Cardiol Clin 24 (2006) 427437

The 12-Lead Electrocardiogram in Supraventricular Tachycardia

Uday 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 is essential for the perpetuation of the tachyarrhythmia [1]. Because of misdiagnosis and inconsistent classication, the exact prevalence of SVT is not clear but may be as high as six to eight per 1000 people in the United States [2]. SVT aects patients of varied ages, often can lead to symptoms, and may occur in patients with or without structural heart disease. The diagnosis of SVT is made primarily by using the 12-lead electrocardiogram (ECG). Correct ECG diagnosis of SVT is important for several reasons. First, because symptomatic patients who may have SVT often require rapid and accurate treatment, misidentication of the type of SVT can lead to inappropriate acute management. Second, making the correct ECG diagnosis of the type of SVT is important for long-term prognosis and treatment strategies, including the selection of eective medications or the decision to refer a patient for catheter ablation. Finally, for patients who do go on to catheter ablation, a correct ECG diagnosis of the type of SVT facilitates the appropriate choice of ablation strategy. The correct choice is essential because the risk, duration, complexity, and success rate of catheter ablation varies based on the type of SVT [3]. Despite its importance, making the correct ECG diagnosis of SVT type may be dicult for

numerous reasons. First, during the acute care of highly symptomatic or unstable patients who have possible SVT, the health care provider may be pressed for time. Second, the correct diagnosis may also be elusive when only a rhythm strip (as opposed to a 12-lead ECG) is available. Similarly, SVT may be suspected in hospitalized patients who are monitored on telemetry, but such monitoring equipment may not be able to generate a true 12-lead ECG. Third, the ECG morphology may be more unusual in patients taking antiarrhythmic medications or in patients who have had prior ablation or surgical procedures. For instance, patients who have congenital heart disease and have undergone corrective surgeries frequently develop SVT as a late complication [4,5]. Fourth, variability in the placement of ECG electrodes may aect the ECG tracing. Finally, the ECG computer diagnosis of arrhythmias is unreliable. These potential diculties represent just a few of the challenges to accurate ECG diagnosis of SVT. General points This article provides a stepwise approach to the 12-lead ECG diagnosis of SVT. It rst presents an initial approach to categorization and diagnosis. Then, the common ECG manifestations of each type of SVT are discussed individually. Finally, it presents a systematic algorithm for diagnosing suspected SVT based on the ECG. The various forms of SVT include sinus tachycardia (ST), focal atrial tachycardia (AT), multifocal atrial tachycardia (MAT), atrial brillation (AF), atrial utter (AFl), AV node reentrant
cardiology.theclinics.com

* Corresponding author. E-mail address: [email protected] (M.M. Scheinman).

0733-8651/06/$ - see front matter 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.ccl.2006.04.004

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tachycardia (AVNRT), AV reentrant tachycardia (AVRT), junctional tachycardia (JT), and permanent junctional reciprocating tachycardia (PJRT). The rst step in diagnosing SVT is to categorize the rhythm as narrow complex (QRS ! 120 milliseconds) or wide complex (QRS R 120 milliseconds) and as regular (xed R-R cycle lengths) or irregular (variable R-R cycle lengths) (Table 1). Some tachycardias are represented in more than one category. The next step is to look for evidence of atrial activity. If a discrete P wave is visible, the relationship of the P wave to the QRS complex should be evaluated. This relationship is characterized as either a short-RP tachycardia or a long-RP tachycardia. In short-RP tachycardia, the time from the P wave to 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 dierentiate the various types of SVT: heart rate during tachycardia; mechanism of initiation/termination; P wave/QRS/ST morphology; changes in cycle length with the appearance of bundle-branch block; and ECG changes in response to maneuvers such as carotid sinus massage or adenosine administration. One study reports that viewing

the ECG at both normal (25 mm/s) and faster (50 mm/s) paper speeds may improve diagnostic accuracy [6]. The ndings and criteria helpful in the diagnosis of each particular SVT are discussed in greater detail later. Sinus tachycardia ST is a long-RP tachycardia that presents with a heart rate over 100 beats/min (bpm). The P wave morphology is identical to that of normal sinus rhythm. There usually is a gradual onset and termination that often can be appreciated on Holter or telemetry monitoring. A variant of ST, sinus node reentrant tachycardia, comprises a reentrant loop originating in the sinus node, behaves clinically like an SVT, and has a sudden onset and abrupt termination. In sinus node reentry tachycardia, the PR interval during tachycardia may dier from normal sinus rhythm, although the P wave morphology is identical. True sinus node reentrant tachycardia seems to be uncommon, with most of the reported cases originating from high in the crista terminalis [7]. Patients who have another variant of ST, termed inappropriate sinus tachycardia, show persistent tachycardia during the day with marked increases in heart rate in response to exercise. This diagnosis is made from the 24-hour Holter recording, and beta-blockers are the drugs of choice.

Table 1 Initial categorization of tachycardic rhythms using the 12-lead electrocardiogram Rhythm Regular Narrow Short-RP Typical (slow-fast) AVNRT Atypical (slow-slow) AVNRT (usually) Orthodromic AVRT JT AT (less commonly) Long-RP Atypical (fast-slow) AVNRT Orthodromic AVRT (slowly conducting accessory pathway) ST AT (more commonly) PJRT Flutter waves AFl (xed AV block) AF AFl (variable AV block) MAT Wide ST, JT, AT, AVNRT, orthodromic AVRT, or AFl with aberrancy Antidromic AVRT Monomorphic ventricular tachycardia

Irregular

AF, AFl, or MAT with aberrancy AF, AFl with pre-excitation Polymorphic ventricular tachycardia

Abbreviations: AF, atrial brillation; AFl, atrial utter; AT, atrial tachycardia; AVNRT, atrioventricular node reentrant tachycardia; AVRT, atrioventricular reentrant tachycardia; JT, junctional tachycardia; MAT, multifocal atrial tachycardia; PJRT, permanent junctional reciprocating tachycardia; ST, sinus tachycardia.

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Focal atrial tachycardia AT is initiated and sustained within the atria and 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 by automaticity, triggered activity, or microreentry [810]. Rarely, digitalis toxicity can result in AT, usually with accompanying AV nodal block [11]. AT is usually a long-RP tachycardia with an atrial rate usually less than 250 bpm and a ventricular rate dependent on the presence or absence of AV nodal block [1]. A classic example of focal AT is shown in Fig. 1. AT caused by abnormal automaticity often exhibits a warm-up phenomenon in which the heart rate gradually speeds up before reaching a xed peak. The diagnosis of AT caused by triggered activity is often made in the electrophysiology laboratory when the AT can be initiated by pacing the atrium at a critical rate. AT caused by microreentry is often seen in patients who have structural heart disease, usually is initiated by a premature atrial beat, and typically is paroxysmal. It often is impossible to distinguish triggered from reentrant AT. For AT caused by abnormal automaticity, adenosine usually results in AV nodal block without terminating the AT. On the ECG, this AT is manifested as discernible P waves continuing at the AT rate with occasionally conducted QRS complexes. In contrast, triggered ATs usually are terminated with adenosine. Although these general aspects of the dierent types of AT can be useful in diagnosis, signicant overlap of these properties exists. To help localize the origin of the AT, one can begin 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 that are positive in V1 usually arise from the left atrium, whereas P waves that are positive in aVL usually arise from the right atrium or occasionally from the right pulmonary vein [12 15]. Positive P wave polarity in leads II, III, and aVF predicts a superior origin; negative P wave polarity in these leads predicts an inferior origin. The polarity of the P wave may be dicult to interpret if the P wave is inscribed upon the ST segment or T wave. Thus, the P wave morphology is interpreted best when the heart rate or ventricular rate is slowed, such as after adenosine administration. The ner points of P wave polarity during AT that are most relevant for the site of ablation are described in Table 2. Multifocal atrial tachycardia MAT is thought to be caused by enhanced automaticity of multiple competing atrial foci. MAT is almost always associated with pulmonary disease and rarely, if ever, is seen in the setting of digitalis toxicity. To make the diagnosis of MAT, at least three dierent P wave morphologies must be observed, which typically do not have a xed relationship to one another. The heart rate is greater than 100 bpm and usually is irregular (varying R-R intervals); the PR intervals may vary; and AV nodal block may be present. Atrial utter AFl is caused by a rapid macroreentrant circuit occurring in the atria. The atrial rate is usually 240 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 diers from that of sinus rhythm.

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Table 2 P wave morphology in atrial tachycardiadgeneral principles Location Right atrium or in aVL and in V1 P wave polarity during atrial tachycardia Crista terminalis (CT) May be , , or in II, II, aVF in the high, mid, and inferior CT, respectively; or in V1; in aVR in V1-V2; in aVL and frequently in I Insucient data in V1V6; in I; narrow P wave in V1 in V1V6; /isoelectric in aVL; broad or notched P wave in V1 with initially narrow negative deection in V1; /isoelectric in I, aVL; slightly /isoelectric in II, III, aVF Broadly in V1V6; in I, aVL; in II, III, aVF in V1; isoelectric in I; in II, III, aVF; in aVL, aVR / in V1; / in II, III, aVF / in V1; in two of three inferior leads (II, III, aVF) Uncommon; variable ndings

Left atrium

in aVL and in V1

Tricuspid annulus Right atrial appendage Right pulmonary veins Left pulmonary veins Mitral annulus

Left atrial appendage Interatrial septum and adjacent structures Specic to location Coronary sinus ostium Anteroseptum Mid septum Left septum Abbreviations: , positive; , negative; , biphasic. From Refs. [12,15,42].

depending on the degree of AV nodal block. Of note, chronic antiarrhythmic therapy may prolong 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 nodal block is variable. Unless the atrial rate is relatively slow, 1:1 conduction is unusual unless it occurs by an accessory pathway, which can result in wide pre-excited QRS complexes. The nomenclature of AFl is based on electroanatomic relationships observed during electrophysiology studies; if the circuit is dependent upon the cavotricuspid isthmus, it is dened as typical AFl [1720]. The reentrant circuit in typical AFl traverses the musculature around the tricuspid valve. If this circuit activates the lateral right atrium from superior to inferior and the septum from inferior to superior, it is termed counterclockwise typical AFl. If the lateral and septal activations occur in reverse, while still being dependent on the cavotricuspid isthmus, it is termed clockwise typical AFl. In contrast to discrete P waves, typical AFl usually results in utter waves having a saw-tooth pattern. An analysis of their polarity demonstrates that counterclockwise typical utter waves are positive in V1 and negative in leads II, III, and aVF

(Fig. 2). Clockwise typical utter waves are negative in V1 and positive in leads II, III, and aVF. Of note, although the macroreentrant circuit is located in the right atrium, the saw-tooth pattern and its polarity primarily reect the axis and sequence of left atrial activation. In contrast to typical AFl, atypical AFl is any other AFl that does not display a typical activation sequence. On the ECG, the saw-tooth utter waves may be absent, and the utter wave polarity diers from typical AFl. The utter waves may be quite varied in appearance and may appear similar to discrete P waves. For example, in atypical AFl arising from the left atrial septum, the utter waves are prominent in V1 but are at in 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 spatial extent of the macroreentrant circuit. Atypical AFl can originate in the left or right atrium, around a scar or surgical site, or around other structures, which partly explains the variability in its morphology and rate. The administration of adenosine can be important in the diagnosis of any type of AFl by virtue of its eect on the AV node: the slowing of the ventricular rate can make utter waves more readily discernible.

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Fig. 2. Typical, counterclockwise atrial utter. The utter waves are marked with arrows. Four-to-one atrioventricular block is present, which facilitates examination of the utter wave morphology. Note the characteristic saw-tooth appearance in the inferior leads (II, III, aVF) and the positive utter wave polarity in lead V1.

ECG diagnosis of typical versus atypical utter is clinically relevant, because the approach and success rate of catheter ablation dier [3,23,24]. Atrial brillation The ECG hallmarks of AF include an irregularly irregular variation in R-R interval and the absence of organized atrial activity. Underlying AF may still be present even if the R-R intervals are regular when concomitant complete AV nodal block with a junctional or subjunctional escape rhythm is present (occasionally seen with digitalis toxicity). Coarse AF may be confused with AFl; very ne AF may be confused with atrial paralysis. In addition to AF, irregular junctional rhythms, MAT, and AFl with variable block are also in the dierential diagnosis for irregularly irregular rhythms (see Table 1). The atrial rates in AF are variable but are usually greater than 350 bpm. The ventricular rate is usually signicantly slower and varies depending on AV nodal function, unless an accessory pathway capable of antegrade conduction is present. Atrioventricular node reentrant tachycardia Initiation of AVNRT is dependent on the presence of dual AV node physiology, with two pathways having diering conduction and refractory times. AVNRT can be divided into typical and atypical forms, with the typical form being more common [2,25]. Typical AVNRT, also known as slow-fast AVNRT, uses a slow AV nodal pathway for antegrade conduction and a fast pathway for retrograde conduction

(Fig. 3). Atypical AVNRT can be slow-slow AVNRT, using a slow antegrade and another slow retrograde pathway (with dierent properties), or fast-slow, using a fast antegrade and a 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 in AVRT [26]. There typically is a 1:1 AV relationship in AVNRT, but because the reentrant circuit resides within the area of the AV node, 2:1 AV block can be seen. Retrograde AV nodal atrial block can occur also, although less commonly. Typical AVNRT is initiated with an atrial premature beat and terminates with a P wave (antegrade slow pathway). AVNRT is terminated by adenosine (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 is detected on the septum, near the AV node. The RP interval is usually less than 70 milliseconds [28]. Because retrograde atrial activation occurs over a fast pathway, the retrograde P wave is superimposed on the QRS and appears as a pseudo S wave (present during AVNRT but not during normal sinus rhythm) that is best seen in leads II, III, and aVF. Similarly, a pseudo R0 may also be present in lead V1. These ECG ndings are important because they are infrequently seen in AVRT [29,30]. Having a pseudo S, a pseudo R0 , or both is 90% to 100% specic for typical AVNRT and has an 81% positive predictive value for typical AVNRT [29,30]. These criteria are only 42% sensitive for typical AVNRT, however [29]. Occasionally in typical AVNRT (20% of the time), the P wave is buried

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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 common in AVNRT and is seen to a lesser extent and in fewer leads than in AVRT [29]. In contrast to AVRT, QRS alternans is an uncommon nding in AVNRT and may be related more to the rapidity of the heart rate than to the underlying SVT mechanism [29,31]. Taking into account the pseudo S/R0 waves, the RP interval, and the lack of signicant ST depression in multiple leads (the Jaeggi algorithm), a correct diagnosis of typical AVNRT can be made by ECG analysis 76% of the time [28,29]. In atypical (slow-slow) AVNRT, the retrograde atrial activation usually is seen rst near the coronary sinus ostium. The P wave may be distinct from the QRS and appears negative in leads II, III, and aVF and positive in leads V1, V2, aVR, and aVL [32]. Atypical (slow-slow) AVNRT is usually a short-RP tachycardia and often cannot 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 or in the coronary sinus. This form of AVNRT is thought to use the same pathways as in typical AVNRT, but in reverse [34]. The P wave precedes the QRS and is negative in leads II, III, and aVF and is positive in leads V1, V2, aVR, and aVL. Atypical (fast-slow) AVNRT may be indistinguishable from a low AT or orthodromic AVRT with a posteroseptal pathway.

Orthodromic atrioventricular reentrant tachycardia The reentrant loop in AVRT is comprised of the atria, AV node, ventricle, and accessory pathway. In orthodromic AVRT, conduction occurs antegrade through the AV node and retrograde through an accessory pathway. Orthodromic AVRT is usually a short-RP tachycardia with an RP interval greater than 100 milliseconds [28,29]. If the accessory pathway has slow retrograde conduction, however, the RP is signicantly longer, consistent with a long-RP tachycardia. Orthodromic AVRT also is a narrow complex tachycardia, unless bundle-branch block or aberrancy is 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 ventricular premature beats and usually terminates with a QRS complex. AVRT can be terminated by adenosine (O90% of the time) or vagal maneuvers [27]. In normal sinus rhythm, antegrade conduction over an accessory pathway resulting in a short PR interval and a delta wave on the surface ECG is the hallmark of the Wol-Parkinson-White ECG pattern (Fig. 5). The delta wave is the ECG manifestation of ventricular pre-excitation. If no antegrade conduction is evident, but the pathway is capable of retrograde conduction, the pathway is dened as concealed. In Wol-Parkinson-White, the disappearance of the delta wave during tachycardia is caused by orthodromic AVRT. The loss

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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 from the loss of pre-excitation caused by a poorly conducting accessory pathway incapable of conducting 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 amplitude) is common (45% of cases), unlike AVNRT [29]. Also unlike AVNRT, ST segment depression of R2 mm is common in AVRT, particularly in patients who have no visible P wave or who have 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 Jaeggi algorithm, which takes into account the absence of pseudo S/R0 waves, an RP interval greater than 100 milliseconds, and the presence of ST depression of R2 mm, a correct diagnosis of AVRT can be made using the surface ECG 88% of the time [28,29].

After diagnosing AVRT, it is helpful to localize the pathway because the feasibility, approach, and success of catheter ablation depend on the pathway site. In Wol-Parkinson-White syndrome, the polarity of the delta wave during normal sinus rhythm often predicts accessory pathway location unless multiple accessory pathways are present (an occasional nding) [36,37]. Accessory pathway localization based on the delta wave during normal sinus rhythm has been described in detail previously [38,39]. The polarity and morphology of the retrograde P wave during orthodromic AVRT also may assist in pathway localization [14,32,35]. In general, a positive P wave in leads II, III, and aVF suggests an anterior accessory pathway; a negative P wave in leads II, III, and aVF suggests an inferior accessory pathway; a positive P wave in lead V1 or a negative P wave in lead I suggests a left-sided accessory pathway; and a negative P wave in lead V1 or a positive P wave in lead I suggests a right-sided accessory pathway.

Fig. 5. Wol-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).

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The development of bundle-branch block aberrancy during SVT also can be a helpful clue. If the tachycardia cycle length slows when bundlebranch block appears, then the SVT is an AVRT and not AVNRT or AT, because the ventricle is not an integral component of the circuit in these latter two arrhythmias. More importantly, the slowing of the tachycardia cycle length in with the appearance of bundle branch block proves that this AVRT uses an accessory pathway with the pathway on the same side as the blocked bundle branch. The increase in cycle length can be explained by the additional conduction time required for the depolarization wave front to go from the normally conducting bundle branch (on the contralateral side) across the ventricular septum and into the accessory pathway and atrium. Focal junctional tachycardia JT is uncommon in adults and often is a diagnosis of exclusion. This arrhythmia is more common in children and often is irregular. In adults, JT manifests as a regular, short-RP tachycardia (if ventriculo-atrial [VA] conduction is present) with a narrow QRS complex, unless bundle-branch aberrancy is present. It can be caused by enhanced automaticity or triggered activity. The VA relationship may be dissociated, associated with 1:1 retrograde conduction, or associated with various degrees of VA retrograde block [36]. When dissociation is present, the P waves seen on the ECG are most likely caused by sinus rhythm. If the P waves appear associated with the QRS rhythm, they typically are negative in leads II, III, and aVF because of retrograde atrial activation. The diagnosis of JT is based primarily on tachycardia initiation without the need for a critical AV nodal delay. Beta-blockers are

the initial drug of choice, and ablation may be recommended for drug-refractory cases. Permanent junctional reciprocating tachycardia PJRT is an incessant long-RP tachycardia, typically seen in children but occasionally seen in adults, which may lead to tachycardia cardiomyopathy [37]. The cardiomyopathy frequently abates after successful treatment of the arrhythmia. In PJRT the heart rate is usually between 100 and 200 bpm but can vary signicantly because of autonomic inuences [37]. The arrhythmia uses the atria, AV node, the ventricle, and an accessory pathway and is similar to orthodromic AVRT. PJRT enters into the dierential diagnosis of atypical AVNRT or AT originating from the inferior atrium. The accessory pathway usually is concealed and possesses decremental conduction properties. In most cases, the accessory pathway is within or near the coronary sinus ostium. PJRT usually starts spontaneously after a sinus beat and does not require a premature beat or a change in the PR interval for initiation. On the ECG, the QRS complexes usually are narrow and have a 1:1 AV relationship. The P waves usually are broad and negative in leads II, III, and aVF [38]. The RP interval is much longer in PJRT than in most orthodromic AVRTs. PJRT usually terminates in the retrograde limb, which is sensitive to vagal maneuvers [38,39]. Wide-complex supraventricular tachycardias caused by pre-excitation It is important to dierentiate patients who have pre-excited wide-complex tachycardia (WCT) from those who have SVT with aberrancy or ventricular tachycardia. Of particular concern are patients who have AF and AFl with antegrade

Fig. 6. Wide-complex tachycardia caused by atrial brillation in a dierent patient who had Wol-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.

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conduction through an accessory pathway. Because the accessory pathway does not possess the same decremental conduction properties as the AV node, AF or AFl with antegrade conduction through an accessory pathway may conduct rapidly, often with ventricular rates greater than 280 to 300 bpm, and may degenerate into ventricular brillation. An irregular, rapid WCT should 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 preexcitation. In all cases, delta waves should be present during tachycardia but may be overshadowed by the wide-complex morphology. In AF, AFl, or AT, varying degrees of fusion through the pathway and through the AV node may produce beat-to-beat variation in the QRS morphology. If the rhythm is maximally pre-excited, the QRS morphology may appear similar to that of patients who have ventricular tachycardia, but conversion to sinus rhythm will produce the preexcitation pattern in patients who have WolParkinson-White syndrome. Antidromic AVRT is a WCT that exhibits maximal pre-excitation (Fig. 7). In antidromic AVRT, conduction occurs antegrade through an accessory pathway and retrograde through the AV node. Delta waves should be evident both during normal sinus rhythm and during tachycardia. The retrograde P waves in antidromic AVRT are frequently seen in a 1:1 VA relationship preceding the QRS [40]. Because dual AV node physiology (having both fast and slow pathways) is common in patients who have accessory pathways, retrograde conduction may occur during antidromic AVRT by a slow AV nodal pathway,

a fast AV nodal pathway, or alternate between fast and slow AV nodal pathways [41]. Thus, the characteristics of the P wave and PR interval may 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 sinus rhythm  Evaluate the AV relationship (eg, 1:1, 2:1, dissociated) 4. If utter waves are seen or suspected  Evaluate their morphology, preferably if the ventricular rate can be slowed 5. If no P waves are seen  Look for irregularity or the absence of an isoelectric baseline, both suggesting AF  Look for a pseudo S/R0 to suggest AVNRT 6. Assess the underlying atrial and ventricular rates. 7. Examine the initiation (atrial premature beat, ventricular premature beat, warm-up, no initiating factors) and termination. (Does the SVT 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 happens 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.

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