Differential Diagnosis of Supraventricular Tachycardia from the Electrocardiogram

ECG documentation of the tachycardia is essential for the proper diagnosis and management of SVT. SVT may sometimes present with wide QRS complexes, and a clinical EPS is helpful in determining if the cause is bundle branch block (BBB) or aberrent conduction. Differentiating PSVT from ventricular tachycardia (VT), particularly when pre-excitation is present, is definitively accomplished at EPS.

Electrophysiological Study of Supraventricular Tachycardia

An EPS is used for diagnostic and therapeutic purposes. During these procedures the underlying atrial and ventricular substrate is assessed. PSVT initiation during these procedures allows ECG documentation of the underlying symptoms of the tachycardia, such as evanescent palpitations, if it has not been previously recorded; definition of the mechanism of the tachycardia and the critical components of the circuit; evaluation of symptoms and hemodynamics during the arrhythmia; and, if indicated, performance of radiofrequency ablation or evaluation of the efficacy of antiarrhythmic therapy.

Atrioventricular Re-entrant Tachycardia and Atrioventricular Node Re-entrant Tachycardia

The methods of catheter placement and programmed electrical stimulation are discussed in detail in Chapter 20 and are not revisited here in detail. In brief, multipolar electrode catheters are placed in the right atrium, His bundle region, coronary sinus, and right ventricle. Recordings are obtained from these regions as well as the right and left AV ring for bypass tract mapping or more detailed septal pathway localization. Programmed atrial stimulation is usually performed from the high right atrium, coronary sinus, right ventricular apex, and the atrial or ventricular insertion site of a bypass tract as needed. In some instances, alternate pacing sites can include the left atrium, right ventricular outflow tract, right ventricular septum, or left ventricle. For the study of propagation and induction of tachycardia, the extrastimulus technique is widely used, although burst pacing is an alternative. These techniques are discussed in Chapter 20. Facilitiation of induction may require the administration of pharmacologic agents such as isoproterenol or atropine (see Chapter 72). Other pharmacologic agents such as adenosine may be used for diagnostic purposes to evaluate the presence of accessory pathway conduction or termination of PSVT involving the AV node (see Chapter 72).

Most SVTs are caused by a re-entrant mechanism and may be induced in the laboratory by using programmed electrical stimulation. In A-V junctional tachycardias, electrophysiological study permits induction of tachycardia in more than 90% of patients with AVRT or AVNRT. In patients with AVNRT, premature atrial stimulation can demonstrate dual AV nodal conduction and induce the tachycardia to determine its mechanism. The arrhythmias associated with WPW syndrome include reciprocating or circus movement tachycardias and atrial arrhythmias. In some instances of AVNRT, concomitant pre-excited QRS complexes may exist because of passive conduction over an accessory pathway that may serve as a passive bystander. Tachycardias related to Mahaim fibers have a particular electrocardiographic presentation with LBBB and left-axis deviation. The ECG in sinus rhythm shows the features of WPW syndrome (Figure 24-1). The electrophysiological study often demonstrates decremental conduction over the accessory pathway.

FIGURE 24-1 Tachycardias with pre-excited QRS complexes. Top to bottom, Electrocardiogram leads I, II, and V1; high right atrium (HRA); and left atrium (LA1 and LA2). A, Consistent with an antidromic reciprocating tachycardia. B, Atrial fibrillation conducted over a left-sided accessory atrioventricular (AV) pathway termination of supraventricular tachycardia with vagal maneuvers.

Dual Atrioventricular Nodal Pathway

During electrophysiological evaluation, typical AVNRT manifests antegrade conduction via a “slow” pathway and retrograde conduction via a “fast” pathway.^1–10 The electrophysiological characteristic is the presence of dual AV nodal pathway physiology demonstrated by a discontinuous AV node functional curve. Discontinuous AV nodal conduction is defined as a sudden increment of 50 ms or greater in the A-H or H-A interval (“jump”), with a decrement in prematurity of the extrastimulus by 10 to 20 ms. In some patients, a jump (>50 ms) of any consecutive A-H intervals during incremental atrial pacing is found, which might be a manifestation of dual AV nodal pathways. Typically, the jump phenomenon is followed by induction of a slow-fast AVNRT (Figure 24-2). During tachycardia in typical slow-fast AVNRT, a long A-H interval with a short V-A interval can be documented (Figure 24-3). When performing endocardial mapping, the earliest atrial activation during tachycardia can be detected at the slow pathway area around the coronary sinus ostium. In contrast, atypical AVNRT has antegrade conduction through a “fast” or “slow” pathway and retrograde conduction through a “slow” pathway.^2,3

FIGURE 24-2 Induction atrioventricular nodal re-entrant tachycardia (AVNRT). Atrial extra stimulus pacing with an A-H jump and induction of typical slow-fast AVNRT. HRA, High right atrium.

FIGURE 24-3 Typical slow-fast atrioventricular nodal re-entrant tachycardia with a short V-A interval.

To differentiate AVNRT from AVRT, the following maneuvers can be used^4–6:

FIGURE 24-4 Miller stimulation. AVNRT, Atrioventricular nodal re-entrant tachycardia; RV, right ventricle; RVA, right ventricular apex.

FIGURE 24-5 Miller stimulation. AV, Atrioventricular; RVA, right ventricular apex.

FIGURE 24-6 Programmed stimulation. AP, Accessory pathway; AVNRT, atrioventricular nodal re-entrant tachycardia; RVA, right ventricular apex.

FIGURE 24-7 Programmed stimulation. AP, Accessory pathway; AV, Atrioventricular.

Two important concepts of dual AV nodal pathways have been further clarified by provocative pharmacologic testing and catheter ablation in patients with AVNRT. One major question has been whether dual AV nodal pathways are fully intranodal and caused by longitudinal dissociation of AV nodal tissue or extranodal, involving separate atrial inputs into the AV node. From clinical studies of slow pathway potentials, LH (low followed by high) frequency potentials are observed during asynchronous activation of muscle bundles above and below the coronary sinus orifice. HL (high followed by low) frequency potentials are caused by asynchronous activation of atrial cells and a band of nodal-type cells that may represent the substrate of the slow pathway.^7–10 Thus the slow and fast pathways are likely to be atrionodal approaches or connections rather than discrete intranodal pathways. The results of catheter ablation indicate that the fast and slow pathways have their origins outside the limits of the compact AV node and that the tissues targeted during successful ablation are composed of ordinary working atrial myocardium surrounding the AV node itself.^11–14 Furthermore, AV or VA conduction block during AVNRT favors the concept that atrial and ventricular tissues are not involved in the maintenance of this tachycardia (Figures 24-8 and 24-9).^15,16

FIGURE 24-8 A, Right ventricular stimulus induces atrioventricular nodal re-entrant tachycardia (AVNRT). Although the last pacing beat (vertical line) does not conduct to the atrium, AVNRT still occurs. B, AVNRT with occasional retrograde conduction to the atrium (arrows). HRA, High right atrium; HIS-P, proximal portion of the His bundle; HIS-M, medial portion of the His bundle; HIS-D, distal portion of the His bundle; CSO, coronary sinus ostium.

FIGURE 24-9 Infra-His block during typical slow-fast atrioventricular nodal re-entrant tachycardia. HIS, Quadrupolar catheter in His position; HRA, quadrupolar catheter in high right atrium.

Unusual Physiology of Dual Atrioventricular Nodal Pathways

Some patients with AVNRT have multiple antegrade and retrograde AV nodal pathways with multiple discontinuities in the AV node function curve or dual AV nodal pathways with a continuous curve during programmed electrical stimulation.^13,17 Furthermore, variant forms (slow-slow, slow-intermediate, fast-intermediate) of AVNRT have been noted (Figures 24-10 and 24-11).^11–13 Whether multiple antegrade and retrograde AV nodal pathways originate from anatomically different pathways or represent anisotropic conduction–induced functional pathways is still being debated. Several investigators have demonstrated the marked heterogeneity of the transitional cells surrounding the compact AV nodal pathway. The non-uniform properties of the AV node can produce anisotropic conduction and suggest that the antegrade and retrograde fast pathways are anatomically distant from the multiple “antegrade slow” and “retrograde slow” or intermediate pathways, respectively. Clinical studies have demonstrated that successful ablation or modification of retrograde slow and intermediate pathways occurs at different sites from the antegrade fast or slow pathway, and the possibility of anatomically different antegrade or retrograde multiple pathways should be considered. Furthermore, in the patients who have successful ablation of multiple antegrade slow pathways or retrograde slow and intermediate pathways at a single site, anisotropic conduction over the low septal area of the right atrium is a possible explanation for the presence of multiple antegrade and retrograde AV nodal pathways.^11–1317

FIGURE 24-10 A to D, Atrioventricular (AV) nodal conduction curve with multiple jumps. Five patterns of tachycardia (slow-fast form) induction demonstrated by AV node conduction curves (A₂H₂ vs. A₁A₂). A₂H₂, atrio–His bundle conduction interval in response to atrial extra stimulus; A₁A₂, coupling interval of atrial extra stimulus. Purple circles indicate fast pathway conduction; blue circles indicate slow pathway conduction without initiation or maintenance of sustained tachycardia; red circles indicate slow pathway conduction with initiation and maintenance of sustained tachycardia. A, Only the first slow pathway is used for induction and maintenance of sustained tachycardia (pattern 1). B, Only the second slow pathway is used for induction and maintenance of sustained tachycardia (pattern 2). C, The first slow pathway is used during sustained tachycardia; either the first or the second slow pathway is used for initiation of tachycardia (pattern 3). D, The first slow pathway is used during sustained tachycardia; any of the three slow pathways is used for initiation of tachycardia (pattern 4). E, The third slow pathway is used during sustained tachycardia; either the second or third slow pathway is used for initiation of tachycardia (pattern 5). F, AV nodal conduction curve without AH jump. Curve relating A₂H₂ interval to prematurity of atrial extra stimuli (A₁A₂). Before ablation, a smooth curve without evidence of dual AV nodal pathway is present (s). After critical AH delay, tachycardia also is induced (green triangles). Ablation in the slow pathway zone eliminates the “tail” of the curve.

(E, From Tai CT, Chen SA, Chiang CE, et al: Multiple anterograde atrioventricular node pathways in patients with atrioventricular node reentrant tachycardia, J Am Coll Cardiol 28:725–731, 1996. F, From Tai CT, Chen SA, Chiang CE, et al: Complex electrophysiological characteristics in atrioventricular nodal reentrant tachycardia with continuous atrioventricular node function curves, Circulation 95:2541–2547, 1997.)

FIGURE 24-11 Recordings show four types of atrioventricular nodal re-entrant tachycardia (AVNRT) and echo. A and B, The baseline state. C and D, Intravenous infusion of isoproterenol. A, Induction of slow-fast form of AVNRT by atrial extra stimulus, with the earliest atrial activation at the ostium of the coronary sinus (OCS). D, A slow-slow form AVNR echo before termination of slow-intermediate form of AVNRT. A₂ and H₂, Atrial and His bundle response to the atrial extra-stimulus (S₂), respectively; HRA, high right atrium; HBE₁, distal bundle of His area; HBE₂, proximal bundle of His area; PCS, proximal coronary sinus; MCS, middle coronary sinus; S₁, basic paced beats; S₂, extra stimulus.

(From Tai CT, Chen SA, Chiang CE, et al: Electrophysiologic characteristics and radiofrequency catheter ablation in patients with multiple atrioventricular nodal reentry tachycardias, Am J Cardiol 77:52–58, 1996.)

Patients with AVNRT can have continuous AV node conduction curves. These patients do not exhibit an A-H jump with two extrastimuli and two drive cycle lengths during atrial pacing from the high right atrium and the coronary sinus ostium. The possible mechanisms of the continuous AV node function curves in AVNRT include the following: (1) the functional refractory period of the atrium limits the prematurity with which atrial premature depolarization will encounter the refractoriness in the AV node, which, in turn, produces inability to dissociate the fast and slow AV node pathways; and (2) fast and slow AV nodal pathways have similar refractory periods and conduction times.¹⁷

Anatomy and Electrophysiology of Accessory Pathways

The oblique orientation of most accessory pathways has been demonstrated by detailed endocardial and epicardial mapping techniques.^18–20 The locations of atrial and ventricular insertion sites of accessory pathways can differ by up to 2 cm; furthermore, some accessory pathways have antegrade and retrograde conduction fibers at different locations. This finding has been proven by different ablation sites for antegrade as well as retrograde conduction.²¹ Thus the anatomic and functional dissociation of the accessory pathway into atrial and ventricular insertions and antegrade and retrograde components is possible. Approximately 90% of AV accessory pathways have fast conduction properties, and the other accessory pathways (including Mahaim fibers) show decremental conduction properties during atrial or ventricular stimuli with shorter coupling intervals.^22–25 These pathways with decremental conduction may be sensitive to several antiarrhythmic drugs, including verapamil and adenosine. Accessory pathways in the right free wall and posteroseptal areas have a higher incidence of decremental conduction properties. When decremental conduction is present, the possibility of Mahaim fibers, such as atriofascicular or nodoventricular pathways, must be considered. Several studies have demonstrated that most of the ventricular insertion sites of these particular bypass tracts are close to the right bundle branch and that the typical Mahaim fiber potential can be recorded along the tricuspid annulus in patients with the atriofascicular pathways (Figure 24-12).^26–29

FIGURE 24-12 A, A mapping catheter along the posterolateral aspect of tricuspid annulus records the Mahaim fiber potential (arrow). B, Application of radiofrequency (RF) energy on this point (arrow) eliminates Mahaim fiber conduction with disappearance of ventricular pre-excitation. HRA, High right atrium; ABL, ablation; CSO, coronary sinus ostium; CSP, proximal coronary sinus; RVA, right ventricular apex.

Electrophysiological Findings in Atrioventricular Re-entry Tachycardia

The manifest accessory pathway can be diagnosed from the 12-lead surface ECG with a typical δ wave and is confirmed by a reduced, absent, or negative H-V interval. During the electrophysiological study, recordings should be obtained from the tricuspid annulus and the mitral annulus directly or indirectly from the coronary sinus as well as the normal AV nodal–His conduction system. Atrial and ventricular pacing and extrastimulation, isoproterenol provocation, and induction of atrial fibrillation (AF) to assess antegrade conduction over an accessory pathway are essential elements of the electrophysiological study. Ventricular pacing and extrastimulation can define retrograde conduction properties such as refractoriness and conduction time and the location of the pathway. Switching of conduction between the accessory pathway and the AV nodal–His axis can be demonstrated on reaching the effective refractoriness of one or the other conduction pathway. Atrial pacing or extrastimulation can accentuate antegrade pre-excitation up to the refractoriness of the pathway. Tachycardia induction requires unidirectional block in one of the AV conduction pathways (AV node–His axis or accessory pathway) coupled with critical conduction delay in the circuit.

For the diagnosis of accessory pathway–mediated AVRT, a premature ventricular depolarization can be delivered during the tachycardia when the bundle of His is refractory and the impulse still conducts to the atrium; this indicates that retrograde propagation conducts to the atrium over a pathway other than the normal AV conduction system. The definition of AVRT involves re-entry over one or more AV accessory pathways and the AV node, and the classic classification of AVRT includes orthodromic and antidromic tachycardias.^29–31 For the initiation of orthodromic tachycardia, a critical degree of delay in the A-V or V-A interval, which can be in the AV node or His-Purkinje system, is usually necessary. However, dual AV nodal pathway physiology, with or without AVNRT, can be noted in some patients (Figure 24-13). Ventricular pacing from different sites can provide valuable information about retrograde conduction through the AV node or via a septal pathway (Figure 24-14). The incidence of antidromic AVRT is much lower than orthodromic AVRT. Comparison with sinus rhythm shows a fully pre-excited QRS complex. Rapid conduction in retrograde AV nodal–His axis is necessary for the initiation and maintenance of antidromic tachycardia. The atrial premature beat usually can advance the next pre-excited ventricular complex through the antegrade accessory pathway, or it can terminate the AVRT through collision with the previous retrograde wavefront (Figure 24-15). The incidence of multiple accessory pathways is approximately 5% to 20%, and antidromic tachycardia is common in this situation.

FIGURE 24-13 Right ventricular extrastimulus (S₁S₂) with V3 phenomenon induces atrioventricular (AV) re-entry tachycardia with retrograde conduction through the left lateral accessory pathway. Left, The first and second tachycardia beats show antegrade conduction time (A-H interval) of 133 and 180 ms, respectively. Right, The S₁S₂ coupling interval is shorter than that on the left, and the antegrade conduction time is much longer in the first tachycardia beat than the second tachycardia beat (256 vs. 178 ms), with the difference larger than 50 ms suggesting the possibility of antegrade conduction through the slow pathway in the first tachycardia beat. HRA, High right atrium; HIS-P, proximal portion of the His bundle; HIS-M, medial portion of the His bundle; HIS-D, distal portion of the His bundle; CSO, coronary sinus ostium; CSD, distal portion of the coronary sinus; RVA, right ventricular apex.

FIGURE 24-14 Left, Delivery of two right ventricular apex stimuli during tachycardia without changing the tachycardia cycle length (417 ms) or atrial cycle length. The earliest atrial activation is on the proximal part of the coronary sinus. Middle, Ventricular stimuli from the right ventricular apex with the same pacing cycle length as tachycardia cycle length, and the interval from stimulus to atrial activation on the coronary sinus is 220 ms. Right, Ventricular stimuli from the basal part of the right ventricle with the same pacing cycle length as tachycardia cycle length. The interval from stimulus to atrial activation on the CS is 220 ms. The retrograde bundle of His potential is found before atrial activation. The stimulus to the A interval (220 ms) is much longer than the QRS-A interval during tachycardia. These findings suggest atrioventricular nodal re-entrant tachycardia with demonstration of a lower common pathway during ventricular pacing and exclude the possibility of retrograde accessory pathway in the posteroseptal area.

FIGURE 24-15 A, A 12-lead electrocardiogram (ECG) during sinus rhythm. B, Surface 12-lead ECG of antidromic tachycardia.

C, Rapid atrial pacing (S) induces antidromic atrioventricular (AV) re-entry tachycardia with antegrade conduction through right free wall accessory pathway and retrograde conduction through slow AV nodal pathway (earliest retrograde atrial activation in the coronary sinus ostium [CSO]). D, One atrial premature beat pre-excites the ventricle through the accessory pathway; however, this atrial premature beat (S) also collides with retrograde atrial activation, and AV re-entry tachycardia is terminated. HRA, High right atrium.

The most difficult situation for the differential diagnosis of AVRT is the so-called Mahaim tachycardia, which includes atriofascicular or nodofascicular (or nodoventricular) re-entry tachycardia and AVNRT with an “innocent bystander” bypass tract. These arrhythmias often appear as wide-complex tachycardias with LBBB and left-axis deviation. However, the presence of ventriculoatrial dissociation favors nodofascicular tachycardia. Sternick et al recently described a simple parameter to distinguish between decremental or rapidly conducting pathways during pre-excited tachycardia: An AV interval of more than 150 ms during pre-excited tachycardia is reliable for detecting a decrementally conducting accessory pathway.³²