CHAPTER 2 • ELECTRICAL ACTIVITY OF THE HEART
21
Arrhythmias Caused by Abnormal
Action Potential Generation
ABNORMAL AUTOMATICITY
“Fast response” nonpacemaker action poten-
tials do not ordinarily display automatic-
ity because they are characterized as having
a true resting membrane potential that does
not undergo spontaneous depolarization. If
the fast sodium channels that are responsible
for the rapid depolarization during phase 0
are blocked pharmacologically, or inactivated
by depolarization caused by cellular hypoxia,
the slope and amplitude of phase 0 are sig-
nificantly depressed, and the action potential
appears much like a “slow response” action
potential. The depolarization phase of the
action potential under these conditions is
brought about by slow inward calcium cur-
rents carried through L-type calcium channels.
Furthermore, like SA nodal pacemakers, these
cells may display spontaneous depolarization
during phase 4. This abnormal automaticity
in these transformed “fast response” cells can
result in spontaneous action potential genera-
tion, thereby producing arrhythmias.
TRIGGERED ACTIVITY
A second mechanism that can lead to abnormal
generation of action potentials is called triggered
activity.
Nonpacemaker
cells
may undergo
spontaneous depolarizations either during phase
3 or early in phase 4, triggering abnormal action
potentials. These spontaneous depolarizations
(termed afterdepolarizations), if of sufficient
magnitude, can trigger self-sustaining action
potentials resulting in tachycardia (Fig. 2.8).
Early afterdepolarizations occur during phase
3 and are more likely to occur when action
potential durations are prolonged. Because these
afterdepolarizations occur at a time when fast
Na+ channels are still inactivated, slow inward
Ca++ carries the depolarizing current. Another
type of afterdepolarization, delayed afterdepo-
larization, occurs at the end of phase 3 or early
in phase 4. It, too, can lead to self-sustaining
action potentials and tachycardia. This form of
triggered activity appears to be associated with
elevations in intracellular calcium, as occurs
Early Afterdepolarizations
■ FIGURE 2.8 Early (top panel) and delayed
(bottom panel) afterdepolarizations. If the m agni-
tude of spontaneous depolarization is sufficient, it
can trigger self-sustaining action potentials.
during ischemia, digoxin toxicity, and excessive
catecholamine stimulation.
CONDUCTION OF ACTION
POTENTIALS WITHIN THE HEART
Electrical Conduction within
the Heart
The action potentials generated by the SA node
spread throughout the atria primarily by cell-
to-cell conduction (Fig. 2.9). When a single
■ FIGURE 2.9 Cell-to-cell conduction. Cardiac
cells are connected together by low-resistance
gap junctions between the cells, form ing a
functional syncytium. When one cell depolarizes,
depolarizing currents can pass through the gap
junctions
(redarrow s)
and depolarize adjacent
cells, resulting in a cell-to-cell propagation of
action potentials.
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