Page 359 - Cardiac Nursing

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C HAPTER 1 6 / Arrhythmias and Conduction Disturbances 335
hypomagnesemia, hypothermia, high PCO 2 , catecholamines, mental conduction is a normal function of the AV node, delaying
many drugs, and in ventricular hypertrophy and HF. 2,4 Gene mu- the impulse in the AV node long enough for atrial contraction to
tations that alter sodium and potassium ion channel activity and contribute to ventricular filling. Decremental conduction normally
result in prolonged action potential duration have been identified occurs in areas of the heart where resting potentials are low and ac-
and shown to cause EADs. The congenital long QT syndrome tion potentials depend on slow channels, such as the AV and SA
(LQTS) associated with torsades de pointes (TdP), a polymorphic nodes. It can also occur in areas where resting potentials are low
VT (PVT) associated with sudden cardiac death (SCD), has been due to ischemia, disease, or drugs. Under such circumstances, con-
shown to be due to genetic mutations that affect ion channel duction velocity is slow because of the slower rate of rise of the ac-
function and prolong repolarization, thus leading to EAD forma- tion potential that occurs when cells are stimulated at reduced rest-
tion. Triggered activity due to EADs occurs at slow heart rates, ing potentials. At times, decremental conduction can be so
and arrhythmias thought to be due to EAD often occur during pronounced that the impulse fails to conduct, thus leading to
bradycardia or after a pause in rhythm. The proarrhythmic effects block. This failure of conduction can occur in the SA node, lead-
of many drugs, especially class IA and class III antiarrhythmics, ing to sinus exit block; in the AV node, leading to AV block; or in
are due to their ability to prolong repolarization in cardiac cells the bundle-branch system, causing bundle-branch block.
and cause EADs. Clinical arrhythmias thought to be due to EAD Phase 3 Block. When a cell is stimulated during phase 3 of
include both the acquired and congenital types of TdP, and many the action potential, conduction is impaired because the mem-
arrhythmias that occur with hypertrophy and HF.
brane has not yet returned to its resting level. Whenever a cell is
Delayed Afterdepolarizations. DADs occur after the mem- stimulated at a less negative membrane potential, the rate of rise of
brane has repolarized to its original level after an action potential the action potential, and thus conduction velocity, is slow because
but before the next propagated impulse. Subthreshold afterdepo- most sodium channels are inactivated at reduced membrane po-
larizations do not result in triggered activity, but, if the DAD is tentials. Figure 16-3 illustrates phase 3 block occurring in the right
large enough to reach threshold, a triggered impulse arises. This bundle branch, resulting in aberrant conduction of the impulse
triggered impulse may also be followed by its own afterdepolariza- with a right bundle-branch block (RBBB) pattern.
tion, leading to trains of triggered beats. Again, the mechanism dif- Phase 3 block, also called short-cycle aberrancy 11 or tachycar-
3
fers from automaticity in that afterdepolarizations depend on and dia-dependent block, can occur in normal hearts if impulses are
arise as a result of preceding action potentials. DADs occur in as- premature enough to reach fibers during their normal refractory
sociation with increased intracellular calcium levels. There is a di- period, resulting in aberrant conduction of premature beats. It is
rect relation between amplitude of DAD and heart rate: as the also responsible for rate-dependent bundle-branch blocks and for
heart rate increases, so does afterdepolarization amplitude. Thus, the aberration that commonly occurs when cycle lengths are very
triggered activity tends to occur after premature beats or at rapid irregular, as in atrial fibrillation (AF). Phase 3 block can occur
heart rates. Factors that increase DAD amplitude and contribute to pathologically if the refractory period is abnormally prolonged by
triggered arrhythmias include high concentrations of catecholamines drugs or disease.
and digitalis and hypokalemia. 1–4 Clinical arrhythmias that may be
Phase 4 Block. Phase 4 block, also called long-cycle aber-
due to DAD include digitalis toxic rhythms like accelerated junc- 11 3
rancy or bradycardia-dependent block, occurs late in diastole
tional rhythm and AT, idiopathic VT originating in the right ven-
when fibers are stimulated at reduced membrane potentials sec-
tricular outflow tract (RVOT), accelerated idioventricular rhythm af-
ondary to spontaneous phase 4 depolarization. In this case, the
ter MI, and tachycardias originating in the coronary sinus.
membrane has begun to depolarize spontaneously during its nor-
mal phase 4. By the time a stimulus arrives, the resting potential
Abnormal Impulse Conduction has been reduced enough to cause slow conduction. Again, when-
ever a cell is stimulated at a reduced membrane potential, only
Abnormal impulse conduction can result in bradyarrhythmias or
some of the sodium channels are available, and slow conduction re-
aberrancy when impulses are blocked, or premature beats and
sults. Figure 16-4 shows a normal right bundle-branch action po-
tachyarrhythmias when reentrant excitation occurs.
tential followed by spontaneous phase 4 depolarization. By the
time the second impulse arrives in that bundle, membrane poten-
Conduction Block
tial has been reduced enough to cause slow conduction and RBBB.
The electrical impulse can be prevented from propagating through
Phase 4 block is responsible for abnormal conduction that oc-
the heart for a variety of reasons. If the propagating impulse is not
curs only at the end of long cycles or for so-called bradycardia-de-
strong enough to excite the tissue ahead of it, conduction will fail
pendent bundle-branch block. Phase 4 block is uncommon and is
(see section below titled “Decremental Conduction”). If an im-
considered pathologic when it occurs.
pulse arrives at an area where the tissue is still refractory after a pre-
vious depolarization, it will not be able to conduct further (see sec- Reentry
tion below titled “Phase 3 Block”). If an impulse reaches tissue that
Reentry is a type of conduction abnormality that leads to the oc-
is abnormally depolarized due to ischemia, disease, or drugs, it may
currence of premature beats or sustained tachycardias rather than
not be able to conduct at all or will conduct with delay (see section
to a block. Reentry can occur in areas of the heart where conduc-
below titled “Phase 4 Block”). Scar tissue from previous MI, sur-
tion velocity is abnormally slow because of ischemia, electrolyte
gery, or catheter ablation also prevents conduction.
abnormalities, drugs, or disease. Reentry means that an impulse
Decremental Conduction. Decremental conduction is the can travel through an area of myocardium, depolarize it, and then
progressive decrease in conduction velocity of an impulse as it trav- reenter the same area to depolarize it again. For anatomic reentry
els through a region of myocardium and occurs when an action to occur, there must be an area of unidirectional block in which
potential loses its ability to stimulate the tissue ahead of it. Decre- an impulse can conduct in one direction but not in the opposite