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SUPRAVENTRICULAR ON CARDIOVASCULAR
TACHYCARDIA: DISEASES
DIAGNOSIS AND MANAGEMENT
Supraventricular tachycardia (SVT) includes all forms of tachycar- incidence of coronary artery disease of approximately
dia that either arise above the bifurcation of the bundle of His or
that have mechanisms dependent on the bundle of His. We con- 20%. By contrast, Clarke et al2 analyzed the SVT rate in a
ducted a review of the techniques used to differentiate the mecha- normal disease-free population with an age range of 16 to
nisms of SVT. We searched the PubMed and MEDLINE databases 65 years, reporting a rate of documented SVT of only 12%.
for English-language literature published from 1970 to 2008. Ar-
ticles were selected for either their historical importance or up-to- Harrison et al3 also reported a low SVT incidence rate of
date clinical data. This review focuses on techniques for scrutiniz- only 18%. Research has shown that the incidence of SVT,
ing electrocardiograms of patients, analyzing in particular the in particular the most common forms (ie, atrial
onset of tachycardia, the mode of tachycardia termination, and
the effects of premature ventricular contractions, premature atrial arrhythmias), increases with age and presence of cardiac
contractions, and aberrancy during tachycardia. Both short-term disease.4,5 However, SVT incidence is difficult to quantify
and long-term management of SVT are examined, including the precisely because of the high rate of asymptomatic epi-
urgent treatment of patients in the emergency department. This
review also describes management of patients who have ongoing sodes in patients.
symptomatic SVT, outlining such available treatment options as Although SVT includes such arrhythmias as atrial fibril-
atrioventricular node–blocking drugs, antiarrhythmic drugs, and lation and atrial flutter, the current review focuses on diag-
catheter ablation.
nosis, patient treatment, and management for the 3 most
Mayo Clin Proc. 2008;83(12):1400-1411 commonly encountered forms of paroxysmal (ie, sudden-
AV = atrioventricular; AVNRT = AV nodal reentrant tachycardia; AVRT =
onset) SVT (PSVT). These forms are AV nodal reentrant
AV reentrant tachycardia; BBB = bundle branch block; ECG = electro- tachycardia (AVNRT), AV reentrant tachycardia (AVRT),
cardiography; JET = junctional ectopic tachycardia; PAC = premature and atrial tachycardia.
atrial complex; PJRT = permanent junctional reciprocating tachycardia;
PSVT = paroxysmal supraventricular tachycardia; SVT = supraventricu-
lar tachycardia
METHODS
We searched the PubMed and MEDLINE databases for
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.
SUPRAVENTRICULAR TACHYCARDIA: DIAGNOSIS AND MANAGEMENT
Patients with PSVT may present either to the emergency cardia) longer than the PR interval (the conduction time
department or to the physician’s office. In patients who after the RP interval). During tachycardia, if the distance
have symptoms of tachycardia but no diagnosis based on from the R wave to the next P wave is longer than the
ECG results, appropriate steps need to be taken to ensure distance from that same P wave to the next R wave, the
that the tachycardia is recorded and that a symptom-rhythm condition is termed long RP tachycardia. If the distance
correlation exists. Hence, the use of ambulatory monitoring from the R wave to the next P wave is shorter than the
and event recorders may be required. distance from that same P wave to the next R wave, the
At presentation, PSVT may be associated with pre- condition is termed short RP tachycardia.
syncope, syncope, chest pain, and abnormal pulsations in
the neck.6 Syncope may occur if an episode of PSVT is
CLASSIFICATION AND MECHANISMS OF PSVT
extremely rapid, resulting in compromise in cardiac output,
or it may follow a prolonged pause immediately after spon- Paroxysmal SVT can be classified in several ways. The
taneous termination of tachycardia. Syncope may also be classifications may be based on ECG appearance (ie, long
related to the triggering of a vasovagal response caused by RP tachycardia or short RP tachycardia) or on the underly-
the tachycardia itself.7 The mechanism of chest pain is ing mechanism of tachycardia (ie, AV reentry, AV nodal
unclear. Although chest pain in PSVT is usually unrelated reentry, or atrial tachycardia). It is also clinically useful to
to coronary artery disease, such pain in older patients raises consider PSVT classifications in terms of whether the con-
the possibility of myocardial ischemia. dition is dependent on AV nodal conduction. This type of
By definition, PSVT is paroxysmal, both starting and consideration is useful because it generally allows the ar-
stopping abruptly. However, it may be prolonged because rhythmia to be classified clinically without the need for
of the cardiac adrenergic drive that builds up during PSVT specialized arrhythmia studies.
as a result of hypotension or anxiety. The build-up of Supraventricular tachycardia that persists even when
adrenergic drive results in a less perceptible transition to a AV block is achieved by carotid sinus massage or other
sinus tachycardia after the PSVT has terminated. An atrial interventions is clearly independent of AV nodal conduc-
tachycardia or junctional tachycardia may accelerate more tion. The use of adenosine may terminate some focal atrial
gradually and, thus, would be nonparoxysmal. Some pa- tachycardias, but some degree of AV block usually pre-
tients with PSVT may describe an urge to urinate, possibly cedes this termination, allowing the diagnosis of AV nodal
as a result of atrionatriuretic peptide release, which pro- independence. By contrast, if an intervention that causes
duces an intrinsic diuretic effect. AV block terminates the tachycardia, the SVT is clearly
In a less common scenario, some patients with SVT may AV node–dependent. Atrioventricular nodal dependence is
present with chronic cardiac failure and cardiomyopathy. more commonly encountered in the clinical setting than is
In such cases, patients generally do not experience palpita- AV nodal independence.
tions during tachycardia and will have excessive heart rates
until cardiac decompensation occurs. The tachycardia in
AV NODE–DEPENDENT ARRHYTHMIAS
these patients likely takes weeks or months to cause heart
failure, depending on the patient’s heart rate and on the The two most common forms of PSVT (ie, AVNRT and
amount of time that the patient experiences tachycardia AVRT) are both dependent on AV nodal conduction to
episodes. Ventricular dysfunction is usually reversible, maintain the tachycardia circuit. Any interruption of AV
even, to some degree, in patients who have not been treated nodal conduction will normally terminate tachycardia.
for long-standing tachycardia. These 2 arrhythmias are, of course, reentrant. In the case of
The mechanism of SVT is usually AV reentry involv- AVNRT, the reentrant circuit is small (ie, microreentrant)
ing a decremental accessory pathway, atypical AV nodal and is in or closely related to the AV node. In the case of
reentry, or atrial tachycardia.8 All these types of AV reen- AVRT, the reentrant circuit is large (ie, macroreentrant)
try are frequently referred to as permanent junctional and involves the atria, AV node, and ventricles.
reciprocating tachycardia (PJRT); strictly speaking, how- A much less common form of AV node–dependent ar-
ever, this term refers only to atypical AV nodal reentry.9,10 rhythmia is junctional ectopic tachycardia (JET).12,13 This
More recently, PJRT has become synonymous with AV arrhythmia is most common in childhood and may be associ-
reentry involving a slowly conducting decremental acces- ated with congenital heart disease. It may also be seen in the
sory pathway.11 early phase after surgery for congenital heart disease.12,13 The
The ECG appearance of PJRT is similar to that of SVT, mechanism of JET is abnormal automaticity in the AV nodal
but with the RP interval (the distance from the peak of the region. The ECG findings in JET show a tachycardia that, in
QRS to the onset of the next visible P wave during tachy- some cases, has identical ventricular and atrial rates, and, in
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.
SUPRAVENTRICULAR TACHYCARDIA: DIAGNOSIS AND MANAGEMENT
other cases, has a ventricular rate that is faster than the atrial procedures for assessing the role of the AV node in the
rate, with ventriculoatrial block. Tachycardia myopathy has tachycardia mechanism. Pharmacologic interventions are
been observed in cases in which the AV rate or rhythm has most useful for quickly determining the mechanism of an
not been adequately controlled.14,15 arrhythmia.
Features to consider in ECG interpretation include the
following: (1) tachycardia rate; (2) mode of onset and
AV NODE–INDEPENDENT ARRHYTHMIAS
termination of the tachycardia; (3) relative position of the P
Less commonly encountered forms of PSVT, including wave within the R-R interval; (4) morphology of the P
atrial tachycardia, are independent of AV nodal conduc- wave; (5) change in QRS morphology, including variabil-
tion. These arrhythmias may persist during AV block. The ity in cycle length and relative movement of the atrial ECG
source of these arrhythmias is usually a small focus, and the and ventricular ECG during variability in tachycardia rate;
mechanism is usually abnormal automaticity or triggered and (6) effect of intermittent BBB on the tachycardia.
activity. The mechanism is usually microreentrant, espe-
cially in diseased atria. TACHYCARDIA RATE
Atrial tachycardias (commonly called flutters, if suffi- Careful analysis of the R-R interval should be performed to
ciently rapid) may also occur as a result of a macroreentrant determine the rate of the tachycardia. A rate of 150 beats/
mechanism. However, the reentrant circuit in these min raises the suspicion of atrial flutter with 2:1 AV block
tachycardias lies within the atrium (eg, a surgical atriotomy because the usual atrial rate during flutter is 300 beats/
scar) and is not dependent on the AV node. Although PSVT min. In general, a tachycardia with an atrial rate of less
may be related to reentry in and around the sinus node than 160 to 170 beats/min and without a visible P wave
region, this type of reentry is rarely observed as a clinically implies the presence of the slow-pathway component of
relevant SVT. the AV node.
Technically, multifocal atrial tachycardia, atrial flutter, The most frequently encountered PSVT of this type is
and atrial fibrillation are all AV node–independent arrhyth- typical AV nodal reentry (ie, AVNRT), a schematic of
mias. However, these conditions are not discussed further which is shown in Figure 1. Atrial tachycardia or AVRT
in the current review. involving a slow AV nodal pathway for anterograde con-
duction are considerably less frequently observed than
AVNRT. Faster rates of tachycardia are not generally help-
INTERPRETATION OF ECG FINDINGS IN PSVT
ful in narrowing the differential diagnosis.
Most PSVTs are represented on ECGs as narrow QRS-
complex tachycardias, with the QRS duration being less MODE OF ONSET AND TERMINATION OF TACHYCARDIA
than 90 ms (ie, normal QRS duration). Tachycardia-contin- Onset. The physician should check if the onset of the
gent BBB (ie, aberrancy) is relatively frequent in patients patient’s tachycardia is captured on the ECG. Most PSVTs
with PSVT. Many of these patients may have preexistent are triggered by a premature atrial complex (PAC). If the
BBB, interventricular conduction delays, or some other PAC conducts to the ventricle with a very long PR interval at
QRS abnormality. These abnormalities carry over to the initiation of tachycardia (ie, a “jump” in the PR interval), the
tachycardia. physician can safely postulate that the tachycardia is
An initial analysis of ECG findings for a patient with dependent on anterograde slow-pathway conduction of the
PSVT is best followed by a methodical approach to ECG AV node to the ventricle. Atrioventricular nodal reentrant
interpretation, in which the physician reviews the elements tachycardia is the typical tachycardia that begins with this
of the differential diagnosis, either mentally or in writing, mechanism. It is important to remember that a PAC, if
and examines the evidence supporting each diagnostic pos- coupled closely enough, generally results in a longer PR
sibility. A high-quality12-lead ECG is much more useful in interval in the premature cycle because of normal decremen-
the clinical setting than limited presentations or individual tal AV nodal physiologic factors. Supraventricular tachy-
cardiac rhythm strips. The main ECG findings of interest cardias that start with a ventricular premature complex are
are compelling atrial activity and zones of transition, such usually AV node–dependent tachycardias. Supraventricular
as ectopy, cycle length change, or intermittent aberrant tachycardias are almost never atrial tachycardias.
conduction. Termination. Tachycardias in which the last event at
Interventions may be helpful if the mechanism of the termination is a P wave are highly unlikely to be atrial
tachycardia is unclear from examination of the routine tachycardias. If such conditions were atrial tachycardias, it
ECG or rhythm strips. Vagal stimulation maneuvers, such would be necessary to postulate that the last atrial beat
as carotid sinus massage or Valsalva maneuver, are classic 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 close comparison of P-wave morphology during sinus
tachycardia to terminate and, consequently, that the rhythm vs during the tachycardia.
condition is an AV node–dependent tachycardia. These guidelines for ECG interpretation have been vali-
Although an atrial tachycardia almost always terminates dated with electrophysiologic data. Kalbfleisch et al16 re-
with a ventricular complex, this observation may not be ported that more than 90% of AVNRTs and 87% of
helpful in diagnosis because some AV node–dependent AVRTs are short RP tachycardias. By contrast, only 11%
tachycardias also terminate in this manner. Figure 2 shows of atrial tachycardias present as short RP tachycardias.16
a schematic of 2 terminations of tachycardias.
MORPHOLOGY OF THE P WAVE
RELATIVE POSITION OF THE P WAVE WITHIN THE R-R INTERVAL P waves may be difficult to distinguish in ECGs, especially
When analyzing ECGs of any PSVT, the physician should during more rapid tachycardia, because of overlap with the
attempt to identify the presence of P waves. A widely used
classification nomenclature of PSVT morphology, as pre-
viously 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 si-
multaneous atrial and ventricular activation occurs, this
classification system can be used to rule out AVRT, point-
ing 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 distin-
guish 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 FIGURE 2. Schematic of 2 terminations of paroxysmal supraven-
morphologies, shown in the bottom panel of Figure 3, may tricular tachycardia (PSVT) as recorded on electrocardiograms. The
also represent atypical AVNRT or AVRT. Finally, sinus top panel demonstrates PSVT terminating with a ventricular com-
plex. The bottom panel shows PSVT terminating with an atrial
tachycardia is technically a long RP tachycardia, but it can complex, indicating that this patient is highly unlikely to have atrial
often be differentiated from atrial tachycardia through tachycardia.
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SUPRAVENTRICULAR TACHYCARDIA: DIAGNOSIS AND MANAGEMENT
QRS and T waves. If P waves are visible during tachycar- is negative or isoelectric (ie, electrically neutral) in lead
dia, comparison with P waves in sinus rhythm is useful. aVL. In addition, a positive P wave (ie, from the back to the
Although all available ECG leads require inspection, front) is observed in lead V1 in left atrial foci. This contrasts
evaluation of the inferior ECG leads (particularly lead II), with the negative or biphasic P wave observed in lead V1
as well as lead V1, is likely to be the most productive. A when the atrial tachycardia is of right atrial origin.
normal P wave has a positive QRS morphology in the In the long RP tachycardias caused by atrial tachy-
inferior leads because normal atrial activation begins at the cardias, the P-wave morphology provides the first approxi-
sinus node during sinus rhythm, with a wave of electrical mation of the site of the abnormal focus.17-19 These algo-
propagation moving toward the AV node (ie, high to low rithms may be useful if the physician attempts to ablate the
sequence). As this impulse moves toward the inferior leads, tachycardia.
it produces an upright P wave in leads II, III, and aVF. By
contrast, junctional-dependent rhythms, such as AVNRT CHANGE IN QRS MORPHOLOGY
and AVRT, and atrial tachycardias with origins in the A ventricular rate that is irregularly irregular (ie, a rate that
lower atrium result in negative P waves in the inferior is variable in unpredictable ways), including having an
leads. The negative P waves occur because these irregular baseline, suggests a diagnosis of atrial fibrillation.
tachycardias activate the atrium in the opposite direction The cycle length in most cases of PSVT is reasonably
(ie, low to high sequence). regular; however, it may oscillate in a patient who has dual
Careful analyses of other ECG leads can help physicians or multiple anterograde AV nodal pathways. In fact, most
to determine if the atria are being activated from left to oscillation in cycle length occurs in the anterograde part of
right or vice versa. This conclusion can be achieved by the circuit. Patients with atrial tachycardias may present
examining the morphology of the P wave in leads I and with a notably irregular ventricular rate if there is variable
aVL. In right atrial tachycardia foci, the P wave is positive block in the AV node.
or biphasic (ie, first negative, then positive) in lead aVL. A more subtle oscillation in cycle length can be diagnos-
That is because the right atrium is activated first, with the tically useful. If the ECG shows that the QRS change
wave of depolarization moving toward the left atrium and, initiates the P-wave change during SVT (ie, if the VV
thus, to lead aVL. In left atrial tachycardia foci, the P wave 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 Furthermore, BBB that occurs in either AVNRT or
reentrant tachycardia instead. The converse (ie, if the AA atrial tachycardia has no effect on the tachycardia cycle
change precedes the VV change) is less useful for diagnos- length because the bundle branches are not integral parts of
tic purposes, although such an observation usually suggests these tachycardia mechanisms.
an atrial tachycardia.
QRS alternans is a phasic alteration of the amplitude of
BROAD COMPLEX TACHYCARDIA
the QRS complex, of unclear mechanism, that is observed
SECONDARY TO PSVT
in 1 or more ECG leads. It is a nonspecific finding in faster
tachycardias regardless of mechanism. Thus, it most com- A PSVT may present as a broad complex tachycardia for 3
monly occurs in conjunction with AVRT (25%-38% of main reasons. First, a preexisting BBB, intraventricular
orthodromic AVRT, in which the usual direction of traffic conduction disturbance, or other QRS abnormality in sinus
is to the AV node). QRS alternans also occurs with rhythm will usually be manifested during tachycardia. Sec-
AVNRT (13%-23% of AVNRT), but it is virtually never ond, tachycardia-contingent BBB may occur if either the
seen with atrial tachycardia.16,20-22 right- or left-sided bundle branch reaches its effective re-
fractory period and cannot conduct impulses to match the
EFFECT OF INTERMITTENT BBB ON TACHYCARDIA rapid rate of the tachycardia. This condition is also called
A change in AV rate with the development of BBB aberra- functional BBB or rate-related BBB. Subtle features of the
tion can mean only that a bundle branch is part of the bundle branch may point to PSVT-related broad complex
tachycardia circuit. This characteristic excludes every SVT tachycardia rather than ventricular tachycardia. For ex-
mechanism except AV reentry. ample, in a patient with PSVT and a structurally normal
Bundle branch block that occurs ipsilateral to an acces- heart, the bundle branch pattern will usually have a typical
sory pathway results in prolongation of the ventriculoatrial appearance, virtually identical to conventional bundle
conduction time, which is generally reflected in the tachy- branch morphology.24 Statistically, this is by far the most
cardia cycle length.23 This association exists because those common cause of wide QRS morphology on ECG in pa-
bundle branches are active (if not obligatory) components tients with SVT. Third, the QRS morphology will be wide
of the tachycardia circuit. The converse is also true. If left- during SVT if the tachycardia is related to preexcitation or
sided BBB resolves during tachycardia and the cycle length conduction over an accessory pathway. The most common
decreases, an ipsilateral accessory pathway is suggested. preexcited tachycardia, other than atrial fibrillation, is anti-
By contrast, the development of right-sided BBB with a dromic tachycardia, in which the tachycardia proceeds in an
left-sided accessory pathway, or vice versa, will have no anterograde manner over an accessory pathway and returns
effect on the tachycardia cycle length because that bundle via the normal AV conduction system. The accessory path-
is not an integral part of the tachycardia circuit. Figure 4 way may also serve as a route for some other tachycardia
shows an ECG indicative of the sudden development of mechanism (eg, an atrial tachycardia conducted over an
right-sided BBB in a case of AVNRT. accessory pathway). In such a case, the accessory pathway is
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SUPRAVENTRICULAR TACHYCARDIA: DIAGNOSIS AND MANAGEMENT
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SUPRAVENTRICULAR TACHYCARDIA: DIAGNOSIS AND MANAGEMENT
VENTRICULAR PREEXCITATION
Preexcitation of the ventricles is indicated by the presence FIGURE 6. Schematic of orthodromic and antidromic tachycardia,
showing the relationship between the atrioventricular node (AVN) and
in the ECG of a shortened PR interval in association with the accessory pathway (AP) and the associated QRS morphology. The
slurring of the upstroke of the QRS complex.25 Preexci- top panel demonstrates anterograde conduction through the AV node
tation occurs as the sinus impulse travels to the ventricle and retrograde conduction to the atria via the accessory pathway.
This condition is an orthodromic tachycardia, which usually has a
via both the AV node and the accessory pathway, resulting narrow complex QRS morphology. The bottom panel demonstrates
in a fusion of ventricular activation via both the conven- anterograde conduction via an accessory pathway and retrograde
tional His-Purkinje system and the accessory pathway. Be- conduction via the AV node. This condition is an antidromic tachycar-
dia, presenting with a wide complex QRS morphology.
cause 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 Accessory pathways may conduct only intermittently or
ventricle first, forming a delta wave on the ECG. This be so far lateral as to ensure that the bulk of anterograde
slurring persists until AV nodal conduction propagates into ventricular activation during sinus rhythm occurs via the
the ventricle, activating the ventricles rapidly and resulting sinus node, resulting in an ECG that does not show
in a terminal QRS complex that is closer to normal in preexcitation. Although most accessory pathways are ca-
morphology. The greater the ventricular activation over an pable of bidirectional conduction, some are concealed,
accessory pathway, the more preexcitation occurs (thus, meaning that they are capable only of retrograde conduc-
the broader the QRS) and vice versa. tion. These accessory pathways never produce preexci-
Many algorithms used in diagnosis allow approximate tation on ECGs, and they can result only in orthodromic
localization of accessory pathways along the AV rings on tachycardia.
the basis of preexcited ECG morphology. These algo-
rithms are more reliable when the preexcitation is pre-
PREEXCITED ATRIAL FIBRILLATION
dominant. A minimally preexcited ECG makes precise
localization difficult; however, such ECG results gener- An association exists between accessory pathways and an
ally suggest a left lateral pathway that is much farther increased risk of atrial fibrillation. A classic feature of
away from the source of normal atrial activation than the preexcited atrial fibrillation is an irregularly irregular cycle
AV node.26,27 Accessory pathways are most commonly length in conjunction with an irregularly irregular QRS
located in the left lateral position (Figure 7), where the duration. This feature develops because the atrial fibrilla-
ECG shows a delta wave that is positive in lead V1 and tion wave fronts conduct to the ventricle via both the AV
negative in lead I. In right-sided pathways, the delta wave node and the accessory pathway, causing a fusion of ven-
is usually negative in lead V1 (with a QS pattern) and tricular activation over both structures. Unlike the conduc-
positive in lead I. tion properties of the AV node, the conduction properties
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SUPRAVENTRICULAR TACHYCARDIA: DIAGNOSIS AND MANAGEMENT
of accessory pathways are usually nondecremental. If the tachycardia-induced myopathy. Figure 8 shows an ECG
pathway has a short refractory period, conduction to the indicative of incessant postpartum atrial tachycardia.
ventricles at extremely rapid rates (>250 beats/min) is
possible and may lead to ventricular fibrillation.28
EMERGENCY MANAGEMENT OF PSVT
Accessory pathways are also capable of anterograde
conduction in cases of atrial tachycardia, AVNRT, and As with any emergency cardiac situation, the “golden rule
atrial flutter. In such cases, the pathway acts like a by- of ABC” (airway, breathing, circulation) should be fol-
stander, not participating in the mechanism driving the lowed in emergency management of PSVT. A rapid assess-
tachycardia. ment of the patient’s airway, breathing, and circulation
should be conducted, and all vital signs should be docu-
mented. If the patient is hemodynamically compromised or
PSVT SECONDARY
in cardiovascular collapse (both of which are unusual con-
TO ATRIAL TACHYCARDIA
ditions in PSVT), urgent direct-current cardioversion
Patients may present with atrial tachycardia at any age. should be performed without delay.29
Younger patients, especially those in the pediatric age Most patients who present with PSVT are hemody-
group, are most likely to have a focal atrial tachycardia namically stable, allowing enough time for physicians to
suggestive of abnormal automaticity or triggered activity. perform a thorough history, physical examination, and
Older patients, especially those with cardiac disease and 12-lead ECG examination. Patients should also ideally
such comorbidities as cardiorespiratory problems, are more undergo noninvasive blood pressure assessment, measure-
likely to have an atrial tachycardia substrate related to such ment of oxygen saturation levels, and continuous ECG
conditions as atrial stretch or scarring. monitoring. Oxygen supplementation should be used
Atrial tachycardia is usually revealed on an ECG as a long when necessary.
RP tachycardia, as in the bottom panel in Figure 3. The The initial strategy for terminating a PSVT is generally
mechanism of atrial tachycardia usually includes enhanced a vagotonic maneuver, such as carotid sinus massage.
automaticity, triggered activity, or reentry. If conduction However, the physician should evaluate the patient for the
happens conventionally to the ventricle via the AV node, presence of a carotid bruit (ie, abnormal sound) before
variable AV block may result. Atrial tachycardias may also attempting this maneuver, especially in elderly patients.
conduct in an anterograde manner over an accessory path- The Valsalva maneuver or possibly facial immersion in
way, resulting in a preexcited broad complex tachycardia. cold water may also be attempted. These methods serve to
Once again, the accessory pathway acts like a bystander, not increase vagal tone, which may prolong AV nodal refracto-
participating in the driving mechanism of the tachycardia. riness to the point of AV block, thereby terminating the
Atrial tachycardias can be incessant. In such cases, pa- tachycardia. It should be noted that vagotonic maneuvers
tients may present with chronic cardiac failure caused by will not terminate atrial tachycardia, but they may create
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SUPRAVENTRICULAR TACHYCARDIA: DIAGNOSIS AND MANAGEMENT
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SUPRAVENTRICULAR TACHYCARDIA: DIAGNOSIS AND MANAGEMENT
electrophysiologic study is performed to fully elucidate the department and in the physician’s office. In the emer-
nature of the SVT. gency department setting, the physician should conduct a
Catheter ablation has a high procedural success rate of thorough assessment of the patient, followed by close
approximately 95% for patients with clinical tachycardia, inspection of all available ECGs or cardiac rhythm strips.
particularly AVNRT and AVRT. As many as 5% of pa- Comorbid conditions and current drug therapies should
tients may experience a recurrence of tachycardia and re- be considered before any decision is made regarding
quire a second procedure. treatment for patients with arrhythmia. When sinus
In the case of AVNRT, the patient can be treated by rhythm is restored, the physician should consider the
performing careful ECG mapping and delivering radio- long-term management options for the patient, including
frequency energy to the slow-pathway area of the heart (ie, conservative pharmacologic and ablative strategies.
the posteromedial tricuspid annulus, near the coronary si-
nus ostium). In patients with AVNRT and in some patients
with accessory pathways, the site of ablation is extremely REFERENCES
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plantation of a permanent pacemaker. the normal human heart. Lancet. 1976;1(7984):508-512.
3. Harrison DC, Fitzgerald JW, Winkle RA. Contribution of ambulatory
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PSVT, regardless of the mechanism. Research indicates 1978;41(6):996-1004.
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