast
sodium (Na
+
) channels, (2) slow calcium (Ca
++
) chan-
nels, and (3) potassium (K
+
) channels.
During
phase 0
in atrial and ventricular muscle and
in the Purkinje conduction system, opening of the fast
Na
+
channels for a few ten-thousandths of a second is
responsible for the spikelike onset of the action poten-
tial. The point at which the Na
+
gates open is called the
depolarization threshold.
When the cell has reached this
threshold, a rapid influx of Na
+
to the interior of the cell
membrane causes the membrane potential to shift from
a resting membrane potential of approximately −90 mV
to +20 mV.
Phase 1
occurs at the peak of the action potential and
signifies inactivation of the fast Na
+
channels with an
SA node
AV
node
Bundle of
His
Left
posterior
fascicle
Left
anterior
fascicle
Purkinje
fibers
Right bundle
branch Left bundle
branch
A
B
C
FIGURE 17-11.
Conduction system of the heart
and action potentials.
(A)
Action potential of
sinoatrial (SA) and atrioventricular (AV) nodes.
(B)
Atrial muscle action potential.
(C)
Action
potential of ventricular muscle and Purkinje
fibers.
