Orthodromic Reciprocating Tachycardia



Orthodromic Reciprocating Tachycardia








MECHANISM

ORT is a macroreentrant AP-mediated tachycardia utilizing the atrio-ventricular (AV) node-His-Purkinje axis as the antegrade limb (true or “ortho”) and an AP as the retrograde limb of the circuit. The ventricles are activated by the His-Purkinje system, and therefore, QRS complexes are normal. After activation of the ventricle, the AP and atrium are activated sequentially (“in series”). P waves result from retrograde activation of the AP, and their axis reflects AP location.


ELECTROPHYSIOLOGIC FEATURES


12-LEAD ECG

The 12-lead ECG of ORT is a 1) regular narrow complex tachycardia (NCT), 2) short RP interval ≥70 ms, and 3) P-wave axis (generally superior) that reflects the AP location.1,2 Retrograde AP conduction is typically rapid, but because the ventricles and atria are sequentially activated, the RP interval ≥70 ms with P wave buried within the ST segment. An NCT with an RP interval <70 ms therefore excludes ORT. Rightward (aVR [+], aVL [−]) and leftward (aVR [−], aVL [+]) P-wave axes identify left- and right-sided APs, respectively. A midline, superior P-wave axis (aVR [+], aVL [+]) suggests a septal AP. Anteroseptal APs can produce inferior P-wave axes.3


ELECTROPHYSIOLOGIC STUDY

The electrophysiologic features of ORT are 1) antegrade His bundle electrograms preceding QRS complexes, 2) VA interval ≥70 ms, and 3) earliest atrial activation at the site of the AP (Figs. 10-1 and 10-2).1,2 The VA interval is the intracardiac equivalent of the surface RP interval and is ≥70 ms. Atrial activation is either concentric or eccentric depending on AP location.4 Septal APs generate concentric (antero- or posteroseptal) activation patterns, while right and left free wall APs produce right and left eccentric patterns, respectively. Because APs span the tricuspid or mitral annuli, earliest atrial activation occurs at the annulus. In general, a NCT with earliest atrial activation far from an annular site argues against ORT and suggests diagnosis of atrial tachycardia (AT), although nonannular APs (e.g., atrial appendage AP) have been described.


AV Relationship

Except for ORT using a nodo-fascicular/nodo-ventricular AP (nodo-fascicular reentrant tachycardia [NFRT]), all ORT requires participation of both the atrium and ventricle (obligatory 1:1 AV relationship).5 ORT, therefore, cannot occur with AV block (see Figs. 9-21 and 9-22).6,7 ORT, however, can occur with AV dissociation (NFRT) (see Figs. 11-11 and 11-12).8 Because ORT is dependent on the AV node and retrograde AP conduction is generally rapid and fixed, oscillations in AH and HH intervals precede and predict VV and subsequent AA intervals.


Bundle Branch Block

Aberration-induced cycle length changes during NCT reflect His-Purkinje participation in tachycardia and are unique to ORT. ORT uses the shortest functional circuit capable of sustained reentry and, therefore, incorporates the bundle branch ipsilateral to the AP as an integral part of its circuit. During tachycardia, development of bundle branch block (BBB) ipsilateral to the AP forces antegrade conduction over the contralateral bundle and enlarges the circuit with transeptal conduction (Fig. 10-3). The addition of transeptal conduction causes an 1) obligatory increase in VA interval and generally 2) nonobligatory increase in tachycardia cycle length (TCL) (Coumel’s sign) (Figs. 10-4, 10-5, 10-6 and 10-7).9,10,11,12,13 The degree of VA interval increase depends on the



AP location: Free wall APs increase the VA interval >35 ms, and septal APs increase the VA interval <25 ms.10 TCL prolongs with ipsilateral BBB provided that the increase in VA interval is not counterbalanced by an equivalent decrease in the AV (generally, AH) interval. Conversely, loss of BBB ipsilateral to the AP causes tachycardia acceleration. Rarely, loss of BBB might cause paradoxical slowing of tachycardia if the decrease in VA interval is counterbalanced by a greater increase in the AV interval (decrement in the AV node or switch from fast pathway [FP] to slow pathway [SP]) (Figs. 10-5 and 10-6).14 The VA interval (not TCL), therefore, is the important variable when assessing the effect of BBB on ORT. Once established, BBB is perpetuated by repetitive, concealed, transeptal conduction from unblocked to blocked bundle (transeptal linking).15






FIGURE 10-1 ORT using a left anterolateral (top), lateral (middle), and posterolateral (bottom) AP. Earliest site of atrial activation during retrograde AP conduction is depicted in white.






FIGURE 10-2 ORT using an anteroseptal (top) and posterior-posteroseptal (bottom) AP. Earliest site of atrial activation during retrograde AP conduction is depicted in red.






FIGURE 10-3 Schematic diagram illustrating Coumel’s sign. ORT using a left free wall AP. LBBB (ipsilateral to the AP) forces antegrade conduction over the RB and across the septum enlarging the circuit and obligating an increase in the VA interval. Concealed transeptal retrograde conduction (“transeptal linking”) perpetuates BBB. Right bundle branch block (RBBB) (contralateral to the AP) does not affect the circuit.






FIGURE 10-4 Coumel’s sign (ORT using a left free wall AP). Atrial activation is left eccentric. Loss of LBBB causes a 36 ms shortening of the VA interval and acceleration of tachycardia.






FIGURE 10-5 Coumel’s sign (ORT using a left free wall AP). Atrial activation is left eccentric. Loss of LBBB results in 36 ms shortening of the VA interval but 67 ms lengthening of the AH interval (due to decremental conduction over the AV node), causing paradoxical slowing of tachycardia. The VA interval is more important than TCL to assess the effect of BBB on ORT.


ZONES OF TRANSITION


INITIATION


Atrial Stimulation

Induction of ORT by atrial stimulation (programmed extrastimulation or burst pacing) requires that an impulse falls into the tachycardia window (defined as the difference in antegrade refractory periods between the AV node and AP). A critically timed impulse 1) fails to conduct over the AP (unidirectional block) and 2) conducts exclusively over the AV node-His-Purkinje system (slow conduction). For manifest APs, this atrial stimulus blocks in the AP, causing abrupt PR prolongation and normalization of the QRS complex at tachycardia onset. Critical AV delay over the AV node-His-Purkinje axis allows recovery of AP excitability and initiation of tachycardia.16 This critical AV delay can occur in the 1) AV node, 2) His bundle, and/or 3) bundle branches (particularly, BBB ipsilateral to the AP) (Figs. 10-8, 10-9 and 10-10). Sufficient AV node delay (AH prolongation) can occur by two mechanisms: physiologic decrement or switch from FP to SP. Delay in the His-Purkinje system facilitating ORT is manifested by HV prolongation and/or BBB ipsilateral to the AP. Ipsilateral BBB forces antegrade conduction over the contralateral bundle, and the addition of transeptal conduction to the circuit allows additional time for the AP to recover excitability. Restitution (cycle length dependency) and longitudinal dissociation of bundle branch refractory periods provide the conditions favorable to induce functional BBB using long-short sequences inherent in

programmed atrial extrastimulation, particularly at long drive cycle lengths.17






FIGURE 10-6 Coumel’s sign (ORT using a left free wall AP). Atrial activation is left eccentric. Top: A His refractory right ventricular extrastimulus crosses the septum, advances the atrium (asterisk) over the AP, and breaks the transeptal link perpetuating LBBB. Loss of LBBB results in 60 ms shortening of the VA interval but 80 ms lengthening of the AH interval (due to decremental conduction over the AV node), causing paradoxical slowing of tachycardia. Bottom: A His refractory ventricular extrastimulus advances the atrium (asterisk) over the AP, breaks the transeptal link perpetuating LBBB, and induces dual AV node physiology (FP/SP alternans). Loss of LBBB results in 36 ms shortening of the VA interval, but FP/SP decrement causes paradoxical slowing of tachycardia and cycle length alternans.






FIGURE 10-7 Coumel’s sign with 3:2 LBBB Wenckebach (ORT using a left posterior AP). The earliest site of atrial activation is at CS md. VA intervals accompanying normal and incomplete LBBB are similar (VA = 93 ms) but longer with complete LBBB (VA = 147 ms). Note the repeating sequence of AA prolongation for three successive cycles accompanying LBBB Wenckebach as AA intervals bracketing normal and complete LBBB are the shortest and longest, respectively.


Ventricular Stimulation

Induction of ORT by ventricular stimulation (programmed extrastimulation or burst pacing) require that an impulse fall into the tachycardia window (defined by the difference in retrograde refractory periods between the His-Purkinje-AV node axis and AP). A critically timed impulse 1) fails to conduct retrogradely over the His-Purkinje-AV node axis (unidirectional block) and 2) conducts exclusively over the AP.18 A critical VA delay allows recovery of the AV node-His-Purkinje axis and initiation of tachycardia. The site of unidirectional block occurs either in the 1) His-Purkinje system or 2) AV node and can be determined by 1) retrograde His bundle potentials and 2) first AH(ORT) versus second AH(ORT) (Figs. 10-11, 10-12, 10-13, 10-14 and 10-15). Absence of a retrograde His bundle potential following the last pacing stimulus (when retrograde His bundle potentials are otherwise present) and first AH(ORT) less than the second AH(ORT) indicates block in the His-Purkinje system and failure to retrogradely penetrate the AV node. Presence of a retrograde His bundle potential after the last pacing stimulus and first AH(ORT) greater than the second AH(ORT) indicates penetration of the AV node prior to block (unless the His bundle is orthodromically activated, [Fig. 10-13]).


Bundle Branch Reentrant Beats (“V3 Response”)

A characteristic feature of ORT using a left-sided AP is its induction by bundle branch reentrant (BBR) beats during programmed ventricular extrastimulation (Figs. 10-16 and 10-17). Typical BBR beats 1) follow a “VH jump,” 2) manifest left bundle branch block (LBBB) morphology, and 3) are preceded by His bundle electrograms (HV[BBR]≥HV[nonpreexcited NSR]). A single ventricular extrastimulus fails to conduct over the right bundle (retrograde right bundle effective refractory period) and crosses the interventricular septum to activate the left and His bundle (“VH jump”). Sufficient retrograde delay allows the RB to recover excitability, conduct antegradely, and induce a single BBR beat (“V3 response”). The single BBR beat crosses the septum, fails to conduct over the left bundle (unidirectional block), and conducts exclusively over the left-sided AP to initiate tachycardia (conditions similar to left-sided ORT induction by atrial stimulation with LBBB).


TERMINATION

The weak links for ORT are the AV node-His bundle axis and AP where block at either site terminates tachycardia.


Spontaneous

The obligatory 1:1 AV relationship during ORT implies that either AV or VA block precludes tachycardia induction or causes termination. Antegrade block occurs either in the 1) AV node or 2) His-Purkinje system. Spontaneous termination with block in the AV node demonstrates tachycardia dependence on the AV node and excludes AT (Fig. 10-18). The rare spontaneous termination with block below the AV node demonstrates tachycardia dependence on the His-Purkinje system and excludes both AV nodal reentrant tachycardia (AVNRT)










and AT (Fig. 10-19).7 Retrograde AP block can occur either at its atrial or ventricular insertion sites (Fig. 10-20).6,19,20






FIGURE 10-8 ORT induction facilitated by SP conduction. At a coupling interval of 360 ms, conduction occurs over the FP (AH = 154 ms). At 350 ms, the extrastimulus encounters FP refractoriness (antegrade FP ERP) and conducts over the SP (AH = 342 ms) with sufficient AV delay to initiate ORT using a left free wall AP.






FIGURE 10-9 ORT induction facilitated by ipsilateral BBB. Top: During sinus rhythm, a spontaneous APC encroaches on His-Purkinje refractoriness, conducts with HV prolongation (119 ms)/right bundle branch block (RBBB), and induces a single orthodromic reciprocating echo over a left free wall AP that fails to initiate ORT because of infrahisian AV block. Bottom: A similarly coupled APC preceded by a slightly longer sinus cycle length conducts with HV prolongation (127 ms)/LBBB. LBBB increases the VA interval of the reciprocating echo, allowing sufficient time for the otherwise refractory His-Purkinje system to recover partial excitability initiating ORT with LBBB.

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Oct 13, 2019 | Posted by in CARDIOLOGY | Comments Off on Orthodromic Reciprocating Tachycardia
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