Dual Atrioventricular Nodal Non–Re-Entrant Tachycardia

Abstract

A patient presented with symptoms of palpitations. Her standard 12-lead electrocardiogram captured 3 potential causes of her symptoms (premature atrial contractions, junctional rhythm, and narrow complex tachycardia). Further workup uncovered dual atrioventricular node physiology with 1:2 sinus conduction and resultant alternating QRS from a slow and fast conduction pathway. (Level of Difficulty: Intermediate.)

Central Illustration

A 43-year-old female patient with a history of palpitations and intermittent supraventricular tachycardia (SVT) presented with an abnormal electrocardiogram (ECG) during her routine annual physical. Transthoracic echocardiography was previously normal, and she did not take any cardiac medications. She had palpitations but otherwise did not have alarm symptoms such as syncope, near syncope, typical angina, or exercise impairment. From the Holter monitor and ECG obtained after the patient’s appointment (Figure 1), which of the following is the most likely cause of these findings? 1) SVT with long RP interval; 2) junctional rhythm with atrioventricular (AV) dissociation; 3) premature atrial contractions; 4) dual AV node physiology. The correct answer is number 4.

Figure 1.

Holter Monitor and 12-Lead Electrocardiogram With Ladder Diagram

(A) Baseline sinus rhythm with (B) an intermittent junctional rhythm blocking sinus-activated beats. (C) Premature atrial contractions interrupt sinus rhythm leading brief supraventricular tachycardia followed by a sinus-activated narrow complex tachycardia with 2 narrow QRS complex morphologies. (D) Each of these is demonstrated on 12-lead electrocardiography. Blue arrow indicates blocked sinus beat.

Discussion/Rationale

The patient’s Holter monitor demonstrated multiple ECG anomalies that could be responsible for her symptomology (Figures 1A to 1C). The patient had a baseline sinus rhythm (Figure 1A) with an intermittent junctional rhythm, which blocked her sinus impulses from reaching the ventricles (Figure 1B). On the Holter, the patient’s normal sinus rhythm was also interrupted by ectopic atrial beats (premature atrial contractions) with a subsequent 3-beat episode of a narrow complex tachycardia (right bundle branch block morphology) followed by a narrow complex tachycardia with 2 distinct, narrow QRS morphologies (Figure 1C). In review of the patient’s 12-lead ECG (Figure 1D), this same, narrow complex tachycardia with alternating QRS morphology was observed. After 7 beats, a blocked sinus beat (Figure 1D, blue arrow) was followed by a junctional rhythm. Eventually, the atrial activity was faster than the junctional rhythm, and this narrow complex tachycardia with alternating morphologies returned.

While the patient had a history of SVT, which could result in palpitations and discomfort, there was dissociation between the junctional beats and the atrial activation on the 12-lead ECG, which would argue against an SVT with a consistent P-wave conduction/association. The junctional rhythm with AV dissociation, while present, could have caused the patient’s symptoms even at slower rates (near 90-100 beats/min) as atrial contraction against a closed mitral or tricuspid valve may result in symptoms of palpitations or pounding sensation. However, there was a separate narrow complex tachycardia on ECG and Holter (rate near 150 beats/min) with alternating QRS morphology, which was thought to be the culprit. Initially, it was suspected that concealed retrograde conduction from underlying junctional rhythm may have caused the alternating QRS morphology with intermittent sinus rhythm. The fast pathway conduction PR interval gets progressively longer until the portion at which the A blocks and the junctional comes in. This could be due to retrograde concealed conduction from the slow pathway impulse turning around and climbing back into the fast pathway. However, there was clear evidence of dual AV node physiology (1:2 ratio of sinus to ventricular activation) during electrophysiology study (Supplemental Figures 1 and 2). We demonstrated this complex physiology by our ladder diagram, as each sinus node activation was followed by 2 ventricular responses from fast and slow pathway conduction (Figures 1C and 1D).¹ During electrophysiologic study, a 1:2 ratio of sinus to ventricular activation was noted on intracardiac electrogram. On the second beat of each complex, His activation reliably occurred proximal to distal (Supplemental Figures 1 and 2). Ventricular decremental pacing and ventricular extrastimuli did not demonstrate ventriculoatrial conduction, and atrial extrastimulus testing demonstrated dual AV node physiology. Junctional ectopic beats were also seen concurrently during the study, as oftentimes a junctional focus can emanate from around the slow pathway. Ablation, in some cases, can resolve both problems. Slow pathway ablation was performed, eliminating the dual AV node physiology even with programed atrial stimulation with and without isoproterenol. The previously seen junctional beats were no longer seen after ablation as well. The patient reported resolution of symptomology during a follow-up phone call 2 months postprocedure.

Funding Support and Author Disclosures

Dr Deshmukh has served as a consultant for GE Healthcare. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.