affect conduction velocity by altering autonomic
influences or direcdy altering intercellular con-
duction. For example, antiarrhythmic drugs that
block fast sodium channels decrease conduction
velocity in nonnodal tissue; digoxin activates
vagal influences on the conduction system, par-
ticularly at the AV node; and fi-adrenoceptor
agonists or antagonists can increase or decrease
conduction velocity, respectively.
A drug is found to partially inactivate
fast sodium channels. How would this
drug alter the action potential in a
ventricular myocyte? How would the
drug alter conduction velocity within the
Abnormal Conduction
When electrical activation of the heart does
not follow the normal pathways outlined ear-
lier, the efficiency of ventricular contraction
may be reduced, and arrhythmias may be pre-
cipitated. For example, if the AV node becomes
completely blocked by ischemic damage or
excessive vagal stimulation, impulses cannot
travel from the atria into the ventricles. For-
tunately, latent pacemakers within the ven-
tricular conduction system usually take over
to activate the ventricles; however, the lower
firing rate of these pacemakers results in ven-
tricular bradycardia and decreased cardiac
output. As another example, if one of the
bundle branches is blocked, ventricular depo-
larization still occurs, but the depolarization
pathways will be altered, leading to a delay in
ventricular activation and reduced contraction
efficiency. An ectopic beat originating within
the ventricle can cause altered pathways of
conduction as well. When this occurs outside
of the normal fast conducting system, it alters
the pathway of depolarization, and ventricular
depolarization has to rely on the relatively slow
cell-to-cell conduction between myocytes.
Tachycardia Caused by Reentry
Reentry is an important mechanism in the gen-
eration of tachycardias. Reentry occurs when a
conducting pathway is stimulated prematurely
by a previously conducted action potential,
leading to a rapid, cyclical reactivation as
described in Figure 2.11. In this illustration,
if a single Purkinje fiber forms two branches
(1 and 2), the action potential will divide and
travel down each branch (left panel). If these
branches then come together into a common
branch (3), the action potentials will cancel
each other out, and reentry will not occur. An
electrode (*) recording from branch 3 would
record single, normal action potentials as they
are conducted in this branch.
To model what occurs during reentry, sup-
pose that branch 2 (right panel) has a unidi-
rectional block (impulses can travel retrograde
but not orthograde) caused by partial depo-
larization. An action potential traveling down
branch 1, after entering the common distal
path (branch 3), travels in retrograde fashion
through the unidirectional block in branch 2.
Within the block, the conduction velocity is
reduced because the tissue is depolarized. As
the action potential exits the block, if it finds
the tissue excitable (i.e., beyond the refrac-
tory period), then the action potential will
once again be conducted down branch 1 (i.e.,
reenter branch 1). If the action potential exits
the block more rapidly and finds the tissue
unexcitable (i.e., within its refractory period),
then the action potential will cease to propa-
FIGURE 2.11 Mechanism of reentry. With normal
conduction of action potentials, impulses traveling
down branches 1 and 2 cancel out each other in
branch 3. Reentry can occur if branch 2 has impaired
conduction and blocks orthograde impulses, but
slowly conducts retrograde impulses. If a retrograde
impulse emerging from branch 2 reaches excitable
tissue (after the ERP, but before the next normal
impulse), a premature action potential can be con-
ducted down branch 1. If this occurs with successive
action potentials, tachycardia occurs.
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