CHAPTER 2 • ELECTRICAL ACTIVITY OF THE HEART
23
traveling through the AV node and activating
the ventricle. This is important in atrial flutter
and fibrillation, in which excessively high atrial
rates, if transmitted to the ventricles, can lead
to a very high ventricular rate. This can reduce
cardiac output because of inadequate time for
ventricular filling (see Chapter 4).
Action potentials leaving the AV node
enter the base of the ventricle at the bundle of
His and then follow the left and right bundle
branches along the interventricular septum
that separates the two ventricles. These spe-
cialized bundle branch fibers conduct action
potentials at a high velocity (about 2 m/s).
The bundle branches divide into an exten-
sive system of Purkinje fibers that conduct
the impulses at high velocity (about 4 m/s)
throughout the ventricles. The Purkinje fiber
cells
connect
with
ventricular
myocytes,
which become the final pathway for cell-to-
cell conduction within the ventricles.
The conduction system within the heart is
important because it permits rapid, organized,
near-synchronous depolarization and contrac-
tion of ventricular myocytes, which is essen-
tial to generate pressure efficiently during
ventricular
contraction.
If the
conduction
system becomes damaged or dysfunctional, as
can occur during ischemic conditions or myo-
cardial infarction, this can lead to altered path-
ways of conduction and decreased conduction
velocity within the heart. The functional con-
sequence is that it diminishes the ability of the
ventricles to generate pressure. Furthermore,
damage to the conducting system can precipi-
tate arrhythmias as described later.
Regulation of Conduction
Velocity
The rate of cell-to-cell conduction is deter-
mined by several intrinsic and extrinsic fac-
tors. Intrinsic factors include the electrical
resistance between cells and the nature of the
action potential, particularly in the initial rate
of depolarization (phase 0). As discussed ear-
lier in this chapter, fast sodium channels are
responsible for the rapid upstroke velocity of
nonpacemaker action potentials. Increasing
the number of activated fast sodium chan-
nels increases the rate of depolarization. The
more rapidly one cell depolarizes, the more
quickly an adjoining cell depolarizes. There-
fore, conditions that decrease the availability
of fast sodium channels (e.g., depolarization
caused by cellular hypoxia), decrease the rate
and magnitude of phase 0, thereby decreas-
ing conduction velocity within the heart. In
AV nodal tissue in which slow inward calcium
primarily determines phase 0 of the action
potential, alterations in calcium conductance
alter the rate of depolarization and therefore
the rate of conduction between AV nodal cells.
Extrinsic factors can influence conduction
velocity, including autonomic nerves, circulat-
ing hormones (particularly catecholamines),
and various drugs (Table 2-3). Autonomic nerve
activity significantly influences the conduction
of electrical impulses throughout the heart, par-
ticularly in the specialized conduction system.
An increase in sympathetic firing (or increased
circulating catecholamines) increases conduc-
tion velocity via norepinephrine binding to
P1-adrenoceptors. The activation of parasym-
pathetic (vagal) nerves decreases conduction
velocity via the action of acetylcholine on M2
receptors. This is most prominent at the AV
node, which has a high degree of vagal inner-
vation. The signal transduction mechanisms
coupled to P1-adrenoceptors and M2 receptors
(Gs- and Gi-proteins) are the same as described
in Chapter 3 (see Fig. 3.6) for the regulation
of cardiac contraction. A number of drugs can
TABLE 2-3
EXTRINSIC FACTORS
INCREASING OR DECREASING
CONDUCTION VELOCITY
WITHIN THE HEART
IN C R E A S IN G
( d e c r e a s in g
Sympathetic
stimulation
Parasympathetic
stimulation
Muscarinic recep-
tor antagonists
Muscarinic receptor
agonists
b-Adrenoceptor
agonists
b-Blockers
Circulating
catecholamines
Ischemia/hypoxia
Hyperthyroidism
Sodium and calcium
channel blockers
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