Atrio-ventricular Nodal Reentrant Tachycardia



Atrio-ventricular Nodal Reentrant Tachycardia








DUAL AV NODE PHYSIOLOGY

Both the AV node and His bundle are located within the triangle of Koch, which is formed by the 1) septal leaflet of the tricuspid valve, 2) tendon of Todaro, and 3) coronary sinus (CS) ostium. The penetrating His bundle is located at the apex of the triangle. The compact AV node is a subendocardial structure in the right atrium located posterior and inferior to the His bundle along the interatrial septum. Dual AV node physiology (longitudinal dissociation of the AV node) refers to anatomically and functionally distinct inputs (or approaches) to the AV node: the slow pathway (SP, or right inferior extension) and fast pathway (FP, or superior extension).1 The SP is located along the posteroseptal right atrium near the ostium of the CS and demonstrates slow conduction/short refractoriness (α limb). The FP is located along the anteroseptal right atrium superior to the His bundle and exhibits rapid conduction/long refractoriness (β limb). When the refractoriness of each pathway complements the conduction properties of the other, they can create the substrate for AVNRT. Left atrio-nodal connections (left inferior extensions) also exist and are generally found within 2 cm of the CS os.2


ECG MANIFESTATIONS OF DUAL AV NODE PHYSIOLOGY

12-Lead ECG manifestations of dual AV node physiology include 1) two distinct families of PR intervals for a given sinus rate, 2) PR alternans, 3) dual antegrade response tachycardia (DART, also called “double fire,” “1:2” tachycardia, and paroxysmal non-reentrant tachycardia), and 4) AVNRT (Figs. 7-1, 7-2, 7-3, 7-4, 7-5, 7-6, 7-7, 7-8, 7-9, 7-10 and 7-11).3 Two families of PR intervals can occur spontaneously or be unmasked by critically timed atrial or ventricular premature depolarizations (VPDs) that conceal into a longitudinally dissociated AV node (sequential FP/SP conduction) (Figs. 7-1, 7-2 and 7-3). Sustained conduction over the SP (or FP) is maintained by repetitive concealment from SP to FP (or vice versa), rendering the latter refractory with each subsequent sinus impulse.4 A rare manifestation is PR alternans (alternating FP and SP conduction after each sinus complex) (Figs. 7-4 and 7-5).5 PR alternans result from 2:1 block in the FP when the SP is capable of 1:1 conduction. SP conduction is only manifest when FP conduction is absent. Isolated or sustained dual antegrade responses result from simultaneous conduction over the FP and SP, generating two QRS complexes for each P wave—the latter potentially causing a tachycardia-mediated cardiomyopathy (simultaneous FP/SP conduction) (Figs. 7-6, 7-7, 7-8, 7-9, 7-10 and 7-11).6,7,8,9,10 RR irregularity generated by 2:1 and 1:1 conduction can be mistaken for atrial fibrillation. Determinants of DART are 1) sufficient difference between SP and FP conduction times (generally, AHSP – AHFP >300 ms), 2) HSP-HFP interval is greater than the His-Purkinje effective refractory period (ERP), 3) absence of retrograde conduction over each AV nodal pathway following antegrade conduction over its counterpart, and 4) appropriate timing of sinus impulses relative to preceding AV nodal conduction (critical HA interval).8,9 Dual antegrade responses often require AHSP >400 ms. The HSP-HFP interval must exceed His-Purkinje refractoriness to allow consecutive activation of the His-Purkinje by a single sinus input. Aberration is common
because of longitudinal dissociation within the His-Purkinje system (Fig. 7-9).






FIGURE 7-1 Dual AV node physiology (FP/SP alternans induced by PVCs). Sinus P waves conduct over the FP with mild PR prolongation (260 ms). An interpolated PVC conceals retrogradely into both the FP and SP. Because the FP has a longer refractory period, the subsequent P wave finds it refractory and conducts over the SP with a long PR interval (520 ms). Repetitive concealment from SP to FP (“linking”) maintains SP conduction until another PVC. This second PVC again conceals into both the FP and SP rendering them refractory upon arrival of the next sinus impulse. The subsequent compensatory pause allows both pathways to recover, but FP then preempts SP conduction. Solid and dashed lines represent FP and SP conduction, respectively.


Dual Antegrade Response versus His Bundle Extrasystole

His bundle extrasystoles can mimic isolated dual antegrade responses. Similar to dual antegrade responses, His bundle extrasystoles can be associated with aberration due either to its prematurity relative to His-Purkinje refractoriness or site of origin within the His bundle (committed fibers in the His bundle destined for specific bundle branches). A short HV interval and retrograde His bundle activation sequence (His ds to px) suggest an extrasystole arising from the His bundle distal to the recording site (Fig. 7-12).11 Antegrade His bundle activation, however, is not specific to a dual antegrade response and can occur with an extrasystole arising from the AV node or proximal His bundle. While the target ablation site for DART is the SP, ablation of His bundle extrasystoles carries a greater risk of AV block depending on its location along the AV node-His bundle axis.


ELECTROPHYSIOLOGIC STUDY

During programmed atrial extrastimulation, dual AV node physiology is defined by ≥50 ms increment in the AH interval (“AH jump” or discontinuity) for a 10 ms decrement in the A1A2 coupling interval.12 An AH jump ≥50 ms arbitrarily differentiates physiologic decrement over the FP from SP conduction, and the A1A2 interval defines the antegrade FP ERP. During rapid atrial pacing, conduction over the SP is suggested when the PR interval exceeds the atrial pacing cycle length (crossover phenomenon).13 During programmed ventricular extrastimulation, retrograde dual AV node physiology is manifested by an increase in the VA interval accompanied by a switch from a midline atrial activation pattern earliest along the anteroseptum (FP) to the posteroseptum (SP).


ATRIO-VENTRICULAR NODAL REENTRANT TACHYCARDIA CIRCUIT

For typical (slow-fast) AVNRT, the antegrade and retrograde limbs of the circuit are the SP and FP, respectively, and reversed for its atypical counterpart (fast-slow AVNRT). The presence of variable AV nodal pathways (e.g., intermediate SP, “superior” SP, left atrio-nodal inputs), however, can produce other atypical AVNRTs (slow-slow, fast-slow with “superior” SP, and AVNRT with left atrio-nodal inputs mimicking ORT with a left-sided AP).14,15,16 The conduction time over each pathway must exceed the refractory period of its counterpart to allow the depolarizing wavefront to constantly encounter excitable tissue. At the lower turnaround point of the circuit, the wavefront splits to activate the ventricle antegradely while simultaneously activating the atrium retrogradely (simultaneous ventriculo-atrial activation). At the upper turnaround point, the wavefront activates the atrium retrogradely while simultaneously activating the ventricle antegradely. The existence of an upper common final pathway (UCFP) separate from the atrium is controversial.17,18 Occurrence of JA block during AVNRT supports the



presence of a UCFP. A lower common final pathway (LCFP) is less controversial.19,20,21,22 Wenckebach-type and 2:1 blocks above the His bundle recording site during AVNRT support a LCFP that involves the distal AV node/proximal His bundle.






FIGURE 7-2 Dual AV node physiology (FP/SP alternans induced by APCs). Sinus impulses conduct over the FP. An APC is delivered, which encounters FP refractoriness and conducts over the SP. Repetitive concealment from SP to FP (“linking”) maintains SP conduction. Spontaneous FP conduction resumes coincident with a pacing stimulus delivered during a sinus beat.






FIGURE 7-3 Dual AV node physiology. Spontaneous conversion from SP to FP conduction (sinus rhythm with two families of PR intervals).






FIGURE 7-4 PR alternans. Alternating conduction over the FP and SP produces two sets of PR intervals (180 and 380 ms) changing on a beat-to-beat basis. Conduction over the SP becomes manifest only when FP conduction is absent. Solid and dashed lines represent FP and SP conduction, respectively.






FIGURE 7-5 DART transitioning to PR alternans. During DART, retrograde concealment from SP into FP renders the FP relatively and absolutely refractory, abolishing the dual antegrade response after the second and fourth sinus beats, respectively. Isolated SP conduction after the fourth sinus beat is followed by alternating SP/FP conduction with prolonged AHFP due to concealment from SP into FP (“linking”) and relative FP refractoriness.






FIGURE 7-6 Intermittent dual antegrade responses followed by isolated SP Wenckebach conduction.


ELECTROPHYSIOLOGIC FEATURES OF AVNRT


12-LEAD ECG

The 12-lead ECG of typical AVNRT is a 1) regular, narrow complex tachycardia; 2) short RP interval <70 ms; and a 3) midline, superior P-wave axis (Figs. 7-13 and 7-14).23,24,25 Antegrade activation of the ventricle simultaneously with retrograde activation of FP and atrium results in a short RP interval <70 ms. Retrograde P waves are buried within or distort the terminal portion of the QRS complex causing pseudo S waves in the inferior leads and pseudo r′ in V1. Because atrial activation originates from the FP along the interatrial septum, P waves are narrow and have a midline, superior axis (negative in inferior leads, positive in aVR and aVL). Atypical AVNRT is a regular, narrow complex tachycardia with a long RP interval and a midline superior P-wave axis because retrograde conduction occurs over the SP (Figs. 7-13 and 7-15).


ELECTROPHYSIOLOGIC STUDY

The electrophysiologic features of typical AVNRT are 1) antegrade His bundle electrograms preceding QRS complexes, 2) VA interval <70 ms, and 3) earliest site of atrial activation at the FP (His bundle region) (Fig. 7-14).23,24,25 The VA interval is short (<70 ms) because activation of the ventricle is simultaneous with the atrium (“A on V” tachycardia). A negative VA interval occurs when the antegrade conduction time to the ventricle exceeds the retrograde conduction time to the atrium. Atrial activation is concentric and earliest at the His bundle region. Atypical AVNRT manifests a long VA interval and earliest site of atrial activation at the SP (CS os region) (Fig. 7-15). Variability of AV nodal pathways, however, can cause different types of AVNRT with midline or left eccentric atrial activation patterns occurring anywhere within the tachycardia cycle length (TCL).


AV Relationship

The existence of a LCFP and UCFP allows AVNRT to persist despite block to the ventricle and atrium, respectively. Therefore, AVNRT does not have an obligatory 1:1 AV relationship.19,21,22 Physiologic block to the ventricle can occur either above or below the His bundle and is often a transient phenomenon induced by abrupt changes (long-short sequences) in cycle length (e.g., tachycardia initiation) (Figs. 7-16, 7-17, 7-18, 7-19, 7-20, 7-21, 7-22, 7-23, 7-24 and 7-25). An ECG clue to typical AVNRT with 2:1 LCFP block is the finding of a P wave (narrow, superior axis) buried exactly between two QRS complexes (mid-diastole). AVNRT with Wenckebach-type block above the His bundle suggests that the LCFP can involve the distal AV node (Fig. 7-20). AVNRT can also be induced despite pathologic AV block in the His-Purkinje system (Figs. 7-26 and 7-27).26 Block to the atrium is less common and supports the existence of an UCFP (Figs. 7-28, 7-29 and 7-30). Concealed AVNRT results from transient block in both UCFP and LCFP resulting in a pause, which is a multiple of the TCL.27







FIGURE 7-7 DART. Every P wave (asterisks) except the fourth conduct over the FP and SP producing two sets of PR intervals (160 and 460 ms). The fourth P wave is preceded by the shortest RP interval on the tracing, falls into the relative refractory period of the FP (due to preceding concealment from the SP), and conducts with delay over the FP (PR = 280 ms). Reduction in the difference between SP and FP conduction causes momentary loss of the dual antegrade response. His bundle recordings show each sinus impulse generating two His bundle potentials (AHFP = 75 ms, AHSP = 383 ms) and QRS complexes.

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Oct 13, 2019 | Posted by in CARDIOLOGY | Comments Off on Atrio-ventricular Nodal Reentrant Tachycardia
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