Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common type of supraventricular tachycardia (excluding atrial fibrillation) with a normal resting 12-lead ECG and accounts for about 60% of all narrow complex tachycardias in the adult population. AVNRT occurs in the presence of a reentrant circuit involving two electrophysiologically distinct limbs that connect to the AV node; they are known as the fast and slow pathways. The fast pathway is an anterior structure and lies near the compact AV node along the tendon of Todaro, whereas the slow pathway is a posterior structure and can usually be identified along the tricuspid valve annulus near the os of the coronary sinus (Figure 1). During sinus rhythm, atrioventricular conduction typically occurs over the fast pathway. Initiation of AVNRT may follow an appropriately-timed premature atrial beat that blocks in the fast pathway due to its longer effective refractory period (ERP), allowing conduction to travel antegrade over the slow pathway to the AV node. Because the slow pathway has a longer conduction time than the fast pathway, the impulse is delayed. This delay allows sufficient time for retrograde activation at the fast pathway insertion site, which has now recovered and is ready to conduct. Activation then quickly reenters the slow pathway in the antegrade direction, completing the loop causing tachycardia (typical slow-fast AVNRT). Case Study A 63-year-old woman presented to her local hospital for evaluation of chest pain. Upon further investigation of her symptoms, she complained of multiple episodes of tachy-palpitations. These episodes often occurred at night, waking her from sleep. She described the palpitations as regular and fast with an average duration of ten to fifteen minutes. She stated that she was able to terminate these episodes with Valsalva maneuvers. While hospitalized, she experienced a typical spell. A 12-lead electrocardiogram showed a narrow complex tachycardia with a heart rate of 150 beats per minute (Figure 2). Examination of the electrocardiogram did not reveal obvious P-waves preceding the QRS complexes. However, close inspection of the terminal portion of the QRS complex, especially in the inferior leads II and III, suggested the presence of a retrograde P-wave. The most likely differential diagnosis for this type of short RP tachycardia is AVNRT. The patient underwent an electrophysiologic study. Electrode catheters were introduced and advanced to the high right atrium, His bundle region, and right ventricular apex. A 20-pole catheter was placed in the coronary sinus with pole 13, 14 marking the location of the ostium. Baseline intervals were obtained, which were within normal limits (Figure 3). Standard pacing maneuvers were performed beginning with programmed ventricular stimulation. Ventricular burst pacing along with ventricular extrastimulus testing (VEST) revealed concentric activation (earliest atrial activation seen in the His bundle electrogram), and decrement in retrograde activation without a change in activation sequence, likely excluding the possibility of a concealed accessory pathway. Atrial pacing maneuvers followed. Atrial extrastimulus testing (AEST) was utilized to assess for the presence of two functional pathways, also known as dual AV nodal physiology. Dual AV nodal physiology has been defined as an increase of 50 msec or greater in the A2-H2 interval when the atrial extrastimulus coupling interval (A1-A2) is shortened by 10 msec decrements. This abrupt increase in the AH interval is termed a jump. During AEST, an 85 msec jump was recorded. Along with the increase in the AH interval, an echo beat was observed (Figure 4). The AV nodal echo beat occurred as rapid retrograde activation conducted back up the fast pathway. Continued AEST resulted in the induction of a sustained narrow complex tachycardia with a cycle length of 390 msec (Figure 5). While in tachycardia, VA conduction appeared almost simultaneous with a VA time of 40 msec (short RP), highly suggestive of AVNRT. To confirm the diagnosis, differential pacing maneuvers were conducted. During tachycardia, the introduction of sensed premature ventricular contractions (PVCs) at progressively shorter coupling intervals were used in an attempt to advance, or pre-excite retrograde atrial activation. If inserted at the time of His bundle refractoriness, advanced atrial activation and tachycardia reset could only occur as a result of conduction via an alternate means other than the normal AV conduction system. This would prove diagnostic for the presence of an accessory pathway. Sensed PVCs did not advance atrial depolarizations or reset the tachycardia. A pre-excitation index (PI) was obtained by subtracting the tightest coupling interval of the PVC that captured the atrium retrogradely from the tachycardia cycle length. A PI of less than 100 msec suggests the presence of an accessory pathway; the PI in this case was measured at greater than 170 msec. The inability to pre-excite the atrium once again supported the impression that this tachycardia did not utilize an accessory pathway as a part of the circuit. Entrainment of this tachycardia (Morady maneuver) was also performed and demonstrated a V-A-H-V or V-A-V response (Figure 6). While in tachycardia, ventricular pacing was initiated at a CL slightly faster than the tachycardia CL and revealed no change in retrograde activation sequence. The resultant V-A-H-V response largely excluded the presence of atrial tachycardia (supported by a V-A-A-V response), but did not differentiate between alternate AV nodal dependent rhythms such as AVNRT and AVRT. To help distinguish retrograde conduction via the AV node or concealed accessory pathway, parahisian pacing was also performed. This involved high output pacing in the region of the His bundle and revealed retrograde activation to the atrium via the AV node, excluding the presence of an accessory pathway. During parahisian pacing, high output pacing created a strong enough current to capture the His bundle directly. The impulse spread directly to the AV node in the retrograde direction and to the ventricles over the His bundle causing a narrow QRS complex. With a reduction in pacing output, direct capture of the His bundle no longer occurred and the ventricle was depolarized from the high septal myocardium causing a wide QRS complex. This impulse traveled to the right ventricular apex, and then back to the His bundle in the retrograde direction. The increased travel time greatly increased the time to get back to the atrium. However, in the presence of an accessory pathway, the atrium can be rapidly activated retrogradely from the pacing site independent of the AV node. This rapid activation occurs whether the His is directly stimulated or not. The two different types of paced beats, wide and narrow complex, are illustrated in Figure 7. The stimulus artifact to A with His non-capture (wide complex beat) is longer than the stimulus artifact to A where His capture is present (narrow complex beat). The stimulus artifact to A with His non-capture is longer than the stimulus artifact to A where His capture is present. This confirmed that activation to the atrium utilized the AV node alone excluding the presence of an accessory pathway. Based on the summary of evidence, radiofrequency (RF) ablation was performed at the slow pathway region. The response to ablation is shown in Figure 8. With the application of RF energy, accelerated junctional rhythm was recorded. The presence of an accelerated junctional rhythm corresponds highly to successful ablation of slow pathway conduction. Observation for the presence of continuous one-to-one retrograde atrial activation during junctional rhythm is critical. If retrograde VA block is observed, ablation therapy should be immediately terminated because of the possibility of incurring AV block. The induction of rapid junctional rhythm during ablation has also been associated with AV block and should result in energy termination. This ablation was successful, and no further tachycardia was induced despite isoproterenol infusion. Summary This case served to illustrate the common (typical) form of AV nodal reentrant tachycardia. The symptoms, termination with Valsalva maneuvers, and 12-lead ECG were classic findings associated with this arrhythmia. Several diagnostic criteria, including the presence of dual AV node physiology, initiation of tachycardia dependent on a critical A-H interval, and exclusion of atrial tachycardia and reciprocating tachycardia with pacing maneuvers, confirmed the final diagnosis. While the success rate of catheter ablation in the treatment of this arrhythmia ranges up to 98%, this diagnosis and subsequent ablative therapy should not be taken lightly. Complications, while rare, can and do occur. One of the more serious of these complications is AV block, which occurs in around 1 - 2% of cases. Full knowledge of the anatomy of the right atrium is critical with emphasis on the triangle of Koch. The recognition of intracardiac electrograms and their relationship to anatomical location is also crucial. The patient should be consented with full knowledge of the low risk of heart block in addition to the risks accompanying vascular access and catheter placement. Variants of typical AVNRT can also occur and include forms that utilize the fast pathway or anterior approach to the AV node as the antegrade limb of the circuit and the slow pathway region near the coronary sinus ostium as the retrograde limb. Slow-slow AVNRT and left-sided forms have also been described. Successful treatment of all forms can in most cases be achieved with modification of the slow pathway region. Because of the relative safety of the procedure and high rate of effectiveness, ablation is considered a Class I indication and first-line therapy for patients in whom treatment is deemed necessary. It is also recommended in patients who have failed one or more types of antiarrhythmic therapy or who are otherwise intolerant of medical treatment.