The 12-Lead Electrocardiogram in Supraventricular Tachycardia

Cardiol Clin 24 (2006) 427–437

The 12-Lead Electrocardiogramin Supraventricular TachycardiaUday N. Kumar, MD, Rajni K. Rao, MD,

Melvin M. Scheinman, MD*Division of Cardiology, Department of Medicine, 500 Parnassus Avenue, Box 1354, University of California,

San Francisco, San Francisco, California 94143, USA

The term supraventricular tachycardia (SVT)encompasses a range of common arrhythmias in

which the atrial or atrioventricular (AV) node isessential for the perpetuation of the tachyarrhyth-mia [1]. Because of misdiagnosis and inconsistentclassification, the exact prevalence of SVT is not

clear but may be as high as six to eight per 1000people in the United States [2]. SVT affects pa-tients of varied ages, often can lead to symptoms,

and may occur in patients with or without struc-tural heart disease.

The diagnosis of SVT is made primarily by

using the 12-lead electrocardiogram (ECG). Cor-rect ECG diagnosis of SVT is important forseveral reasons. First, because symptomatic pa-

tients who may have SVT often require rapid andaccurate treatment, misidentification of the typeof SVT can lead to inappropriate acute manage-ment. Second, making the correct ECG diagnosis

of the type of SVT is important for long-termprognosis and treatment strategies, including theselection of effective medications or the decision to

refer a patient for catheter ablation. Finally, forpatients who do go on to catheter ablation,a correct ECG diagnosis of the type of SVT

facilitates the appropriate choice of ablation strat-egy. The correct choice is essential because the risk,duration, complexity, and success rate of catheterablation varies based on the type of SVT [3].

Despite its importance, making the correctECG diagnosis of SVT type may be difficult for

* Corresponding author.

E-mail address: [email protected]

(M.M. Scheinman).

0733-8651/06/$ - see front matter � 2006 Elsevier Inc. All r

doi:10.1016/j.ccl.2006.04.004

numerous reasons. First, during the acute care ofhighly symptomatic or unstable patients who have

possible SVT, the health care provider may bepressed for time. Second, the correct diagnosismay also be elusive when only a rhythm strip (asopposed to a 12-lead ECG) is available. Similarly,

SVT may be suspected in hospitalized patientswho are monitored on telemetry, but such mon-itoring equipment may not be able to generate

a true 12-lead ECG. Third, the ECG morphologymay be more unusual in patients taking antiar-rhythmic medications or in patients who have had

prior ablation or surgical procedures. For in-stance, patients who have congenital heart diseaseand have undergone corrective surgeries frequently

develop SVT as a late complication [4,5]. Fourth,variability in the placement of ECG electrodesmay affect the ECG tracing. Finally, the ECGcomputer diagnosis of arrhythmias is unreliable.

These potential difficulties represent just a few ofthe challenges to accurate ECG diagnosis of SVT.

General points

This article provides a stepwise approach to

the 12-lead ECG diagnosis of SVT. It firstpresents an initial approach to categorizationand diagnosis. Then, the common ECG manifes-tations of each type of SVT are discussed in-

dividually. Finally, it presents a systematicalgorithm for diagnosing suspected SVT basedon the ECG.

The various forms of SVT include sinus tachy-cardia (ST), focal atrial tachycardia (AT), multifo-cal atrial tachycardia (MAT), atrial fibrillation

(AF), atrial flutter (AFl), AV node reentrant

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428 KUMAR et al

tachycardia (AVNRT), AV reentrant tachycardia(AVRT), junctional tachycardia (JT), and perma-nent junctional reciprocating tachycardia (PJRT).

The first step in diagnosing SVT is to catego-rize the rhythm as narrow complex (QRS ! 120milliseconds) or wide complex (QRS R 120milliseconds) and as regular (fixed R-R cycle

lengths) or irregular (variable R-R cycle lengths)(Table 1). Some tachycardias are represented inmore than one category. The next step is to look

for evidence of atrial activity. If a discrete Pwave is visible, the relationship of the P wave tothe QRS complex should be evaluated. This rela-

tionship is characterized as either a ‘‘short-RPtachycardia’’ or a ‘‘long-RP tachycardia.’’ Inshort-RP tachycardia, the time from the P waveto the preceding R wave is less than the time

from the P wave to the following R wave (RP !PR). In long-RP tachycardia, the opposite is true(RP O PR) (see Table 1).

In addition to cycle regularity and QRS width,the following ECG criteria may help differentiatethe various types of SVT: heart rate during

tachycardia; mechanism of initiation/termination;P wave/QRS/ST morphology; changes in cyclelength with the appearance of bundle-branch

block; and ECG changes in response to maneu-vers such as carotid sinus massage or adenosineadministration. One study reports that viewing

the ECG at both normal (25 mm/s) and faster(50 mm/s) paper speeds may improve diagnosticaccuracy [6]. The findings and criteria helpful in

the diagnosis of each particular SVT are discussedin greater detail later.

Sinus tachycardia

ST is a long-RP tachycardia that presents witha heart rate over 100 beats/min (bpm). The

P wave morphology is identical to that of normalsinus rhythm. There usually is a gradual onset andtermination that often can be appreciated on

Holter or telemetry monitoring. A variant of ST,sinus node reentrant tachycardia, comprises a re-entrant loop originating in the sinus node, behavesclinically like an SVT, and has a sudden onset and

abrupt termination. In sinus node reentry tachy-cardia, the PR interval during tachycardia maydiffer from normal sinus rhythm, although the

P wave morphology is identical. True sinus nodereentrant tachycardia seems to be uncommon,with most of the reported cases originating from

high in the crista terminalis [7]. Patients who haveanother variant of ST, termed ‘‘inappropriate si-nus tachycardia,’’ show persistent tachycardiaduring the day with marked increases in heart

rate in response to exercise. This diagnosis ismade from the 24-hour Holter recording, andbeta-blockers are the drugs of choice.

Table 1

Initial categorization of tachycardic rhythms using the 12-lead electrocardiogram

Rhythm Narrow Wide

Regular Short-RP ST, JT, AT, AVNRT, orthodromic AVRT,

or AFl with aberrancyTypical (slow-fast) AVNRT

Atypical (slow-slow) AVNRT (usually) Antidromic AVRT

Orthodromic AVRT Monomorphic ventricular tachycardia

JT

AT (less commonly)

Long-RP

Atypical (fast-slow) AVNRT

Orthodromic AVRT (slowly conducting

accessory pathway)

ST

AT (more commonly)

PJRT

Flutter waves

AFl (fixed AV block)

Irregular AF AF, AFl, or MAT with aberrancy

AFl (variable AV block) AF, AFl with pre-excitation

MAT Polymorphic ventricular tachycardia

Abbreviations: AF, atrial fibrillation; AFl, atrial flutter; AT, atrial tachycardia; AVNRT, atrioventricular node reen-

trant tachycardia; AVRT, atrioventricular reentrant tachycardia; JT, junctional tachycardia; MAT, multifocal atrial

tachycardia; PJRT, permanent junctional reciprocating tachycardia; ST, sinus tachycardia.

429THE 12-LEAD ECG IN SUPRAVENTRICULAR TACHYCARDIA

Focal atrial tachycardia

AT is initiated and sustained within the atriaand is manifested by a single P wave morphology.The P wave morphology depends of the site of

origin of the tachycardia. AT may be caused byautomaticity, triggered activity, or microreentry[8–10]. Rarely, digitalis toxicity can result in AT,usually with accompanying AV nodal block [11].

AT is usually a long-RP tachycardia with an atrialrate usually less than 250 bpm and a ventricularrate dependent on the presence or absence of

AV nodal block [1]. A classic example of focalAT is shown in Fig. 1.

AT caused by abnormal automaticity often

exhibits a ‘‘warm-up’’ phenomenon in which theheart rate gradually speeds up before reachinga fixed peak. The diagnosis of AT caused bytriggered activity is often made in the electrophys-

iology laboratory when the AT can be initiated bypacing the atrium at a critical rate. AT caused bymicroreentry is often seen in patients who have

structural heart disease, usually is initiated bya premature atrial beat, and typically is paroxys-mal. It often is impossible to distinguish triggered

from reentrant AT. For AT caused by abnormalautomaticity, adenosine usually results in AVnodal block without terminating the AT. On the

ECG, this AT is manifested as discernible P wavescontinuing at the AT rate with occasionallyconducted QRS complexes. In contrast, triggeredATs usually are terminated with adenosine. Al-

though these general aspects of the different typesof AT can be useful in diagnosis, significantoverlap of these properties exists.

To help localize the origin of the AT, one canbegin by analyzing the P wave polarity. To

distinguish a right atrial from a left atrial location,aVL and V1 are the essential leads. P waves thatare positive in V1 usually arise from the leftatrium, whereas P waves that are positive in

aVL usually arise from the right atrium oroccasionally from the right pulmonary vein [12–15]. Positive P wave polarity in leads II, III, and

aVF predicts a superior origin; negative P wavepolarity in these leads predicts an inferior origin.The polarity of the P wave may be difficult to in-

terpret if the P wave is inscribed upon the ST seg-ment or T wave. Thus, the P wave morphology isinterpreted best when the heart rate or ventricular

rate is slowed, such as after adenosine administra-tion. The finer points of P wave polarity duringAT that are most relevant for the site of ablationare described in Table 2.

Multifocal atrial tachycardia

MAT is thought to be caused by enhancedautomaticity of multiple competing atrial foci.MAT is almost always associated with pulmonarydisease and rarely, if ever, is seen in the setting of

digitalis toxicity. To make the diagnosis of MAT,at least three different P wave morphologies mustbe observed, which typically do not have a fixed

relationship to one another. The heart rate isgreater than 100 bpm and usually is irregular(varying R-R intervals); the PR intervals may

vary; and AV nodal block may be present.

Atrial flutter

AFl is caused by a rapid macroreentrant circuitoccurring in the atria. The atrial rate is usually240 to 340 bpm; the ventricular rate varies,

Fig. 1. Focal atrial tachycardia with 1:1 conduction. Note the narrow, regular tachycardia. The P waves are marked

with arrows (long-RP interval), and the P wave morphology differs from that of sinus rhythm.

430 KUMAR et al

Table 2

P wave morphology in atrial tachycardiadgeneral principles

Location P wave polarity during atrial tachycardia

Right atrium þ or � in aVL

and � in V1

Crista terminalis (CT) May be þ, �, or � in II, II, aVF in the high,

mid, and inferior CT, respectively; � or � in V1;

� in aVR

Tricuspid annulus � in V1-V2; þ in aVL and frequently in I

Right atrial appendage Insufficient data

Left atrium � in aVL and Right pulmonary veins þ in V1–V6; þ in I; narrow P wave in V1

þ in V1 Left pulmonary veins þ in V1–V6; �/isoelectric in aVL; broad or

notched P wave in V1

Mitral annulus � with initially narrow negative deflection

in V1; �/isoelectric in I, aVL; slightly

þ/isoelectric in II, III, aVF

Left atrial appendage Broadly þ in V1–V6; � in I, aVL; þ in II,

III, aVF

Interatrial septum

and adjacent

structures

Specific to

location

Coronary sinus ostium þ in V1; isoelectric in I; � in II, III, aVF; þ in aVL,

aVR

Anteroseptum �/� in V1; þ/� in II, III, aVF

Mid septum �/� in V1; � in two of three inferior

leads (II, III, aVF)

Left septum Uncommon; variable findings

Abbreviations: þ, positive; �, negative; �, biphasic.From Refs. [12,15,42].

depending on the degree of AV nodal block. Of

note, chronic antiarrhythmic therapy may pro-long atrial refractoriness and slow the AFl rate[16]. The atrial-to-ventricular ratio can be regular

(eg, 2:1, 4:1) or irregular if the degree of AV nodalblock is variable. Unless the atrial rate is relativelyslow, 1:1 conduction is unusual unless it occurs by

an accessory pathway, which can result in widepre-excited QRS complexes.

The nomenclature of AFl is based on electro-

anatomic relationships observed during electro-physiology studies; if the circuit is dependentupon the cavotricuspid isthmus, it is defined astypical AFl [17–20]. The reentrant circuit in typ-

ical AFl traverses the musculature around the tri-cuspid valve. If this circuit activates the lateralright atrium from superior to inferior and the

septum from inferior to superior, it is termedcounterclockwise typical AFl. If the lateral andseptal activations occur in reverse, while still be-

ing dependent on the cavotricuspid isthmus, it istermed clockwise typical AFl. In contrast to dis-crete P waves, typical AFl usually results in flut-

ter waves having a saw-tooth pattern. Ananalysis of their polarity demonstrates that coun-terclockwise typical flutter waves are positive inV1 and negative in leads II, III, and aVF

(Fig. 2). Clockwise typical flutter waves are neg-

ative in V1 and positive in leads II, III, and aVF.Of note, although the macroreentrant circuit islocated in the right atrium, the saw-tooth pattern

and its polarity primarily reflect the axis and se-quence of left atrial activation.

In contrast to typical AFl, atypical AFl is any

other AFl that does not display a typical activa-tion sequence. On the ECG, the saw-tooth flutterwaves may be absent, and the flutter wave polarity

differs from typical AFl. The flutter waves may bequite varied in appearance and may appearsimilar to discrete P waves. For example, inatypical AFl arising from the left atrial septum,

the flutter waves are prominent in V1 but are flatin the other leads and may appear similar to AT[21,22]. The atrial rate of atypical AFl may also be

quite varied, depending on the location and spa-tial extent of the macroreentrant circuit. AtypicalAFl can originate in the left or right atrium,

around a scar or surgical site, or around otherstructures, which partly explains the variabilityin its morphology and rate. The administration

of adenosine can be important in the diagnosisof any type of AFl by virtue of its effect on theAV node: the slowing of the ventricular rate canmake flutter waves more readily discernible.


Fig. 2. Typical, counterclockwise atrial flutter. The flutter waves are marked with arrows. Four-to-one atrioventricular

block is present, which facilitates examination of the flutter wave morphology. Note the characteristic saw-tooth appear-

ance in the inferior leads (II, III, aVF) and the positive flutter wave polarity in lead V1.

ECG diagnosis of typical versus atypical flutter isclinically relevant, because the approach and suc-

cess rate of catheter ablation differ [3,23,24].

Atrial fibrillation

The ECG hallmarks of AF include an irregu-larly irregular variation in R-R interval and the

absence of organized atrial activity. UnderlyingAF may still be present even if the R-R intervalsare regular when concomitant complete AV nodal

block with a junctional or subjunctional escaperhythm is present (occasionally seen with digitalistoxicity). Coarse AF may be confused with AFl;

very fine AF may be confused with atrial paral-ysis. In addition to AF, irregular junctionalrhythms, MAT, and AFl with variable block arealso in the differential diagnosis for irregularly

irregular rhythms (see Table 1). The atrial ratesin AF are variable but are usually greater than350 bpm. The ventricular rate is usually signifi-

cantly slower and varies depending on AV nodalfunction, unless an accessory pathway capable ofantegrade conduction is present.

Atrioventricular node reentrant tachycardia

Initiation of AVNRT is dependent on thepresence of dual AV node physiology, with twopathways having differing conduction and refrac-

tory times. AVNRT can be divided into typicaland atypical forms, with the typical form beingmore common [2,25]. Typical AVNRT, also

known as slow-fast AVNRT, uses a slow AVnodal pathway for antegrade conduction anda fast pathway for retrograde conduction

(Fig. 3). Atypical AVNRT can be slow-slowAVNRT, using a slow antegrade and another

slow retrograde pathway (with different proper-ties), or fast-slow, using a fast antegrade anda slow retrograde pathway. The heart rate in

AVNRT can vary from 118 to 264 bpm (mean,181 � 35) and is similar to the rates seen inAVRT [26]. There typically is a 1:1 AV relation-

ship in AVNRT, but because the reentrant circuitresides within the area of the AV node, 2:1 AVblock can be seen. Retrograde AV nodal atrialblock can occur also, although less commonly.

Typical AVNRT is initiated with an atrial prema-ture beat and terminates with a P wave (antegradeslow pathway). AVNRT is terminated by adeno-

sine (O90% of the time) or vagal maneuvers,which can be useful in making a diagnosis [27].

Typical AVNRT is a short-RP tachycardia in

which the earliest retrograde atrial activity isdetected on the septum, near the AV node. TheRP interval is usually less than 70 milliseconds[28]. Because retrograde atrial activation occurs

over a fast pathway, the retrograde P wave issuperimposed on the QRS and appears asa pseudo S wave (present during AVNRT but

not during normal sinus rhythm) that is bestseen in leads II, III, and aVF. Similarly, a pseudoR0 may also be present in lead V1. These ECG

findings are important because they are infre-quently seen in AVRT [29,30]. Having a pseudoS, a pseudo R0, or both is 90% to 100% specific

for typical AVNRT and has an 81% positive pre-dictive value for typical AVNRT [29,30]. Thesecriteria are only 42% sensitive for typicalAVNRT, however [29]. Occasionally in typical

AVNRT (20% of the time), the P wave is buried

432 KUMAR et al

Fig. 3. Typical atrioventricular node reentrant tachycardia. Note the rapid, regular, narrow complexes, the pseudo

S wave in leads I, II, and aVF, and the small pseudo R0 wave in lead V1.

within the QRS and is invisible [26]. Additionally,

ST segment depression of R2 mm is less commonin AVNRT and is seen to a lesser extent and infewer leads than in AVRT [29]. In contrast toAVRT, QRS alternans is an uncommon finding

in AVNRT and may be related more to the rapid-ity of the heart rate than to the underlying SVTmechanism [29,31]. Taking into account the

pseudo S/R0 waves, the RP interval, and the lackof significant ST depression in multiple leads(the Jaeggi algorithm), a correct diagnosis of typ-

ical AVNRT can be made by ECG analysis 76%of the time [28,29].

In atypical (slow-slow) AVNRT, the retro-

grade atrial activation usually is seen first nearthe coronary sinus ostium. The P wave may bedistinct from the QRS and appears negative inleads II, III, and aVF and positive in leads V1, V2,

aVR, and aVL [32]. Atypical (slow-slow) AVNRTis usually a short-RP tachycardia and often can-not be distinguished from orthodromic AVRT,

as discussed later [31,33].Atypical (fast-slow) AVNRT is a long-RP

tachycardia in which the earliest retrograde atrial

activity is seen in the posteroseptal right atrium orin the coronary sinus. This form of AVNRT isthought to use the same pathways as in typical

AVNRT, but in reverse [34]. The P wave precedesthe QRS and is negative in leads II, III, and aVFand is positive in leads V1, V2, aVR, and aVL.Atypical (fast-slow) AVNRT may be indistin-

guishable from a low AT or orthodromic AVRTwith a posteroseptal pathway.

Orthodromic atrioventricular reentrant

tachycardia

The reentrant loop in AVRT is comprised ofthe atria, AV node, ventricle, and accessorypathway. In orthodromic AVRT, conduction

occurs antegrade through the AV node andretrograde through an accessory pathway. Ortho-dromic AVRT is usually a short-RP tachycardiawith an RP interval greater than 100 milliseconds

[28,29]. If the accessory pathway has slow retro-grade conduction, however, the RP is significantlylonger, consistent with a long-RP tachycardia. Or-

thodromic AVRT also is a narrow complex tachy-cardia, unless bundle-branch block or aberrancyis present (Fig. 4). The heart rate in AVRT ranges

from 124 to 256 bpm (mean, 183 � 32 bpm) [32].AVRT usually is initiated with one or more ven-tricular premature beats and usually terminateswith a QRS complex. AVRT can be terminated

by adenosine (O90% of the time) or vagal maneu-vers [27].

In normal sinus rhythm, antegrade conduction

over an accessory pathway resulting in a short PRinterval and a delta wave on the surface ECG isthe hallmark of the Wolff-Parkinson-White ECG

pattern (Fig. 5). The delta wave is the ECG man-ifestation of ventricular pre-excitation. If no ante-grade conduction is evident, but the pathway is

capable of retrograde conduction, the pathway isdefined as concealed. In Wolff-Parkinson-White,the disappearance of the delta wave during tachy-cardia is caused by orthodromic AVRT. The loss


Fig. 4. Orthodromic atrioventricular reentrant tachycardia. Note the narrow, regular, rapid tachycardia. The P waves

buried in the ST segment (short-RP interval) are marked with an arrow. No pseudo S/R0 waves are seen.

of the delta wave during sinus rhythm results fromthe loss of pre-excitation caused by a poorly con-ducting accessory pathway incapable of conduct-

ing at higher rates.Most patients who have orthodromic AVRT

(81%–87%) have visible retrograde P waves that

are best seen in leads I, II, III, aVF, and V1[29,32]. QRS alternans (alternating QRS ampli-tude) is common (45% of cases), unlike AVNRT[29]. Also unlike AVNRT, ST segment depression

of R2 mm is common in AVRT, particularly inpatients who have no visible P wave or whohave an RP interval less than 100 milliseconds;

the ST depressions also are seen in several leads(mean, 4.4 � 1.4 leads) [29]. By using the Jaeggialgorithm, which takes into account the absence

of pseudo S/R0 waves, an RP interval greaterthan 100 milliseconds, and the presence of ST de-pression of R2 mm, a correct diagnosis of AVRTcan be made using the surface ECG 88% of the

time [28,29].

After diagnosing AVRT, it is helpful to localizethe pathway because the feasibility, approach, andsuccess of catheter ablation depend on the path-

way site. In Wolff-Parkinson-White syndrome, thepolarity of the delta wave during normal sinusrhythm often predicts accessory pathway location

unless multiple accessory pathways are present (anoccasional finding) [36,37]. Accessory pathwaylocalization based on the delta wave during nor-mal sinus rhythm has been described in detail pre-

viously [38,39]. The polarity and morphology ofthe retrograde P wave during orthodromicAVRT also may assist in pathway localization

[14,32,35]. In general, a positive P wave in leadsII, III, and aVF suggests an anterior accessorypathway; a negative P wave in leads II, III, and

aVF suggests an inferior accessory pathway; a pos-itive P wave in lead V1 or a negative P wave in leadI suggests a left-sided accessory pathway; anda negative P wave in lead V1 or a positive P wave

in lead I suggests a right-sided accessory pathway.

Fig. 5. Wolff-Parkinson-White pattern. Note the short PR interval, the delta waves (pre-excitation), which are positive

in leads I and aVL and negative in leads II, III, and aVF, and the transition of the delta wave axis from lead V1 to V2

(consistent with a right posteroseptal accessory pathway).

434 KUMAR et al

The development of bundle-branch block ab-errancy during SVT also can be a helpful clue. Ifthe tachycardia cycle length slows when bundle-

branch block appears, then the SVT is an AVRTand not AVNRT or AT, because the ventricle isnot an integral component of the circuit in theselatter two arrhythmias. More importantly, the

slowing of the tachycardia cycle length in with theappearance of bundle branch block proves thatthis AVRT uses an accessory pathway with the

pathway on the same side as the blocked bundlebranch. The increase in cycle length can beexplained by the additional conduction time re-

quired for the depolarization wave front to gofrom the normally conducting bundle branch (onthe contralateral side) across the ventricularseptum and into the accessory pathway and

atrium.

Focal junctional tachycardia

JT is uncommon in adults and often is a di-agnosis of exclusion. This arrhythmia is more

common in children and often is irregular. Inadults, JT manifests as a regular, short-RPtachycardia (if ventriculo-atrial [VA] conduction

is present) with a narrow QRS complex, unlessbundle-branch aberrancy is present. It can becaused by enhanced automaticity or triggered

activity. The VA relationship may be dissociated,associated with 1:1 retrograde conduction, orassociated with various degrees of VA retrogradeblock [36]. When dissociation is present, the P

waves seen on the ECG are most likely causedby sinus rhythm. If the P waves appear associatedwith the QRS rhythm, they typically are negative

in leads II, III, and aVF because of retrogradeatrial activation. The diagnosis of JT is based pri-marily on tachycardia initiation without the need

for a critical AV nodal delay. Beta-blockers are

the initial drug of choice, and ablation may be rec-ommended for drug-refractory cases.

Permanent junctional reciprocating tachycardia

PJRT is an incessant long-RP tachycardia,typically seen in children but occasionally seenin adults, which may lead to tachycardia cardio-

myopathy [37]. The cardiomyopathy frequentlyabates after successful treatment of the arrhyth-mia. In PJRT the heart rate is usually between100 and 200 bpm but can vary significantly be-

cause of autonomic influences [37]. The arrhyth-mia uses the atria, AV node, the ventricle, andan accessory pathway and is similar to ortho-

dromic AVRT. PJRT enters into the differentialdiagnosis of atypical AVNRT or AT originatingfrom the inferior atrium. The accessory pathway

usually is concealed and possesses decrementalconduction properties. In most cases, the acces-sory pathway is within or near the coronary sinus

ostium. PJRT usually starts spontaneously aftera sinus beat and does not require a prematurebeat or a change in the PR interval for initiation.On the ECG, the QRS complexes usually are nar-

row and have a 1:1 AV relationship. The P wavesusually are broad and negative in leads II, III, andaVF [38]. The RP interval is much longer in PJRT

than in most orthodromic AVRTs. PJRT usuallyterminates in the retrograde limb, which is sensi-tive to vagal maneuvers [38,39].

Wide-complex supraventricular tachycardiascaused by pre-excitation

It is important to differentiate patients who

have pre-excited wide-complex tachycardia(WCT) from those who have SVT with aberrancyor ventricular tachycardia. Of particular concern

are patients who have AF and AFl with antegrade

Fig. 6. Wide-complex tachycardia caused by atrial fibrillation in a different patient who had Wolff-Parkinson-White

syndrome. Note the very rapid rate, the irregularity, and the wide, bizarre, varying QRS morphology caused by varying

degrees of fusion from AV node conduction and antegrade accessory pathway conduction. The negative delta wave in

lead II suggests a posterior (inferior) accessory pathway location.


conduction through an accessory pathway. Be-cause the accessory pathway does not possess thesame decremental conduction properties as theAV node, AF or AFl with antegrade conduction

through an accessory pathway may conductrapidly, often with ventricular rates greater than280 to 300 bpm, and may degenerate into ven-

tricular fibrillation. An irregular, rapid WCTshould raise suspicion for AF with pre-excitation(Fig. 6). Similarly, AFl or AT with very rapid or

1:1 AV conduction should raise concern for pre-excitation. In all cases, delta waves should be pres-ent during tachycardia but may be overshadowed

by the wide-complex morphology. In AF, AFl, orAT, varying degrees of fusion through the path-way and through the AV node may producebeat-to-beat variation in the QRS morphology.

If the rhythm is maximally pre-excited, theQRS morphology may appear similar to that ofpatients who have ventricular tachycardia, but

conversion to sinus rhythm will produce the pre-excitation pattern in patients who have Wolff-Parkinson-White syndrome.

Antidromic AVRT is a WCT that exhibitsmaximal pre-excitation (Fig. 7). In antidromicAVRT, conduction occurs antegrade through an

accessory pathway and retrograde through theAV node. Delta waves should be evident bothduring normal sinus rhythm and during tachycar-dia. The retrograde P waves in antidromic AVRT

are frequently seen in a 1:1 VA relationship pre-ceding the QRS [40]. Because dual AV node phys-iology (having both fast and slow pathways) is

common in patients who have accessory path-ways, retrograde conduction may occur duringantidromic AVRT by a slow AV nodal pathway,

a fast AV nodal pathway, or alternate betweenfast and slow AV nodal pathways [41]. Thus, thecharacteristics of the P wave and PR intervalmay vary during tachycardia.

Summary of steps required for ECG diagnosis

of SVT

1. Assess QRS width and regularity.2. Look for evidence of atrial activity.

3. If distinct P waves are seen� Determine the RP relationship� Evaluate the P wave morphology during

SVT and, if possible, during normal sinusrhythm� Evaluate the AV relationship (eg, 1:1, 2:1,dissociated)

4. If flutter waves are seen or suspected� Evaluate their morphology, preferably ifthe ventricular rate can be slowed

5. If no P waves are seen� Look for irregularity or the absence of anisoelectric baseline, both suggesting AF

� Look for a pseudo S/R0 to suggest AVNRT6. Assess the underlying atrial and ventricular

rates.7. Examine the initiation (atrial premature beat,

ventricular premature beat, warm-up, no ini-tiating factors) and termination. (Does theSVT terminate with a P wave or a QRS;

does it cool down slowly?)8. Examine the response to adenosine. (Does it

terminate the tachycardia, and, if so, how?

Does it cause AV block, and, if so, what hap-pens to the underlying atrial rhythm?)

Fig. 7. Antidromic atrioventricular reentrant tachycardia in the same patient as in Fig. 5, using a right posteroseptal

accessory pathway. Note the wide-complex, regular rhythm. The delta waves are more prominent because of maximal

pre-excitation.

436 KUMAR et al

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Documents

The 12-Lead Electrocardiogram in Supraventricular Tachycardia