Clin. Cardiol.
12, 586-599 (1989)
Electrophysiology, Pacing, and Arrhythmia
Ventricular Tachycardia
J. A. KASTOR, M.D.
Department of Medicine,University of Maryland School of Medicine, Baltimore, Maryland, USA
Introduction
Ventricular tachycardia (VT), the abnormal, rapid heart
rhythm that originates in the ventricles, has been studied
more intensively in the past 10 years than probably any
other cardiac arrhythmia. As a result, we are now able
to categorize VT more precisely, identify it more easily,
and mat it moxe successfullythan was previously possible.
Key words: ventricular tachycardia, bidirectional
tachycardia, accelerated idioventricular rhythm, cardiac
electmphysiology, antiamhythmic drugs, antiarrhythmic
surgery, automatic implantable cardioverter defibrillator
Electrocardiographic Recognition
VT is conventionally recognized in the electrocardio-
gram as a regular tachycardia of three or more beats at
a rate greater than 100 per minute with QRS complexes
of 120 ms or greater. Why a sequence of three beats in-a-
row, rather than 2, 4,or more? Why a rate greater than
100 beats per minute? W h y a QRS width of 120 ms or
more? These criteria have no sacred value but have be-
come associated with the diagnosis over the years. They
seem to describe most cases of what we have chosen to
define as VT.
Address for reprints:
John A. Kastor, M.D.
University of Maryland Hospital
22 South Greene Street
Baltimore, MD 21201, USA
Received: May 22, 1989
Accepted: June 1, 1989
Types of VT
The currently accepted classification of VT has been
derived from the appearance of the arrhythmta in the elec-
trocardiogram.
Monomorphic VT
Most ventricular tachycardias are monomorphic, which
means that most of the QRS complexes have the same
form. Monomorphic VT is usually divided into three types
based on the duration of the episodes: (1) recurrent sus-
tained, (2) transient or nonsustained, and (3) repetitive.
Recurrent sustained Ventriculartachycardia is the form
which most physicians recognize as typical of VT. It is
characterized by a relatively long sequence of monomorph-
ic ventricular beats which ru~lsfor at least 30 seconds (Fig.
1). Reentry within abnormal ventricular tissue or occa-
sionally within the bundle branches (6% in one series) is
the usual mechanism of recurrent sustained VT. As is
characteristic of clinical reentrant arrhythmias, this form
of VT can be started by programmed stimulation of the
ventricles with 1,2, or 3 premature beats and stopped by
premature beats or rapid stimulation.
In the United States, most patients with recurrent sus-
tained VT have coronary artery disease and acute or healed
myocardial infarctions. Many frequently have ventricu-
lar aneurysms, at the borders of which regions of slow
conduction in partly damaged endocardium form the sub-
strate in which reentry develops. VT also develops in pa-
tients with valvular heart disease and in patients with cardi-
omyopathy, including an unusual, localized variety called
right ventricular dysplasia. VT in patients with cardi-
omyopathy is sustained by bundle-branch reentry in a third
of cases. Occasionally, VT appears in patients without
demonstrable heart disease other than the electrical dis-
turbance.
Transient or nonsustained ventricular tachycardia is a
particularly common form of VT which is frequently en-
countered in healthy people who require no specific treat-
ment (Fig. 2). Transient VT is usually defined as a mono-
morphic tachycardia with wide QRS complexes, the
 J. A. Kastor: Ventricular tachycardia
FIG. 1 Recurrent sustained ventricular tachycardia. A typical ex-
ample with the pattern of right bundle branch block in which the
first positive deflection is taller than the second in lead V,.
paroxysms of which last less than 30 seconds. Many epi-
sodes include no more than 10 beats. As in sustained VT,
the transient form usually occurs in patients with coro-
nary artery disease and cardiomyopathyas well as in those
with no obvious heart disease. Patients with mitral valve
prolapse are sometimes afflicted with transient VT and
occasionally with sustained VT .
Repetitive monomorphic VT is a relatively unusual type
of VT in which short paroxysms of monomorphic
tachycardia occur among periods of sinus rhythm and ven-
tricular premature beats having the same form as the VT.
Patients with repetitive VT frequently have no structural
heart disease and, as one might expect, a good progno-
sis. Ventricular function is well preserved in most of the
patients. Even those with coronary artery disease have
relatively little myocardial damage or ventricular
aneurysms.
The mechanism of repetitive monomorphic VT is not
certain. Patients have features that are characteristic of
FIG.2 Transient (nonsustained) ventricular tachycardia from a
Holter monitor recording of an asymptomatic patient. From Am J
Cardiol 24, 637 (1969) with permission.
5 87
reentry, but also of one or another of the different types
of automaticity. In one report the investigatorscould eas-
ily induce VT by raising the heart rate through rapid atri-
al or ventricular pacing, by exercise or upon administra-
tion of isopmterenol. Furthermore, patients with repetitive
VT may respond relatively well to beta-blocking drugs
or very easily to type I antiarrhythmicagents such as dis-
opyramide, flecainide, quinidine, or pwainamide. These
are not characteristic features of VT in most patients whose
arrhythmia is sustained by reentry.
Polymorphic Ventricular Tachycardia
Some VTs are characterized by wide QRS complexes
whose form changes beat to beat or within gmups of beats.
Torsades de pointes describes in French words the
salient electrocardiographic feature of this form of VT-
wide QRS complexes of continually changing size twist-
ing around the isoelectric baseline (Fig. 3). The phrase
was first used to describe this arrhythmia in patients with
severe bradycardia due to complete heart block. Subse-
quently, clinical investigators observed the tachyarrhyth-
mia in patients whose Q-T intervals in sinus rhythm were
longer than normal. (Part of the long Q-T interval may
actually consist of a large U wave at the end of the T
wave.) Thus, in a few patients, an abnormality in repolar-
ization, the electrophysiological process which transpires
during the Q-T interval and U wave, can give rise by some
manner as yet undefined to torsades de pointes.
Cextain drugs given for both cardiac and noncardiac Con-
ditions can produce the arrhythma, particularly when they
are administered to patients with severe myocardial dis-
ease (Table I). Patients with torsades may have hypokale-
mia or hypomagnesemia or one of the congenital long QT
interval syndromes which may be associated with other
abnormalities such as deafness. A tachycardia with the
same characteristic electrocardiographic features has also
been described in some patients with normal Q-T inter-
vals and severe myocardial disease often from old my-
ocardial infarctions.
Does torsades de pointes define an arrhythmia or a syn-
drome? Both answers have adherents, but I prefer to use
the phrase to describe the electrocardiographic finding.
TABLEI Some of the drugs which have been observed to in-
duce torsades de pointes
Amiodarone
Phenothiazine drugs, particularly Thiondizine
Sotolol
Tricyclic antidepressants
Type IA antiarrhythmic agents
Disopyramide
Procainamide
Quinidine
588 Clin. Cardiol. Vol. 12, October 1989

The words torsades de pointes tell us what the arrhyth- Diagnosis

mia looks like, rather than the setting in which it occurs.
Most tachycardias with wide QRS complexes can be
Bidirectional Tachycardia. One recognizes this unusual diagnosed from the history, the physical examination, and
arrhythmia by its characteristic alternation of the QRS the appearance of electrocardiograms taken during both
complexes (Fig. 4). Usually the QRS complexes look like the arrhythmia and sinus rhythm. Only occasionally are
right bundle-branch block, and the bidirectional appear- intracardiac recordings needed to differentiatebetween VT
ance is due to alternating right- and left-axis deviation in and supraventricular tachycardia (SVT) with bundle-
the frontal plane. Frequently this appearance will only be branch block or antegrade conduction over an anomalous
seen in a few of the electrocardiographic leads. pathway or bypass tract as in the Wolff-Parkinson-White
Bidirectional tachycardia has usually been reported in syndrome.
patients with severe myocardial disease who a~ toxic from
overdoses of digitalis. Their mortality is high. Patients
not taking digitalis and even people with otherwise nor- Clinical Information
mal hearts may occasionally develop the arrhythmia.
From the earliest descriptions, investigators have specu- When a middle-aged or elderly patient presents with a
lated about the mechanism of bidirectional tachycardia. wide QRS complex tachycardia, the diagnosis is most like-
A once popular hypothesis suggested that the tachycardia ly to be ventricular tachycardia, particularly when there
originated in the atrioventricular (AV) junction with al- is a history of a previous myocardial infarction. Recur-
ternating bundle-branch block producing the characteris- rent SVT tends to afflict younger patients since
tic appearance. More recently, intracardiac recordings
have revealed that bidirectional tachycardia starts in the
ventricles in almost all cases. The bidirectional form is
probably produced by different routes of ventricular acti-
vation from the site of origin. However, the cause for the
two morphologieshas not been experimentally established. Lead 2
Furthermore, in those few cases of bidirectional
tachycardia fully studied in the electrophysiologylabora-
tories the mechanism of the arrhythmia-reentry or
automaticity-has not been defined.

Accelerated Idioventricular Rhythm (IVR)

Although not usually a tachycardia-the most common

rates range from 60 to 110 beatdmin-idioventricular
rhythm deserves to be mentioned in a review of VT since
continuous ,
the arrhythmia is sometimes called “slow ventricular
tachycardia” (Fig. 5). IVR is probably an automatic ven-
tricular rhythm and, accordingly, tends to accelerate and
decelerate gradually and not be inducible or suppressible
by programmed ventricular stimulation. Idioventricular FIG.5 Idioventricular rhythm, a “slow VT” in a patient with an
rhythm is most often seen during acute myocardial infarc- inferior myocardial infarction. The last three beats in the top panel
tion or in patients with digitalis intoxication. The prog- and the first two beats in the bottom panel are ventricular. The third
nosis is usually favorable. complex on both the top and bottom strips are fusion beats.
 J. A. Kastor: Ventricular tachycardia
tachycardias associated with AV nodal reentry or
anomalous pathways usually cause symptoms before the
typical age for chronic coronary artery disease. Of course,
such generalizations are not always correct but may be
helpful in leading one toward the right diagnosis.
Physical Examination
General examination of the patient with a wide QRS
complex tachycardia will indicate how rapidly the physi-
cian must institute treatment. Some patients may be se-
verely ill while others can be asymptomatic except for the
awareness of rapid heart action.
The degree of disability relates most closely to the heart
rate and the condition of the myocardium and/or the cardi-
ac valves. In general, the faster the rate, the worse the
symptoms. Although rapid heart rates, of over 200
beats/min for example, may be reasonably well tolerated
if the ventricles and valves are otherwise normal, a pa-
tient with poor myocardial function due to previous my-
ocardial infarctions or cardiomyopathy may become dan-
gerously ill with a relatively slow ventricular tachycardia
of only 120 beatslmin. Therefore, before deliberating long
on the details of the electrocardiogram, the examiner
should search for signs of hypotension, congestive failure,
cerebral hypoxia, or myocardial ischemia. In the presence
of any of these findings, rapid conversion to sinus rhythm,
possibly with cardioversion, is indicated regardless of the
type of tachycardia.
If the patient is comfortable and hemodynamically sta-
ble, time may be devoted to analyzing the arrhythmia be-
fore definitive treatment is administered. Here the cardi-
ovascular physical examination can be quite revealing.
Atrioventricular (AV) dissociation is present in half the
cases of VT but is absent in supraventriculartachycardia
with abberancy. AV dissociation is produced when the
ventricles and the atria beat independently of each other.
TL
VT with 1:1 VA
A
Conduction
A A
FIG.6 Atrioventricular relationships in VT. In the recording to the left, each ventricular beat of VT in lead V , is conducted to the atria
producing a constant relationship between the QRS complex and the retrograde P wave (Pr) in the surface tracing and A wave in the high
right atrial (HRA) tracing. In the example on the right, AV dissociation is present. There is no temporal relationship between the QRS
complexes and the sinus P waves (P, in lead V,) and A waves in the high right atrial recording. From N Engl J Med 304, 1007 (1981)
with permission.
589
This changing relationship between the time of contrac-
tion of the chambers can produce varying levels of sys-
tolic blood pressure, different intensity of the first heart
sound and of heart murmurs and intermittent large can-
non A waves in the neck veins produced by the right atri-
um’s contraction against the closed tricuspid valve.
Electrocardiographic Recognition
We consider several characteristicsof the electrocardi-
ogram in making the diagnosis of VT: the duration of the
QRS complex, the relationship of the P wave to the QRS
complex, the axis deviation, concordance and the form
or morphology of the individual QRS complexes. Features
which are less helpful include the rate and regularity of
the arrhythmia and fusion beats.
Duration of the QRS Complex. Although VT is con-
ventionally recognized by QRS complexes of at least 120
ms, ventricular activation in a few cases may have a short-
er duration. These arrhythmias, often called fascicular
rhythms, are presumed to originate in or near the prox-
imal bundle branches. They prolong ventricular activa-
tion relatively little and consequently produce a QRS pat-
tern which is almost normal. Some VTs due to digitalis
intoxication have such relatively short QRS complexes.
Tachycardias with QRS complexes of greater than 140
ms almost always originate in the ventricles. Consequent-
ly, one has the most difficulty diagnosing arrhythmias with
QRS widths between 120 and 140 ms.
P-QRS Relationships. Most of us have been taught that
AV dissociation characterizes VT. “Cherchez le P,” we
were advised (Fig. 6). Finding the electrocardiographic
manifestation of atrial activation may indeed be helpful
when it is possible, but even when the P waves can be
seen, an incorrect diagnosis may be made.
HRA
HBE
TL
- VT without VA
A
‘V
I
\
Conduction
IV V
590 Clin. Cardiol. Vol. 12, October 1989

When the ventricles are driven by a source within them-

selves, the atria may continue to contract under control
of the sinus node. When this occurs, complete AV dis-
sociation results. The physical signs of this electrical
phenomenon have already been described. In the elec-
trocardiogram one may see P waves “marching through,”
unrelated to the QRS complexes.
Recognizing P waves may not always be possible,
however. At faster ventricular rates, the P waves with their
characteristic low amplitude may be invisible among the
large QRS complexes and T waves. This is particularly
distressing since, in general, AV dissociation is more like-
ly to develop when the heart rate is rapid.
In many cases of VT, the ventricular rhythm may con-
trol the atria, either completely or intermittently. This is
caused by ventriculoatrial (VA) conduction in which the
electrical impulse from the ventricles, traveling retrograde
up the conduction system and through the AV node, drives
the atria and suppresses the pacemaking activity of the
sinus node. Retrograde activation of the atria produces in-
verted P waves in leads 2,3, and aVF. However, the mor-
FIG.7 Concordance. All the beats of VT in leads V , to V, have
phology of the P waves may not always be recognizable a similar appearance. This finding is known as concordance and
in VT, thus often making difficult the diagnosis of retro- appears in some examples of VT. From Wellens HJJ and Culbert-
grade conduction. US HE: What’sNew in Electrocardiography, Boston: Maltinus Nij-
The AV node characteristically slows conduction in the hoff (1981) 193, with permission.
antegrade direction in sinus rhythm and in the retrograde
direction in VT. Therefore, in VT, some of the ventricu-
lar beats may be blocked in the AV node or elsewhere
in the conduction system. When this happens, all the P activation. However, unlike in true bundle-branch block,
waves do not follow the QRS complexes. The P-P inter- the QRS pattern is not produced by a beat which enters
vals, when they can be seen, may, consequently, not be the AV node from the atria and is then transmitted with
regular even when some VA conduction is present. depressed conduction through one or both of the bundle
In a series of patients with VT studied with intracardi- branches.
ac recordings, 1:l VA conduction occurred in 34%, in- The right bundle-branch block form is the more com-
complete VA conduction in 18%, and no VA conduction mon morphology for QRS complexes in VT. It is usually
(AV dissociation) in 48%. produced by VT which begins in the left ventricle or the
interventricular septum.
Axis Deviation. The majority of patients with VT have The following findings in lead V, favor VT over SVT
left axis deviation in their 12-leadelectrocardiograms.This with right bundle-branch block:
finding appears more commonly when the form of the VT
is similar to right bundle-branch block (74% in one ser- The QRS complex has a monophasic, wide R wave;
ies) than when the VT looks like left bundle-branch block The QRS complex is biphasic (qR, QR, or RS pattern)
(59% in the same series). Left-axis deviation appears in- with the larger positive deflection inscribed first (Rr’ );
frequently in supraventricular tachycardia with aberran- A q wave starts the QRS complex.
cy; 3% with right bundle-branch block, 13% with left
bundle-branch block. Lead V6 also provides clues favoring VT:
The R wave, if present, is shorter than the R wave in V1;
Concordance. Occasionally during a tachycardia the The S wave which terminates the QRS complex is deep
form of the QRS complex may appear almost the same, and relatively thin.
either upright or inverted, in several leads. This concor-
dant pattern, usually best seen in leads vI to v6, strongly SVT with right bundle-branch block is more likely i f
suggests VT (Fig. 7). In lead VI, the QRS complex is triphasic, and the larger
positive deflection is inscribed second (rR’ or rsR’);
Form of the Individual QRS Complexes. Intraventncu- The R wave in lead V6 is larger than the R wave in V1;
lar conduction is always abnormal in VT since the ventri- The S wave is v6 is shallow and wide.
cles are depolarized from an ectopic site. As a result, the
beats during VT usually have a form which simulates bun- The left bundle-branch block pattern, which occurs less
dle branch blocks, another cause of abnormal ventricular frequently than the right bundle-branch block pattern dur-
 J. A. Kastor: Ventricular tachycardia
ing VT, can be produced when the arrhythmia starts in
the interventricular septum or the left ventricle in patients
with chronic coronary artery disease. In patients with
otherwise normal hearts, VT with this form may originate
in the right ventricle. VT sustained through bundle-branch
reentry usually has the appearance of left bundle-branch
block (87% in one series).
The following favor VT over SVT with left bundle-
branch block:
In lead VI, the width of the r wave in patients with rS
patterns is 240 ms during the arrhythmia and tends
to be taller and wider than in the same patient during
sinus rhythm (Fig. 8);
In lead V,, a qR or QS pattern is present.
In SVT with left bundle-branch block:
In lead V I ,the duration of the r wave is <40 ms (Fig. 8);
In lead V6, the q wave is absent because of the reversed
(right to left) septal activation characteristic of left
bundle-branch block.
FIG.8 Form ofthe QRS complex. In patients whose VT has the
form of left bundle-branch block, the r wave during VT is usually
wider and taller than the r wave in sinus rhythm (first two beats)
in lead V , . This recording also illustrates how VT characteristical-
ly begins spontaneously (in beat 3) after a relatively long interval
from the previous sinus beat. From Wellens HJJ and Culbems HE:
What's New in Electrocardiography, Boston: Martinus Nijhoff
(1981) 193, with permission.
NSR VT
TL
FIG 9 Fusion beats. In this illustration the His bundle electrograms of a sinus, a ventricular, and a fusion beat are shown. In the fusion
beat, the ventricle begins to be activated from the VT beat before the bundle of His has been depolarized from the sinus beat. From N
En& J Med 304, 1005 (1981) with permission.
59 1
Fusion beats are a well-known feature of VT. They are
formed when a beat of ventricular origin appears at about
the same time as a beat conducted from the atria (Fig.
9). The morphology of fusion beats is produced by the
activation of the ventricles from both sources.
Fusion beats are commonly produced during idioven-
tricular rhythm or during slow VT. However, they are sel-
dom seen when VT is rapid, which is more frequently the
case.
The average ventricular rate of VT is slightly slower
than that of SVT with abberancy. However, so much over-
lap exists that rates cannot be used as useful criteria in
making the diagnosis.
Slight irregularity of the rhythm has been described as
characteristic of VT. Recent studies have shown that this
feature is not particularly helpful in differentiating VT
from SVT.
Clinical Electrophysiology
Much of our current knowledge of VT has been der-
ived from studies in the clinical electrophysiology labora-
tory. In this review, those features with the greatest
relevance to clinical management will be discussed.
Recognition
In most electrophysiologicalstudies of patients with VT,
electrode catheters are inserted to record signals from the
right atrium, right ventricle, and bundle of His. Three
deflections are characteristically recorded from the His
bundle electrode during sinus rhythm: (1) an A wave from
atrial activation, (2) a V wave from electrical depolariza-
tion of the ventricles, (3) a relatively low-amplitude H
deflection which appears between the A and V waves and
is produced by forward (antegrade) conduction through
the bundle of His.
The A-H interval, normally 60-140 ms, indicates the
time from atrial to His bundle activation. The H-V inter-
val shows the time from depolarization of the bundle of
Fusion
592 Clin. Cardiol. Vol. 12, October 1989

SVT VT

HBE

FIG.10 His bundle elecrrogram in SVT with right bundle-branch block abberancy (left) and VT. Notice that in SVT an H deflection pre-
cedes each QRS complex, whereas in VT the H deflection is absent. The QRS complexes in the right example are typical of VT with left
axis deviation and one broad positive deflection in lead V , . From N Engl J Med 304, 1005 (1981) with permission.

His to the beginning of ventricular activation; the normal VT

H-V interval is 35-55 ms.
During VT the bundle of His may be activated retro-
gradely from the ventricles where the arrhythmia originates
(Fig. 10). H deflections (designated H’ during retrograde
conduction) are buried within the V waves and are sel-
dom visible. In bundle-branch reentrant VT, however,
their presence is characteristic.
Fascicular rhythms, the form of VT associated with only
slightly abnormal ventricular activation, can be recognized
by shorr H’ -V intervals on the His bundle recording. The VT
H‘ wave is presumed to be produced by a signal arising
slightly distal to the His bundle recording site which
reaches the electrode retrograde just before ventricular ac-
tivation begins.
If A-V dissociation is present, an antegrade His deflec-
tion may follow the atrial wave, but unless fusion occurs,
the V wave does not follow the H wave as in supraven-
tricular rhythms.

Starting VT VT

Most spontaneous episodes of monomorphic sustained

VT begin with a ventricular beat which appears a rela-
tively long time after the previous, normally conducted
sinus beat (Fig. 8). The coupling interval from the begin-
ning of the sinus QRS complex to the first beat of VT
may be longer than 500 ms (499 f 98 ms according to
one recent study). This first beat of VT does not occur
in the T wave or “vulnerable phase” of the previous si-
nus beat and usually has the same or a very similar mor- FIG 1 1 Starting VT by pacing. A paced ventricular premature beat
introduced at the appropriate time institutes a paroxysm of VT in
phology to that of the other beats of the arrhythmia. the top panel. In the middle panel, two paced beats are required,
In the clinical electrophysiology laboratory, VT is in- and in the bottom panel VT is instituted by rapidly pacing the ven-
itiated by the introduction, after a suitable coupling inter- tricle at 170 per minute. From N Engl J Med 304, 1008 (1981) with
val, of one or more paced ventricular beats (Fig. 11). To permission.
 J. A. Kastor: Ventricular tachycardia 593

Single VPD

-____

Underdrive pacing

FIG.12 Stopping VT with pacing. A single paced premature beat (labeled VPD for ventricular premature depolarization) stops a burst
of sustained ventricular tachycardia in the upper panel. In the lower panel, the VT is terminated by “underdrive” pacing the ventricles
at the relatively slow rate of 88 per minute. These techniques tend to be effective when the rate of the tachycardia is relatively slow, 145
per minute in this case. From N Engl J Med 304, 1009 (1981) with permission.

start the arrhythmia in the laboratory, the interval of the Mapping

stimulated premature beat to the preceding sinus or
ventricular-paced beat must usually be much shorter than
the same interval in spontaneous VT. The electrocardio-
graphic form of the paced premature beat is frequently
different from that of the arrhythmia since the pacing
catheter is usually in the right ventricle distant from the
source of the spontaneous arrhythmia.
How does a properly timed paced beat institute VT? We
believe that it enters a reentrant pathway within ventricu-
lar muscle or Purkinje tissue. The early beat blocks con-
duction in one limb of the circuit, and reentry begins.
Presumably a similar process occurs during spontaneous
onset, although why the coupling intervals of spontane-
ous and paced VT in the same patient should be so differ-
ent is not known.
Stopping VT
Many episodes of VT can be terminated by intmduc-
ing one or more paced ventricular beats or by electrically
driving the ventricles at a relatively rapid rate (Fig. 12).
We presume that the beats enter the reentrant circuit, pre-
excite the tissue, and interrupt the conduction pattern
which sustains the arrhythmia.
VT may also be stopped with extra- or intracardiacelec-
tric shock which terminates reentry by depolarizing the
entire heart. VT has been treated with external cardiover-
sion for over 25 years. More recently, intrathoracic shock
delivered by the automatic implantable cardioverter
defibrillator (AICD) has been used with increasing fre-
quency for treating recurrent VT as well as ventricular
fibrillation for which the device was originally designed.
The origin of VT can be located with reasonable preci-
sion by intracardiac mapping in the electrophysiology
laboratory. Electrode catheters are passed into the cham-
ber where the VT originates. The arrhythmia is induced,
and the signals generated by ventricular depolarization are
then recorded. The origin of the VT is defined by the site
where the earliest activation appears (Fig. 13).
Slow conduction in diseased tissue is characteristic of
regions where reentrant arrhythmias originate. Conse-
quently, the duration of signals recorded in these areas
is frequently abnormally long, and their form is fragment-
ed (Fig. 13).
Mapping is used clinically to locate the origin of VT
for subsequent excision during cardiac surgery or intraven-
tricular catheter oblation.
Late Potentials
Low amplitude electrical signals are generated by tis-
sue in regions of slow conduction where reentrant anhyth-
mias arise. These signals are called late potentials because
they are recorded after normal ventricular depolarization
which produces the QRS pattern on the electrocardiogm
(Fig. 14).
Almost all patients with recurrent sustained ventricular
tachycardia have late potentials, and asymptomatic patients
with late potentials frequently develop clinical VT. Suc-
cessful antiarrhythmicsurgery may abolish late potentials,
but drugs, even those which suppress arrhythmias, do not
usually affect late potentials. Physicians can now identi-
fy patients with late potentials by the use of commercial-
594 Clin. Cardiol. Vol. 12. October 1989

LV
site of
origin

TL.
FIG. 13 Endocardial mapping. Recordings have been taken at the right ventricular (RV) apex and at the site of origin of the tachycardia
in the left ventricle in two cases of VT. Only one beat, recorded at a rapid paper speed, is displayed. Notice that the electrical activity
recorded from the origin precedes the beginning of the QRS complex in lead v,. In the beat on the right, the electrical activity recorded
from the site of origin is broad and fragmented. TL means time lines of 10 ms. From N Engl J Med 304, 1012 (1981) with permission.

ly available equipment which provides suitable amplifi-
cation and signal processing.
Conversion
Clinical VT can be converted to normal rhythm with
chest thump, electric shock, drugs, or pacing. The tech-
nique used is often determined by the state of the patient.
Rapid conversion must be performed when angina, con-
gestive failure, systemic hypotension, or cerebral hypoper-
fusion are present.
Except for patients who are allergic, lidocaine is given
intravenously as the first method of treatment. (For de-
tails on dosage, see Table II.) If this fails, external cardi-
oversion should be administed. Often relatively small
amounts of power, such as 20 or 50 J, may be success-
ful. Whenever possible, analgesia or preferably anesthe-
sia should be given. Sometimes, conversion may be ob-
tained by thumping the chest without a cardioverting shock
being required.
In some patients, other drugs, usually pmainamide or
bretylium, may be infused to convert the arrhythmia.
However, because of the possible development of
hypotension or ventricular fibrillation, a cardioverter
should be available for rapid use.
Some cardiologists favor passing an electrode catheter
into the right ventricle and pacing the patient fmm spon-
taneous VT to sinus rhythm. This technique, however,
can take longer than cardioversion or drugs.

I I I I

1
0 100 200
Time (ms)
FIG. 14 Late potenrials. These charts show surface electrocardiographicsignals which have been greatly amplified and processed from
2 patients with inferior myocardial infarctions. On the vertical axis is the amplitude in microvolts and on the horizontal axis is the time
in milliseconds. On the left is the record from a patient without VT and on the right from a patient with recurrent sustained VT. The amw
points to the low amplitude late potentials. From Circulation 64, 238 (1981) by permission of the American Heart Association, Inc.
 J. A. Kastor: Ventricular tachycardia 595

TABLE Il Intravenous doses of antiarrhythmic dmgs most fre- suppression of the arrhythmia. If VT can still be started,
quently used to convert or suppress VT in acute settings more of the drug is given until suppression is achieved
or an intolerably large amount has been administered.
~ ~ ~ ~ ~~~~

IV loading dose IV maintenance

Another drug may then be tested with the hope that sup-
Drug (mg/kg) dose (mg/min)
pression can be obtained (Fig. 15).,
Lidocaine 1-3 1-4 Drug testing with electrophysiological techniques
at 20-50 mglmin predicts clinical effect for many of the drugs used in treat-
Procainamide 6-13 2-6 ing VT. Amiodarone is frequently cited as an exception
at 0.2-0.5 mglkglmin since partial or total clinical suppression of the arrhyth-
Bretylium 5-10 0.5-2
mia may be produced in patients whose VT can still be
1-2 mg/kg/min induced in the laboratory after administration of the drug.
Follow-up studies have shown, however, that recurrence

Chronic Treatment Control 230Jmin

After VT has been converted to sinus rhythm, a pro-

gram to suppress recurrences must be developed. In gener-
al, the healthier the ventricular myocardium, the better
will be the prognosis and the more likely will suppres-
sion be successful. Treatment itself is conducted with Lidocaine 5.1 pgtrnl 240imin
drugs, surgery, pacing, catheter ablation, or cadioversion.

Drugs

Before discussing individual drugs, here are some gener- __

al concepts which apply to the pharmacological treatment Phenytoin 17.8pg/ml 230Jmin
of VT.

Dosage. To be effective in suppressing VT, drugs must

be given often enough and in large enough amounts. The
best dose of the right drug will both successfully convert
VT to sinus rhythm and provide the patient with the lon- Procaina
gest period afterward free of the tachycardia.
Blood levels correlate reasonably closely with therapeu-
tic effect.in most patients. Regular review of the amount
of drug in the blood determined just before the dose is
scheduled (trough level) or at the time of maximal effect
(peak level) can provide excellent guidance about the most
effective size of the dose and fEquency of administration.

Electrophysiological Evaluation. When suppression of

VT by empirical administration of drugs fails, testing in
the electrophysiology laboratory may define a more suc-
cessful program. The value of such studies is based on
the observation that when VT cannot be induced in the
laboratory, it is unlikely to appear clinically. The proce-
dure has been applied for more than 10 years and is now
conducted in most university and some community hospi-
tals with clinical electrophysiology laboratories. FIG 15 Electrophysiologicaldrug testing. In each of the panels.
After pacing catheters have been inserted, the arrhyth- an attempt has been made to induce V T by programmed stimula-
mia is induced and converted by programmed ventricular tion of the ventncles. In the presence of no drug (control) and after
administration of lidocaine, phenytoin and disopyramide, the VT
stimulation. The drug to be tested is then administered can still be induced. When procainamide and quinidine are given,
intravenously, a blood level is drawn and reinduction of induction is not possible; these drugs are likely to suppress clinical
the VT is attempted. If the arrhythmia cannot be started, VTinthispatient. FromNEngfJMed304, 1011 (1981) withper-
the drug at the level attained will probably provide chronic mission.
596 Clin. Cardiol. Vol 12, October 1989

of VT or cardiac arrest are likely to develop in those pa-
tients taking amiodamne whose VT cannot be suppressed
in the laboratory.
Side Effects. Antianbythmicdrugs are notorious for their
many side effects, some only annoying but several poten-
tially fatal. The tendency to produce dangerous arrhyth-
mias and further decrease ventricular function constitute
the most womsome cardiac side effects. Unfortunately,
both these effects are more likely to develop in patients
with severe myocardial impairment, the group most in
need of successful suppression of VT.
Proarrhythmia is the word now widely used to describe
the tendency for drugs to produce arrhythmias, often the
ones for which the drug was given. Probably every an-
tiarrhythmic agent can produce this unwanted effect, and
the frequency has been estimated to exceed 15% with
some drugs.
Proarrhythmia can sometimes be detected in the elec-
trophysiology laboratoly. When this technique is not avail-
able, continuous electrocardiographic recording, prefer-
ably in the hospital, may reveal it. Proarrhythmia usually
appears within 5 days after the drug is first given.
To detect the negative inotropic effects of antianhyth-
mic drugs, physicians should specifically look for signs
of worsening congestive heart failure or decreasing cardiac
output by carefully and frequently questioning and examin-
ing their patients.
Which drug to give is not always an easy question to
answer. The relatively large number of agents now avail-
able complicates the decision. Here are some gened com-
ments about the individual drugs. (For details see Table
111.)
Type IA agents such as disopyramide, quinidine, and
procuinamide are among the most commonly employed
antiarrhythmic drugs probably because physicians are
more familiar with them. Each has proarrhythmic poten-.
tial, and disopyramide is particularly prone to decrease
cardiac output in patients with severe myocardial disease.
Type IA agents can be useful in most cases of VT but
are generally avoided in patients who have long Q-T in-
tervals in sinus rhythm.
Flecainide and encainide, relatively recently released
antiarrhythmic agents, have many electrophysiological
similarities to the Type IA agents, but sometimes one of
them will be better tolerated than pmcainamide or quini-

TABLEIII Oral doses, therapeutic levels, and principal side effects of noninvestigational drugs frequently used in chronic treatment
of ventricular tachycardia"

Oral Oral Therapeutic

loading dose maintenance serum or plasma Principal
Drugs (mg) dose (mg) levels (pglml) side effectsb

Type IA agents
Disopyramide 300-400 100-400 q6-8h 2-5 Parasympatholytic effects (urinary
retention, constipation, blurred vision
glaucoma, dry mouth)
Procainamide 500-lo00 350-1000 q3-6h 4-10 Lupus-like syndrome, agranulocytosis ,
rashes
Quinidine 600- 1OOO 300-600 q6h 3-6 GI symptoms (nausea, vomiting, diarrhea),
cinchonism (tinnitus, visual disturbances,
confusion), thrombocytopenia, raises
digoxin levels
Encainide 25-75 q6-8h 0.5-1.0 Blurred vision, dizziness, diploplia,
vertigo, paresthesia, metabolic taste
Flecainide 100-300 q12h 0.2-0.8 Blurred vision, dizziness, nausea
Oral lidocaine-like
Mexiletine 400-600 200-300 q6-8h 1-2 CNS symptoms (tremor, dysarthria,
dizziness, confusion), nausea, vomiting
Tocainide 400-600 400-800 q8-12h 6-12 Agranulocytosis, pulmonary fibrosis,
otherwise like mexiletine
Amiodarone 800-1200iday 200-800Iday 1-5 Pulmonary fibrosis, blue-grey skin,
for 7-14 days hyperthyroidism, hypothyroidism,
photosensitivity, raises digoxin levels

"Many brands of beta-blocking and calcium blocking drugs are also available for treatment of the occasional patient with VT who
may respond to these agents.
addition to proarrhythmia, negative inotropy, sinus slowing, and AV block which each drug can produce.
 J. A. Kastor: Ventricular tachycardia
dine. However, both have become infamous for their
proarrhythmic effects, and flecainide’s negative inotrop-
ic action can produce cardiovascular collapse in patients
with badly diseased ventricles.
Mexiletine and tocainide are similar to lidocaine. Their
value alone in treating VT is relatively limited, but occa-
sionally combining them with other drugs may be effec-
tive. Mexiletine and tocainide seem to have somewhat less
proarrhythmic and negative inotropic action than most
other drugs used to treat VT. However, tocainide’s ten-
dency to produce marrow suppression in a small number
of patients has limited its use.
Amiodarone has become the principal drug now used
for the most recalcitrant cases of VT. It can be quite ef-
fective, but side effects are many, including such unusual
problems as pulmonary fibrosis, hyper- and
hypothyroidism and bluish-grey discoloration of the skin.
The half-life of amiodarone is exceedingly long.
Beta-blocking drugs are seldom useful in suppressing
VT in patients with coronary artery disease and cardi-
omyopathy, the settings in which most cases occur in the
United States. However, these agents can be highly ef-
fective in those few patients whose VT is produced by
exercise or sympathetic stimulation and in patients with
torsades de pointes or long Q-T intervals.
Calcium channel-blockingdrugs. The mechanism for
the arhythmia in some patients whose VT can be produced
by catecholamine administration or exercise may be quite
responsive to calcium channel-blocking drugs. In such
cases, the VT, which cannot usually be instituted by ven-
tricular stimulation, may be due to triggered automatici-
ty, a mechanism dependent on calcium.
Surgery
Studies in experimental and clinical electrophysiology
laboratories and in operating rooms have shown that VT
usually originates in the ventricular endocardium in as-
sociation with abnormal tissue. In patients with coronary
artery disease who have VT, ventricular aneurysms have
usually developed from previous myocardial infarctions.
The reentrant circuits in these patients localize at the
periphery of the aneurysms where abnormal but still rela-
tively viable tissues still exist.
With clinical mapping, the sites where VT originates
can be found and then cut away or obliterated by freezing
(cryoablation) at open heart surgery. Many patients will
be cured of their VT by endocardial excision and no longer
have clinical or inducible VT. In some cases, relatively
low doses of antiarrhythmic drugs may still be needed,
but often none are required any longer.
When should operative rather than medical treatment
be recommended for patients with VT? One usually ad-
vises surgery for those patients who also need coronary
artery bypass grafting for angina or when aneurysmecto-
my seems indicated for congestive heart failure or to re-
move endocardial clots which may have produced embo-
597
li. Endocardial excision or cryoablation is seldom suita-
ble for patients whose VT is due to cardiomyopathy.
In general, better results are obtained in patients whose
left ventricular function is reasonably well preserved.
Those with low ejection fractions have a poor prognosis
regardless of treatment, and operation itself is associated
with high morbidity and mortality.
Pacing
Since VT can be terminated by pacing in the elec-
trophysiology laboratory, some patients with VT have
been given permanent pacemakers for chronic treatment.
These units pace at rapid rates either when instructed to
do so by transcutaneous impulse or when they detect an
abnormally fast rate. Rapid pacing can convert recurrent
sustained VT but at the price of occasionally inducing ven-
tricular fibrillation. In the electrophysiologylaboratory this
occurs not infrequently and is treated routinely with ex-
ternal cardioversion. Outside the hospital, the sequence
can be fatal. Because of this complication, permanent
pacers which provide rapid ventricular pacing for recur-
rent VT are seldom installed except with an implanted
defibrillator.
Catheter Ablation
Since endomyocardial reentrant circuits can be excised
by surgery, clinical electrophysiologistshave tried to ob-
tain similar results by ablating the tissue with electric
shocks delivered through electrode catheters. This tech-
nique has been successfully employed to obliterate func-
tioning reentrant circuits sustaining supraventricular
tachycardia.
In bundle-branch reentrant VT, where the arrhythmia
is sustained through the bundle of His and the bundle
branches, catheter ablation of the right bundle branch has
been highly effective in curing patients of VT. However,
in the more common VT sustained by intraventricular
reentry, catheter ablation is seldom successful.
Cardioverter-Defibrillator
The automatic implantable cardioverter-defibrillator
(AICD) detects ventricular tachycardia or ventricular fibril-
lation and cardioverts the arrhythmia with internal shock
(Fig. 16). Units now being developed can also pace rapidly
when VT is detected. If the arrhythmia does not respond
or fibrillation develops, the AICD delivers a shock and
converts the patient to sinus rhythm.
The AICD is now an accepted method for treating dan-
gerous tachyarrhythmias, and thousands are being
prescribed for patients in the United States each year.
Cardiologists differ, however, on who should receive
them. There seems little controversy about installing an
AICD in a patient with recurrent syncope whose ventric-
598 Clin. Cardiol. Vol. 12, October 1989
Josephson ME, Horowitz LN, Farshidi A, Kastor JA: Recunent
Josephson ME, Horowitz LN, Farshidi A, Spear JF, Kastor JA,
Liem LB, Swerdlow CD: Value of electropharmacologic testing in
Transient (Non-Sustained) Ventricular Tachycardia
FIG. 16 Automatic implantable cardioverter dejbrillator. Model
1500 Ventak automatic implantable cardioverter-defibrillator
(AICD). Manufactured by Cardiac Pacemakers, Inc.
ular tachycardia or fibrillation, even after administration
of drugs or operation, can still be induced in the elec-
tmphysiology laboratory. Furthermore, few would refuse
an AICD to a patient with similar problems who cannot
tolerate drugs or whose risk for surgery is high.
If, however, the arrhythmia can be rendered uninduci-
ble, should the patient also receive an AICD? Many
authorities say no. Proponents for wider use of the device
assert that some “good risk” patients will still sustain
cardiac arrest which an AICD could treat. More general
application of AICDs will probably become acceptable
when their size decreases fulther, their functions can be
more readily programmed externally, and they can be mu-
tinely inserted without general anesthesia and thoracoto-
my. Each of these features is now being clinically evalu-
ated in experimental models.
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