SYMPOSIUM
CARDIOVASCULAR
DISEASES
SUPRAVENTRICULAR ON
TACHYCARDIA:
DIAGNOSIS AND MANAGEMENT
Supraventricular Tachycardia: Diagnosis and Management
DAVID J. FOX, BMSC, MBCHB, MRCP; ALEXANDER TISCHENKO, MD, FRCPC;
ANDREW D. KRAHN, MD, FRCPC; ALLAN C. SKANES, MD, FRCPC; LORNE J. GULA, MSC, MD, FRCPC;
RAYMOND K. YEE, MD, FRCPC; AND GEORGE J. KLEIN, MD, FRCPC
Supraventricular tachycardia (SVT) includes all forms of tachycardia that either arise above the bifurcation of the bundle of His or
that have mechanisms dependent on the bundle of His. We conducted a review of the techniques used to differentiate the mechanisms of SVT. We searched the PubMed and MEDLINE databases
for English-language literature published from 1970 to 2008. Articles were selected for either their historical importance or up-todate clinical data. This review focuses on techniques for scrutinizing electrocardiograms of patients, analyzing in particular the
onset of tachycardia, the mode of tachycardia termination, and
the effects of premature ventricular contractions, premature atrial
contractions, and aberrancy during tachycardia. Both short-term
and long-term management of SVT are examined, including the
urgent treatment of patients in the emergency department. This
review also describes management of patients who have ongoing
symptomatic SVT, outlining such available treatment options as
atrioventricular node–blocking drugs, antiarrhythmic drugs, and
catheter ablation.
Mayo Clin Proc. 2008;83(12):1400-1411
AV = atrioventricular; AVNRT = AV nodal reentrant tachycardia; AVRT =
AV reentrant tachycardia; BBB = bundle branch block; ECG = electrocardiography; JET = junctional ectopic tachycardia; PAC = premature
atrial complex; PJRT = permanent junctional reciprocating tachycardia;
PSVT = paroxysmal supraventricular tachycardia; SVT = supraventricular tachycardia
S
upraventricular tachycardia (SVT), by definition, includes all forms of tachycardia that either arise above
the bifurcation of the bundle of His or that have mechanisms dependent on the bundle of His. In patients with
SVT, the heart rate is at least 100 beats/min, but ventricular
rates can be lower as a result of atrioventricular (AV)
block. On electrocardiography (ECG), QRS morphology is
usually normal or supraventricular; however, it may be
widened or abnormal because of intrinsic conduction disturbance, myocardial disease, or rate-related bundle branch
block (BBB).
INCIDENCE OF SVT
The incidence of SVT in the general population remains
unclear. Published incidence data from studies vary widely
depending on the characteristics of the enrolled patients,
the diagnostic modality used to identify SVT, and specific
definitions incorporated into the studies.
In a short-term ambulatory monitoring study of 301 men
with a mean age of 56 years, the documented occurrence of
any form of SVT was 76%.1 The study’s population had an
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incidence of coronary artery disease of approximately
20%. By contrast, Clarke et al2 analyzed the SVT rate in a
normal disease-free population with an age range of 16 to
65 years, reporting a rate of documented SVT of only 12%.
Harrison et al3 also reported a low SVT incidence rate of
only 18%. Research has shown that the incidence of SVT,
in particular the most common forms (ie, atrial
arrhythmias), increases with age and presence of cardiac
disease.4,5 However, SVT incidence is difficult to quantify
precisely because of the high rate of asymptomatic episodes in patients.
Although SVT includes such arrhythmias as atrial fibrillation and atrial flutter, the current review focuses on diagnosis, patient treatment, and management for the 3 most
commonly encountered forms of paroxysmal (ie, suddenonset) SVT (PSVT). These forms are AV nodal reentrant
tachycardia (AVNRT), AV reentrant tachycardia (AVRT),
and atrial tachycardia.
METHODS
We searched the PubMed and MEDLINE databases for
English-language literature published from 1970 to 2008.
Articles were selected for either their historical importance
or up-to-date clinical data, particularly in regard to techniques for scrutinizing ECG results of patients with PSVT.
CLINICAL PRESENTATION OF PSVT
Most patients with PSVT present clinically with episodes of
palpitations that are of sudden onset and, in some cases, also
abrupt offset. The duration of palpitations is highly variable
among individuals, with episodes that may last from a few
seconds to several hours. Patients usually cannot identify a
precipitating trigger that provokes their sudden tachycardia.
From the University of Western Ontario, Division of Cardiology, Arrhythmia
Section, University Hospital, London, Ontario, Canada. Dr Fox is now with the
Wythenshawe Hospital, Manchester, United Kingdom.
Address correspondence to David J. Fox, BMSc, MBChB, MRCP, North West
Regional Cardiac Centre, Wythenshawe Hospital, Manchester M23 9LT,
United Kingdom (david.j.fox@talk21.com).
Individual reprints of this article and a bound reprint of the entire Symposium
on Cardiovascular Diseases will be available for purchase from our Web site
www.mayoclinicproceedings.com.
© 2008 Mayo Foundation for Medical Education and Research
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SUPRAVENTRICULAR TACHYCARDIA: DIAGNOSIS AND MANAGEMENT
Patients with PSVT may present either to the emergency
department or to the physician’s office. In patients who
have symptoms of tachycardia but no diagnosis based on
ECG results, appropriate steps need to be taken to ensure
that the tachycardia is recorded and that a symptom-rhythm
correlation exists. Hence, the use of ambulatory monitoring
and event recorders may be required.
At presentation, PSVT may be associated with presyncope, syncope, chest pain, and abnormal pulsations in
the neck.6 Syncope may occur if an episode of PSVT is
extremely rapid, resulting in compromise in cardiac output,
or it may follow a prolonged pause immediately after spontaneous termination of tachycardia. Syncope may also be
related to the triggering of a vasovagal response caused by
the tachycardia itself.7 The mechanism of chest pain is
unclear. Although chest pain in PSVT is usually unrelated
to coronary artery disease, such pain in older patients raises
the possibility of myocardial ischemia.
By definition, PSVT is paroxysmal, both starting and
stopping abruptly. However, it may be prolonged because
of the cardiac adrenergic drive that builds up during PSVT
as a result of hypotension or anxiety. The build-up of
adrenergic drive results in a less perceptible transition to a
sinus tachycardia after the PSVT has terminated. An atrial
tachycardia or junctional tachycardia may accelerate more
gradually and, thus, would be nonparoxysmal. Some patients with PSVT may describe an urge to urinate, possibly
as a result of atrionatriuretic peptide release, which produces an intrinsic diuretic effect.
In a less common scenario, some patients with SVT may
present with chronic cardiac failure and cardiomyopathy.
In such cases, patients generally do not experience palpitations during tachycardia and will have excessive heart rates
until cardiac decompensation occurs. The tachycardia in
these patients likely takes weeks or months to cause heart
failure, depending on the patient’s heart rate and on the
amount of time that the patient experiences tachycardia
episodes. Ventricular dysfunction is usually reversible,
even, to some degree, in patients who have not been treated
for long-standing tachycardia.
The mechanism of SVT is usually AV reentry involving a decremental accessory pathway, atypical AV nodal
reentry, or atrial tachycardia.8 All these types of AV reentry are frequently referred to as permanent junctional
reciprocating tachycardia (PJRT); strictly speaking, however, this term refers only to atypical AV nodal reentry.9,10
More recently, PJRT has become synonymous with AV
reentry involving a slowly conducting decremental accessory pathway.11
The ECG appearance of PJRT is similar to that of SVT,
but with the RP interval (the distance from the peak of the
QRS to the onset of the next visible P wave during tachyMayo Clin Proc.
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cardia) longer than the PR interval (the conduction time
after the RP interval). During tachycardia, if the distance
from the R wave to the next P wave is longer than the
distance from that same P wave to the next R wave, the
condition is termed long RP tachycardia. If the distance
from the R wave to the next P wave is shorter than the
distance from that same P wave to the next R wave, the
condition is termed short RP tachycardia.
CLASSIFICATION AND MECHANISMS OF PSVT
Paroxysmal SVT can be classified in several ways. The
classifications may be based on ECG appearance (ie, long
RP tachycardia or short RP tachycardia) or on the underlying mechanism of tachycardia (ie, AV reentry, AV nodal
reentry, or atrial tachycardia). It is also clinically useful to
consider PSVT classifications in terms of whether the condition is dependent on AV nodal conduction. This type of
consideration is useful because it generally allows the arrhythmia to be classified clinically without the need for
specialized arrhythmia studies.
Supraventricular tachycardia that persists even when
AV block is achieved by carotid sinus massage or other
interventions is clearly independent of AV nodal conduction. The use of adenosine may terminate some focal atrial
tachycardias, but some degree of AV block usually precedes this termination, allowing the diagnosis of AV nodal
independence. By contrast, if an intervention that causes
AV block terminates the tachycardia, the SVT is clearly
AV node–dependent. Atrioventricular nodal dependence is
more commonly encountered in the clinical setting than is
AV nodal independence.
AV NODE–DEPENDENT ARRHYTHMIAS
The two most common forms of PSVT (ie, AVNRT and
AVRT) are both dependent on AV nodal conduction to
maintain the tachycardia circuit. Any interruption of AV
nodal conduction will normally terminate tachycardia.
These 2 arrhythmias are, of course, reentrant. In the case of
AVNRT, the reentrant circuit is small (ie, microreentrant)
and is in or closely related to the AV node. In the case of
AVRT, the reentrant circuit is large (ie, macroreentrant)
and involves the atria, AV node, and ventricles.
A much less common form of AV node–dependent arrhythmia is junctional ectopic tachycardia (JET).12,13 This
arrhythmia is most common in childhood and may be associated with congenital heart disease. It may also be seen in the
early phase after surgery for congenital heart disease.12,13 The
mechanism of JET is abnormal automaticity in the AV nodal
region. The ECG findings in JET show a tachycardia that, in
some cases, has identical ventricular and atrial rates, and, in
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SUPRAVENTRICULAR TACHYCARDIA: DIAGNOSIS AND MANAGEMENT
other cases, has a ventricular rate that is faster than the atrial
rate, with ventriculoatrial block. Tachycardia myopathy has
been observed in cases in which the AV rate or rhythm has
not been adequately controlled.14,15
AV NODE–INDEPENDENT ARRHYTHMIAS
Less commonly encountered forms of PSVT, including
atrial tachycardia, are independent of AV nodal conduction. These arrhythmias may persist during AV block. The
source of these arrhythmias is usually a small focus, and the
mechanism is usually abnormal automaticity or triggered
activity. The mechanism is usually microreentrant, especially in diseased atria.
Atrial tachycardias (commonly called flutters, if sufficiently rapid) may also occur as a result of a macroreentrant
mechanism. However, the reentrant circuit in these
tachycardias lies within the atrium (eg, a surgical atriotomy
scar) and is not dependent on the AV node. Although PSVT
may be related to reentry in and around the sinus node
region, this type of reentry is rarely observed as a clinically
relevant SVT.
Technically, multifocal atrial tachycardia, atrial flutter,
and atrial fibrillation are all AV node–independent arrhythmias. However, these conditions are not discussed further
in the current review.
INTERPRETATION OF ECG FINDINGS IN PSVT
Most PSVTs are represented on ECGs as narrow QRScomplex tachycardias, with the QRS duration being less
than 90 ms (ie, normal QRS duration). Tachycardia-contingent BBB (ie, aberrancy) is relatively frequent in patients
with PSVT. Many of these patients may have preexistent
BBB, interventricular conduction delays, or some other
QRS abnormality. These abnormalities carry over to the
tachycardia.
An initial analysis of ECG findings for a patient with
PSVT is best followed by a methodical approach to ECG
interpretation, in which the physician reviews the elements
of the differential diagnosis, either mentally or in writing,
and examines the evidence supporting each diagnostic possibility. A high-quality12-lead ECG is much more useful in
the clinical setting than limited presentations or individual
cardiac rhythm strips. The main ECG findings of interest
are compelling atrial activity and zones of transition, such
as ectopy, cycle length change, or intermittent aberrant
conduction.
Interventions may be helpful if the mechanism of the
tachycardia is unclear from examination of the routine
ECG or rhythm strips. Vagal stimulation maneuvers, such
as carotid sinus massage or Valsalva maneuver, are classic
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procedures for assessing the role of the AV node in the
tachycardia mechanism. Pharmacologic interventions are
most useful for quickly determining the mechanism of an
arrhythmia.
Features to consider in ECG interpretation include the
following: (1) tachycardia rate; (2) mode of onset and
termination of the tachycardia; (3) relative position of the P
wave within the R-R interval; (4) morphology of the P
wave; (5) change in QRS morphology, including variability in cycle length and relative movement of the atrial ECG
and ventricular ECG during variability in tachycardia rate;
and (6) effect of intermittent BBB on the tachycardia.
TACHYCARDIA RATE
Careful analysis of the R-R interval should be performed to
determine the rate of the tachycardia. A rate of 150 beats/
min raises the suspicion of atrial flutter with 2:1 AV block
because the usual atrial rate during flutter is 300 beats/
min. In general, a tachycardia with an atrial rate of less
than 160 to 170 beats/min and without a visible P wave
implies the presence of the slow-pathway component of
the AV node.
The most frequently encountered PSVT of this type is
typical AV nodal reentry (ie, AVNRT), a schematic of
which is shown in Figure 1. Atrial tachycardia or AVRT
involving a slow AV nodal pathway for anterograde conduction are considerably less frequently observed than
AVNRT. Faster rates of tachycardia are not generally helpful in narrowing the differential diagnosis.
MODE OF ONSET AND TERMINATION OF TACHYCARDIA
Onset. The physician should check if the onset of the
patient’s tachycardia is captured on the ECG. Most PSVTs
are triggered by a premature atrial complex (PAC). If the
PAC conducts to the ventricle with a very long PR interval at
initiation of tachycardia (ie, a “jump” in the PR interval), the
physician can safely postulate that the tachycardia is
dependent on anterograde slow-pathway conduction of the
AV node to the ventricle. Atrioventricular nodal reentrant
tachycardia is the typical tachycardia that begins with this
mechanism. It is important to remember that a PAC, if
coupled closely enough, generally results in a longer PR
interval in the premature cycle because of normal decremental AV nodal physiologic factors. Supraventricular tachycardias that start with a ventricular premature complex are
usually AV node–dependent tachycardias. Supraventricular
tachycardias are almost never atrial tachycardias.
Termination. Tachycardias in which the last event at
termination is a P wave are highly unlikely to be atrial
tachycardias. If such conditions were atrial tachycardias, it
would be necessary to postulate that the last atrial beat
caused the block in the AV node. It is more logical to
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SUPRAVENTRICULAR TACHYCARDIA: DIAGNOSIS AND MANAGEMENT
FIGURE 1. Schematic of typical atrioventricular nodal reentry. The panel on the left demonstrates
anterograde conduction from the atrium (ATR) to the ventricle (VTR) over both slow and fast pathways.
The ventricle is activated initially in sinus rhythm by the fast pathway. The panel in the center shows the
effect of a premature atrial complex (PAC). Although the fast pathway conducts rapidly, it repolarizes
slowly. In this hypothetical scenario, the fast pathway is refractory to the PAC, allowing the PAC to
proceed via the slow pathway, which has a shorter refractory period. In the panel on the right, conditions
are such that anterograde conduction of the PAC occurs via the slow pathway, with subsequent recovery
of the fast pathway. These conditions allow retrograde conduction into the atrium via the fast pathway,
thereby creating the first beat of typical slow-fast atrioventricular nodal reentrant tachycardia.
postulate that the block in the AV node caused the
tachycardia to terminate and, consequently, that the
condition is an AV node–dependent tachycardia.
Although an atrial tachycardia almost always terminates
with a ventricular complex, this observation may not be
helpful in diagnosis because some AV node–dependent
tachycardias also terminate in this manner. Figure 2 shows
a schematic of 2 terminations of tachycardias.
RELATIVE POSITION OF THE P WAVE WITHIN THE R-R INTERVAL
When analyzing ECGs of any PSVT, the physician should
attempt to identify the presence of P waves. A widely used
classification nomenclature of PSVT morphology, as previously mentioned, is the long RP tachycardia vs the short
RP tachycardia. This nomenclature is purely descriptive
and in most cases does not help the physician to narrow the
differential diagnosis. Nevertheless, in cases in which simultaneous atrial and ventricular activation occurs, this
classification system can be used to rule out AVRT, pointing to typical slow-fast AVNRT. This type of AVNRT is
depicted in the center panel of Figure 3.
With any extremely rapid PSVT, both the RP interval
and PR interval become short, making it difficult to distinguish between the two. However, at slower PSVT rates, a
shorter RP interval is usually indicative of AVRT, as
shown in the top panel of Figure 3, and a long RP interval
most commonly represents atrial tachycardia. Long RP
morphologies, shown in the bottom panel of Figure 3, may
also represent atypical AVNRT or AVRT. Finally, sinus
tachycardia is technically a long RP tachycardia, but it can
often be differentiated from atrial tachycardia through
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close comparison of P-wave morphology during sinus
rhythm vs during the tachycardia.
These guidelines for ECG interpretation have been validated with electrophysiologic data. Kalbfleisch et al16 reported that more than 90% of AVNRTs and 87% of
AVRTs are short RP tachycardias. By contrast, only 11%
of atrial tachycardias present as short RP tachycardias.16
MORPHOLOGY OF THE P WAVE
P waves may be difficult to distinguish in ECGs, especially
during more rapid tachycardia, because of overlap with the
FIGURE 2. Schematic of 2 terminations of paroxysmal supraventricular tachycardia (PSVT) as recorded on electrocardiograms. The
top panel demonstrates PSVT terminating with a ventricular complex. The bottom panel shows PSVT terminating with an atrial
complex, indicating that this patient is highly unlikely to have atrial
tachycardia.
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SUPRAVENTRICULAR TACHYCARDIA: DIAGNOSIS AND MANAGEMENT
FIGURE 3. Schematic representing appearances of long RP tachycardia and short RP tachycardia
morphologies. The electrocardiogram (ECG) in the top panel indicates a short RP tachycardia. The
3 examples of this condition shown to the right of the ECG are (left to right) atrioventricular
reentrant tachycardia (AVRT), atrial tachycardia, and atrioventricular nodal reentrant tachycardia
(AVNRT). The ECG in the panel in the center also indicates a short RP morphology, with a very
short ventriculoatrial time. Examples shown for this condition are (left to right) typical AVNRT and
atrial tachycardia with anterograde slow-pathway conduction. The ECG in the bottom panel
indicates a long RP morphology. Examples shown for this condition are (left to right) atypical
AVNRT, atrial tachycardia, and AVRT. Theoretically, junctional ectopic tachycardia can present as
any of the morphologies shown in this figure.
QRS and T waves. If P waves are visible during tachycardia, comparison with P waves in sinus rhythm is useful.
Although all available ECG leads require inspection,
evaluation of the inferior ECG leads (particularly lead II),
as well as lead V1, is likely to be the most productive. A
normal P wave has a positive QRS morphology in the
inferior leads because normal atrial activation begins at the
sinus node during sinus rhythm, with a wave of electrical
propagation moving toward the AV node (ie, high to low
sequence). As this impulse moves toward the inferior leads,
it produces an upright P wave in leads II, III, and aVF. By
contrast, junctional-dependent rhythms, such as AVNRT
and AVRT, and atrial tachycardias with origins in the
lower atrium result in negative P waves in the inferior
leads. The negative P waves occur because these
tachycardias activate the atrium in the opposite direction
(ie, low to high sequence).
Careful analyses of other ECG leads can help physicians
to determine if the atria are being activated from left to
right or vice versa. This conclusion can be achieved by
examining the morphology of the P wave in leads I and
aVL. In right atrial tachycardia foci, the P wave is positive
or biphasic (ie, first negative, then positive) in lead aVL.
That is because the right atrium is activated first, with the
wave of depolarization moving toward the left atrium and,
thus, to lead aVL. In left atrial tachycardia foci, the P wave
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is negative or isoelectric (ie, electrically neutral) in lead
aVL. In addition, a positive P wave (ie, from the back to the
front) is observed in lead V1 in left atrial foci. This contrasts
with the negative or biphasic P wave observed in lead V1
when the atrial tachycardia is of right atrial origin.
In the long RP tachycardias caused by atrial tachycardias, the P-wave morphology provides the first approximation of the site of the abnormal focus.17-19 These algorithms may be useful if the physician attempts to ablate the
tachycardia.
CHANGE IN QRS MORPHOLOGY
A ventricular rate that is irregularly irregular (ie, a rate that
is variable in unpredictable ways), including having an
irregular baseline, suggests a diagnosis of atrial fibrillation.
The cycle length in most cases of PSVT is reasonably
regular; however, it may oscillate in a patient who has dual
or multiple anterograde AV nodal pathways. In fact, most
oscillation in cycle length occurs in the anterograde part of
the circuit. Patients with atrial tachycardias may present
with a notably irregular ventricular rate if there is variable
block in the AV node.
A more subtle oscillation in cycle length can be diagnostically useful. If the ECG shows that the QRS change
initiates the P-wave change during SVT (ie, if the VV
change precedes the AA change), the patient’s condition
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SUPRAVENTRICULAR TACHYCARDIA: DIAGNOSIS AND MANAGEMENT
FIGURE 4. Electrocardiograms indicative of paroxysmal supraventricular tachycardia, with no visible P wave. Left, normal QRS morphology; right,
sudden development of right-sided bundle branch block (without any change in cycle length). The tachycardia shown in this electrocardiogram
was verified as atrioventricular nodal reentrant tachycardia during electrophysiologic testing.
cannot be an atrial tachycardia and must be a junctional
reentrant tachycardia instead. The converse (ie, if the AA
change precedes the VV change) is less useful for diagnostic purposes, although such an observation usually suggests
an atrial tachycardia.
QRS alternans is a phasic alteration of the amplitude of
the QRS complex, of unclear mechanism, that is observed
in 1 or more ECG leads. It is a nonspecific finding in faster
tachycardias regardless of mechanism. Thus, it most commonly occurs in conjunction with AVRT (25%-38% of
orthodromic AVRT, in which the usual direction of traffic
is to the AV node). QRS alternans also occurs with
AVNRT (13%-23% of AVNRT), but it is virtually never
seen with atrial tachycardia.16,20-22
EFFECT OF INTERMITTENT BBB ON TACHYCARDIA
A change in AV rate with the development of BBB aberration can mean only that a bundle branch is part of the
tachycardia circuit. This characteristic excludes every SVT
mechanism except AV reentry.
Bundle branch block that occurs ipsilateral to an accessory pathway results in prolongation of the ventriculoatrial
conduction time, which is generally reflected in the tachycardia cycle length.23 This association exists because those
bundle branches are active (if not obligatory) components
of the tachycardia circuit. The converse is also true. If leftsided BBB resolves during tachycardia and the cycle length
decreases, an ipsilateral accessory pathway is suggested.
By contrast, the development of right-sided BBB with a
left-sided accessory pathway, or vice versa, will have no
effect on the tachycardia cycle length because that bundle
is not an integral part of the tachycardia circuit. Figure 4
shows an ECG indicative of the sudden development of
right-sided BBB in a case of AVNRT.
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Furthermore, BBB that occurs in either AVNRT or
atrial tachycardia has no effect on the tachycardia cycle
length because the bundle branches are not integral parts of
these tachycardia mechanisms.
BROAD COMPLEX TACHYCARDIA
SECONDARY TO PSVT
A PSVT may present as a broad complex tachycardia for 3
main reasons. First, a preexisting BBB, intraventricular
conduction disturbance, or other QRS abnormality in sinus
rhythm will usually be manifested during tachycardia. Second, tachycardia-contingent BBB may occur if either the
right- or left-sided bundle branch reaches its effective refractory period and cannot conduct impulses to match the
rapid rate of the tachycardia. This condition is also called
functional BBB or rate-related BBB. Subtle features of the
bundle branch may point to PSVT-related broad complex
tachycardia rather than ventricular tachycardia. For example, in a patient with PSVT and a structurally normal
heart, the bundle branch pattern will usually have a typical
appearance, virtually identical to conventional bundle
branch morphology.24 Statistically, this is by far the most
common cause of wide QRS morphology on ECG in patients with SVT. Third, the QRS morphology will be wide
during SVT if the tachycardia is related to preexcitation or
conduction over an accessory pathway. The most common
preexcited tachycardia, other than atrial fibrillation, is antidromic tachycardia, in which the tachycardia proceeds in an
anterograde manner over an accessory pathway and returns
via the normal AV conduction system. The accessory pathway may also serve as a route for some other tachycardia
mechanism (eg, an atrial tachycardia conducted over an
accessory pathway). In such a case, the accessory pathway is
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SUPRAVENTRICULAR TACHYCARDIA: DIAGNOSIS AND MANAGEMENT
FIGURE 5. Cardiac rhythm strips demonstrating (top) sinus rhythm
and (bottom) paroxysmal supraventricular tachycardia. The P wave
is seen as a pseudo-R wave (circled in bottom strip) in lead V1 during
tachycardia. By contrast, the pseudo-R wave is not seen during
sinus rhythm (it is absent from circled area in top strip). This very
short ventriculoatrial time is frequently seen in typical atrioventricular nodal reentrant tachycardia.
not part of the mechanism that causes the atrium to beat
rapidly.
Patients with accessory pathways may present on different occasions with either antidromic or orthodromic tachycardia because many pathways are capable of bidirectional
conduction. Ventricular tachycardia needs to be considered
in the differential diagnosis of any tachycardia, but especially a tachycardia represented by a wide QRS morphology. The hallmarks of ventricular tachycardia (eg, AV
dissociation, capture and fusion beats, extreme axis deviation, atypical bundle branch morphology) should be investigated in the diagnosis. A useful rule of thumb is that, for
patients who present with a broad complex tachycardia and
a history of coronary artery disease/myocardial infarction,
the arrhythmia should be considered to be a ventricular
tachycardia until proven otherwise.
PSVT SECONDARY TO AVNRT
Patients with PSVT secondary to AVNRT are typically
young (20-35 years) and generally healthy, with no history
of structural heart disease. However, PSVT secondary to
AVNRT also occurs in older individuals. Slightly more
women than men have this type of PSVT. Typical AVNRT
is seldom incessant and, hence, does not generally present as
tachycardia myopathy or portend an adverse prognosis for
patients. Unless either preexistent or rate-related BBB is
present, the QRS morphology of AVNRT typically appears
narrow and without clearly discernible P waves on ECG.
In some cases, P waves can be seen as pseudo-R waves,
particularly in lead V1 and in the inferior leads II, III and
aVF (Figure 5). Rarely, P waves can also manifest as
pseudo-Q waves, when retrograde atrial depolarization precedes ventricular depolarization. In such cases, a direct com1406
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parison with QRS morphology in sinus rhythm is required to
establish the presence of pseudo-Q waves. The ventricular
rate during AVNRT is usually between 160 and 180 beats/
min. The most common form of AVNRT (ie, slow-fast
AVNRT) is also the most frequent cause of any PSVT.
The mechanism of tachycardia is related to the presence
of dual AV nodal pathways (ie, functionally or anatomically separate routes of AV node conduction). Typical AV
nodal reentry is thought to be related to a fast pathway
(anteriorly near the AV node’s junction with the bundle of
His) and to a slow pathway (at the entrance to the AV node
between the coronary sinus orifice and the tricuspid annulus). Atrioventricular nodal reentry begins if these 2 pathways become dissociated (Figure 1).
Normal AV nodal conduction occurs in an anterograde
manner over both the fast and slow pathway. However, a
PAC may reach the fast pathway early when it is refractory.
The PAC will then act to block conduction in this pathway.
Subsequent conduction occurs more slowly over the slow
pathway, resulting in PR prolongation. The impulse may
then find the distal end of the fast pathway recovered
enough for retrograde conduction (ie, reentry) to the
atrium, resulting in the first beat of tachycardia.
Hence, the anterograde limb of the tachycardia occurs
via the slow AV nodal pathway, whereas the retrograde
limb occurs via the fast AV nodal pathway. Because the
atria and ventricles are generally activated simultaneously
as a result of this small circuit in the middle of the heart, the
P wave is often obscured by, buried within, or very close to
the QRS complex on the ECG.
PSVT SECONDARY TO AVRT
Patients who present with PSVT secondary to AVRT are
generally similar demographically to those with AVNRT.
However, individuals with AVRT are less likely to present
in middle age or later than those with AVNRT.
A narrow complex tachycardia is seen in the ECGs of
patients with AVRT, because anterograde conduction usually proceeds via the AV node and His-Purkinje system to
the ventricle. Retrograde conduction then occurs via the
accessory pathway, which may be located on the right, left,
or septal AV areas. This type of tachycardia is an orthodromic tachycardia and is the most common type of SVT
observed in accessory pathways. In contrast to AVNRT, in
which the atria and ventricles are typically activated nearly
simultaneously, in AVRT, first the ventricles and then the
atria are activated in sequence. Subsequently, the P wave is
usually in the ST segment or T wave of an ECG and is often
visible between successive R waves.
Patients with accessory pathways may also present with
broad complex tachycardia resulting from aberrancy or
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SUPRAVENTRICULAR TACHYCARDIA: DIAGNOSIS AND MANAGEMENT
preexcited tachycardia (ie, antidromic AVRT) or from ventricular tachycardia. However, the most common wide
QRS tachycardia observed in patients with accessory pathways is orthodromic SVT with aberrant ventricular conduction. Preexcited tachycardia, in which the pathway conducts in an anterograde manner, occurs less frequently. The
most common form of preexcited tachycardia uses the
accessory pathway as the anterograde limb and the AV
node as the retrograde limb of the circuit (Figure 6). Because the ventricle is activated via myocardium rather than
specialized conduction tissue of the His-Purkinje system,
ventricular depolarization happens slowly, resulting in the
broad complex preexcited rhythm.
Electrocardiograms of patients with accessory pathway
arrhythmias may or may not show delta waves (ie, initial
slurring of the QRS) in sinus rhythm. The presence of a
delta wave in sinus rhythm usually suggests that the SVT is
related to the accessory pathway.
AP
AVN
QRS
MORPHOLOGY
IN
TACHYCARDIA
VENTRICULAR PREEXCITATION
Preexcitation of the ventricles is indicated by the presence
in the ECG of a shortened PR interval in association with
slurring of the upstroke of the QRS complex.25 Preexcitation occurs as the sinus impulse travels to the ventricle
via both the AV node and the accessory pathway, resulting
in a fusion of ventricular activation via both the conventional His-Purkinje system and the accessory pathway. Because AV nodal conduction is decremental and, hence,
relatively slow, the first part of the QRS is slurred—that is,
the anterograde accessory pathway conduction reaches the
ventricle first, forming a delta wave on the ECG. This
slurring persists until AV nodal conduction propagates into
the ventricle, activating the ventricles rapidly and resulting
in a terminal QRS complex that is closer to normal in
morphology. The greater the ventricular activation over an
accessory pathway, the more preexcitation occurs (thus,
the broader the QRS) and vice versa.
Many algorithms used in diagnosis allow approximate
localization of accessory pathways along the AV rings on
the basis of preexcited ECG morphology. These algorithms are more reliable when the preexcitation is predominant. A minimally preexcited ECG makes precise
localization difficult; however, such ECG results generally suggest a left lateral pathway that is much farther
away from the source of normal atrial activation than the
AV node.26,27 Accessory pathways are most commonly
located in the left lateral position (Figure 7), where the
ECG shows a delta wave that is positive in lead V1 and
negative in lead I. In right-sided pathways, the delta wave
is usually negative in lead V1 (with a QS pattern) and
positive in lead I.
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FIGURE 6. Schematic of orthodromic and antidromic tachycardia,
showing the relationship between the atrioventricular node (AVN) and
the accessory pathway (AP) and the associated QRS morphology. The
top panel demonstrates anterograde conduction through the AV node
and retrograde conduction to the atria via the accessory pathway.
This condition is an orthodromic tachycardia, which usually has a
narrow complex QRS morphology. The bottom panel demonstrates
anterograde conduction via an accessory pathway and retrograde
conduction via the AV node. This condition is an antidromic tachycardia, presenting with a wide complex QRS morphology.
Accessory pathways may conduct only intermittently or
be so far lateral as to ensure that the bulk of anterograde
ventricular activation during sinus rhythm occurs via the
sinus node, resulting in an ECG that does not show
preexcitation. Although most accessory pathways are capable of bidirectional conduction, some are concealed,
meaning that they are capable only of retrograde conduction. These accessory pathways never produce preexcitation on ECGs, and they can result only in orthodromic
tachycardia.
PREEXCITED ATRIAL FIBRILLATION
An association exists between accessory pathways and an
increased risk of atrial fibrillation. A classic feature of
preexcited atrial fibrillation is an irregularly irregular cycle
length in conjunction with an irregularly irregular QRS
duration. This feature develops because the atrial fibrillation wave fronts conduct to the ventricle via both the AV
node and the accessory pathway, causing a fusion of ventricular activation over both structures. Unlike the conduction properties of the AV node, the conduction properties
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SUPRAVENTRICULAR TACHYCARDIA: DIAGNOSIS AND MANAGEMENT
FIGURE 7. Electrocardiogram showing a positive dominant R wave in lead V1, with
slurring of the initial deflection of the QRS complex (ie, the delta wave indicated by the
arrow), and ventricular preexcitation resulting from a left lateral accessory pathway.
of accessory pathways are usually nondecremental. If the
pathway has a short refractory period, conduction to the
ventricles at extremely rapid rates (>250 beats/min) is
possible and may lead to ventricular fibrillation.28
Accessory pathways are also capable of anterograde
conduction in cases of atrial tachycardia, AVNRT, and
atrial flutter. In such cases, the pathway acts like a bystander, not participating in the mechanism driving the
tachycardia.
PSVT SECONDARY
TO ATRIAL TACHYCARDIA
Patients may present with atrial tachycardia at any age.
Younger patients, especially those in the pediatric age
group, are most likely to have a focal atrial tachycardia
suggestive of abnormal automaticity or triggered activity.
Older patients, especially those with cardiac disease and
such comorbidities as cardiorespiratory problems, are more
likely to have an atrial tachycardia substrate related to such
conditions as atrial stretch or scarring.
Atrial tachycardia is usually revealed on an ECG as a long
RP tachycardia, as in the bottom panel in Figure 3. The
mechanism of atrial tachycardia usually includes enhanced
automaticity, triggered activity, or reentry. If conduction
happens conventionally to the ventricle via the AV node,
variable AV block may result. Atrial tachycardias may also
conduct in an anterograde manner over an accessory pathway, resulting in a preexcited broad complex tachycardia.
Once again, the accessory pathway acts like a bystander, not
participating in the driving mechanism of the tachycardia.
Atrial tachycardias can be incessant. In such cases, patients may present with chronic cardiac failure caused by
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tachycardia-induced myopathy. Figure 8 shows an ECG
indicative of incessant postpartum atrial tachycardia.
EMERGENCY MANAGEMENT OF PSVT
As with any emergency cardiac situation, the “golden rule
of ABC” (airway, breathing, circulation) should be followed in emergency management of PSVT. A rapid assessment of the patient’s airway, breathing, and circulation
should be conducted, and all vital signs should be documented. If the patient is hemodynamically compromised or
in cardiovascular collapse (both of which are unusual conditions in PSVT), urgent direct-current cardioversion
should be performed without delay.29
Most patients who present with PSVT are hemodynamically stable, allowing enough time for physicians to
perform a thorough history, physical examination, and
12-lead ECG examination. Patients should also ideally
undergo noninvasive blood pressure assessment, measurement of oxygen saturation levels, and continuous ECG
monitoring. Oxygen supplementation should be used
when necessary.
The initial strategy for terminating a PSVT is generally
a vagotonic maneuver, such as carotid sinus massage.
However, the physician should evaluate the patient for the
presence of a carotid bruit (ie, abnormal sound) before
attempting this maneuver, especially in elderly patients.
The Valsalva maneuver or possibly facial immersion in
cold water may also be attempted. These methods serve to
increase vagal tone, which may prolong AV nodal refractoriness to the point of AV block, thereby terminating the
tachycardia. It should be noted that vagotonic maneuvers
will not terminate atrial tachycardia, but they may create
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SUPRAVENTRICULAR TACHYCARDIA: DIAGNOSIS AND MANAGEMENT
transient AV block, clarifying the underlying mechanism
by allowing visualization of the P wave.
If these efforts are unsuccessful in terminating PSVT,
the next step in treatment is pharmacologic intervention.
Previous strategies of using infusions of sympathomimetic
medications (eg, methoxamine hydrochloride, phenylephrine), parasympathomimetic medications (eg, neostigmine,
edrophonium), or digoxin are now rarely, if ever, used. The
use of intravenous verapamil and adenosine has become
standard treatment. Adenosine has a rapid half-life of only
a few seconds, and it produces intense but transient AV
block. Adenosine is safe to use in patients who have structural heart disease because it does not produce a negatively
inotropic effect. The standard starting dose of adenosine is
a 6-mg bolus, which should be administered rapidly
through a free-flowing intravenous line. Doses of 12 mg or
even 18 mg may also be used.
The physician needs to ensure that the patient does not
have asthma or reversible obstructive pulmonary disease
before administering adenosine because this drug can
cause acute bronchospasm. Adenosine can be potentiated
by dipyridamole. Hence, much smaller doses of adenosine
should be used if the patient is taking dipyridamole to avoid
prolonged AV block. Patients should be warned that administration of adenosine may cause transient sensations of
chest tightness, nausea, and flushing. Despite these minor
adverse effects, adenosine is a safe drug for patients in all
age groups.30,31 Adenosine will usually terminate AV node–
dependent rhythms, such as AVNRT and AVRT, and it
may also terminate some types of atrial tachycardias.32
In some cases of PSVT, calcium channel blockers and
!-blockers may be useful. However, the dihydropyridine
class of calcium channel blockers should not be used because they have no effect on AV nodal conduction. Typical
intravenous calcium channel blockers that may be effective
include verapamil and diltiazem. Among !-blockers,
metoprolol and atenolol may be effective. If the physician
is concerned about the patient’s ability to tolerate a !blocker, intravenous esmolol, which has a very short halflife, may be used.
Verapamil is the medication most commonly used as an
alternative to adenosine. Verapamil is especially useful if
adenosine is contraindicated or if the PSVT terminates
rapidly but is immediately recurrent.
The use of vagal maneuvers, adenosine, or verapamil
will convert most AV node–dependent SVTs and some
atrial tachycardias. If atrial tachycardia persists, however,
such intravenous medications as procainamide may be
needed. If control of atrial tachycardia is not achieved with
any of these interventions, the physician should consider
using elective cardioversion, particularly if conversion is
expediently desired.
Mayo Clin Proc.
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FIGURE 8. Electrocardiogram showing incessant atrial tachycardia in
a young woman who presented with postpartum tachycardia-induced
myopathy. Arrows indicate evidence of atrial activity.
Management strategies for PSVT should not change for
patients who are known to have accessory pathways, but
physicians should be aware that atrial fibrillation with rapid
ventricular response can develop during the treatment process. If this response occurs, intravenous procainamide or
ibutilide may be useful. However, if their use is not feasible
or successful, the threshold for using elective cardioversion
should be low.
LONG-TERM TREATMENT
If sufficiently symptomatic, the patient with PSVT should
be offered pharmacologic therapy or catheter ablation for
long-term treatment. Catheter ablation should be considered early in the management of PSVT because of its
proven efficacy and low procedural risk, particularly if the
patient has not responded to medication or is reluctant to
take medication. Catheter ablation is generally performed
on an outpatient basis with a combination of local anesthesia and conscious sedation. Catheters are introduced into
the heart via femoral and subclavian venous access, and an
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SUPRAVENTRICULAR TACHYCARDIA: DIAGNOSIS AND MANAGEMENT
electrophysiologic study is performed to fully elucidate the
nature of the SVT.
Catheter ablation has a high procedural success rate of
approximately 95% for patients with clinical tachycardia,
particularly AVNRT and AVRT. As many as 5% of patients may experience a recurrence of tachycardia and require a second procedure.
In the case of AVNRT, the patient can be treated by
performing careful ECG mapping and delivering radiofrequency energy to the slow-pathway area of the heart (ie,
the posteromedial tricuspid annulus, near the coronary sinus ostium). In patients with AVNRT and in some patients
with accessory pathways, the site of ablation is extremely
close to the compact AV node. Therefore, these patients
should be informed of a small risk (0.1%-1%) of potential
damage to the AV node. Such damage would require implantation of a permanent pacemaker.
Catheter ablation is highly effective in most cases of
PSVT, regardless of the mechanism. Research indicates
that ablation may be more effective for AVRT and AVNRT
(>95% success rate) than for the atrial tachycardias (>80%
success rate). Nevertheless, certain considerations, such as
a patient’s very advanced age or comorbidities, may lead a
physician to reject the use of catheter ablation. Cryoablation (ie, using extreme cold to produce a “lesion”) is
another procedure that can be used to ablate either AVNRT
or AVRT. Cryoablation may have a lower risk of inadvertent AV block than catheter ablation.33-36
Some patients with PSVT may prefer using medications
instead of undergoing ablation. Traditionally, AV nodal
blocking agents, such as verapamil and diltiazem, or !blockers are used first. Class I antiarrhythmic agents, such
as flecainide and propafenone, may also be effective. Such
drugs are preferable for patients with known WolffParkinson-White syndrome because they generally prolong
the effective refractory period of the accessory pathway.
Class I antiarrhythmic agents may also have some efficacy
in the prophylaxis of atrial fibrillation.
Patients with atrial tachycardia generally require the
use of an AV nodal blocking drug for atrial rate control. A
membrane-active drug can be used for prevention of atrial
tachycardia. Sotalol is a !-blocker with antiarrhythmic
properties that may be useful in any case of PSVT.
Amiodarone is effective in the management of PSVT, but
it is rarely indicated because of its potential toxicity over
the long term and because of the availability of effective
alternatives.
CONCLUSION
Paroxysmal SVT is a common presenting diagnosis among
patients with cardiac conditions, both in the emergency
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department and in the physician’s office. In the emergency department setting, the physician should conduct a
thorough assessment of the patient, followed by close
inspection of all available ECGs or cardiac rhythm strips.
Comorbid conditions and current drug therapies should
be considered before any decision is made regarding
treatment for patients with arrhythmia. When sinus
rhythm is restored, the physician should consider the
long-term management options for the patient, including
conservative pharmacologic and ablative strategies.
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The Symposium on Cardiovascular Diseases will continue in the January issue.
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