Simultaneous dual AV node antegrade conduction (2 for 1) and lower common pathway (2–1) block illustrate AVNRT physiology

Abstract

We report a rare case of spontaneous initiation of Atrioventricular nodal reentry tachycardia (AVNRT) via 2 for 1 phenomenon, into a 2:1 AV block due to lower common pathway block and finally transition to 1:1 tachycardia. The premature atrial p wave traverses down both the fast and slow pathway simultaneously during 2 for 1 initiation and is met with subsequent typical AVNRT with 2:1 block. Infranodal location of the block is confirmed on electrophysiologic testing and is also cured by intervention. This rare electrographic presentation is not only pathognomonic for AVNRT with lower common pathway block but also illustrates its dual conduction physiology.

1. Introduction

Atrioventricular nodal reentrant tachycardia (AVNRT) is a regular paroxysmal supraventricular tachycardia based on dual AV nodal pathways which occurs in 2.25/1000 persons [1]. The incidence of 2:1 AV nodal block in adults during electrophysiological study (EPS) for AVNRT is approximately 10% [2], but spontaneous 2:1 block is probably rarer, accounting for only a fifth (6/31) among those who demonstrated the block during EPS in a pediatric series [3]. We report a case illustrating an uncommon variant of typical AVNRT with initiation via a 2 for 1 phenomenon, a 2 to 1 conduction in AVNRT due to lower common pathway block, and transition to 1 to 1 tachycardia.

2. Case report and discussion

A 74 year old gentleman with hypertension, diabetes mellitus and metastatic prostate cancer in remission, presented with atypical chest pain, palpitations and recurrent pre-syncopal episodes. His baseline EKG (Fig. 1) showed sinus rhythm, right bundle branch block and left ventricular hypertrophy with diffuse T wave inversions, concerning for ischemic changes. Echocardiogram revealed normal left ventricular function without structural abnormalities and cardiac catheterization revealed non obstructive coronary artery disease. After short term monitoring was unrevealing, a beta blocker was started and an implantable loop recorder (ILR) was inserted. ILR interrogation revealed recurrent symptomatic (patient triggered) SVT episodes as shown in Fig. 2A and D, which was followed by an electrophysiological study. Fig. 2A shows the onset of the tachycardia, well before the actual ventricular rate increased in Fig. 2D. Fig. 2A reveals an APC after the second QRS complex, followed by another QRS with no precedent P wave. This suggests that the APC conducted down both a fast pathway (FP) AND a slow pathway (SP) simultaneously, with the SP impulse reaching the His-Purkinje system after the conduction system had repolarized allowing a second ventricular event (4th QRS complex) for the same atrial depolarization (Fig. 2B). This is known as 2 for 1 phenomenon, demonstrative of dual AVN physiology. The impulse is then conducted retrogradely to the atrium via the fast pathway initiating typical AVNRT (slow-fast). The impulse then travels back around down the SP but is only conducted to the ventricle every alternate revolution around the circuit (2 to 1 block). This was confirmed on EP testing seen in Fig. 2C during induced SVT. During EP study, 2 for 1 induction did not occur. Of note, the blocked impulses lack a His depolarization and therefore indicate a suprahisian block in the lower common pathway beneath the circuit but above the His bundle. In Fig. 2D and E, the ILR tracing and the corresponding ladder diagram show the transition from the 2 to 1 to the more typical appearing 1 to 1 SVT (AVNRT), again confirmed via EP testing (Fig. 2F). Fig. 3 shows the pathognomonic 12 lead EKG of the 2 to 1 AVNRT during EP study showing a regular rhythm with a right bundle branch block, ventricular rate of 97 bpm, with distinct P waves seen in the mid RR cycle. The differential for this pattern would be sinus rhythm with a first degree atrioventricular block. However, a few clues lead us to an alternate diagnosis. Firstly, the superiorly directed p wave axis rules out a sinus nodal origin. Secondly, there appears to be a second P wave seen at the terminal QRS best visualized in II/aVR, marching out with the P waves visible at the midpoint between QRS deflections. The cycle length is exactly double that when the rate accelerates (at the end of the strip), confirming that it changes from 2:1 to 1:1. Atrial tachycardia with 2:1 AVB is possible. However, with atrial tachycardia there is a focal atrial site or a microrentrant circuit going off by itself, and there is often “wobble” as the ventricular depolarization is not absolutely tied with the atrial depolarization. In our case it was precisely congruent with the R-R cycle length. Hence, along with what was shown on the ILR and EPS, this is pathognomonic for AVNRT with lower common pathway block.

Fig. 1.

Baseline EKG

Fig. 2.

ILR recording, ladder diagram, and EP study. A - Magnified ILR recording of 2 for 1 onset of 2 to 1 AVNRT. B - Ladder diagram explaining ILR recording. C - EP study confirmation of 2 to 1 block during SVT. D - Magnified ILR recording of spontaneous transition of 2 to 1 to 1 to 1 AVNRT. E - Ladder diagram explaining ILR recording. F - EP study confirmation of transition to 1 to 1 block.

Fig. 3.

12 lead EKG of the SVT during EP study.