Color Atlas and Synopsis of Electrophysiology, 1st Ed.


Rakesh Latchamsetty, MD, and Fred Morady, MD


A 60-year-old woman with previous history of supraventricular tachycardia (SVT) and who had undergone two prior ablation procedures for SVT presents with recurrent episodes of palpitations and fatigue. The patient’s most recent ablation procedure had been performed 1 week earlier. She had presented with nearly incessant tachycardia, and the electrophysiology study had revealed orthodromic reciprocating tachycardia (ORT) utilizing two separate left lateral pathways. The two left-sided accessory pathways were successfully ablated, and the patient remained arrhythmia-free for several days. She now presents to the emergency department in a narrow QRS complex tachycardia with a cycle length of 370 to 430 ms that spontaneously terminates and reinitiates with atrial premature depolarizations (APDs).

The patient arrived in the electrophysiology laboratory in narrow QRS complex tachycardia (Figure 14-1). The tachycardia demonstrates frequent cycle length variability with the septal atrial electrogram at times simultaneous with the QRS complex. During the study, the tachycardia occasionally terminated with spontaneous APDs. Spontaneous reinduction would occur soon thereafter with APDs that did not display atrial-His interval (AH) prolongation.


FIGURE 14-1 Patient’s presenting rhythm. The ablation catheter is positioned in the low right atrial septum, and a decapolar catheter is positioned in the coronary sinus (SC). Note the significant cycle length variability of the tachycardia with the septal atrial electrogram at times within the QRS complex. ABL = Ablation; d = distal; p = proximal; RVA = right ventricular apex; SC = coronary sinus.

Cycle length variability as great as 60 ms, as seen in Figure 14-1, is most commonly observed during atrial tachycardia. The occasionally simultaneous activation of the atria and ventricle ruled out orthodromic reciprocating tachycardia (ORT) as a sole diagnosis. Atrioventricular nodal reentrant tachycardia (AVNRT) with multiple slow pathways or multiple coexisting tachycardias could not be ruled out.

Ventricular pacing during the tachycardia revealed a V-A-V response (Figure 14-2). This response eliminates atrial tachycardia as the only mechanism of the tachycardia.1 The postpacing interval (PPI) in this tracing exceeded the tachycardia cycle length (TCL) by 100 msec, which is inconsistent with a diagnosis of AVNRT.2


FIGURE 14-2 Entrainment of the tachycardia by ventricular pacing revealed a V-A-V response, consistent with either atrioventricular nodal reentrant tachycardia (AVNRT) or orthodromic reciprocating tachycardia. The postpacing interval minus the tachycardia cycle length was 100 ms, which is inconsistent with AVNRT. ABL = Ablation; d = distal; p = proximal; RVA = right ventricular apex; SC = coronary sinus.

Induction by atrial pacing (or spontaneous APDs) was not dependent on critical AH prolongation. Figure 14-3 shows an example of initiation with a single ventricular premature depolarization (VPD) with a V-A-A-V response. As is the case upon cessation of ventricular pacing that entrains a tachycardia, induction with a V-A-A-V response is indicative of an atrial tachycardia.


FIGURE 14-3 Tachycardia is initiated with a single ventricular premature depolarization. The method of induction is a V-A-A-V response, strongly indicating atrial tachycardia as the mechanism of the tachycardia. ABL = Ablation; d = distal; p = proximal; RVA = right ventricular apex; SC = coronary sinus.

A single tachycardia mechanism fails to adequately explain all of the findings previously described. The PPI <115 ms following ventricular entrainment made AVNRT unlikely. Initiation of the tachycardia with ventricular pacing followed by a V-A-A-V response as well as the significant tachycardia cycle length variability with lack of stability in the V-A interval confirms the presence of an atrial tachycardia. Entrainment with a V-A-V response with a relatively short PPI-TCL also suggests the presence of an accessory pathway and probable ORT.

Atrial activation mapping during the tachycardia demonstrated earliest atrial activation at the low right atrial septum. Ablation here terminated the tachycardia and rendered it noninducible. Following ablation, ventricular pacing demonstrated VA dissociation, indicating that both the atrial tachycardia and a posteroseptal accessory pathway were ablated at the same target site. The site of origin of the atrial tachycardia had been at or very close to the atrial insertion of the accessory pathway.


Diagnosis of ORT utilizing a concealed septal accessory pathway is made based on tachycardia characteristics and pacing maneuvers during SVT. Differentiation of ORT from atypical AVNRT or in some cases focal atrial tachycardia can be challenging. Here, we describe techniques to differentiate these tachycardia mechanisms.

Para-Hisian pacing can be a valuable tool to confirm the presence of retrograde septal accessory pathway conduction as well as to verify successful septal accessory pathway ablation. The goal of para-Hisian pacing is to pace near the His bundle at high output and to gradually decrease the pacing output to produce complexes with right ventricular plus His capture and complexes with only right ventricular capture. When rapid retrograde conduction proceeds through an accessory pathway, similar conduction times from the pacing stimulus to the atrial electrogram are expected regardless of His capture. When no retrograde accessory pathway conduction is present, conduction proceeds through the atrioventricular node, and conduction time will be abbreviated with His capture. Caution should be used when interpreting results of this maneuver to ascertain that only the right ventricle and His bundle were captured during pacing (Figure 14-4). Furthermore, slowly conducting and nonseptal accessory pathways can also result in a “nodal” response to this maneuver. Following successful accessory pathway ablation, this maneuver can be repeated to demonstrate a nodal response.


FIGURE 14-4 Pacing is performed at the His level with varying outputs. Similar VA conduction times are seen with both right ventricular capture (first three paced complexes) and His + right ventricular capture (remaining paced complexes). However, the VA conduction time <70 ms is highly suggestive of atrial capture,5 and therefore this maneuver does not confirm the presence of a septal accessory pathway. HRA = high right atrium; RVA = right ventricular apex.


With spontaneous tachycardia cycle length variability, changes in atrial electrogram intervals (A-A) will precede and predict changes in the His electrogram intervals (H-H) during atrial tachycardia. Changes in the H-H interval predicting changes in the A-A interval rules out atrial tachycardia as a mechanism and strongly favors ORT or typical AVNRT. Repeated spontaneous termination of the SVT with an atrial electrogram also eliminates atrial tachycardia from the diagnosis, as maintenance of an atrial tachycardia is independent of atrioventricular nodal conduction. When atrioventricular block is observed during tachycardia, ORT is eliminated as a diagnosis.

Ventricular pacing during SVT that entrains the SVT with resumption of the tachycardia upon pacing termination is a valuable maneuver for differentiating ORT from atrial tachycardia. When a V-A-V response upon pacing termination is elicited, atrial tachycardia can be eliminated as a diagnosis. During this maneuver, a diagnosis of AVNRT can also be excluded when the corrected postpacing interval (PPI) exceeds the tachycardia cycle length (TCL) by <115 msec,2 or if upright P waves in the inferior surface ECG leads are revealed. Even when ventricular pacing fails to entrain the tachycardia, the results may still be helpful. AV dissociation without interruption of the tachycardia during ventricular pacing eliminates ORT as a tachycardia mechanism (Figure 14-5) and strongly favors an atrial tachycardia or AVNRT with retrograde lower common pathway block. Termination of the tachycardia during ventricular pacing can also be useful to differentiate mechanisms of the tachycardia. When termination occurs with a paced ventricular stimulus at a time when the His-Purkinje system is refractory, the presence of an accessory pathway is verified. If termination occurs in this setting without advancement of the next atrial electrogram, a diagnosis of ORT is established (Figure 14-6).


FIGURE 14-5 Ventricular pacing fails to entrain the tachycardia; however, this produces atrioventricular dissociation with continuation of the tachycardia. This is incompatible with a diagnosis of orthodromic reciprocating tachycardia. In this example, the upright P waves in the inferior leads also rules out a diagnosis of atrioventricular nodal reentrant tachycardia and establishes atrial tachycardia as the tachycardia mechanism. d = distal; HRA = high right atrium; m = middle; p = proximal; RVA = right ventricular apex.


FIGURE 14-6 A premature ventricular stimulus is delivered at a time when the His bundle is refractory. Termination of the tachycardia without advancement of the next atrial electrogram establishes orthodromic reciprocating tachycardia as the mechanism of this tachycardia. ABL = ablation; d = distal; HRA = high right atrium; p = proximal; RV = right ventricle.

If ventricular pacing during the tachycardia fails to establish a diagnosis, atrial pacing during the tachycardia at a slightly faster cycle length than the TCL can also be useful. Consistent resumption of the tachycardia with a constant VA conduction time (“VA linking”) supports a diagnosis of ORT (or AVNRT), whereas a variable VA relationship strongly favors an atrial tachycardia (Figure 14-7).


FIGURE 14-7 Following cessation of atrial pacing during tachycardia, the interval between the last entrained ventricular complex and the next atrial electrogram (A) is compared with the interval between the first ventricular complex of the tachycardia to the following atrial electrogram (B). The difference in these measurements here (or lack of “VA linking”) supports a diagnosis of atrial tachycardia. d = distal; HRA = high right atrium; m = middle; p = proximal; RVA = right ventricular apex.

In the majority of cases, the previously described techniques will definitively differentiate ORT from atrial tachycardia. If these pacing maneuvers or tachycardia characteristics fail to establish a clear-cut diagnosis, mapping for the earliest atrial electrogram during the tachycardia can be performed to identify a successful ablation target for either arrhythmia.


In an SVT with concentric retrograde atrial activation, ORT utilizing a septal accessory pathway can often be distinguished from typical AVNRT using retrograde VA conduction times. Simultaneous atrial and ventricular activation eliminates the possibility of ORT. If atrial activation follows ventricular activation but the interval between the onset of the QRS complex and the septal atrial electrogram is <70 ms, ORT is very unlikely. A longer retrograde VA conduction time can be seen with ORT, typical AVNRT with slower retrograde fast pathway conduction, or atypical AVNRT.

The postpacing interval upon cessation of ventricular pacing that entrains the SVT is a valuable tool for distinguishing AVNRT from ORT. When there is a V-A-V response, a corrected PPI-TCL interval <115 ms essentially rules out AVNRT (Figure 14-8). The PPI is corrected by subtracting any increment in AH interval in the first beat following ventricular pacing compared to the AH intervals during tachycardia.3A corrected PPI-TCL >115 ms strongly favors AVNRT as the mechanism, but ORT utilizing a very decremental or nonseptal accessory pathway is not ruled out.


FIGURE 14-8 Following entrainment of the SVT by ventricular pacing, the SVT resumes with a V-A-V response. This coupled with a short postpacing interval (PPI) minus tachycardia cycle length (TCL) of 60 ms establishes a diagnosis of ORT. d = distal; HRA = high right atrium; m = middle; p = proximal; RV = right ventricle.

Two other observations during ventricular pacing that entrains the SVT are also helpful in making a diagnosis. A recent study4 demonstrated that during entrainment, a highly sensitive and specific criteria for ORT is advancement of the atrial electrograms with the first nonfused ventricular paced beat. Also, if fusion between the paced ventricular beat and the tachycardia QRS complex is observed during entrainment, this proves the presence of an extra-nodal pathway.

As in the case highlighted above, multiple mechanisms may be at play and can lead to seemingly contradictory findings. In these cases, one must consider a combination of SVT mechanisms that can explain all the observations noted during tachycardia and with pacing maneuvers.


1. Knight BP, Zivin A, Souza J, et al. A technique for the rapid diagnosis of atrial tachycardia in the electrophysiology laboratory. J Am Coll Cardiol. 1999;33(3):775-781.

2. Michaud GF, Tada H, Chough S, et al. Differentiation of atypical atrioventricular node re-entrant tachycardia from orthodromic reciprocating tachycardia using a septal accessory pathway by the response to ventricular pacing. J Am Coll Cardiol. 2001;38(4):1163-1167.

3. González-Torrecilla E, Arenal A, et al. First postpacing interval after tachycardia entrainment with correction for atrioventricular node delay: a simple maneuver for differential diagnosis of atrioventricular nodal reentrant tachycardias versus orthodromic reciprocating tachycardias. Heart Rhythm. 2006;3(6):674-679.

4. Dandamudi G, Mokabberi R, Assal C, et al. A novel approach to differentiating orthodromic reciprocating tachycardia from atrioventricular nodal reentrant tachycardia. Heart Rhythm. 2010;7(9):1326-1329.

5. Obeyesekere M, Leong-Sit P, Skanes A, et al. Determination of inadvertent atrial capture during para-Hisian pacing. Circ Arrhythm Electrophysiol. 2011;(4)4:510-514.