Junctional Tachycardia

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Junctional Tachycardia




Junctional tachycardia (JT), alternatively known as junctional ectopic tachycardia (JET), originates from the atrioventricular (AV) junction—encompassing the AV node and the bundle of His. Junctional tachycardia is rarely encountered, especially in the adult population, and its pathogenesis remains incompletely understood. Furthermore, its presentation can be widely variable, and its diagnosis and therapy are often challenging. This chapter will focus on tachycardic forms of junctional arrhythmia, although escape rhythms arising from the AV junction in the setting of severe bradycardia and AV block may also occur.



Electrocardiographic Features and Diagnosis


The surface electrocardiographic findings of JET can be variable, depending on whether the tachycardia is paroxysmal or incessant, and on whether ventriculo-atrial (VA) conduction occurs during tachycardia. An incessant JT with 1 : 1 VA conduction will present as a regular narrow-QRS tachycardia with short RP interval and retrograde P waves, mimicking typical AV nodal reentrant tachycardia (AVNRT). By contrast, in paroxysmal JET without VA conduction, the electrocardiogram (ECG) will show an irregular narrow-QRS tachycardia with intermittent sinus capture beats. During periods of frequent irregular junctional ectopy without obvious P waves or with variable distortion of sinus P waves, the surface ECG can mimic the appearance of multifocal atrial tachycardia or atrial fibrillation. Finally, JT with bundle branch block can mimic ventricular tachycardia involving the specialized conduction system, particularly if VA conduction is absent. Because of its relative rarity in the adult population, JET may not always be considered in the differential diagnosis and therefore may be underdiagnosed.


When VA conduction is present, JET most often demonstrates short RP intervals, although it is possible for the retrograde P wave to slightly precede the QRS; this same pattern is also seen in typical AVNRT, which is much more common. To differentiate JET from AVNRT on the basis of surface ECG, the pattern of initiation of tachycardia can be informative, that is, it can indicate whether critical prolongation of the PR interval is seen on the initiating beat (this would suggest that AVNRT is more likely). Bursts of short RP tachycardia without initiation by premature atrial contractions (PACs) or PR prolongation suggest that JET is more likely. Finally, complete absence of VA conduction would also favor JET as the diagnosis, because AVNRT with complete block of the upper common pathway is less likely.



Differentiation During Electrophysiological Study


The electrophysiological hallmark of JT is the presence of a His bundle electrogram preceding the QRS complex. The HV interval may be normal or prolonged (in the setting of infra-Hisian conduction system disease). A short HV interval (<35 ms) should prompt suspicion of a fascicular tachycardia, bundle branch reentry, or the presence of a nodofascicular accessory pathway. Differentiation of JET with aberrant conduction from myocardial ventricular tachycardia (VT) is based primarily on the presence of the His bundle electrogram preceding the QRS. When VA conduction is present, differentiation of JET from atrial tachycardia can be based on observation of H-H interval variability driving A-A interval variability. Ventricular overdrive pacing yields a V-A-H-V response, also ruling out atrial tachycardia.


As indicated earlier, the most challenging differential diagnosis is between JET and AVNRT, as the two arrhythmias present with similar HV intervals recorded during tachycardia and sinus rhythm. Each arrhythmia may also be associated with VA block.1 Several maneuvers can help to differentiate JT from AV node reentry but require the presence of VA conduction. Atrial overdrive pacing yields an A-H-H-A response in JET because of the focal nature of this tachycardia; the maneuver yields an A-H-A response in AVNRT because entrainment proceeds via the same anterograde limb as the reentry circuit (Figure 79-1).2 Another useful maneuver involves the introduction of premature atrial complexes (PACs) during tachycardia. A late-coupled PAC delivered during His-refractoriness does not affect JET but can preexcite or delay the subsequent ventricular beat in AVNRT by engaging the anterograde slow AV nodal pathway (Figure 79-2, A, B). An early-coupled PAC that captures the His and ventricle usually allows JET to continue but should terminate AVNRT because it conducts anterogradely down the fast pathway (Figure 79-2, C, D).3




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Figure 79-2 Premature Atrial Complex (PAC) Response to Differentiate Junctional Tachycardia (JT) from Atrioventricular Nodal Reentrant Tachycardia (AVNRT)
Left, Response to PAC delivered when junction is refractory (local atrial activation from PAC occurs at or after His activation). A, During JT, a PAC delivered at a time the junction focus has already depolarized blocks at the AV node (AVN) and is unable to influence the immediate or the next junction beat. Solid circles represent junction focus. Black lines show conduction through AVN, His (H), and atrium (A). B, During AVNRT, a similarly timed PAC can influence the next beat of AVNRT by early engagement of the slow pathway. Black lines show conduction through AVN, His (H), and atrium (A), and red lines show PAC and its response. Although this figure shows advancement of the next beat (x-n), delay of the next beat or termination of tachycardia is also specific to AVNRT. Red arrow indicates PAC and its response. FP, Fast AV nodal pathway; SP, slow AV nodal pathway; x and x-n, H-H intervals. Right, Response to earlier-coupled PACs. C, During JT, an early PAC advances the immediate JT beat, and His timing by AV nodal fast pathway activation and JT continues. Open circle represents the anticipated JT beat timing if no PAC is delivered. D, During AVNRT, an early PAC may advance the immediate His by activation of the AV nodal fast pathway. However, this makes the fast pathway refractory and unavailable for retrograde conduction, thus terminating the AVNRT circuit. (From Padanilam BJ, Manfredi JA, Steinberg LA, et al: Differentiating junctional tachycardia and atrioventricular node re-entry tachycardia based on response to atrial extrastimulus pacing. J Am Coll Cardiol 52:1711-1717, 2008.)



Mechanisms


There is a dearth of data regarding the electrophysiological mechanism of junctional ectopic tachycardia. Given the lack of dependence on a critical coupling interval for tachycardia initiation, the often irregular tachycardia rate, and inability to entrain the arrhythmia, the electrophysiological behavior of JET is consistent with a focal non-reentrant arrhythmia. With regard to cellular mechanisms, most published case series of JET have postulated that enhanced automaticity is responsible for the arrhythmia.4–6 However, recent evidence suggests that at least two other mechanisms may be responsible for cases of JET: abnormal automaticity and triggered activity.7


In contrast with enhanced automaticity, tissue with abnormal automaticity generally does not demonstrate overdrive suppression because of its reduced resting membrane potential (typically ≤−60 mV) and the inactivated state of the sodium current and the electrogenic sodium pump. Abnormal automaticity is then dependent on the slow inward calcium current and is therefore sensitive to inhibition of this current by calcium channel blockers.8 Adenosine has no effect on abnormal automaticity, whereas it transiently suppresses enhanced normal automaticity (Figure 79-3).9 Therefore, sensitivity of an automatic tachycardia to calcium channel blockade as well as insensitivity to adenosine is consistent with abnormal automaticity rather than enhanced “normal” automaticity (Figure 79-4).


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Jun 5, 2016 | Posted by in CARDIAC SURGERY | Comments Off on Junctional Tachycardia

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