Premature Ventricular Complexes (PVCs)
Few cardiac arrhythmias have created as much consternation and confusion,
among both doctors and patients, as premature ventricular complexes
(PVCs). In various doctors’ offices, and at various points in time, PVCs have
been regarded as either harbingers of impending death, or as completely
benign phenomena that require no attention whatsoever.
PVCs are extra electrical impulses arising from one of the cardiac ventricles,
usually the left ventricle.
Normally, the heart rhythm is controlled by electrical impulses arising in the
sinus node portion of the right atrium. These impulses travel across both
atria, then enter the ventricles through the AV node and the His bundle. This
normal pattern of electrical activation causes the atria to contract first,
emptying their blood into the ventricles, and then causes the ventricles to
contract. The normal heart rhythm, then, maintains optimal synchrony
between atria and ventricles.
PVC is caused by a spontaneous electrical impulse arising in the ventricle.
This impulse occurs earlier than the normal impulse would (hence it is
“premature.”) Sometimes the presence of PVCs indicates an inherent
electrical instability in the heart, and therefore indicates an increased risk of
sudden death from its more dangerous cousins, ventricular tachycardia and
ventricular fibrillation. These “dangerous” PVCs are generally limited to
patients with significant underlying heart disease. More often, PVCs do not
indicate any inherent problem with electrical stability, and are completely
benign.
The significance of PVCs –
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In patients with underlying heart disease (such as prior heart attacks
or cardiomyopathy), the presence of many PVCs indicates an
increased risk of sudden death. Sometimes measures must be taken
to reduce that risk, but the measures will not include suppressing the
PVCs themselves.
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While PVCs are fairly common in the general population, they are far
more common (and more frequent) in people with heart disease. Thus,
the presence of PVCs on a routine, screening ECG sometimes
indicates unrecognized cardiac disease.
Tests for Detecting PVCs
Electrocardiogram (ECG or EKG). A record of the electrical activity of the
heart. The types of ECGs are:
--- Resting ECG. The patient lies down for a few minutes while a record is
made. In this type of ECG, disks are attached to the patient's arms and legs
as well as to the chest.
--- Exercise ECG (stress test). The patient exercises either on a treadmill
machine or bicycle while connected to the ECG machine. This test tells
whether exercise causes arrhythmias or makes them worse or whether there
is evidence of inadequate blood flow to the heart muscle ("ischemia").
--- 24-hour ECG (Holter) monitoring. the patient goes about his or her usual
daily activities while wearing a small, portable tape recorder that connects to
the disks on the patient's chest. Over time, this test shows changes in rhythm
(or "ischemia") that may not be detected during a resting or exercise ECG.
--- Transtelephonic monitoring. The patient wears the tape recorder and disks
over a period of several days to several weeks. When the patient feels an
arrhythmia, he or telephones a monitoring station where the record is made. If
access to a telephone is not possible, the patient has the option of activating
the monitor's memory function. Later, when a telephone is accessible, the
patient can transmit the recorded information from the memory to the
monitoring station. Transtelephonic monitoring can reveal arrhythmia that
occur only once every few days or weeks.
Electrophysiologic study (EPS). A test for arrhythmias that involves
catheterization. Very thin, flexible tubes (catheters) are placed in a vein of an
arm or leg and advanced to the right atrium and ventricle. This procedure
allows doctors to find the site and type of arrhythmia and how it responds to
treatment.
PVC characteristics
Since PVCs originate in the ventricle, the normal sequence of ventricular
depolarization is altered, i.e., instead of the two ventricles depolarizing
simultaneously, they depolarize sequentially. In addition, conduction occurs
more slowly through the myocardium than through specialized conduction
pathways. This results in a wide (0.12 second or greater) and bizarreappearing QRS. The sequence of repolarization is also altered, usually
resulting in an ST segment and T wave in a direction opposite to the QRS
complex.
The interval between the previous normal beat and the PVC (the coupling
interval) usually remains constant when PVCs are due to reentry from the
same focus (uniform VCs). When the coupling interval and the QRS
morphology vary, the PVCs may be arising from different areas within the
ventricles, or if the PVCs are arising from a single focus, ventricular
conduction may vary. Such PVCs are referred to as multifocal or more
appropriately, multiformed.
A PVC may occur nearly simultaneously with the firing of the sinus node. The
antegrade impulse originating in the sinus node (resulting in normal atrial
depolarization) and the retrograde impulse traveling toward the atria from the
ventricles may meet in the AV node. Then neither can spread further because
of the other's refractory period. Since the rhythm of the sinus node is
undisturbed, a fully compensatory pause usually results (i.e., the next P wave
should occur at the proper time.) However, on occasion, retrograde
conduction can spread to the atria and reset the SA node.
PVCs may occur as isolated complexes, or they may occur repetitively in
pairs (two PVCs in a row). When three or more PVCs occur in a row, VT is
present. When VT lasts for more than 30 seconds, it is arbitrarily defined as
sustained ventricular tachycardia.
If every other beat is a PVC, ventricular bigeminy is present. If every third beat
is a PVC, the term ventricular trigeminy is used. If every fourth beat is a PVC,
ventricular quadigeminy is present, and so forth.
A PVC that falls on the T wave (during the so-called vulnerable period of
ventricular repolarization) may precipitate VT or VF. However, PVCs occurring
after the T wave may also initiate such VT.
As mentioned above, PVCs may be unifocal (see above), multifocal (see
below) or multiformed. Multifocal PVCs have different sites of origin, which
means their coupling intervals (measured from the previous QRS complexes)
are usually different. Multiformed PVCs usually have the same coupling
intervals (because they originate in the same ectopic site but their conduction
through the ventricles differ. Multiformed PVCs are common in digitalis
intoxication.
PVCs may occur as isolated single events or as couplets, triplets, and salvos
(4-6 PVCs in a row), also called brief ventricular tachycardias.
Simple PVCs
Simple PVCs have the following characteristics:
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Occur beyond the T wave of the preceding QRS complex
Morphology is uniform
Occur in an isolated fashion and do not present in pairs or triplets
Generally exhibit constant coupling intervals with the preceding QRS
complex.
Complex PVCs
Complex ventricular ectopy can be defined as PVCs that:
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Occur in pairs, triplets or more prolonged runs of ventricular
tachycardia
Fall in the vulnerable period of the cardiac cycle
(R on T)
Have more than one morphology
PVCs may occur early in the cycle (R-on-T phenomenon), after the T wave
(as seen above), or late in the cycle - often fusing with the next QRS (fusion
beat). R-on-T PVCs may be especially dangerous in an acute ischemic
situation, because the ventricles may be more vulnerable to ventricular
tachycardia or fibrillation. Examples are seen below.
In the above example, "late" (end-diastolic) PVCs are illustrated with varying
degrees of fusion. For fusion to occur the sinus P wave must have made it to
the ventricles to start the activation sequence, but before ventricular activation
is completed the "late" PVC occurs. The resultant QRS looks a bit like the
normal QRS, and a bit like the PVC; i.e., a fusion QRS.
The events following a PVC are of interest. Usually a PVC is followed by
a complete compensatory pause because the sinus node timing is not
interrupted; one sinus P wave isn't able to reach the ventricles because
they are still refractory from the PVC; the following sinus impulse occurs
on time based on the sinus rate. In contrast, PACs are usually followed
by an incomplete pause because the PAC usually enters the sinus node
and resets its timing; this enables the following sinus P wave to appear
earlier than expected. These concepts are illustrated below.
Not all PVCs are followed by a pause. If a PVC occurs early enough
(especially if the heart rate is slow), it may appear sandwiched in
between two normal beats. This is called an interpolated PVC. The
sinus impulse following the PVC may be conducted with a longer PR
interval because of retrograde concealed conduction by the PVC into
the AV junction slowing subsequent conduction of the sinus impulse.
Finally a PVC may retrogradely capture the atrium, reset the sinus node, and
be followed by an incomplete pause. Often the retrograde P wave can be
seen on the ECG, hiding in the ST-T wave of the PVC.
The most unusual post-PVC event is when retrograde activation of the AV
junction re-enters the ventricles as a ventricular echo. This is illustrated
below. The "ladder" diagram below the ECG helps us understand the
mechanism. The P wave following the PVC is the sinus P wave, but the PR
interval is too short for it to have caused the next QRS. (Remember, the PR
interval following an interpolated PVC is usually longer than normal, not
shorter!).
PVCs usually stick out like "sore thumbs", because they are bizarre in
appearance compared to the normal complexes. However, not all premature
sore thumbs are PVCs. In the example below 2 PACs are seen, #1 with a
normal QRS, and #2 with RBBB aberrancy - which looks like a sore thumb.
The challenge, therefore, is to recognize sore thumbs for what they are,
and that's the purpose of this project!
Summary of ECG criteria
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QRS: Not normal looking. Usually broadened to more than 0.12
second.
Rhythm: Irregular.
P waves: The sinus P wave is usually obscured by the QRS, ST
segment or T wave of the PVC. It may, however, sometimes be
recognized as a notching during the ST segment or T wave.
Retrograde P waves may occur. The presence of a sinus P wave
(when it cannot be seen) may be inferred by the presence of a fully
compensatory pause.