NCTs are categorized by the length of its RP interval (onset of QRS complex to onset of P wave) into short and long RP tachycardias. Short RP tachycardias (RP < PR) include typical (slow-fast) AVNRT, ORT, AT with PR prolongation, and JT with retrograde fast pathway (FP) conduction. During typical (slow-fast) AVNRT, simultaneous activation of the atrium and ventricle produces a very short RP interval (<70 ms) (“A on V” tachycardia) with P waves buried within the QRS complex or distorting its terminal portion (pseudo S waves in II, III, aVF; pseudo r′ wave in V1) (see Fig. 7-13).⁵,⁶ Sequential activation from ventricle to atrium during ORT imposes a mandatory finite VA interval during tachycardia (≥70 ms; ≥50 ms for pediatric populations) so that P waves are generally buried within the ST segment.⁶,⁷ Therefore, a NCT with an RP interval <70 ms essentially excludes ORT. Long RP tachycardias (RP > PR) include atypical (fast-slow) AVNRT, ORT using a slowly conducting, decremental accessory pathway (AP) (permanent form of junctional reciprocating tachycardia [PJRT] or nodo-fascicular reentrant tachycardia [NFRT]), and AT (see Chapter 6). A mid-RP tachycardia with P waves buried exactly between QRS complexes (RP = PR) should raise suspicion of typical AVNRT with 2:1 block in the lower common final pathway (LCFP) (Fig. 5-1). NCTs without identifiable P waves

include typical AVNRT (P waves buried within QRS complexes) and atrial flutter with 2:1 AV conduction (flutter waves buried within QRS complexes and T waves) especially when the ventricular rate is ˜150 bpm.

The site of atrial origin during tachycardia determines its P-wave morphology. P waves originating from the septum tend to be narrower than those from the free wall. In general, low septal origin (AVNRT, ORT using a septal AP, septal AT) have a superior (inverted in leads II, III, aVF) and midline (aVR P [+] ˜ aVL P [+]) axis. Left atrial origin (ORT using a left-sided AP, left AT, AVNRT with left atrio-nodal inputs) has an anterior (V1 P [+]) and rightward (aVR P [+], aVL P [−]) axis. Right atrial origin (ORT using a right-sided AP, right AT) have a posterior (V1 P [−]) and leftward (aVR P [−], aVL P [+]) axis. P waves with an inferior axis (upright in leads II, III, aVF) are generally due to AT, although ORT using an anteroseptal AP can produce positive P waves inferiorly.⁸

QRS alternans is the beat-to-beat variation in R-wave amplitude (≥1 mm) during stable tachycardia. While some evidence suggests that QRS alternans favors ORT with slower rates (<180 bpm), it is likely a rate-related phenomenon and not specific for a particular tachycardia mechanism.⁴,⁹,¹⁰

Because of the large overlap in rates of different NCT, a specific rate criterion is generally not helpful for discrimination. However, a ventricular rate of 150 bpm suggests the possibility of atrial flutter with 2:1 AV conduction. An extremely rapid (“ultrafast”) SVT (>250 bpm) should raise suspicion of atrial flutter with 1:1 AV conduction.

The VA interval (onset of QRS complex to earliest site of atrial activation) is the intracardiac equivalent of the RP interval. A VA <70 ms (<50 ms in pediatric populations) excludes ORT.⁶,⁷

Atrial activation patterns dictate P-wave morphology and are either concentric (midline) or eccentric.¹¹,¹²,¹³ Concentric patterns show earliest activation along the interatrial septum near the coronary sinus ostium (posteroseptum) or His bundle region (anteroseptum). NCTs with earliest activation at the anteroseptum include typical AVNRT, ORT using an anteroseptal AP, AT arising near the His bundle (e.g., noncoronary cusp), and JT with retrograde conduction over the FP. NCT with earliest activation at the posteroseptum include atypical AVNRT; ORT using a posteroseptal AP; AT arising near the coronary sinus ostium; and theoretically, JT with retrograde conduction over the slow pathway (SP). Eccentric patterns show earliest activation away from the septum and generally argue against retrograde AV nodal conduction except with left atrio-nodal inputs. NCTs with left eccentric atrial activation include ORT using a left-sided AP, left AT, and uncommonly AVNRT with left atrio-nodal inputs.¹⁴ NCT with right eccentric atrial activation includes ORT using a right-sided AP and right AT. Because both the typical (AV) AP and the AV node are annular structures, an NCT with early activation from a nonannular site is most likely an AT.

ORT is the only NCT that incorporates the ventricle as an integral part of its reentrant circuit, and therefore, a NCT with AV block excludes ORT. AV block, on the other hand, is possible but uncommon during AVNRT and common during AT. AVNRT with LCFP block is generally a transient phenomenon precipitated by abrupt changes (long-short sequence) in cycle length (particularly at SVT initiation) (Fig. 5-1).¹⁵,¹⁶ A NCT
with sustained and varying degrees of AV block is likely AT. During 1:1 AV association, changes in AH intervals that precede and predict VV and subsequent AA intervals indicate an AV node-dependent tachycardia (AVNRT or ORT) and argue against AT. Constant AA intervals despite changes in AH and VV intervals demonstrate AV node independence (AT).

In contrast to NCT with AV block, NCT with AV dissociation is rare and includes 1) AVNRT with upper common final pathway (UCFP) block, 2) JT with JA block, 3) ORT using a nodo-fascicular/nodo-ventricular AP with nodo-atrial block, and 4) intrahisian reentry with His-atrial block (see below).¹⁷,¹⁸ While ORT using an AV AP obligates a 1:1 AV relationship, ORT using a nodo-fascicular/ventricular AP does not and can show AV dissociation (but not AV block).

ORT is the only NCT that incorporates the His-Purkinje system as an integral part of its reentrant circuit and specifically uses the bundle branch and Purkinje fibers ipsilateral to the AP to form the shortest functional circuit sustaining reentry. Block in the bundle branch ipsilateral to the AP forces antegrade conduction over the contralateral bundle enlarging the circuit with transeptal conduction.¹⁹,²⁰,²¹,²² The addition of transeptal conduction time to the tachycardia increases its 1) VA interval and, generally, 2) cycle length (Coumel’s sign) (Figs. 5-2 and 5-3). VA intervals increase by >35 ms for free wall AP and <25 ms for septal AP.²⁰ Therefore, cycle length deceleration with BBB (or conversely, cycle length acceleration with loss of BBB) indicates that the His-Purkinje system is an integral part of the circuit and establishes a diagnosis of ORT using an AP ipsilateral to the blocked bundle. By contrast, failure of cycle length deceleration with BBB is not specific for a tachycardia mechanism and even does not exclude ORT using an AP ipsilateral to BBB. The increase in VA interval can be compensated by an equivalent shortening of the AV interval, generally due to a decrease in the AH interval (see Figs. 10-5 and 10-6).

Important clues to tachycardia diagnosis during spontaneous initiation include its 1) mode of onset and 2) initiating complexes. Gradual onset (warm-up phenomenon) occurs with automatic tachycardias (e.g., automatic AT). Abrupt onset is observed with triggered activity and reentry (e.g., AVNRT, ORT). NCTs whose initial P wave is identical to tachycardia P waves include automatic AT (where an ectopic focus drives all tachycardia P waves) and PJRT (which occurs spontaneously during sinus rhythm without the need for atrial prematurity).

NCTs triggered by an atrial premature depolarization (APD) (initial P wave ≈ tachycardia P waves) include AVNRT, ORT, and triggered and reentrant AT. NCT initiated by a ventricular premature depolarization (VPD) (particularly, late-coupled VPDs) favors ORT because the ventricle is an integral part of the circuit. Rarely, NCT can be induced upon termination of atrial fibrillation (Fig. 5-4).

Programmed atrial extrastimulation facilitates induction of reentrant tachycardias by providing triggers that fall into the tachycardia window (difference in refractory periods between the two limbs of the reentrant circuit). The premature impulse fails to conduct over the β limb with longer refractoriness (unidirectional block) and conducts with sufficient delay
(slow conduction) over its counterpart α limb allowing sufficient time to recover excitability and initiate reentry. Induction of intra-atrial reentrant tachycardia, AVNRT, and ORT requires a critical degree of slow conduction within the atrium, the AV node, and along the AV node-His-Purkinje axis, respectively.²³ The critical AH interval for typical AVNRT is achieved by switch from FP to SP conduction (see Figs. 7-32 and 7-33). The critical AV interval for ORT can occur within the AV node, His bundle, and/or bundle branches (particularly BBB ipsilateral to the AP) (see Figs. 10-8, 10-9 and 10-10). While programmed ventricular extrastimulation can induce both AVNRT and ORT, atypical AVNRT is more easily induced from the ventricle than its typical counterpart. A feature characteristic of ORT using a left-sided AP is induction following typical bundle branch reentrant (BBR) complexes (Fig. 5-5). Single, typical BBR complexes cross the lower interventricular septum, fail to conduct over the AV node due to retrograde left bundle (LB) refractoriness (unidirectional block), and reach the AP with sufficient VA delay (transeptal conduction) to initiate tachycardia.

When single-site atrial and ventricular extrastimulation fail to induce tachycardia, several techniques might facilitate induction: 1) stimulation from different sites (site-dependent induction), 2) extrastimulation following different drive cycles or during sinus rhythm (simulating clinical APD or VPDs), 3) double atrial extrastimulation, and 4) drug provocation (isoproterenol or atropine).

Important clues during spontaneous termination of tachycardia include the 1) mode of termination and 2) terminating complexes. Gradual deceleration preceding termination (cool-down period) suggests an automatic tachycardia (e.g., automatic AT), while sudden termination occurs with triggered and reentrant mechanisms. Spontaneous termination with AV block (tachycardia termination with a P wave) demonstrates tachycardia dependence on the AV node (AVNRT, ORT) and excludes AT (Figs. 5-6 and 5-7). Tachycardia termination by a VPD that fails to reach the atrium (VA block) also excludes AT (Figs. 5-8 and 5-9). Electrocardiographically, VA block is suggested by early return of a sinus beat (less than the sinus cycle length) following the VPD. Termination of tachycardia by a late-coupled VPD (≥85% of tachycardia cycle length [TCL]) favors diagnosis of ORT.

Late-coupled VPDs delivered when the His bundle has been antegradely depolarized (“committed”) by tachycardia are “His refractory” and do not affect AVNRT (unless a nodo-fascicular/nodo-ventricular AP is present) or AT (unless an AV AP with its atrial insertion site at the AT site of origin is present). Tachycardia termination by His refractory VPD that fails to reach the atrium (VA block) excludes pure AVNRT and AT and strongly favors a diagnosis of ORT (Fig. 5-10). Tachycardia termination by early-coupled (non-His refractory) VPD that fails to reach the atrium (VA block) excludes AT (Figs. 5-8 and 5-9).

Programmed ventricular extrastimulation with tightly coupled extrastimuli can induce a “VH jump” when retrograde right bundle (RB) refractoriness (retrograde right bundle branch block [RBBB]) is reached (particularly at long drive cycles when RB effective refractory period [ERP] is greater than RV ERP). During the VH jump, retrograde RBBB forces retrograde activation to cross the interventricular septum and conduct retrogradely over

the LB to activate the His bundle. Taking advantage of the VH jump allows determination of whether retrograde atrial activation is associated (AV node) or dissociated (AP) from the His bundle.²⁶ With retrograde AV node conduction, the increase in VH interval is accompanied by an equivalent (fully excitable AV node) or longer (relative refractory AV node) increase in VA interval (HA is unchanged or longer) (Fig. 5-11). With retrograde AP conduction, the increase in the VH interval is accompanied by no change in the VA interval (nondecremental AP) (HA becomes shorter or paradoxically negative). A negative HA interval (retrograde atrial activation preceding retrograde His bundle activation) shows that atrial activation is not linked to retrograde activation of the His bundle and identifies the presence of an extranodal AP (Figs. 5-12, 5-13 and 5-14).

Differential RV pacing takes advantage of the site dependency of retrograde atrial activation, which differs between the AV node and AP.²⁷,²⁸ The VA interval is directly related to the proximity of the RV pacing site to the entrance site of the retrogradely conducting structure. Because retrograde conduction over the AV node is linked to the His bundle, the VA interval at the RV apex (near the RB terminus) is shorter than at the base (Fig. 5-15). In contrast, the VA interval for AP at the RV base (near its ventricular insertion site) is shorter than at the apex (Figs. 5-15 and 5-16).

Parahisian pacing takes advantage of the ability to directly capture the His-Purkinje system and therefore determines whether retrograde atrial activation is dependent on capture of the His bundle/RB (AV node) or myocardium (AP).²⁹ High-output pacing is delivered near the His bundle at the RV anterobasal septum directly capturing the His bundle/RB complex and myocardium (His/RV capture). The stimulation strength is lowered until His bundle/RB capture is lost and stimulation only captures the RV (RV-only capture). Loss of direct His bundle/RB capture delays activation of the His bundle by forcing the depolarizing wavefront to travel from the basal pacing site to the terminus of the RB (RV base → apex) and then retrogradely over the RB back to the His bundle (RV apex → base). With retrograde conduction over the AV node, loss of His bundle capture causes 1) prolongation of the stimulus-A (St-A) interval at the expense of the stimulus-H (St-H) interval (demonstrating dependency of retrograde atrial activation on His bundle activation), 2) no change in the HA interval, and 3) no change in the atrial activation pattern (AV node response) (Figs. 5-17 and 5-18). With retrograde conduction over an AP, loss of His bundle capture causes 1) no change in the St-A interval (demonstrating dependency of retrograde atrial activation on myocardial not His bundle activation), 2) shortening or reversal of the HA interval, and 3) no change in the atrial activation pattern (AP response) (Figs. 5-17 and 5-18). With retrograde

fusion over both the AV node and an AP, loss of His bundle capture shows a possible increase in St-A intervals (depending on the relative conduction times over the AV node and AP) but a change in the retrograde atrial activation pattern (Fig. 5-19). Because a finite amount of time (generally ≥35 ms) is required for the pacing stimulus that only captures the right ventricle to retrogradely activate the His bundle, small increases (<35 ms) in St-A interval with loss of His bundle capture should raise suspicion for presence of an AP. The addition of pure His bundle pacing (selective His only capture) can identify other APs not identified by parahisian pacing alone.³⁰