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

C 2012, The Authors. Journal compilation 

 C 2012 Wiley Periodicals, Inc.

PACE, Vol. 35 June 2012 757

 VEENHUYZEN, ET AL.
Figure 1. Advancement of atrial activation by a fused
His-refractory ventricular premature beat (HRVPB).
Panel A: During supraventricular tachycardia with a
stable cycle length of 444 ms, one-to-one atrioven-
tricular relationship, and an earlier atrial electrogram
recorded in the right atrium (where the ablation
catheter, ABLp/d, is located) than in the septum
(d/pHIS) or coronary sinus (proximal CS 9,10 through
distal CS 1,2), a paced premature beat is delivered
by electrodes at the right ventricular apex (RVd). The
subsequent atrial activation is advanced by 19 ms.
The paced premature ventricular beat is His-refractory
(HRVPB) because (1) it is fused: note QRS complex
morphology features and duration (122 ms) that are
intermediate between those of the conducted SVT
(narrow complex) and of a purely paced QRS complex
(Panel B, QRS complex duration = 144 ms) and (2) the
pacing stimulus is delivered at precisely the time of
the expected His bundle potential (arrow). A ventricular
paced beat can be considered His-refractory if it occurs
up to 35–55 ms earlier than the anticipated His bundle
potential. Advancement of atrial activation without a
change in the atrial activation sequence by an HRVPB
indicates that an accessory pathway (AP) is present and
almost certainly participating in orthodromic AVRT, in
this case, employing a right-sided AP.
stimulated wavefront is fusing with in ventricular
myocardium must have exited the His-Purkinje
network (Fig. 1). If the pacing stimulus occurs
just after a discernible antegrade His potential,
then the paced VPB is obviously His-refractory.
Finally, if the paced VPB occurs no more than
35–55 ms earlier than the anticipated timing of
the antegrade His potential, in the time that would
be required for that stimulated wavefront to enter
the distal arborization of the His-Purkinje network
and travel retrogradely to the His bundle, the
tachycardia wavefront would have reached the His
bundle where these wavefronts would collide.2
When the paced VPB occurs more than 35–55 ms
758 June 2012
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
so that if conduction to the atrium does not
occur via the AP, the circuit is interrupted.
This cannot be the case with AT or AVNRT,
even if a bystander AV AP is present. That is,
the AP must also be participating in the SVT
mechanism. Theoretically, this response could be
observed given the coexistence of AVNRT and a
bystander nodoventricular AP, but this occurrence
has not been convincingly demonstrated to our
knowledge, and would have to be extremely rare.
As we discussed in Part 1, sometimes VOP
results in an apparently noninterpretable response
when VOP repeatedly terminates the SVT. VOP
may be considered as a series of consecutive
VPBs. When the SVT repeatedly stops during
VOP because of VA block, if the paced beat that
precedes VA block is His-refractory, and the atrial
timing has not changed prior to that VPB, this
constitutes an equivalent of an HRVPB terminating
SVT without conduction to the atrium, thereby
establishing a diagnosis of AVRT (see “What if the
response to VOP is not interpretable?” in Part I).
(2) Atrial activation is delayed without a
change in the atrial activation sequence. This
response indicates a diagnosis of AVRT employing
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
indicates that atrial activation is decrementally
linked to ventricular activation. This cannot be
the case with either AT or AVNRT even if a
bystander AV AP is present; the decremental AP
must also be participating in the SVT mechanism.
Note that for this response to be appreciated,
the degree of decremental conduction slowing
must exceed the prematurity of the HRVPB; if
they are matched, AVRT employing a decremental
AP could be present but because no change in
atrial timing would occur, one would conclude
that the VPB had no effect on the SVT and the
diagnosis could be missed. Accordingly, it is
worth studying the effects of multiple HRVPBs
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 DIAGNOSTIC SVT PACING MANEUVERS 2
Figure 2. Delay of atrial activation by a His-refractory
ventricular premature beat (HRVPB). During a long R-P
interval supraventricular tachycardia with a stable cycle
length of 473 ms, a paced premature beat is delivered by
electrodes at the right ventricle. The subsequent atrial
activation is delayed by 20 ms without a change in
the atrial activation sequence. The paced premature
ventricular beat is His-refractory because it occurs
virtually simultaneously with and certainly not more
than 35–55 ms earlier than the expected inscription
of the anterograde His bundle potential (arrow). This
response indicates that an accessory pathway (AP) is
present and participating in orthodromic AVRT, in this
case, employing a slowly conducting concealed septal
AP. (Tracing courtesy of Dr. G. Neal Kay.)
introduced throughout the His-refractory diastolic
window to minimize this potential pitfall of
studying only one HRVPB that had no apparent
effect. Theoretically, delayed atrial timing after an
HRVPB could be observed in the setting of AVNRT
with a bystander nodoventricular AP.3 This is
so rare that delay of atrial timing by an HRVPB
without a change in the atrial activation sequence
should be considered extremely strong evidence
that the SVT mechanism is AVRT employing a
decremental AP.
It is often the case that AVRT employing a
decremental AP manifests as a long RP interval
SVT. If the AP used for retrograde conduction
has decremental conduction properties, entrain-
ment by VOP could be associated with long
corrected postpacing interval-tachycardia cycle
length (cPPI-TCL) and stimulus-atrial (SA)-VA
interval values that would normally be considered
evidence of atypical AVNRT. Fusion during
entrainment would still provide proof that the
mechanism is AVRT but, if fusion is not present,
it is important to scan diastole with VPBs during
PACE, Vol. 35 June 2012
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
confidence, but not with certainty, that the AP is
participating in the SVT mechanism, establishing
a diagnosis of AVRT (Fig. 1). Theoretically, AT
or AVNRT could be advanced by conduction
over a bystander AP, and if the bystander AP
were close to the AT origin or atrionodal exit,
respectively, the atrial activation sequence may
not change appreciably. This situation is so rare
that this finding is considered very strong evidence
(but not proof) that the SVT mechanism is
AVRT.
As before, application of this maneuver
requires that any apparent change in atrial timing
exceeds the degree of spontaneous variability in
the SVT CL. Accordingly, this maneuver may not
be reliable in irregular SVTs.
Unfortunately, while these responses to
HRVPBs are specific (or, in the third case, nearly
specific) for AVRT, they are not particularly
sensitive. If the pacing site is far from the
participating AP, the orthodromic wavefront of the
VPB may not have had enough time to reach the AP
and affect the AVRT circuit when delivered late
enough to be His-refractory. The classic situation
in which an HRVPB delivered from the right
ventricular (RV) apex does not affect an AVRT
circuit because of the distance of the RV apex to
the AP occurs when a left free wall AP is operative;
nevertheless, this problem may arise when a
relatively nearby septal AP is involved.4 As is the
case with fusion during VOP, the sensitivity of the
three responses to HRVPBs described earlier can
be increased by moving the pacing site close to
the AP, that is, to a basal ventricular site close
to the site of earliest atrial activation. This is not
surprising, since fusion during VOP constitutes
the continuous resetting of an AVRT circuit by
a series of consecutive HRVPBs; the fact that they
are fused proves that they are His-refractory, as
discussed earlier.
759
 VEENHUYZEN, ET AL.
It is commonly taught that if none of the
three responses to HRVPBs described earlier
is observed, no conclusion regarding the SVT
mechanism can be drawn. However, it has been
suggested that, in the case of a short RP interval
SVT, advancing the local ventricular activation
adjacent to the earliest atrial activation by more
than 30 ms without affecting atrial timing should
exclude the participation of a conventional AP
from the SVT mechanism.5 Similarly, in the case
of a long RP interval SVT, advancing the local
ventricular activation adjacent to the earliest atrial
activation by more than 60 ms without affecting
atrial timing should exclude the participation of a
decremental AP from the SVT mechanism.5
Regarding the HRVPB maneuver, one point
seems to be underappreciated: if an SVT that
resembles typical AVNRT is induced (central
atrial activation and septal VA < 70 ms),
this maneuver will not add further diagnostic
information as it cannot distinguish AVNRT from
AT (see one exception for this in the section on
AV-dissociated SVT). If the diagnosis is not clear
from findings during spontaneous perturbations in
the SVT, the pacing maneuver of choice in this
situation is VOP.
Para-Hisian & Pure-Hisian Pacing
The pacing maneuvers described earlier
rely on studying the response to an induced
perturbation (VOP or single premature beats) of
a stable tachycardia. However, it is common
to encounter SVTs that are difficult to induce,
nonsustained, irregular, or repeatedly terminate
during pacing protocols. Such circumstances may
prevent diagnostic pacing maneuvers from being
performed, or can limit interpretation of their
results.
In a patient with documented SVT, but
no preexcitation on their baseline ECG, one of
the goals at an electrophysiologic study is to
determine the presence or absence of a concealed
AP. Sometimes programmed stimulation from the
RV apex (or even catheter-induced PVCs) can
quickly give a clue: if the atrial activation sequence
is clearly “eccentric” (either right or left free wall),
then an AP is very likely to be present. Further
characterization of the conduction properties
will be required to be more certain, but with
little effort, something of interest will have been
discovered and further investigations can be
directed accordingly. A CS catheter is commonly
placed at the start of an electrophysiology study, so
this works well for detecting nonseptal left-sided
APs, which account for around 50% of all APs.6
The remainder of APs can be harder to
detect by this method. With “standard” catheter
positions there is not usually a catheter recording
760 June 2012
from sites all around the tricuspid annulus, so
both septal and right free wall APs, as well as
retrograde AV nodal conduction, can show earliest
atrial activation on the His catheter or at the
proximal CS. Another pacing maneuver—para-
Hisian pacing—can be useful in these circum-
stances.7 The basic concept is simple—pacing
is performed next to the His bundle/proximal
right bundle (HB-RB) and the response is studied
when the HB-RB and adjacent myocardium are
captured, versus when local myocardium alone
is captured. This is usually achieved by varying
the pacing output and examining the surface
QRS duration and, where possible, the stimulus-
His (SH) interval. HB-RB capture will produce
a narrow QRS complex and short SH interval,
whereas loss of HB-RB capture will produce a
wider QRS complex and lengthening of the SH
interval. In the latter circumstance, the His bundle
will only be activated after excitation has traveled
through ventricular myocardium, penetrated the
distal Purkinje network, and traveled retrogradely
through the conduction system. Often, with HB-
RB capture, the His potential is difficult to discern
(particularly when a single catheter is used for
pacing and recording), either due to saturation of
the His channel by the pacing stimulus, or masking
by the local ventricular potential. Appearance of a
clear retrograde His potential, however, is usually
an indication that HB-RB capture has been lost.
We can now consider the response (timing
and pattern of retrograde atrial activation) in the
absence and presence of an AP (Fig. 3). If AV nodal
conduction alone is present then loss of HB-RB
capture will cause a lengthening of the stimulus-
atrial (SA) interval (because excitation has a longer
path to travel back to the atrium), without a
change in the atrial activation sequence. The
change in SA interval should match the change
in the SH interval, when this can be measured,
and the His-atrial (HA) interval should be the
same. If AP conduction alone is responsible for
retrograde atrial activation (i.e. no VA conduction
is present through the AV node), then loss of
HB-RB capture should have little or no effect on
the SA interval and no change in the pattern
of atrial activation. The SH interval will still
lengthen when HB-RB capture is lost, thus the HA
interval will shorten, since atrial timing depends
only on conduction over the AP. When both AV
nodal and AP conduction is present then a more
complex response may be obtained, depending on
the proximity of the AP to the pacing site and
the conduction properties of the AP and the AV
node/conduction system. Generally, a change in
the retrograde atrial activation sequence should
be seen, although this will depend on how much
of the atrium is activated via the AP versus the
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 DIAGNOSTIC SVT PACING MANEUVERS 2
Figure 3. Responses to para-Hisian pacing. In both
panels, pacing is being performed from the distal poles
of the His catheter (dHis). The first beat in each
panel captures the His bundle and local ventricular
myocardium (narrow QRS complex), whereas the
second beat loses His capture and only stimulates ven-
tricular myocardium. Panel A shows the response when
retrograde conduction is occurring over a concealed
accessory pathway; with loss of His capture there is
no change in the SA interval (the time from stimulus
[dotted line] to earliest atrial activation [dashed line]),
nor is there a change in the atrial activation sequence.
In this case, a right para-Hisian pathway was present,
with earliest atrial activation on the HRA catheter. Panel
B shows the response after successful ablation of the
accessory pathway, demonstrating the response when
purely AV nodal retrograde conduction is present. With
loss of His capture the SA interval extends by 61 ms
since the stimulated wavefront must now travel through
ventricular myocardium, penetrate the distal branches
of the His-Purkinje system, then travel retrogradely
through the AV node. Earliest atrial activation is tied
between the proximal bipole of the His catheter (pHis)
and the CS os (CS 9–10). HRA = high right atrium; CS =
coronary sinus; RVA = right ventricular apex; QRSd =
QRS complex duration (ms); SA = time from stimulus
to atrial electrogram (ms).
AV node, relative to the position of the recording
sites in the atrium (i.e. where fusion is occurring
in the atrium in each case). Demonstrating this
change is facilitated by having a catheter close
to the site of earliest retrograde atrial activation
(i.e. some additional mapping in the atrium may
be required). If the AP is close enough to the
pacing site and has sufficiently rapid conduction
then the SA interval should remain the same with
loss of HB-RB capture, but there will be a change
in the atrial activation sequence. For example, if
a posteroseptal AP is present then loss of HB-
RB capture may lead to a similar SA interval on
PACE, Vol. 35 June 2012
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
pacing or programmed stimulation.
(2) Slowly-conducting APs: Similarly, if
conduction over an AP is slow relative to AV
nodal conduction then the response to para-Hisian
pacing may falsely suggest AV nodal conduction
alone.7,8
(3) Lack of ventricular capture during HB-
RB pacing: Occasionally, pure-Hisian pacing can
occur, without capture of the local ventricular
myocardium (sometimes called “reverse para-
Hisian pacing”). This phenomenon is usually
transient, but can be associated with changes in
the QRS duration and if not recognized can lead
to a misinterpretation of the response. If it is
recognized, then the response can be analyzed and
can also give diagnostic information.9
(4) Presence of a fasciculoventricular con-
nection: These rare pathways connect the prox-
imal conduction system to basal septal my-
ocardium and, if present, can prevent low output
pacing from capturing myocardium alone; even
with loss of direct His bundle capture, excitation
can still reach the conduction system so little
change in QRS duration may be seen.10
(5) Loss of capture of the proximal left
bundle branch alone: This can cause QRS
widening without loss of retrograde conduction
to the AV node and if not recognized could lead to
misinterpretation of the response.11
(6) Inadvertent atrial capture: This can give
the impression that retrograde conduction is via
the AV node when a septal AP is present, and
it can also give the impression that retrograde
conduction is via a septal AP when no such AP
is present. Atrial capture is best identified by
noting a change in atrial timing when adjusting
the catheter basally (to deliberately capture the
atrium and reduce the interval from the pacing
stimulus to a septal atrial electrogram) or apically
(to deliberately lose capture of the atrium and
prolong the interval from the pacing stimulus
to a septal atrial electrogram by more than
761
 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
review.13
Apex versus Base Pacing
Another pacing maneuver that can help to
disclose the presence of a retrogradely conducting
septal AP even in the absence of inducible sus-
tained SVT is apex versus posterobasal pacing.14
This maneuver is, in our opinion, easier to
perform and easier to interpret than para-Hisian
pacing. Just like para-Hisian pacing, apex versus
posterobasal pacing takes advantage of the shorter
VA conduction time expected with VA conduction
via a septal AP during basal pacing than apical
pacing. This maneuver was first described by
Martinez-Alday in an elegant study where apical
and right posterobasal pacing were performed
either in sinus rhythm or as VOP during SVT
in patients with posteroseptal APs (resulting in
entrainment with fusion in the majority of cases)
and patients without posteroseptal APs. Care was
taken to avoid atrial capture during pacing at the
right posterobasal site.14 The VA index (VAI) was
defined as the VA interval (measured from the
pacing stimulus artifact to a stable reference at the
high right atrium) after pacing from the RV apex
minus the VA interval after pacing from the RV
base (Fig. 4). All patients with a septal AP had a
positive VAI. While most patients without septal
APs had negative VAIs, surprisingly, a couple of
patients without septal APs had VAIs of 0 or +5
ms, most likely indicating some anatomic and/or
physiologic heterogeneity in the retrograde input
of the His-Purkine network. Nevertheless, a VAI >
10 ms had 100% sensitivity and specificity for a
septal AP in that small study. This discriminatory
value is close to the VAI of 0–5 ms observed in
two patients without septal APs, so care should
762 June 2012
Figure 4. Apex versus base pacing consistent with the
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)
interval of 142 ms measured from the pacing stimulus
to the earliest atrial electrogram recorded by electrodes
along the middle of the coronary sinus catheter (CS1,2 =
distal; CS 9,10 = proximal). Panel B shows pacing from
the basal RV (note the inferior QRS complex frontal
plane axis) with a resulting VA interval of 120 ms. The
difference between these values is the VA Index (+22
ms), which is consistent with VA conduction over an
accessory pathway.
probably be taken in reaching firm conclusions
based on borderline VAI values.
Like para-Hisian pacing, this maneuver can
be limited in the detection of a slowly conducting
AP. Also, because retrograde conduction can fuse
over an AP and the normal AV conduction system,
this maneuver should probably be limited to
the identification of posteroseptal APs. Because
differential entrainment (discussed in Part 1 of this
Review) employs the same retrograde pathway as
the tachycardia, this limitation may not apply, and
differential entrainment certainly did appear to be
diagnostically useful in patients with nonseptal
APs.15
AVNRT versus AT
Distinguishing AVNRT from AT is usually
problematic when VOP does not accelerate
the atria to the pacing CL (the ventricles are
dissociated from the atria) and the SVT has a 1:1
AV relationship with central atrial activation. The
ability to dissociate the ventricles from the SVT
mechanism excludes the participation of an AP
in the SVT mechanism, but AVNRT must still be
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 DIAGNOSTIC SVT PACING MANEUVERS 2
distinguished from a septal AT. It is noteworthy
that in approximately 80% of such cases, the
diagnosis is AT,16 but the AT mechanism is by no
means proven. Strictly speaking, the VA interval
cannot differentiate septal AT from AVNRT as any
VA interval is possible with either mechanism.
Nevertheless, virtually simultaneous atrial and
ventricular activation, as is observed in typical
AVNRT, has a very high positive predictive
value for that diagnosis, largely because AVNRT
is so much more common than AT (predictive
accuracy of a test is influenced by prevalence).16
Nevertheless, it is possible for the AV relationship
in a septal AT to coincidentally mimic that of
typical AVNRT.17 Other SVT features that may be
useful to distinguish AVNRT from AT include:
(1) The termination (either spontaneously, or
after a vagal maneuver or adenosine administra-
tion) of SVT on a nonpremature atrial electrogram
implies that termination is associated with AV
block. This observation favors AVNRT but could
occur by coincidence in AT.
(2) Termination of SVT on a nonpremature
atrial electrogram by ice-mapping in the region of
the slow AVN pathway implies that termination
is associated with AV block and also favors
AVNRT.18
(3) Continuation of the SVT despite AV block
favors AT but AVNRT with AV block (usually
infranodal) can occur.
(4) Termination of SVT after a VPB that does
not conduct to the atrium favors AVNRT but could
occur by coincidence in AT.
(5) When there are small variations in TCL,
if HH or VV interval changes precede and predict
AA interval changes (i.e. the HA or VA interval is
constant despite HH or VV interval changes), then
a diagnosis of AVNRT can be made.
(6) The apparent requirement of SVT induc-
tion upon a “jump” to the AVN slow pathway
favors AVNRT but does not prove this diagnosis.
(7) An AV Wenckebach CL that exceeds the
tachycardia CL favors AVNRT.
In addition to the features described earlier,
atrial overdrive pacing (AOP) may be useful in
this situation (Fig. 5). If, after AOP at a CL 10–40
ms shorter than the SVT CL, the VA interval
on the first return beat of the entrained SVT is
within 10 ms of the VA interval of the SVT
(“VA linking”), a diagnosis of AVNRT is favored.
Linking of atrial and ventricular activation would
not be expected in AT.16 Unfortunately, it is not
uncommon for the VA interval on the first return
beat of AVNRT to vary by more than 10 ms (just
as it can in the first few beats after the induction
of AVNRT).16 Moreover, on rare occasions, the
PACE, Vol. 35 June 2012
appearance of VA linking could occur during an
AT by coincidence.16 Accordingly, this finding
should be considered strong evidence, rather than
proof, that the SVT mechanism is AVNRT. The
strength of that evidence can be increased if
AOP is performed repeatedly and from different
atrial sites, all yielding similar results. Variability
in the postpacing VA interval after AOP from
multiple distant atrial sites would be expected
in the case of AT because the timing of the first
return atrial impulse will depend on the proximity
of the pacing site to the AT origin, and not on
the timing of the first return ventricular beat.
One small study suggested that first return VA
intervals all within 14 ms of each other after
“differential AOP” (AOP from two or three atrial
sites: right atrial appendage, coronary sinus [CS]
os, and distal CS) is consistent with a diagnosis of
AVNRT (or AVRT) while VA interval differences
obtained after differential AOP exceeding 14 ms is
consistent with a diagnosis of septal AT.19
Typical AVNRT versus JT
The only certain way to distinguish typical
AVNRT from JT would be to record from the
limbs of an AVNRT circuit within the AVN and
demonstrate fusion in those recordings during
resetting or entrainment of AVNRT, which would
not occur in JT since its mechanism is not reentry.
At present, this is not possible. Fortunately,
typical AVNRT is both much more common than
JT and is strongly favored when there is other
evidence of dual AVN pathway physiology. In
particular, AVNRT is strongly favored when the
initiation of SVT appears to require a “jump”
to the slow AVN pathway. Nevertheless, not all
AVNRTs have demonstrable discontinuities in
their AV nodal refractory curves and JT could
appear to require a critical Atrio-His (AH) interval
for its initiation by coincidence. An AH response
would be expected after VOP in the case of either
tachycardia.
AOP is helpful in distinguishing AVNRT from
JT.20 The last atrial paced beat would be expected
to conduct with a long AH interval (slow AV
nodal pathway conduction) to the last ventricular
electrogram that is accelerated to the pacing CL
before SVT resumes (Fig. 5). A prospective study
has recently confirmed that this is the case.21 The
obvious pitfall for this maneuver would be the
exceptional circumstance where JT coexists with
dual AVN physiology and where the last paced
beat conducts to the ventricles via the slow AVN
pathway and echoes back to the atria via the fast
AVN pathway before JT resumes. As we will see,
the coexistence of JT with dual AVN physiology is
a common caveat for pacing maneuvers employed
to distinguish AVNRT from JT.
763
 VEENHUYZEN, ET AL.

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

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 DIAGNOSTIC SVT PACING MANEUVERS 2

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
of AVNRT, but the same caveat discussed earlier
would apply if dual AVN physiology coexisted
with JT.23
Padanilam and colleagues also suggested that
the continuation of SVT after advancement of His
bundle depolarization by an APB delivered prior
to His bundle depolarization (which is again acting
as a surrogate for fast pathway depolarization)
identifies a diagnosis of JT.22 An APB delivered
prior to fast pathway depolarization can advance
the immediate His bundle depolarization via
antegrade conduction down the fast pathway,
but that would leave the fast pathway refractory
and unable to participate in an ongoing AVNRT
circuit (Fig. 7). Thus, both JT and AVNRT could
terminate when an APB that occurs prior to His
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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 DIAGNOSTIC SVT PACING MANEUVERS 2

proposed, but we are not aware of any cases
demonstrating the existence of this mechanism,
and it will not be discussed further. (Of course,
ventricular tachycardia, including bundle branch
reentry, would have to be excluded, but the means
to do so are beyond the scope of this review.)
The ability of an HRVPB to terminate the
SVT or to advance/delay (reset) the timing of
the subsequent His potential would exclude
AVNRT and JT. Resetting by a VPB and
entrainment by VOP with evidence of fusion
would exclude AVNRT, JT, and ONFRT, because
fusion would specifically indicate collision of
the stimulated antidromic wavefront with the
orthodromic wavefront from the preceding beat
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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 VEENHUYZEN, ET AL.
As with conventional orthodromic AVRT circuits,
basal pacing sites close to the ventricular insertion
of the nodoventricular AP would be expected to
increase the likelihood of detecting fusion, and
also decrease the postpacing interval (PPI)-TCL
difference and could, theoretically, be used as a
method of mapping the ventricular insertion of
the AP; sites closest to the ventricular insertion
would be expected to have the shortest PPI-TCL
difference (provided that decremental conduction
through the AVN does not influence the result,
so the VOP CL should be as consistent as
possible) and a QRS complex morphology closest
to that of the native SVT, possibly even revealing
entrainment with concealed fusion. Haı̈ssaguerre
and colleagues have described the use of single
ventricular extrasystoles to accomplish the same
discriminatory goals.25
It is noteworthy that ONVRT and ONFRT
need not be AV dissociated. Indeed, if AV
associated, either could have any VA interval,
including one short enough to mimic typical
AVNRT. Clues to their presence may include
an SVT that otherwise appears consistent with
AVNRT but where: (1) VOP yields cPPI-TCL
and SA-VA interval values that are too short to
be consistent with AVNRT; (2) VOP results in
manifest entrainment (which should not be pos-
sible in AVNRT or ONFRT, therefore indicating
a diagnosis of ONVRT); or (3) HRVPBs terminate
the SVT or affect the timing of the next His
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
AVNRT.
AVNRT with Eccentric Left Atrial Activation
AVNRT with eccentric left atrial activation is
an uncommon SVT whose existence is well doc-
umented.26–32 Although it is widely recognized
that the atrial exit of the AVN is not always
in the superior septum but may also be in the
inferior septum where it can extend along the left
inferior aspect of the mitral annulus, it is not as
well recognized that AVNRT can rarely have its
earliest atrial activation along the lateral mitral
annulus. Normally, this atrial activation sequence
would lead one to exclude AVNRT and to consider
AVRT employing a left free wall AP or a left-sided
AT. If one entertains the possibility of AVNRT
with a left atrionodal extension in the differential
diagnosis, then one faces a similar diagnostic
challenge to that posed by SVT with concentric
atrial activation: all SVT mechanisms are possible.
The usual ventricular pacing maneuvers may be
helpful, but the yield is likely to be lower if they
are only performed from the RV apex, which is
relatively far from the lateral mitral annulus. As
768 June 2012
discussed earlier, an HRVPB may not be capable
of resetting AVRT employing a left free wall AP
because the stimulated wavefront may not have
enough time to reach the operative AP if delivered
late enough to be His refractory. In the setting
of AVRT employing a left free wall AP, VOP is
unlikely to result in manifest entrainment, and the
cPPI-TCL and SA-VA interval differences may be
long by virtue of the distance of the RV apical
pacing site from the circuit (this would not be
the case if there was left bundle branch block
during SVT, as the RV would be part of the
circuit in this circumstance). Thus, if the usual
ventricular pacing maneuvers are not helpful,
one should consider scanning diastole with VPBs
delivered from basal sites in the left ventricle
(LV) or performing VOP from basal sites in the
LV (which can be stimulated via a branch of the
CS, obviating the need to access the systemic
circulation prior to making a diagnosis in at least
one-third of cases). Alternatively, “differential
entrainment,” as described in Part 1 of this
review, could be performed.1 It is noteworthy that
differential entrainment has only been studied in
a few cases of AVRT employing left free wall
APs and we consider it at least theoretically
possible that a patient could have a considerably
shorter conduction time from the RV apex to a left
posterior AP than from the basal infundibulum
to such an AP, potentially making the results of
differential entrainment misleading.
Conclusion
In Part 1 of this review, we explored how
attempts to continuously reset (i.e. entrain) SVT
by VOP can be used to provide a diagnosis in
the majority of sustained, regular SVTs. In this
part, we have explored other diagnostic pacing
maneuvers that might be helpful when VOP is
not diagnostic or appropriate including attempts
to reset SVT with single atrial or ventricular
beats, para-Hisian pacing, apex versus base
pacing, and AOP. We have also discussed some
specific diagnostic SVT challenges encountered
in the electrophysiology lab. To be sure, there
are other pacing maneuvers that we have not
addressed, but this review should serve as a
thorough foundation for SVT diagnosis and for
understanding the strengths and weaknesses of
those other maneuvers. We hope that by gaining a
thorough understanding of how these maneuvers
exploit differences in the underlying anatomy and
physiology of the various SVT mechanisms, one
will gain an appreciation of which diagnostic pac-
ing maneuvers constitute “proof” and which are
merely “evidence” in favor of one mechanism or
another.
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