Long RP Tachycardias

Long RP Tachycardias


Because the retrograde limb of the AV node-dependent long RP tachycardia involves the SP (atypical AVNRT, NFRT AP-SP) or a slowly conducting decremental AP, which are often (but not always) posteroseptal in location (PJRT), atrial activation is generally midline and earliest along the posteroseptum (Figs. 6-2, 6-3 and 6-4). Both the AV node and slowly conducting APs are adenosine-sensitive postulating that these decremental APs contain accessory AV nodal or depolarized atrial tissue.2 While transition zone clues (spontaneous termination with AV block excluding AT, VA/tachycardia cycle length [TCL] prolongation with bundle branch block [BBB]) still apply to long RP tachycardias, such observations are less common than with their short RP counterpart (Fig. 6-5). Spontaneous termination commonly occurs in the retrograde limb (SP or slowly conducting AP), which is unhelpful for diagnosis. Additionally, BBB-induced VA/TCL changes are difficult to appreciate or even absent with long RP ORT because 1) tachycardia is slower and less susceptible to aberration, 2) the septal location of most APs increases VA intervals only slightly (≤25 ms), and 3) any enlargement of the macroreentrant circuit by the addition of transeptal conduction is counterbalanced by faster conduction over the decremental AP, or conversely, reduction of the macroreentrant circuit by the loss of transeptal conduction (loss of BBB ipsilateral to the AP) is counterbalanced by slower conduction over the decremental AP (VA prolongation). Pacing maneuvers are therefore required to establish a more definitive diagnosis.


For the AV node-dependent long RP tachycardias, pacing maneuvers from the ventricle during sinus rhythm (parahisian, differential RV pacing) are less useful than those during tachycardia (His refractory ventricular premature depolarizations [VPDs], entrainment) because 1) VA Wenckebach block might exist despite pacing at the slowest rate allowable by sinus rhythm, 2) fast pathway (FP) might preempt
slower SP or AP conduction and prevent identification of the slowly-conducting retrograde limb of the circuit responsible for tachycardia, and 3) reproducible tachycardia induction with onset of ventricular stimulation can interfere with pacing maneuvers.3 Additionally, an “AV nodal response” during parahisian pacing can occur with a NF AP, while an “AV nodal response” during differential RV pacing can be seen with a long, insulated AV or NF/NV AP inserting closer to the RV apex than base (Figs. 6-6 and 6-7).4,5

FIGURE 6-1 The four AV node-dependent long RP tachycardias. The upper and lower limbs of the circuit are determined by pacing maneuvers in the atrium and ventricle, respectively. Asterisk denotes that NF/NV AP inserts into the SP.

His Refractory VPDs (Identifying Presence of a Decremental AP)

For long RP tachycardias, a positive response to His refractory VPDs is the single most useful maneuver to identify the existence of an AP.1 With long RP tachycardias, positive responses include reproducible 1) termination with VA block, 2) resetting with advancement, and 3) resetting with delay—the latter occurring only in APs with significant decremental properties (Figs. 6-8, 6-9, 6-10, 6-11, 6-12, 6-13 and 6-14).6,7,8,9,10,11,12,13 A positive response, however, proves the presence of an AP but not necessarily its participation in the tachycardia mechanism (participant versus bystander).8,9 It is possible for a His refractory VPD to terminate or reset atypical AVNRT in the presence of a concealed, bystander NF AP inserting into the SP (retrograde limb) of the AV node (Figs. 6-12 and 6-13; see also Fig. 11-16).8,9,10 Such a VPD conducts over the NF AP-SP and penetrates the excitable gap in the SP ahead of the tachycardia wavefront, which had just crossed the lower turnaround point of the circuit. The paced antidromic wavefront collides with tachycardia, while its orthodromic wavefront finds absolute or relative distal SP refractoriness terminating or resetting tachycardia with delay, respectively.

His refractory VPDs that reset tachycardia with delay (“post-excitation”) identify an AP with severe decremental properties (degree of AP delay > degree of VPD prematurity resulting in a more than fully compensatory pause) that can also generate long post-pacing intervals (PPIs) and pseudo AAV responses during entrainment from the ventricle, resulting in a potential misdiagnosis of AVNRT and AT, respectively (Fig. 6-14).11,14 Additionally, it is important to deliver multiple VPDs because apparent absence of resetting following a single VPD (false negative) can occur if the degree of VPD prematurity is offset by an equal degree of AP delay (full compensation) (Fig. 6-15).


The different mechanisms of the AV node-dependent long RP tachycardias are complex. The lower limb of its circuit can involve the His-Purkinje system/ventricle (ORT: PJRT/NFRT) or not (AVNRT). The upper limb of its circuit can be confined to the AV node (“nodal tachycardias”: AVNRT/NFRT) or not (PJRT).1 Therefore, diagnosis requires separate pacing maneuvers in the atrium and ventricle to delineate the upper and lower limbs of the circuit, respectively (Fig. 6-1).

Entrainment from the Ventricle (Delineation of the Lower Circuit: Atypical ORT [PJRT/NFRT] Versus Atypical AVNRT)

In contrast to entrainment of short RP tachycardias from the ventricles, long RP tachycardias often demonstrate atypical responses (AAV patterns, long PPIs) because of the decremental properties of its retrograde limb (SP or AP). Additionally,

oscillations in the cycle length and pacing-induced VA prolongation make interpretation of entrainment criteria difficult.

FIGURE 6-2 Atypical AVNRT. P waves are inverted inferiorly and slightly positive in V1. Atrial activation is midline (earliest along the posteroseptum).

FIGURE 6-3 PJRT. P waves are inverted inferiorly and slightly negative in V1 (in contrast to the slight positivity in V1 of atypical AVNRT). Atrial activation is midline (nearly simultaneous between the antero- and posteroseptum).

FIGURE 6-4 Atypical AVNRT with a concealed, bystander NF AP. P waves are inverted inferiorly and slightly positive in V1. The AH interval is very short (33 ms—the end of the atrial electrogram overlaps the His bundle potential) because it is actually a pseudo-interval that represents simultaneous activation of the atrium and His bundle (excludes PJRT). His refractory VPDs delayed the atrium proving the presence of an AP (Fig. 6-13).

AAV Patterns

An AAV response is generally considered diagnostic of AT, but AAV patterns are common with AV node-dependent long RP tachycardias causing potential misdiagnosis of AT. The AAV pattern can either be a 1) pseudo AAV (true AV) response or 2) true AAV response resulting from retrograde “double fire” (see Table 5-2) (Figs. 6-12, 6-13 and 6-14 and 6-16).8,9,11,15,16,17,18,19 Classic pseudo AAV responses are more common with atypical AVNRT than ORT because of its longer paced VA interval and occur when significant pacing-induced decrement over the SP or AP cause the paced VA interval to exceed the pacing cycle length (VV interval). In this case, the first atrial electrogram after entrainment is actually driven by the penultimate (second to last) pacing stimulus. Identifying the last entrained atrium after pacing demonstrates a true “AV” response and an

atrial activation pattern identical to tachycardia. Other rare causes of pseudo AAV responses during atypical AVNRT are seen when long AH intervals exceed the TCL or momentary lower common final pathway block develops upon cessation of pacing.15,17,19 True AAV responses result from dual retrograde responses (“double fire”) with simultaneous conduction over the FP and SP/slowly conducting AP. This is different from the true AAV response of AT where retrograde atrial activation over the AV node is followed by the first return beat of AT after pacing. In contrast to pseudo AAV responses, first and second atrial activation patterns with true AAV responses generally differ. One mechanism to explain dual retrograde responses during atypical AVNRT/ORT is the presence of a large excitable gap with collision between antidromic and orthodromic wavefronts in the SP or AP (orthodromic or retrograde limb) of the circuit. The last (n) paced antidromic wavefront conducts completely over the FP to the atrium (first A) while colliding with the previous (n − 1) orthodromic wavefront in the SP or AP. The last (n) paced orthodromic wavefront has no antidromic wavefront with which to collide, conducts slowly over the SP or AP to activate the atrium (second A) before conducting antegradely over the FP to the His bundle/ventricle. An alternative mechanism is tachycardia termination and subsequent re-initiation. With onset of ventricular pacing, retrograde block occurs in the SP/AP effectively terminating tachycardia and conducts exclusively over the FP. When pacing stops, retrograde conduction occurs over both the FP and SP/AP, the latter re-initiating tachycardia with a dual retrograde response.

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Oct 13, 2019 | Posted by in CARDIOLOGY | Comments Off on Long RP Tachycardias
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