REVIEW

Diagnostic Pacing Maneuvers for Supraventricular

Tachycardias: Part 2
GEORGE D. VEENHUYZEN, M.D., F. RUSSELL QUINN, M.R.C.P., PH.D.,
STEPHEN B. WILTON, M.D., ROBIN CLEGG, M.D., and L. BRENT MITCHELL, M.D.
From the Libin Cardiovascular Institute of Alberta, University of Calgary and Calgary Health Region, Alberta, Canada

The approach to supraventricular tachycardia (SVT) diagnosis can be complex because it involves
synthesizing baseline electrophysiologic features, features of the SVT, and the response(s) to pacing
maneuvers. In this two-part review, we will mainly explore the latter while recognizing that neither of
the former can be ignored, for they provide the context in which diagnostic pacing maneuvers must
be correctly chosen and interpreted. Part 1 involved a detailed consideration of ventricular overdrive
pacing, since this pacing maneuver provides the diagnosis in the majority of cases. In Part 2, other
diagnostic pacing maneuvers that might be helpful when ventricular overdrive pacing is not diagnostic or
appropriate, including attempts to reset SVT with single atrial or ventricular beats, para-Hisian pacing,
apex versus base pacing, and atrial overdrive pacing, are discussed, as are some specific diagnostic SVT
challenges encountered in the electrophysiology lab. There is considerable literature on this topic, and
this review is by no means meant to be all-encompassing. Rather, we hope to clearly explain and illustrate
the physiology, strengths, and weaknesses of what we consider to be the most important and commonly
employed diagnostic pacing maneuvers, that is, those that trainees in cardiac electrophysiology should
be well familiar with at a minimum. (PACE 2012; 35:757–769)
ablation, electrophysiology - clinical, SVT, pacing

In part 1 of this review on diagnostic pac- Scanning diastole with ventricular premature
ing maneuvers for supraventricular tachycardia beats (VPBs)
(SVT), we explored ventricular overdrive pacing Single VPB introduced decrementally during
(VOP) in detail, since it provides a firm SVT diastole in SVT offer an opportunity to determine
diagnosis in the majority of cases.1 We will now the relationship between altered timing of ven-
consider pacing maneuvers that can be performed tricular depolarization and the timing of atrial
when VOP is not diagnostic, including ones that depolarization. For example, if a VPB is able to
can be performed when sustained, regular SVT terminate tachycardia without atrial depolariza-
cannot be induced. These will include single- tion, then AT can be excluded, provided this
paced ventricular beats during ongoing SVT, para- is not a coincidence. Furthermore, VPBs that
Hisian pacing, and apex versus base pacing. occur during SVT at a time when the stimulated
We will also explore some challenging specific wavefront would be expected to collide with the
situations in SVT diagnosis including differen- SVT wavefront in the His-Purkinje network or
tiating atrioventricular node reentry tachycardia in ventricular myocardium cannot possibly affect
(AVNRT) from atrial tachycardia (AT) and junc- atrial timing during either AVNRT or AT (unless a
tional tachycardia (JT), SVT with atrioventricular bystander AP is present). Accordingly, such His-
(AV) dissociation, and differentiating AVNRT refractory VPBs (HRVPBs) should only be capable
with a leftward atrionodal exit from orthodromic of affecting AVRT circuits (again, in the absence
atrioventricular reciprocating tachycardia (AVRT) of a bystander AP). VPBs that occur before His
employing a left-sided accessory pathway (AP). bundle refractoriness are potentially capable of
affecting atrial timing (including terminating SVT)
in any of AT, AVNRT, or AVRT.
How does one determine if a paced VPB is
Address for reprints: George D. Veenhuyzen, M.D., F.R.C.P.C., His-refractory? If the QRS complex morphology
Libin Cardiovascular Institute of Alberta, University of Calgary of the VPB shows evidence of fusion (i.e., the
and Calgary Health Region, Foothills Medical Centre, Rm C836, QRS complex morphology of the VPB shows some
1403-29 St. N.W., Calgary, Alberta, T2N 2T9, Canada. Fax: 403-
944-1592; e-mail: [email protected] features of the QRS complex morphology of a
paced VPB and some features of the QRS complex
Received September 19, 2011; revised December 22, 2011;
morphology of the SVT), then the paced VPB must
accepted January 5, 2012.
be His-refractory, since the SVT wavefront that the
doi: 10.1111/j.1540-8159.2012.03352.x

C 2012, The Authors. Journal compilation 

 C 2012 Wiley Periodicals, Inc.

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 VEENHUYZEN, ET AL.

earlier than the anticipated timing of the antegrade

His potential, it would not be considered to be
His-refractory, but rather, prior to His bundle
refractoriness.
There are three responses to an HRVPB that
are diagnostically useful:

(1) SVT terminates without conduction to

the atrium. This response indicates a diagnosis
of AVRT, provided that this event is not a
coincidence, as could be the case if the SVT
frequently spontaneously terminates. The fact that
an HRVPB can affect the SVT indicates that an AP
is present, and the fact that the SVT terminates
with ventriculoatrial (VA) block indicates that
ventricular and atrial activation must be linked
Figure 1. Advancement of atrial activation by a fused so that if conduction to the atrium does not
His-refractory ventricular premature beat (HRVPB). occur via the AP, the circuit is interrupted.
Panel A: During supraventricular tachycardia with a This cannot be the case with AT or AVNRT,
stable cycle length of 444 ms, one-to-one atrioven- even if a bystander AV AP is present. That is,
tricular relationship, and an earlier atrial electrogram the AP must also be participating in the SVT
recorded in the right atrium (where the ablation mechanism. Theoretically, this response could be
catheter, ABLp/d, is located) than in the septum observed given the coexistence of AVNRT and a
(d/pHIS) or coronary sinus (proximal CS 9,10 through bystander nodoventricular AP, but this occurrence
distal CS 1,2), a paced premature beat is delivered has not been convincingly demonstrated to our
by electrodes at the right ventricular apex (RVd). The knowledge, and would have to be extremely rare.
subsequent atrial activation is advanced by 19 ms. As we discussed in Part 1, sometimes VOP
The paced premature ventricular beat is His-refractory results in an apparently noninterpretable response
(HRVPB) because (1) it is fused: note QRS complex when VOP repeatedly terminates the SVT. VOP
morphology features and duration (122 ms) that are may be considered as a series of consecutive
intermediate between those of the conducted SVT VPBs. When the SVT repeatedly stops during
(narrow complex) and of a purely paced QRS complex VOP because of VA block, if the paced beat that
(Panel B, QRS complex duration = 144 ms) and (2) the precedes VA block is His-refractory, and the atrial
pacing stimulus is delivered at precisely the time of timing has not changed prior to that VPB, this
the expected His bundle potential (arrow). A ventricular constitutes an equivalent of an HRVPB terminating
paced beat can be considered His-refractory if it occurs SVT without conduction to the atrium, thereby
up to 35–55 ms earlier than the anticipated His bundle establishing a diagnosis of AVRT (see “What if the
potential. Advancement of atrial activation without a response to VOP is not interpretable?” in Part I).
change in the atrial activation sequence by an HRVPB (2) Atrial activation is delayed without a
indicates that an accessory pathway (AP) is present and change in the atrial activation sequence. This
almost certainly participating in orthodromic AVRT, in response indicates a diagnosis of AVRT employing
this case, employing a right-sided AP. a decremental AP (Fig. 2). As above, the fact
that an HRVPB can affect the SVT indicates
that an AP is present and delay of atrial timing
stimulated wavefront is fusing with in ventricular indicates that atrial activation is decrementally
myocardium must have exited the His-Purkinje linked to ventricular activation. This cannot be
network (Fig. 1). If the pacing stimulus occurs the case with either AT or AVNRT even if a
just after a discernible antegrade His potential, bystander AV AP is present; the decremental AP
then the paced VPB is obviously His-refractory. must also be participating in the SVT mechanism.
Finally, if the paced VPB occurs no more than Note that for this response to be appreciated,
35–55 ms earlier than the anticipated timing of the degree of decremental conduction slowing
the antegrade His potential, in the time that would must exceed the prematurity of the HRVPB; if
be required for that stimulated wavefront to enter they are matched, AVRT employing a decremental
the distal arborization of the His-Purkinje network AP could be present but because no change in
and travel retrogradely to the His bundle, the atrial timing would occur, one would conclude
tachycardia wavefront would have reached the His that the VPB had no effect on the SVT and the
bundle where these wavefronts would collide.2 diagnosis could be missed. Accordingly, it is
When the paced VPB occurs more than 35–55 ms worth studying the effects of multiple HRVPBs

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long RP interval SVTs, even if entrainment by

VOP is associated with long cPPI-TCL and SA-
VA interval values. In such a situation, the finding
that an HRVPB delays atrial timing (indicating
a diagnosis of AVRT, Fig. 2) has a greater
diagnostic value than the finding of long cPPI-TCL
or SA-VA interval values (suggesting a diagnosis
of AVNRT).
Application of this maneuver requires that
any apparent delay in atrial timing exceeds the
spontaneous variability in the SVT cycle length
(CL). Accordingly, this maneuver may not be
reliable in irregular SVTs.
(3) Atrial activation is advanced without a
change in the atrial activation sequence. The fact
that an HRVPB can affect atrial timing indicates
that an AP is present. If the atrial activation
sequence is unaltered, one can conclude with
Figure 2. Delay of atrial activation by a His-refractory confidence, but not with certainty, that the AP is
ventricular premature beat (HRVPB). During a long R-P participating in the SVT mechanism, establishing
interval supraventricular tachycardia with a stable cycle a diagnosis of AVRT (Fig. 1). Theoretically, AT
length of 473 ms, a paced premature beat is delivered by or AVNRT could be advanced by conduction
electrodes at the right ventricle. The subsequent atrial over a bystander AP, and if the bystander AP
activation is delayed by 20 ms without a change in were close to the AT origin or atrionodal exit,
the atrial activation sequence. The paced premature respectively, the atrial activation sequence may
ventricular beat is His-refractory because it occurs not change appreciably. This situation is so rare
virtually simultaneously with and certainly not more that this finding is considered very strong evidence
than 35–55 ms earlier than the expected inscription (but not proof) that the SVT mechanism is
of the anterograde His bundle potential (arrow). This AVRT.
response indicates that an accessory pathway (AP) is As before, application of this maneuver
present and participating in orthodromic AVRT, in this requires that any apparent change in atrial timing
case, employing a slowly conducting concealed septal exceeds the degree of spontaneous variability in
AP. (Tracing courtesy of Dr. G. Neal Kay.) the SVT CL. Accordingly, this maneuver may not
be reliable in irregular SVTs.
Unfortunately, while these responses to
introduced throughout the His-refractory diastolic HRVPBs are specific (or, in the third case, nearly
window to minimize this potential pitfall of specific) for AVRT, they are not particularly
studying only one HRVPB that had no apparent sensitive. If the pacing site is far from the
effect. Theoretically, delayed atrial timing after an participating AP, the orthodromic wavefront of the
HRVPB could be observed in the setting of AVNRT VPB may not have had enough time to reach the AP
with a bystander nodoventricular AP.3 This is and affect the AVRT circuit when delivered late
so rare that delay of atrial timing by an HRVPB enough to be His-refractory. The classic situation
without a change in the atrial activation sequence in which an HRVPB delivered from the right
should be considered extremely strong evidence ventricular (RV) apex does not affect an AVRT
that the SVT mechanism is AVRT employing a circuit because of the distance of the RV apex to
decremental AP. the AP occurs when a left free wall AP is operative;
It is often the case that AVRT employing a nevertheless, this problem may arise when a
decremental AP manifests as a long RP interval relatively nearby septal AP is involved.4 As is the
SVT. If the AP used for retrograde conduction case with fusion during VOP, the sensitivity of the
has decremental conduction properties, entrain- three responses to HRVPBs described earlier can
ment by VOP could be associated with long be increased by moving the pacing site close to
corrected postpacing interval-tachycardia cycle the AP, that is, to a basal ventricular site close
length (cPPI-TCL) and stimulus-atrial (SA)-VA to the site of earliest atrial activation. This is not
interval values that would normally be considered surprising, since fusion during VOP constitutes
evidence of atypical AVNRT. Fusion during the continuous resetting of an AVRT circuit by
entrainment would still provide proof that the a series of consecutive HRVPBs; the fact that they
mechanism is AVRT but, if fusion is not present, are fused proves that they are His-refractory, as
it is important to scan diastole with VPBs during discussed earlier.

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It is commonly taught that if none of the from sites all around the tricuspid annulus, so
three responses to HRVPBs described earlier both septal and right free wall APs, as well as
is observed, no conclusion regarding the SVT retrograde AV nodal conduction, can show earliest
mechanism can be drawn. However, it has been atrial activation on the His catheter or at the
suggested that, in the case of a short RP interval proximal CS. Another pacing maneuver—para-
SVT, advancing the local ventricular activation Hisian pacing—can be useful in these circum-
adjacent to the earliest atrial activation by more stances.7 The basic concept is simple—pacing
than 30 ms without affecting atrial timing should is performed next to the His bundle/proximal
exclude the participation of a conventional AP right bundle (HB-RB) and the response is studied
from the SVT mechanism.5 Similarly, in the case when the HB-RB and adjacent myocardium are
of a long RP interval SVT, advancing the local captured, versus when local myocardium alone
ventricular activation adjacent to the earliest atrial is captured. This is usually achieved by varying
activation by more than 60 ms without affecting the pacing output and examining the surface
atrial timing should exclude the participation of a QRS duration and, where possible, the stimulus-
decremental AP from the SVT mechanism.5 His (SH) interval. HB-RB capture will produce
Regarding the HRVPB maneuver, one point a narrow QRS complex and short SH interval,
seems to be underappreciated: if an SVT that whereas loss of HB-RB capture will produce a
resembles typical AVNRT is induced (central wider QRS complex and lengthening of the SH
atrial activation and septal VA < 70 ms), interval. In the latter circumstance, the His bundle
this maneuver will not add further diagnostic will only be activated after excitation has traveled
information as it cannot distinguish AVNRT from through ventricular myocardium, penetrated the
AT (see one exception for this in the section on distal Purkinje network, and traveled retrogradely
AV-dissociated SVT). If the diagnosis is not clear through the conduction system. Often, with HB-
from findings during spontaneous perturbations in RB capture, the His potential is difficult to discern
the SVT, the pacing maneuver of choice in this (particularly when a single catheter is used for
situation is VOP. pacing and recording), either due to saturation of
the His channel by the pacing stimulus, or masking
Para-Hisian & Pure-Hisian Pacing by the local ventricular potential. Appearance of a
The pacing maneuvers described earlier clear retrograde His potential, however, is usually
rely on studying the response to an induced an indication that HB-RB capture has been lost.
perturbation (VOP or single premature beats) of We can now consider the response (timing
a stable tachycardia. However, it is common and pattern of retrograde atrial activation) in the
to encounter SVTs that are difficult to induce, absence and presence of an AP (Fig. 3). If AV nodal
nonsustained, irregular, or repeatedly terminate conduction alone is present then loss of HB-RB
during pacing protocols. Such circumstances may capture will cause a lengthening of the stimulus-
prevent diagnostic pacing maneuvers from being atrial (SA) interval (because excitation has a longer
performed, or can limit interpretation of their path to travel back to the atrium), without a
results. change in the atrial activation sequence. The
In a patient with documented SVT, but change in SA interval should match the change
no preexcitation on their baseline ECG, one of in the SH interval, when this can be measured,
the goals at an electrophysiologic study is to and the His-atrial (HA) interval should be the
determine the presence or absence of a concealed same. If AP conduction alone is responsible for
AP. Sometimes programmed stimulation from the retrograde atrial activation (i.e. no VA conduction
RV apex (or even catheter-induced PVCs) can is present through the AV node), then loss of
quickly give a clue: if the atrial activation sequence HB-RB capture should have little or no effect on
is clearly “eccentric” (either right or left free wall), the SA interval and no change in the pattern
then an AP is very likely to be present. Further of atrial activation. The SH interval will still
characterization of the conduction properties lengthen when HB-RB capture is lost, thus the HA
will be required to be more certain, but with interval will shorten, since atrial timing depends
little effort, something of interest will have been only on conduction over the AP. When both AV
discovered and further investigations can be nodal and AP conduction is present then a more
directed accordingly. A CS catheter is commonly complex response may be obtained, depending on
placed at the start of an electrophysiology study, so the proximity of the AP to the pacing site and
this works well for detecting nonseptal left-sided the conduction properties of the AP and the AV
APs, which account for around 50% of all APs.6 node/conduction system. Generally, a change in
The remainder of APs can be harder to the retrograde atrial activation sequence should
detect by this method. With “standard” catheter be seen, although this will depend on how much
positions there is not usually a catheter recording of the atrium is activated via the AP versus the

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proximal poles of the CS catheter but some delay

in atrial timing on the His catheter.

Pitfalls

(1) APs distant from the pacing site: Inter-

pretation of the response to para-Hisian pacing has
been shown to be reliable for septal and right free
wall APs, but can be misleading for left lateral APs.
In the latter case, the pathway may be so far from
the pacing site that the atria are entirely activated
via the AV node whether the HB-RB is captured or
not (assuming AV nodal conduction is sufficiently
rapid). However, as previously mentioned, an
eccentric atrial activation sequence may be clearly
apparent for left-sided APs simply with RV apical
Figure 3. Responses to para-Hisian pacing. In both pacing or programmed stimulation.
panels, pacing is being performed from the distal poles (2) Slowly-conducting APs: Similarly, if
of the His catheter (dHis). The first beat in each conduction over an AP is slow relative to AV
panel captures the His bundle and local ventricular nodal conduction then the response to para-Hisian
myocardium (narrow QRS complex), whereas the pacing may falsely suggest AV nodal conduction
second beat loses His capture and only stimulates ven- alone.7,8
tricular myocardium. Panel A shows the response when (3) Lack of ventricular capture during HB-
retrograde conduction is occurring over a concealed RB pacing: Occasionally, pure-Hisian pacing can
accessory pathway; with loss of His capture there is occur, without capture of the local ventricular
no change in the SA interval (the time from stimulus myocardium (sometimes called “reverse para-
[dotted line] to earliest atrial activation [dashed line]), Hisian pacing”). This phenomenon is usually
nor is there a change in the atrial activation sequence. transient, but can be associated with changes in
In this case, a right para-Hisian pathway was present, the QRS duration and if not recognized can lead
with earliest atrial activation on the HRA catheter. Panel to a misinterpretation of the response. If it is
B shows the response after successful ablation of the recognized, then the response can be analyzed and
accessory pathway, demonstrating the response when can also give diagnostic information.9
purely AV nodal retrograde conduction is present. With (4) Presence of a fasciculoventricular con-
loss of His capture the SA interval extends by 61 ms nection: These rare pathways connect the prox-
since the stimulated wavefront must now travel through imal conduction system to basal septal my-
ventricular myocardium, penetrate the distal branches ocardium and, if present, can prevent low output
of the His-Purkinje system, then travel retrogradely pacing from capturing myocardium alone; even
through the AV node. Earliest atrial activation is tied with loss of direct His bundle capture, excitation
between the proximal bipole of the His catheter (pHis) can still reach the conduction system so little
and the CS os (CS 9–10). HRA = high right atrium; CS = change in QRS duration may be seen.10
coronary sinus; RVA = right ventricular apex; QRSd = (5) Loss of capture of the proximal left
QRS complex duration (ms); SA = time from stimulus bundle branch alone: This can cause QRS
to atrial electrogram (ms). widening without loss of retrograde conduction
to the AV node and if not recognized could lead to
misinterpretation of the response.11
AV node, relative to the position of the recording (6) Inadvertent atrial capture: This can give
sites in the atrium (i.e. where fusion is occurring the impression that retrograde conduction is via
in the atrium in each case). Demonstrating this the AV node when a septal AP is present, and
change is facilitated by having a catheter close it can also give the impression that retrograde
to the site of earliest retrograde atrial activation conduction is via a septal AP when no such AP
(i.e. some additional mapping in the atrium may is present. Atrial capture is best identified by
be required). If the AP is close enough to the noting a change in atrial timing when adjusting
pacing site and has sufficiently rapid conduction the catheter basally (to deliberately capture the
then the SA interval should remain the same with atrium and reduce the interval from the pacing
loss of HB-RB capture, but there will be a change stimulus to a septal atrial electrogram) or apically
in the atrial activation sequence. For example, if (to deliberately lose capture of the atrium and
a posteroseptal AP is present then loss of HB- prolong the interval from the pacing stimulus
RB capture may lead to a similar SA interval on to a septal atrial electrogram by more than

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 VEENHUYZEN, ET AL.

20 ms).12 Aditionally, it seems that when the

interval from the pacing stimulus to the atrial elec-
trogram recorded by the proximal CS electrodes
is < 60 ms (or < 70 ms to the atrial electrogram
recorded by the high right atrial electrodes), atrial
capture is almost certainly present, and when
these intervals exceed 90 and 100 ms, respectively,
atrial capture is almost certainly not present.12

Another fundamental issue with para-Hisian

pacing is that demonstrating the presence of an
AP does not prove that it participates in SVT—
the maneuver alone cannot distinguish between
an AP that participates in AVRT from one which
is a bystander. However, in the presence of a stable
sustained tachycardia, entrainment pacing can
also be performed from the para-Hisian region and
the response can demonstrate whether an AP is
part of the SVT circuit (para-Hisian entrainment),
though the details remain beyond the scope of this Figure 4. Apex versus base pacing consistent with the
review.13 presence of an accessory pathway. Panel A shows right
ventricular (RV) apical pacing (note the superior QRS
complex frontal plane axis) with a ventriculoatrial (VA)
Apex versus Base Pacing
interval of 142 ms measured from the pacing stimulus
Another pacing maneuver that can help to to the earliest atrial electrogram recorded by electrodes
disclose the presence of a retrogradely conducting along the middle of the coronary sinus catheter (CS1,2 =
septal AP even in the absence of inducible sus- distal; CS 9,10 = proximal). Panel B shows pacing from
tained SVT is apex versus posterobasal pacing.14 the basal RV (note the inferior QRS complex frontal
This maneuver is, in our opinion, easier to plane axis) with a resulting VA interval of 120 ms. The
perform and easier to interpret than para-Hisian difference between these values is the VA Index (+22
pacing. Just like para-Hisian pacing, apex versus ms), which is consistent with VA conduction over an
posterobasal pacing takes advantage of the shorter accessory pathway.
VA conduction time expected with VA conduction
via a septal AP during basal pacing than apical
pacing. This maneuver was first described by probably be taken in reaching firm conclusions
Martinez-Alday in an elegant study where apical based on borderline VAI values.
and right posterobasal pacing were performed Like para-Hisian pacing, this maneuver can
either in sinus rhythm or as VOP during SVT be limited in the detection of a slowly conducting
in patients with posteroseptal APs (resulting in AP. Also, because retrograde conduction can fuse
entrainment with fusion in the majority of cases) over an AP and the normal AV conduction system,
and patients without posteroseptal APs. Care was this maneuver should probably be limited to
taken to avoid atrial capture during pacing at the the identification of posteroseptal APs. Because
right posterobasal site.14 The VA index (VAI) was differential entrainment (discussed in Part 1 of this
defined as the VA interval (measured from the Review) employs the same retrograde pathway as
pacing stimulus artifact to a stable reference at the the tachycardia, this limitation may not apply, and
high right atrium) after pacing from the RV apex differential entrainment certainly did appear to be
minus the VA interval after pacing from the RV diagnostically useful in patients with nonseptal
base (Fig. 4). All patients with a septal AP had a APs.15
positive VAI. While most patients without septal
APs had negative VAIs, surprisingly, a couple of AVNRT versus AT
patients without septal APs had VAIs of 0 or +5 Distinguishing AVNRT from AT is usually
ms, most likely indicating some anatomic and/or problematic when VOP does not accelerate
physiologic heterogeneity in the retrograde input the atria to the pacing CL (the ventricles are
of the His-Purkine network. Nevertheless, a VAI > dissociated from the atria) and the SVT has a 1:1
10 ms had 100% sensitivity and specificity for a AV relationship with central atrial activation. The
septal AP in that small study. This discriminatory ability to dissociate the ventricles from the SVT
value is close to the VAI of 0–5 ms observed in mechanism excludes the participation of an AP
two patients without septal APs, so care should in the SVT mechanism, but AVNRT must still be

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distinguished from a septal AT. It is noteworthy appearance of VA linking could occur during an
that in approximately 80% of such cases, the AT by coincidence.16 Accordingly, this finding
diagnosis is AT,16 but the AT mechanism is by no should be considered strong evidence, rather than
means proven. Strictly speaking, the VA interval proof, that the SVT mechanism is AVNRT. The
cannot differentiate septal AT from AVNRT as any strength of that evidence can be increased if
VA interval is possible with either mechanism. AOP is performed repeatedly and from different
Nevertheless, virtually simultaneous atrial and atrial sites, all yielding similar results. Variability
ventricular activation, as is observed in typical in the postpacing VA interval after AOP from
AVNRT, has a very high positive predictive multiple distant atrial sites would be expected
value for that diagnosis, largely because AVNRT in the case of AT because the timing of the first
is so much more common than AT (predictive return atrial impulse will depend on the proximity
accuracy of a test is influenced by prevalence).16 of the pacing site to the AT origin, and not on
Nevertheless, it is possible for the AV relationship the timing of the first return ventricular beat.
in a septal AT to coincidentally mimic that of One small study suggested that first return VA
typical AVNRT.17 Other SVT features that may be intervals all within 14 ms of each other after
useful to distinguish AVNRT from AT include: “differential AOP” (AOP from two or three atrial
sites: right atrial appendage, coronary sinus [CS]
(1) The termination (either spontaneously, or os, and distal CS) is consistent with a diagnosis of
after a vagal maneuver or adenosine administra- AVNRT (or AVRT) while VA interval differences
tion) of SVT on a nonpremature atrial electrogram obtained after differential AOP exceeding 14 ms is
implies that termination is associated with AV consistent with a diagnosis of septal AT.19
block. This observation favors AVNRT but could
occur by coincidence in AT. Typical AVNRT versus JT
(2) Termination of SVT on a nonpremature The only certain way to distinguish typical
atrial electrogram by ice-mapping in the region of AVNRT from JT would be to record from the
the slow AVN pathway implies that termination limbs of an AVNRT circuit within the AVN and
is associated with AV block and also favors demonstrate fusion in those recordings during
AVNRT.18 resetting or entrainment of AVNRT, which would
(3) Continuation of the SVT despite AV block not occur in JT since its mechanism is not reentry.
favors AT but AVNRT with AV block (usually At present, this is not possible. Fortunately,
infranodal) can occur. typical AVNRT is both much more common than
(4) Termination of SVT after a VPB that does JT and is strongly favored when there is other
not conduct to the atrium favors AVNRT but could evidence of dual AVN pathway physiology. In
occur by coincidence in AT. particular, AVNRT is strongly favored when the
(5) When there are small variations in TCL, initiation of SVT appears to require a “jump”
if HH or VV interval changes precede and predict to the slow AVN pathway. Nevertheless, not all
AA interval changes (i.e. the HA or VA interval is AVNRTs have demonstrable discontinuities in
constant despite HH or VV interval changes), then their AV nodal refractory curves and JT could
a diagnosis of AVNRT can be made. appear to require a critical Atrio-His (AH) interval
(6) The apparent requirement of SVT induc- for its initiation by coincidence. An AH response
tion upon a “jump” to the AVN slow pathway would be expected after VOP in the case of either
favors AVNRT but does not prove this diagnosis. tachycardia.
(7) An AV Wenckebach CL that exceeds the AOP is helpful in distinguishing AVNRT from
tachycardia CL favors AVNRT. JT.20 The last atrial paced beat would be expected
to conduct with a long AH interval (slow AV
In addition to the features described earlier, nodal pathway conduction) to the last ventricular
atrial overdrive pacing (AOP) may be useful in electrogram that is accelerated to the pacing CL
this situation (Fig. 5). If, after AOP at a CL 10–40 before SVT resumes (Fig. 5). A prospective study
ms shorter than the SVT CL, the VA interval has recently confirmed that this is the case.21 The
on the first return beat of the entrained SVT is obvious pitfall for this maneuver would be the
within 10 ms of the VA interval of the SVT exceptional circumstance where JT coexists with
(“VA linking”), a diagnosis of AVNRT is favored. dual AVN physiology and where the last paced
Linking of atrial and ventricular activation would beat conducts to the ventricles via the slow AVN
not be expected in AT.16 Unfortunately, it is not pathway and echoes back to the atria via the fast
uncommon for the VA interval on the first return AVN pathway before JT resumes. As we will see,
beat of AVNRT to vary by more than 10 ms (just the coexistence of JT with dual AVN physiology is
as it can in the first few beats after the induction a common caveat for pacing maneuvers employed
of AVNRT).16 Moreover, on rare occasions, the to distinguish AVNRT from JT.

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Figure 5. Atrial overdrive pacing to distinguish AVNRT from AT and JT. The termination of high right atrial pacing
(from the electrode pair labeled ABLd) at a cycle length of 340 ms during SVT at a CL of 350 ms is shown, revealing
the continuation of SVT after pacing stops. Atrial and ventricular activation during SVT is virtually simultaneous.
The star indicates the last entrained His and ventricular electrograms and QRS complex. This beat and subsequent
beats of the SVT demonstrate “VA linking”: the atrial activation sequence and VA interval on the last entrained beat
is the same as during the tachycardia, suggesting that ventricular and atrial activation are mechanistically linked,
which would not be expected if the diagnosis were atrial tachycardia (AT). During pacing, the PR interval exceeds the
RR interval. This is consistent with antegrade conduction over a slow AV node pathway during pacing, which would
not be the expected if the diagnosis were junctional tachycardia (JT). The AH interval, including the last entrained
AH interval, is long, and the tachycardia resumes as the last entrained impulse echoes back up the fast AV node
pathway. Again, this would not be expected if the diagnosis were JT.

Padanilam and colleagues suggested that JT focus since the stimulated wavefront would
scanning diastole with atrial premature beats collide with the JT wavefront in or proximal to
(APBs) can often be helpful to distinguish AVNRT the fast AVN pathway. On the other hand, an
from JT.22 A His-refractory APB (HRAPB) that APB that occurs when the FP is refractory can
affects the timing of the next His potential in affect an AVNRT circuit by engaging the slow AVN
any way (i.e. that advances or delays the next pathway. Accordingly this response is specific for
His potential, or that terminates the SVT) is AVNRT. As with AOP, the coexistence of JT with
consistent with a diagnosis of AVNRT (Fig. 6). dual AVN physiology represents a caveat since it
An HRAPB should not be able to reach the AVN could permit an HRAPB to advance (but not delay)
focus of a JT if retrograde conduction from that the timing of the next His bundle depolarization
focus proceeds with roughly the same timing if conducted via the slow pathway, leading to an
as antegrade conduction to the His bundle. The echo beat via the fast pathway, only to have JT
timing of His bundle depolarization is actually a resume afterwards. Hamdan and colleagues have
surrogate for the timing of retrograde fast AVN suggested that resetting by an APB delivered close
pathway conduction. An APB that occurs when to the AVN slow pathway region at a time when the
the fast pathway is refractory cannot affect a

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Figure 6. PAC response in AVNRT. Panel A: During supraventricular tachycardia with cycle length of 412 ms and
simultaneous atrial and ventricular activation, a paced atrial premature beat (APB) is delivered by electrodes at
the ostium of the coronary sinus (pCS) timed to junctional (His) refractoriness. The arrow points to the local atrial
activation (A) occurring at the expected time of His bundle depolarization ([H]). Delay of the subsequent His by 16 ms
indicates a diagnosis of atrioventricular nodal reentry tachycardia (AVNRT) where the APB prematurely activated
the slow AVN pathway, delaying the subsequent beat due to decremental conduction slowing. Panel B: Schematic
depiction of this response in AVNRT—the paced wavefront (square wave & solid arrow) can enter the excitable gap in
the AV nodal circuit and activate the slow pathway. Delay of the subsequent His timing (as shown in Panel A) should
be specific for AVNRT. Advancement of the subsequent His timing, or termination of the SVT, are also very specific
for AVNRT, but could be observed in the case of JT with dual AV node physiology. Panel C: Schematic depiction of
the response to an APB timed to junctional refractoriness in junctional tachycardia (JT); in the absence of dual AV
nodal pathways the paced wavefront will collide with the retrograde wavefront from the JT focus (star) somewhere in
the AV node or proximal conduction system (black bar), so His timing cannot be affected.

septum is being depolarized indicates a diagnosis identifies a diagnosis of JT.22 An APB delivered
of AVNRT, but the same caveat discussed earlier prior to fast pathway depolarization can advance
would apply if dual AVN physiology coexisted the immediate His bundle depolarization via
with JT.23 antegrade conduction down the fast pathway,
Padanilam and colleagues also suggested that but that would leave the fast pathway refractory
the continuation of SVT after advancement of His and unable to participate in an ongoing AVNRT
bundle depolarization by an APB delivered prior circuit (Fig. 7). Thus, both JT and AVNRT could
to His bundle depolarization (which is again acting terminate when an APB that occurs prior to His
as a surrogate for fast pathway depolarization) bundle depolarization advances the immediate
His potential, but only JT would be expected

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 VEENHUYZEN, ET AL.

Figure 7. PAC response in JT. Panel A: During supraventricular tachycardia (SVT) with a cycle length of 560 ms and
simultaneous atrial and ventricular activation, a paced atrial premature beat (APB) is delivered by electrodes at the
high right atrium (HRA) prior to anticipated junctional (His) refractoriness (arrow), advancing the immediate His by
38 ms, and the SVT continues, indicating a diagnosis of junctional tachycardia (JT). Panel B: Schematic depiction of
this response in JT; an early paced APB can advance the timing of His activation, while resetting the JT focus (faded
star), after which the JT will resume. Panel C: Schematic depiction of the response to an early paced APB in AVNRT;
the paced wavefront may advance the subsequent His timing by conducting via the AV nodal fast pathway, but will
also collide with the AVNRT circuit in the AV nodal slow pathway (black bar) or leave the fast pathway refractory,
terminating the tachycardia.

to be able to continue in these circumstances AV-dissociated SVT

(Fig. 7). The caveat to this situation again includes The differential diagnosis of an AV-
the coexistence of dual AVN physiology with dissociated SVT includes AVNRT with block
JT where the early APB results in a so-called to the atrium, JT with block to the atrium,
“dual response.” The immediate His potential is orthodromic nodoventricular reciprocating
advanced via conduction down the fast pathway, tachycardia (ONVRT), and orthodromic
but simultaneous conduction down the slow nodofascicular reciprocating tachycardia
pathway resets an AVNRT circuit. (ONFRT). Intra-Hisian reentry has also been

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proposed, but we are not aware of any cases the subsequent His potential would exclude
demonstrating the existence of this mechanism, AVNRT and JT. Resetting by a VPB and
and it will not be discussed further. (Of course, entrainment by VOP with evidence of fusion
ventricular tachycardia, including bundle branch would exclude AVNRT, JT, and ONFRT, because
reentry, would have to be excluded, but the means fusion would specifically indicate collision of
to do so are beyond the scope of this review.) the stimulated antidromic wavefront with the
The ability of an HRVPB to terminate the orthodromic wavefront from the preceding beat
SVT or to advance/delay (reset) the timing of occurring in ventricular myocardium (Fig. 8).24

Figure 8. His-refractory ventricular premature beats (HRVPBs) in AV-dissociated SVT. HRVPBs are delivered from
the right ventricular apex (RVA) during a tachycardia with a typical right bundle branch block (RBBB) QRS
morphology and a prolonged His-ventricular interval (Panels A and B). Independent atrial activity (A) is seen,
indicating atrioventricular dissociation. The main differential diagnosis for this AV-dissociated tachycardia includes
(1) AVNRT, (2) junctional tachycardia (JT), (3) intra-Hisian reentry, (4) bundle branch reentry VT (BBRVT), and (5)
a orthodromic reentry using a nodoventricular or nodofascicular connection as the retrograde limb (with retrograde
block to the atrium in each case). In Panels (A) and (B), the HRVPBs advance the next H and V, ruling out possibilities
(1), (2), and (3) since the paced retrograde wavefront would be unable to reach the circuits or ectopic focus if the
His bundle had just been depolarized. These circumstances are depicted in Panels C (for AVNRT) and D (for JT,
but would equally apply for intra-Hisian reentry). Panels E and F show the circuit for BBRVT and reentry using a
nodofascicular connection, respectively. An earlier PVC (Panel B) leads to a 20-ms increase in the stimulus-to-His
interval compared to Panel A, suggesting decremental conduction in the circuit somewhere between the ventricle
and the His. This would be expected if the AV node was part of the circuit (Panel F) but would be unusual if it was
BBRVT (Panel E). Note that the HRVPB in Panel (A) is fused (compare to the QRS complex morphology of the HRVPB
in Panel B), indicating that collision of the stimulated orthodromic wavefront with the antidromic wavefront from
the preceding beat has occurred in ventricular myocardium. This is not possible during orthodromic nodofascicular
reentry, where this collision would be expected to occur within the conduction system. The best explanation for these
findings is orthodromic nodoventricular reciprocation (see Ref. 23).

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As with conventional orthodromic AVRT circuits, discussed earlier, an HRVPB may not be capable
basal pacing sites close to the ventricular insertion of resetting AVRT employing a left free wall AP
of the nodoventricular AP would be expected to because the stimulated wavefront may not have
increase the likelihood of detecting fusion, and enough time to reach the operative AP if delivered
also decrease the postpacing interval (PPI)-TCL late enough to be His refractory. In the setting
difference and could, theoretically, be used as a of AVRT employing a left free wall AP, VOP is
method of mapping the ventricular insertion of unlikely to result in manifest entrainment, and the
the AP; sites closest to the ventricular insertion cPPI-TCL and SA-VA interval differences may be
would be expected to have the shortest PPI-TCL long by virtue of the distance of the RV apical
difference (provided that decremental conduction pacing site from the circuit (this would not be
through the AVN does not influence the result, the case if there was left bundle branch block
so the VOP CL should be as consistent as during SVT, as the RV would be part of the
possible) and a QRS complex morphology closest circuit in this circumstance). Thus, if the usual
to that of the native SVT, possibly even revealing ventricular pacing maneuvers are not helpful,
entrainment with concealed fusion. Haı̈ssaguerre one should consider scanning diastole with VPBs
and colleagues have described the use of single delivered from basal sites in the left ventricle
ventricular extrasystoles to accomplish the same (LV) or performing VOP from basal sites in the
discriminatory goals.25 LV (which can be stimulated via a branch of the
It is noteworthy that ONVRT and ONFRT CS, obviating the need to access the systemic
need not be AV dissociated. Indeed, if AV circulation prior to making a diagnosis in at least
associated, either could have any VA interval, one-third of cases). Alternatively, “differential
including one short enough to mimic typical entrainment,” as described in Part 1 of this
AVNRT. Clues to their presence may include review, could be performed.1 It is noteworthy that
an SVT that otherwise appears consistent with differential entrainment has only been studied in
AVNRT but where: (1) VOP yields cPPI-TCL a few cases of AVRT employing left free wall
and SA-VA interval values that are too short to APs and we consider it at least theoretically
be consistent with AVNRT; (2) VOP results in possible that a patient could have a considerably
manifest entrainment (which should not be pos- shorter conduction time from the RV apex to a left
sible in AVNRT or ONFRT, therefore indicating posterior AP than from the basal infundibulum
a diagnosis of ONVRT); or (3) HRVPBs terminate to such an AP, potentially making the results of
the SVT or affect the timing of the next His differential entrainment misleading.
potential. The latter is the only reason we can
think of to bother scanning diastole with VPBs
during an SVT that appears consistent with typical Conclusion
AVNRT. In Part 1 of this review, we explored how
attempts to continuously reset (i.e. entrain) SVT
AVNRT with Eccentric Left Atrial Activation by VOP can be used to provide a diagnosis in
AVNRT with eccentric left atrial activation is the majority of sustained, regular SVTs. In this
an uncommon SVT whose existence is well doc- part, we have explored other diagnostic pacing
umented.26–32 Although it is widely recognized maneuvers that might be helpful when VOP is
that the atrial exit of the AVN is not always not diagnostic or appropriate including attempts
in the superior septum but may also be in the to reset SVT with single atrial or ventricular
inferior septum where it can extend along the left beats, para-Hisian pacing, apex versus base
inferior aspect of the mitral annulus, it is not as pacing, and AOP. We have also discussed some
well recognized that AVNRT can rarely have its specific diagnostic SVT challenges encountered
earliest atrial activation along the lateral mitral in the electrophysiology lab. To be sure, there
annulus. Normally, this atrial activation sequence are other pacing maneuvers that we have not
would lead one to exclude AVNRT and to consider addressed, but this review should serve as a
AVRT employing a left free wall AP or a left-sided thorough foundation for SVT diagnosis and for
AT. If one entertains the possibility of AVNRT understanding the strengths and weaknesses of
with a left atrionodal extension in the differential those other maneuvers. We hope that by gaining a
diagnosis, then one faces a similar diagnostic thorough understanding of how these maneuvers
challenge to that posed by SVT with concentric exploit differences in the underlying anatomy and
atrial activation: all SVT mechanisms are possible. physiology of the various SVT mechanisms, one
The usual ventricular pacing maneuvers may be will gain an appreciation of which diagnostic pac-
helpful, but the yield is likely to be lower if they ing maneuvers constitute “proof” and which are
are only performed from the RV apex, which is merely “evidence” in favor of one mechanism or
relatively far from the lateral mitral annulus. As another.

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