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Atrial arrhythmias
Mechanisms of arrhythmias
Under certain circumstances cardiac cells in any part of the
heart may take on the role of pacemaker of the heart. Such
a pacemaker is called an ectopic pacemaker (a pacemaker
other than the sinus node). The result can be ectopic beats
or rhythms. These rhythms are identified according to
the location of the ectopic pacemaker (for example, atrial,
junctional, or ventricular). The three basic mechanisms
that are responsible for ectopic beats and rhythms are
altered automaticity, triggered activity, and reentry:
Altered automaticity — Normally the automaticity of the
sinus node exceeds that of all other parts of the conduction
system, allowing it to control the heart rate and rhythm.
Pacemaker cells in other areas of the heart also have the
property of automaticity, including cells in the atria, atrioventricular (AV) junction, and the ventricles. The rates of
these other pacemaker sites are slower. Therefore, they’re
suppressed by the sinus node under normal circumstances.
Because the inherent firing rate of the pacemaker cells of
the sinus node is faster than the other pacemaker sites, it
is the dominant and primary pacemaker of the heart. An
ectopic pacemaker site can take over the role of pacemaker
either because it usurps control from the sinus node by
accelerating its own automaticity (enhanced automaticity)
or because the sinus node relinquishes its role by decreasing its automaticity. Conditions that may predispose
cardiac cells to altered automaticity include myocardial
ischemia or injury, hypoxia, an increase in sympathetic
tone, digitalis toxicity, hypokalemia, and hypocalcemia.
Triggered activity — Triggered activity results from
abnormal electrical impulses that occur during repolarization when cells are normally quiet. The ectopic pacemaker
cells may depolarize more than once after stimulation by
a single electrical impulse. Triggered activity may result in
atrial, junctional, or ventricular beats occurring singly, in
pairs, in runs (3 or more beats), or as a sustained ectopic
rhythm. Causes of triggered activity may include myocardial ischemia or injury, hypoxia, an increase in sympathetic
tone, and digitalis toxicity.
Reentry — Normally an impulse spreads through
the heart only once. With reentry, an impulse can travel
through an area of myocardium, depolarize it, and then
reenter that same area to depolarize it again. Reentry involves a circular movement of the impulse, which
continues as long as it encounters receptive cells. Reentry
(like triggered activity) may result in atrial, junctional, or
ventricular beats occurring singly, in pairs, in runs, or as
a sustained ectopic rhythm. Common causes of reentry
include myocardial ischemia or injury, hyperkalemia, and
the presence of an accessory conduction pathway between
the atria and the ventricles.
Atrial arrhythmias (Figure 7-1) originate from ectopic
sites in the atria. Ectopic P waves from the atrium differ
in morphology (shape) from the normal sinus P waves
(Figure 7-2). For example, in slower atrial rhythms (premature atrial contractions, wandering atrial pacemaker)
the P wave may appear as a small, pointed, and upright
waveform; a small squiggle that is barely visible; or it may
be inverted if the impulse originates from a site in the
lower atrium near the AV junction. In faster atrial rhythms,
the ectopic P wave is either superimposed on the preceding
T wave, appears in a sawtooth pattern (atrial flutter), or is
seen as a wavy baseline (atrial fibrillation).
Some atrial arrhythmias may be associated with rapid
ventricular rates. Increases in heart rate decrease the
length of time spent in diastole. If diastole is shortened,
there is less time for coronary artery perfusion and less
time for adequate ventricular filling. Thus, an excessively
rapid heart rate may lead to myocardial ischemia and may
compromise cardiac output.
Wandering atrial pacemaker
A wandering atrial pacemaker (WAP) (Figure 7-3 and
Box 7-1) occurs when the pacemaker site shifts back and
Box 7-1.
Wandering atrial pacemaker: Identifying ECG
features
Rhythm:
Rate:
Regular or irregular
Usually normal (60 to 100 beats/minute) but may be
slow (< than 60 beats/minute)
P waves:
Vary in size, shape, and direction across rhythm
strip; one P wave precedes each QRS complex
PR interval: Usually normal duration, but may be abnormal
depending on changing pacemaker location
QRS complex: Normal (0.10 second or less)
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Atrial arrhythmias
Figure 7-1. Atrial arrhythmias.
Pointed
T-P wave
Squiggle
Sawtooth
Inverted
Wavy
Figure 7-2. Atrial P waves.
forth between the sinus node and ectopic atrial sites. The
P wave morphology will vary across the rhythm strip as
the pacemaker “wanders” between the multiple sites.
The ectopic P wave may appear as a small, pointed, and
upright waveform; a small squiggle that is barely visible; or
it may be inverted if the impulse originates from a site in
the lower atrium near the AV junction. Generally, at least
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three different P-wave morphologies should be identified
before making the diagnosis of WAP.
The heart rate is usually normal, but may be slow.
The rhythm may be regular or irregular (each impulse
travels through the atria via a slightly different route).
The PR interval is usually normal, but may be abnormal
because of the different sites of impulse formation. The
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Premature atrial contraction
Figure 7-3.
Rhythm:
Rate:
P waves:
PR interval:
QRS complex:
Wandering atrial pacemaker.
Irregular
60 beats/minute
Vary in size, shape, across rhythm strip
0.10 to 0.14 second
0.04 to 0.08 second.
QRS complex is normal in duration. The distinguishing
feature of this rhythm is the changing P-wave morphology
across the rhythm strip.
WAP may be a normal phenomenon seen as a result of
increased vagal effect on the sinoatrial (SA) node, slowing the sinus rate and allowing other pacemaker sites
an opportunity to compete for control of the heart rate.
It can also occur due to enhanced automaticity of atrial
pacemaker cells that usurp pacemaker control from the
SA node. WAP is commonly seen in patients with chronic
obstructive pulmonary disease.
WAP usually isn’t clinically significant, and treatment is
not indicated. If the heart rate is slow, medications should
Figure 7-4.
Rhythm:
Rate:
P waves:
PR interval:
QRS complex:
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be reviewed and discontinued if possible. If the heart rate
is slow and the patient is symptomatic, treatment of the
rhythm is the same as for symptomatic sinus bradycardia.
When WAP is associated with a heart rate greater than
100 beats per minute, the rhythm is called multifocal
atrial tachycardia (MAT) (Figure 7-4). MAT is a relatively
infrequent arrhythmia and is most commonly observed in
patients with severe chronic obstructive pulmonary disease.
Premature atrial contraction
A premature atrial contraction (PAC) (Figures 7-5 through
7-12 and Box 7-2) is an early beat originating from an
Multifocal atrial tachycardia (MAT).
Irregular
140 beats/minute
Vary in size, shape, and direction across rhythm strip
0.10 to 0.14 second
0.04 to 0.08 second.
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