REVIEW

Diagnostic Pacing Maneuvers for Supraventricular

Tachycardia: Part 1
GEORGE D. VEENHUYZEN, M.D., F. RUSSELL QUINN, M.B.B.S., 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, Calgary, Alberta, Canada

This two-part manuscript reviews diagnostic pacing maneuvers for supraventricular tachycardia (SVT).
Part one will involve a detailed consideration of ventricular overdrive pacing (VOP), since this pacing
maneuver provides the diagnosis in the majority of cases. This will include a review of the post-VOP
response, fusion during entrainment, the importance of the VOP site, quantitative results of entrainment
such as the postpacing interval, differential entrainment, and new criteria derived from features found at
the beginning of the VOP train. There is a 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 2011; 34:767–782)
ablation, electrophysiology–clinical, svt, pacing

Introduction post-VOP response, fusion during entrainment,

The approach to supraventricular tachycardia
(SVT) diagnosis can be complex because it
involves synthesizing baseline electrophysiologic
features, features of the SVT, and responses to
pacing maneuvers. In this 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. None
of these are without their limitations, so one
must be comfortable employing and interpreting
a variety of pacing maneuvers to be proficient at
SVT diagnosis.
This review will address distinguishing
among the three most common SVT mechanisms,
namely, atrioventricular node reentry tachycardia
(AVNRT), atrioventricular reciprocating tachycar-
dia (AVRT), and atrial tachycardia (AT). Part
one will involve a detailed consideration of
ventricular overdrive pacing (VOP), since this
pacing maneuver provides the diagnosis in the
majority of cases. This will include a review of the
Dedication: This manuscript is dedicated to the memory of Dr.
Michael Andrew Nault (1972–2010), a contagiously inquisitive
lover of the good, the silly, and the electrocardiologic.
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 August 20, 2010; revised January 30, 2011; accepted
February 07, 2011.
doi: 10.1111/j.1540-8159.2011.03076.x
the importance of the VOP site, quantitative results
of entrainment such as the postpacing interval
(PPI), differential entrainment, and new criteria
derived from features found at the beginning of
the VOP train. Part two will consider pacing
maneuvers that can be performed when VOP is
not diagnostic (scanning diastole with ventricular
and/or atrial premature beats, overdrive atrial
pacing) or when sustained SVT cannot be induced
(apex vs base pacing, para- and pure-Hisian
pacing). Challenges in SVT diagnosis, including
some esoteric ones, will be discussed in Part
two also. There is a considerable literature on
this topic, and this review is by no means
meant to be all-encompassing. Rather, we hope
to clearly explain 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.
Choosing a Pacing Maneuver
or an Ablation Catheter
Let us begin by considering the usual man-
ifestation of SVT: a narrow complex tachycardia
with a normal His-Ventricular (HV) interval. There
are three tachycardia features that are useful to
consider as outlined in Table I, including (a) the
Ventriculo-Atrial (VA) relationship, (b) the VA
interval, and (c) the atrial activation sequence.
Often, three additional features, dependant upon
perturbations in the SVT, provide additional
information: (d) whether, when there are small

C 2011, The Authors. Journal compilation ⃝

⃝ C 2011 Wiley Periodicals, Inc.

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 VEENHUYZEN, ET AL.

Table I.
Six Features of SVT to Consider before Considering a Diagnostic Pacing Maneuver

Feature Details SVT Mechanism(s)

1. VA relationship V=A AVNRT, AVRT, AT

V > A ± AV dissociation ONVRT, ONFRT, AVNRT
V<A AVNRT, AT
2. VA interval VA > 70 ms aAVNRT, AVRT, AT
VA ≤ 70 ms tAVNRT, AT
VA > AV aAVNRT, AT, AVRT using slowly
conducting AP
3. Atrial activation sequence High to low AT
Concentric AVNRT, AVRT, AT
Eccentric AVRT, AT*
4. Spontaneous termination Ends with an “A” AVNRT, AVRT
Ends with a “V” AVNRT, AVRT, AT
5. HH changes precede and predict Yes AVNRT, AVRT
AA changes No AVNRT, AVRT, AT
6. VA increase > 30 ms with Yes AVRT with free wall AP ipsilateral to
functional BBB BBB
No AVNRT, AVRT, AT

aAVNRT = atypical AVNRT; tAVNRT = typical AVNRT; ONVRT = orthodromic nodoventricular reciprocating tachycardia; ONFRT =
orthodromic nodofascicular reciprocating tachycardia. *AVNRT with a Leftward atrionodal exit is uncommon but still possible. AT is most
likely, but AVNRT and AVRT are theoretically still possible.

variations in tachycardia cycle length (TCL), His-
His (HH) or interventricular (VV) interval changes
precede and predict interatrial (AA) interval
changes (i.e., the His-Atrial [HA] or VA interval
is constant despite HH or VV interval changes), (e)
termination of SVT on a nonpremature terminal
atrial electrogram with the same atrial activation
sequence as SVT, and (f) changes in the VA
interval with the appearance or disappearance of
functional bundle branch block. It is noteworthy
that, after studying these features of the SVT, an
ablation catheter rather than a pacing maneuver
may be what is required next. For example, if
SVT has a septal VA interval <70 ms (excluding
AVRT) and HH interval changes precede and
predict AA interval changes, or the SVT stops
with a nonpremature terminal atrial electrogram
(excluding AT, particularly if the latter happens
more than once so that this is not a mere
coincidence), a diagnosis of typical AVNRT can
be made and the slow atrioventricular (AV) nodal
pathway can be targeted for ablation. On the
other hand, it should not be surprising that
differentiating among tachycardias with a 1:1 V-
A relationship, septal V-A interval >70 ms, and
a central atrial activation sequence has received
considerable attention in the literature, since each
of the usual SVT mechanisms may be operative.
One would want to be very sure of the correct
SVT mechanism in these cases before choosing
an ablation target because of the variable risk of
AV block associated with ablation at different
sites in the septum. For example, it would be
unwise to mistake AVNRT for a septal AT or AVRT
employing a septal accessory pathway (AP), since
both of the latter mechanisms require mapping to
the earliest atrial electrogram, which, in the case
of AVNRT, could well lead one to ablate in a
region where the risk of AV block is considerably
higher than targeting the slow AVN pathway in
the region between the coronary sinus os and
the tricuspid valve annulus. It is also noteworthy
that often the correct diagnostic pacing maneuver
must be chosen after some combination of the
features in Table I permits the SVT mechanism
to be narrowed down to only two possibilities.
Quickly Ruling AT In or Out
Since AT can have any atrial activation
sequence and any VA interval, it is in the
differential diagnosis of 12 (80%) of the 15
diagnostic categories found in the extreme right
column of Table I. Overdrive pacing from the
right ventricle (RV) at a cycle length (CL) that is
10–40 ms shorter than the TCL provides a rapid
tool to rule AT in or out.1 If, during overdrive

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Figure 1. Panel A: response after cessation of overdrive ventricular pacing (340 ms) in an atrial
tachycardia (cycle length 360 ms). The atrial cycle length (CL) was accelerated to the ventricular
pacing CL and then slowed immediately after pacing was stopped. The last atrial electrogram
that was accelerated to the pacing CL is the first atrial electrogram labeled “A.” The response
after pacing is stopped is A-A-V, which indicates a diagnosis of AT. Also note that the septal
atrial electrograms (pHIS, CS 9,10) precede the high right atrial (HRA) electrogram during pacing
with 1:1 ventriculoatrial (VA) conduction (low-to-high atrial activation), while that activation is
reversed during the AT (high-to-low atrial activation). A change in the atrial activation sequence
during overdrive ventricular pacing with 1:1 VA conduction is also consistent with a diagnosis
of AT (In fact, a descending pattern of atrial activation during the tachycardia alone is sufficient
to indicate a diagnosis of AT). Panel B: response after cessation of right ventricular overdrive
pacing in an orthodromic atrioventricular reciprocating tachycardia (AVRT) using a concealed
left-sided accessory pathway. The atrial CL was accelerated to the ventricular pacing CL and
then slowed to the prepacing tachycardia atrial CL immediately after pacing was stopped. The
atrial activation sequence during VOP is the same as the atrial activation sequence during SVT.
The last atrial electrogram that was accelerated to the pacing CL is the atrial electrogram labeled
“A.” The response after pacing is stopped is A-V, which excludes a diagnosis of AT. (stimulus-
to-atrial [SA] = 285 ms; VA = 210 ms; SA-VA = 75 ms; PPI = 520 ms; TCL = 380 ms; PPI-TCL =
140 ms; cPPI-TCL = 120 ms. The cPPI-TCL and SA-VA differences are “borderline” because of
the distance of the pacing site from the left sided AVRT circuit.)

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 VEENHUYZEN, ET AL.
ventricular pacing, the atrial CL is accelerated to
the pacing CL, and the tachycardia continues after
pacing is stopped, then a post-VOP response that is
atrial-atrial-ventricular (A-A-V) rules in AT while
a post-VOP response that is atrial-ventricular (A-
V) rules out AT (effectively ruling in AVRT or
AVNRT). The last atrial electrogram accelerated to
the pacing CL is the first atrial electrogram counted
in the interpretation of this response (Fig. 1).
The main shortcoming of this pacing maneuver
is that, in 50–80% of cases of AT, the atria are not
accelerated to the pacing CL (the ventricles are
dissociated from the tachycardia), so the response
is technically not interpretable (though this
particular response still excludes AVRT).2–4 When
this is the case, the diagnosis is usually AT,2,4
though further information would still be required
to prove a diagnosis of AT rather than AVNRT.
It is important to understand why VOP can
rule AT in or out. First consider AT: during VOP,
as long as the VA block CL is not longer than the
TCL, there will eventually be 1:1 VA conduction
over the normal AV conduction system, and
each retrogradely conduced atrial wavefront will
overdrive, suppress, or entrain (if reentrant) the
AT. The last paced retrogradely conducted atrial
wavefront (which will be responsible for the
first atrial electrogram counted in the post-VOP
response) cannot echo back to the ventricle be-
cause the AV conduction system is still refractory
from having just conducted that wavefront to the
atrium. It seems that even when either dual AVN
physiology or a bystander AP happens also to be
present, none of these routes are available for the
last paced retrogradely conducted atrial wavefront
to echo to the ventricle as all are penetrated
by the pacing wavefront and remain refractory
to the antegrade conduction that would lead to
such an echo beat.1 If the AT has not terminated,
the next atrial electrogram (i.e., the second atrial
electrogram counted in the post-VOP response)
will result from the continuation of the AT, and by
then, the AV conduction system will usually have
recovered so that the next electrogram will be a His
electrogram followed by a ventricular electrogram,
hence, an A-A-V response (Fig. 2A).
In orthodromic AVRT, as long as the refrac-
tory periods of the participating ventricle, AP,
and atrium do not exceed the TCL, eventually,
during VOP, there will be 1:1 VA conduction
of the stimulated orthodromic wavefront (so
called because it travels in the same direction
as the tachycardia circuit) via the AP (so the
atrial activation sequence during VOP ought to
be identical to that of the SVT). A portion of
that stimulated wavefront, called the stimulated
antidromic wavefront (because it travels in the
opposite direction of the tachycardia circuit), will
770 June 2011
collide with the orthodromic wavefront from the
preceding beat either in ventricular myocardium
or in the AV conduction system (Fig. 2B). At
this point, each stimulated orthodromic wavefront
is resetting the tachycardia to the pacing CL,
and each stimulated antidromic wavefront is
colliding with, or fusing with, the orthodromic
wavefront from the previous beat. Thus, the
tachycardia is entrained (i.e., continually reset
by the pacing train). If there is fusion in the
QRS complex morphology during VOP (i.e., the
QRS morphology is a fusion beat combining
some aspects of the QRS complex morphology
of a fully paced beat with some aspects of the
QRS complex morphology of the SVT), there
is proof that the SVT is entrained (manifest
entrainment). In the absence of evidence of
fusion, as long as AVRT continues after pacing
is stopped, it is reasonable to assume that AVRT
was entrained (concealed entrainment). The last
paced retrogradely conducted atrial wavefront
(producing the first atrial electrogram counted in
the post-VOP response) can now revolve through
the AVRT circuit and, because there is no new
stimulated antidromic wavefront for it to collide
with, conduct back to the ventricles over the
normal AV conduction system, producing a His
electrogram and a ventricular electrogram, hence,
an A-V response.
Exactly the same thing happens when typical
AVNRT is entrained by VOP, except that the
stimulated wavefront must travel up the His-
Purkinje system to reach the AV node where the
stimulated orthodromic wavefront resets AVNRT
via the fast AV node pathway (and also accelerates
the atria to the pacing CL), and the stimulated an-
tidromic wavefront collides with the orthodromic
wavefront from the previous beat somewhere
in the slow AV node pathway (Fig. 2C). The
last retrogradely conducted stimulated wavefront
produces the first atrial electrogram that is counted
in the post-VOP response, and also revolves
around the AV node circuit to conduct back
down the slow AV node pathway to reach the
lower common pathway, His-Purkinje network,
and ventricles because there is no new stimulated
antidromic wavefront for it to collide with, hence,
an A-V response. Note that, during entrainment of
typical AVNRT, the collision between the stimu-
lated antidromic wavefront and the orthodromic
wavefront from the previous beat occurs in the
AVN and cannot possibly occur in ventricular
myocardium. Accordingly, QRS complex mor-
phology fusion cannot occur, and entrainment
of AVNRT cannot be proven. (See later.)
Thus, a post-VOP response that is A-V
indicates entrainment of AVRT or AVNRT and
excludes AT (though proof of entrainment of
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Figure 2. Responses to ventricular overdrive pacing (VOP) for three common SVT mechanisms.
In each panel, square wave = pacing site, solid arrows = antidromic paced wavefront, dashed
arrows = orthodromic wavefront, dotted arrows = orthodromic wavefront from the previous
beat. Panel A: in atrial tachycardia (AT), VOP causes overdrive suppression (if focal mechanism,
faded star), or entrainment (if reentrant mechanism) of the SVT. The last paced impulse conducts
retrogradely to the atrium and is followed by a beat of AT (star), which then conducts antegradely
to the ventricle—hence an “A-A-V” or “A-A-H” response. Panel B: in orthodromic AVRT (shown
in this case using a right free-wall pathway), the last impulse of VOP conducts via the accessory
pathway to the atrium, then continues around the circuit through the AV node and conduction
system to the ventricle—hence an “A-V” or “A-H” response. The antidromic paced impulse
collides with the orthodromic impulse from the previous beat either in the conduction system
(as shown here, black bar) or in ventricular myocardium. Panel C: In typical AVNRT, the last
paced impulse of VOP conducts retrogradely via the conduction system, enters the excitable gap
in the AV nodal circuit, activates the atrium via the fast pathway, then conducts via the slow
pathway back to the His-Purkinje system to activate the ventricle—hence an “A-V” or “A-H”
response. Collision of the stimulated antidromic wavefront during VOP occurs in the AV nodal
slow pathway (black bar).

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 VEENHUYZEN, ET AL.

Figure 3. A “pseudo A-A-V response.” The atria are accelerated to the overdrive pacing cycle length (CL = 360 ms)
and the tachycardia resumes after pacing is stopped (380 ms). Note that the second atrial electrogram after the last
paced beat is the last atrial electrogram that is accelerated to the pacing CL, so this is an A-V response. Failure to
recognize this could lead to counting the first atrial electrogram after the last paced beat (*) in the post ventricular
pacing response, leading to an erroneous conclusion of an A-A-V response. This was, in fact, a case of fast-slow
AVNRT (PPI = 565 ms; cPPI-TCL = 185 ms; SA = 415 ms; VA = 265 ms; SA-VA = 150 ms). The recordings labeled
pABL and dABL are from the right atrium. The coronary sinus catheter electrodes are labeled 9,10 as proximal and
1,2 as distal.

AVRT is only available when there is evidence
of fusion), while a post-VOP response of A-
A-V indicates that the SVT mechanism is not
capable of echoing the last stimulated retrogradely
conducted atrial wavefront back to the ventricles,
as is the case in AT. Note that the features of,
and criteria for, entrainment can be studied in the
context of familiar SVT circuits.5
Pitfalls in the interpretation of the post-VOP
response include the following:
1. Incorrectly identifying the last atrial
electrogram that is accelerated to the pacing CL.
As mentioned above, the last atrial electro-
gram accelerated to the pacing CL is the first
response that ought to be annotated after pacing
is stopped. When the SVT mechanism is AVRT
or AVNRT, but the retrograde limb of the circuit
conducts slowly, as it might in atypical AVNRT
(aAVNRT) (such as in so-called “slow-slow” or
“fast-slow” AVNRT) or AVRT employing a slowly
conducting AP, the VA interval after the last paced
beat may be longer than the pacing CL such that
the second atrial electrogram after the last paced
ventricular beat may in fact be the last atrial
electrogram that was accelerated to the pacing CL
(Fig. 3). When this is the case, the interval between
the first and second atrial electrograms after the
last paced ventricular beat will be the same as
the pacing CL. If this is not recognized, then
a “pseudo-A-A-V” response may be incorrectly
interpreted as indicating a diagnosis of AT. It is
possible that the first beat of an AT may occur
after the last atrial electrogram resulting from VA
conduction at a time interval that is equal to the
pacing CL by pure coincidence.6 Accordingly, it
is worthwhile to repeat VOP several times and at
decrementally shorter CLs whenever possible to
show that the A-A-V response is reproducible. It
is also necessary to examine whether the atrial
activation sequence during 1:1 V-A conduction
is the same as during SVT,6 as a different atrial
activation sequence in this setting could be the
clue that AT is present (Fig. 1).
2. When the pacing CL is not short enough,
or when the TCL shortens just before or during
pacing, so that 1:1 VA conduction during pacing
is not present and the tachycardia and the pacing
train are just isorhythmically dissociated from
each other.

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Figure 4. Overdrive pacing at a CL of 340 ms during typical AVNRT (CL 380 ms). The electrogram labeled “A” is
the last atrial electrogram accelerated to the pacing CL (340 ms). Note that on the first beat after pacing stops, the
HV interval exceeds the HA interval. The HA interval on the first beat after pacing can be shorter than during stable
SVT because of the preceding decrement in slow pathway conduction induced by VOP, as in this case. One could
be tempted to include the subsequent atrial electrogram (*) in the post overdrive pacing response, but this would be
incorrect. Although it does precede the following ventricular electrogram, it occurs after the His bundle electrogram
indicating that it could not possibly have conducted antegradely through the His-Purkinje system to produce the
ventricular electrogram. Only atrial electrograms that can conduct antegradely to produce the ventricular electrogram
are counted in the post ventricular pacing response. For cases such as these, where the HV interval exceeds the HA
interval, the error of considering this to represent an A-A-V response can be avoided by considering the response as
A-H instead. The recordings labeled pABL and dABL are from the right atrium. The coronary sinus catheter electrodes
are labeled 9,10 as proximal and 1,2 as distal.

Two ways to avoid this problem include
1) performing the maneuver repeatedly and
decrementing the pacing CL by 10–20 ms after
each apparently successful attempt to accelerate
the atria to the pacing CL and 2) checking to see
that after pacing has stopped, the TCL immediately
returns to the longer pre-pacing TCL, or at least a
CL that is longer than that to which the atria were
accelerated during pacing (Fig. 1 and 3).
3. When the HV interval exceeds the HA
interval in AVNRT.
In AVNRT, if the HV interval exceeds the
HA interval (which can happen when the HV
interval is long or when the HA interval is very
short or even a negative value as can occur in
AVNRT with a long lower common pathway), the
last entrained atrial electrogram will be followed
by a ventricular electrogram but that ventricular
electrogram will be preceded by a second atrial
electrogram resulting from the ongoing AVNRT
circuit (and not from pacing) (Fig. 4). This
“pseudo-A-A-V” response could lead to an error
that can easily be avoided by considering the post-
VOP response as A-A-H or A-H rather than as
A-A-V or A-V.7 Doing so should also avoid the
potential for a pseudo-A-A-V response in the rare
case where the first return beat of AVNRT blocks
below the His-bundle. Accordingly, for the rest of
this article, we will refer to the post-VOP response
as A-H or A-A-H.
4. AVNRT with block below the lower
common pathway on the first return beat.
Theoretically, the first return beat after
entrainment of AVNRT could block below the
lower common pathway, but above the His
bundle (so that a His potential would not be
recorded), resulting in an A-A-H response in
AVNRT. Accordingly, the post-VOP response may
be unreliable in cases where there is spontaneous
AV block during SVT. We are not aware of a

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 VEENHUYZEN, ET AL.
case where this has happened, and so we believe
that the chances of block occurring below the
lower common pathway on only the first return
beat after overdrive ventricular pacing are low
enough that such a response should prompt strong
consideration of a diagnosis of AT. Other features
or pacing maneuvers may need to be considered if
AVNRT is otherwise suggested.
5. Coexistence of AVNRT or AVRT with
an AT
An A-H response indicates that either AVNRT
or AVRT are present, but does not exclude the
possibility that an AT may also be present. It
is always prudent to test for the inducibility of
other forms of SVT after one substrate has been
eliminated.
What Next?
If AT is ruled in by VOP, then the next step
would be mapping and ablation of the AT. If AT
is ruled out by VOP, the diagnosis of AVNRT
or AVRT may be clear, based on the features
in Table I. When the atrial activation sequence
is concentric, and the VA interval is >70 ms,
more information will be required to distinguish
between AVRT employing a septal AP and
aAVNRT. Thankfully, that information is often
already present in other features of the response
to VOP. For the remainder of the discussion,
unless otherwise stated, only tachycardias with
concentric atrial activation (aAVNRT with a VA
>70 ms and AVRT employing a septal AP) are
considered.
Fusion during Entrainment
As mentioned above, a post-VOP response
of A-H indicates entrainment of either AVNRT
or AVRT and, in the case of entrainment of
AVRT, there is an opportunity to observe QRS
complex fusion due to collision of the stimu-
lated antidromic wavefront with the orthodromic
wavefront from the previous beat occurring in
ventricular myocardium (Fig. 5). Because QRS
complex fusion is impossible during entrainment
of AVNRT, the presence of QRS complex fusion
distinguishes AVRT from AVNRT. Unfortunately,
like most diagnostic features for SVT, QRS
complex fusion during entrainment is specific for
AVRT, but not sensitive. That is, during VOP,
entrainment of AVRT is usually concealed: the
QRS complex morphology is that of a paced
beat because the orthodromic wavefront from
the previous beat collides with the stimulated
antidromic wavefront in the AV conduction
system, and fusion (and therefore proof of
entrainment) is not present (e.g., as depicted in
Fig. 2B). This is called “concealed entrainment”
(the tachycardia is entrained, but entrainment
774 June 2011
cannot be proven, since proof of entrainment
requires the demonstration of fusion).
To maximize the opportunity to detect fusion
during entrainment of AVRT by VOP (i.e., to
increase the sensitivity of fusion for AVRT),
one can also include evidence of fusion in
the intracardiac tracings rather than just in the
surface QRS complex morphology. The presence
of an orthodromically captured His or right
bundle potential during VOP indicates that the
orthodromic wavefront from the previous beat has
reached the AV conduction system and will surely
collide with the stimulated antidromic wavefront
(Fig. 5). This collision point may occur within the
distal AV conduction system or within ventricular
myocardium before the orthodromic wavefront
from the previous beat has depolarized a sufficient
amount of ventricular myocardium to affect the
paced QRS complex morphology. It is worth
emphasizing this point: in the latter two cases the
QRS complex morphology will either be identical
to, or virtually indistinguishable from, the QRS
complex morphology of a fully paced beat, yet the
presence of an orthodromically captured His po-
tential is intracardiac evidence that fusion is tak-
ing place in the circuit somewhere distal to the His
bundle, thus indicating that the circuit is AVRT.
The Importance of the Pacing Site in Permitting
Fusion during Entrainment of AVRT by VOP
Another way to increase the sensitivity of QRS
complex morphology fusion during entrainment
of AVRT is to permit the orthodromic wavefront
from the previous beat to depolarize as much
ventricular myocardium as possible before col-
liding with the stimulated antidromic wavefront.
Because the orthodromic wavefront from the
previous beat begins to depolarize ventricular
myocardium as it exits the His-Purkinje network,
the pacing location that would permit that
wavefront to depolarize as much ventricular
myocardium as possible before colliding with
the stimulated antidromic wavefront is the one
farthest from the interface of the His-Purkinje
network and ventricular myocardium, while still
close to the AVRT circuit. That is, as close as
possible to the ventricular insertion of the AP,
on the ventricular side of the AV groove opposite
the earliest atrial electrogram in SVT (Fig. 6).
The closer the pacing site is to the ventricular
insertion of the AP, the more likely fusion
becomes, perhaps to the point of concealed fusion
(where the paced QRS complex morphology is
the same as the QRS complex morphology of
the tachycardia) (Fig. 7). Accordingly, when VOP
is performed from the right ventricular apex,
manifest entrainment (QRS complex fusion during
entrainment) is appreciable in the majority of
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Figure 5. Manifest entrainment of orthodromic AVRT employing a left free wall AP (CL = 340 ms)
with fusion. Panel A: The atria are accelerated to the pacing CL (320 ms) and the tachycardia
continues after pacing is stopped. Note that the pacing site is the basal LV via a branch of the
CS. The post-VOP response is A-H. There is an orthodromically captured His potential during
pacing that is visible just after the pacing stimulus, indicating entrainment with intracardiac
electrogram evidence of fusion. The PPI-TCL difference is 90 ms (430–340 ms). The first return
AH interval is 240 ms, which is 60 ms longer than the AH interval during tachycardia (due to
decremental conduction slowing through the AV node at the shorter pacing CL), so the corrected
PPI-TCL difference is only 30 ms (90–60 ms). The SA-VA interval difference is −20 ms. Panel
B: QRS complex morphology of purely paced beats from the same pacing site that was used for
VOP. Note that the QRS complexes during VOP (left side of Panel A) are narrower than those of
a purely paced beat, and have an intermediate morphology between fully paced beats and beats
of the SVT. LA = left atrial; LV = left ventricular. (The PPI is measured from the pacing stimulus
to the first return ventricular electrogram recorded by the pacing channel. The SA interval is
measured from the pacing stimulus to a consistent atrial electrogram, usually the earliest atrial
electrogram. The VA interval is measured from the beginning of the earliest QRS complex in SVT
to the same atrial electrogram that was used to measure the SA interval.)

AVRTs employing septal or right-sided APs, but
is rarely evident for AVRTs employing a left-
sided AP.4 Similarly, when VOP is performed from
the left ventricle (LV), manifest entrainment is
appreciable in the majority of AVRTs employing
left-sided APs.4
Note that when VOP is performed from the
basal septum, inadvertent His bundle capture
(or proximal right or left bundle capture) could
produce a narrow QRS complex that could mimic
fusion. This can be avoided by pacing superior or
inferior to the His and right bundles.
Entrainment, Fusion, and “Bystander” APs
This discussion has indicated that transient
entrainment by VOP that results in manifest
fusion proves that the SVT is reentrant, that an
AP is participating, and that the ventricle is a
required component of the circuit, excluding both
AVNRT and AT. Theoretically, a simultaneous AT
originating close to the atrial aspect of an AP, or
a simultaneous AVNRT with an atrial exit close
to an AP, are not excluded by these findings.
Such an exceptional circumstance would require
a double tachycardia or a double loop tachycardia
where one of the tachycardias is orthodromic
AVRT. Accordingly, such an AP could not
strictly be considered a “bystander.” Ablation
of the AP would ultimately be required both
clinically and to unmask the second tachycardia
mechanism. Thus, entrainment of SVT with fusion
indicates that orthodromic AVRT is present;

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 VEENHUYZEN, ET AL.
Figure 6. Importance of pacing site to demonstration
of QRS complex fusion. In panel A, with VOP from
an apical site, collision of the stimulated antidromic
wavefront (solid arrow) with the orthodromic impulse
from the previous beat (dotted arrow) occurs within
the conduction system (black bar). Thus the ventricle
is activated entirely by the paced wavefront and QRS
complex fusion will not be seen. In panel B, the pacing
site has been moved to the base, close to the site
of earliest atrial activation. In this case, the impulse
from the previous beat (dotted arrow) has the greatest
chance to exit the His-Purkinje system and activate
most of the ventricle. The collision of the antidromic
impulse and the prior orthodromic impulse occurs in
ventricular myocardium. Manifest QRS fusion, or even
concealed fusion (where the QRS morphology matches
that of the tachycardia), will be apparent. The latter
must be distinguished from isorrhythmic dissociation of
the pacing stimulus from the tachycardia (i.e., when the
tachycardia is not actually accelerated to the pacing CL,
but rather, the pacing CL is the same as the tachycardia
CL because an inappropriately long pacing CL was
chosen or the tachycardia accelerated as pacing was
initiated).
nevertheless, other SVT mechanisms could also be
present.
Beyond Fusion: The Need for Quantitative
Features of Entrainment of SVT by VOP
Despite considering evidence of fusion in
intracardiac electrograms and pacing from ventric-
ular sites close to the ventricular insertion of the
operative AP, fusion during entrainment of AVRT
is not always appreciable (i.e., only concealed
entrainment may be possible). Nevertheless,
AVRT and AVNRT can reliably be distinguished
by studying certain quantitative features of their
entrainment, including the difference between
the PPI and the TCL (the PPI-TCL difference),
and the difference between the stimulus to atrial
electrogram (SA) interval and the tachycardia VA
interval (the SA-VA interval difference).
776 June 2011
The PPI-TCL Difference
The PPI is the time required for the last
stimulated orthodromic wavefront to propagate
to an excitable gap in a reentrant circuit, make
one revolution around that circuit, and return to
the pacing site. Accordingly, if the pacing site
is in the circuit, the PPI should approximate
the TCL, and the PPI-TCL difference should
only be 0–30 ms. The PPI-TCL difference should
increase as the distance of the pacing site from
the circuit increases. A portion of ventricular
myocardium is “in circuit” for AVRT, while
ventricular myocardium is relatively far from
AVNRT circuits, separated from them by the
intervening His-Purkinje network that must be
traversed twice during entrainment of AVNRT by
VOP: once to reach the AVN circuit, and once to
get back to ventricular myocardium. Accordingly,
the PPI-TCL difference should be considerably
longer after entrainment of AVNRT than after
entrainment of AVRT by VOP8 (Fig. 8).
The Corrected PPI-TCL Difference
While the PPI will increase as the distance of
the pacing site from the circuit increases, it may
also increase if overdrive pacing causes decremen-
tal (i.e., rate dependent) conduction slowing. This
is most likely to occur in the AV node because
the AV node typically displays decremental
conduction properties. During entrainment of
AVRT by VOP, the atria are accelerated to the
pacing CL. Therefore, the input to the AV node is
also accelerated to the pacing CL and the AV node
conduction time will increase in keeping with its
decremental conduction properties. Thus, when
AVRT is entrained by VOP, the first Atrio-His (AH)
interval (or, assuming that the His-ventricular
interval remains more or less constant, the first
AV interval) after entrainment is often prolonged
compared to the AH (or AV) interval during AVRT.
This increase in the subsequent PPI is unrelated to
the distance of the pacing site to the circuit. The
PPI-TCL difference can be corrected for the degree
of decremental conduction slowing by subtracting
the magnitude of the increase in the AH (or
AV) interval on the first return beat compared
to the AH (or AV) interval during spontaneous
AVRT from the PPI-TCL difference9 (Fig. 5). The
overlap between PPI-TCL differences in patients
with AVNRT and patients with AVRT employing a
septal AP disappears when the corrected PPI-TCL
difference (cPPI-TCL) is considered: a cPPI-TCL
difference <110 ms is consistent with a diagnosis
of AVRT employing a septal AP while a cPPI-TCL
difference >110 ms is consistent with a diagnosis
of AVNRT (Fig. 3).9 The cPPI-TCL difference may
be >110 ms in a case of AVRT if the pacing site
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 DIAGNOSTIC PACING MANEUVERS FOR SVT

Figure 7. Manifest entrainment of orthodromic AVRT employing a left free wall AP with near concealed fusion. The
atria are accelerated to the pacing CL (340 ms) and the tachycardia resumes at a longer CL (355 ms) immediately
after pacing stops. The post-VOP response is AV. Note that the QRS complexes during VOP are almost identical to
the QRS complexes during tachycardia. There is only a slight difference in the end of the QRS complexes in leads III
and V1 during entrainment. Note that the pacing site is the posterobasal LV.

is far from the circuit (as is the case when AVRT
using a left-sided AP is entrained by VOP from
the right ventricular apex—Fig. 1B) or if the AP
has decremental conduction properties (as might
be encountered during a long RP interval SVT).
Correction of the PPI-TCL difference as
described above will also avoid a similar problem
with the uncorrected PPI-TCL difference that
can arise in patients with both dual AV node
physiology and AVRT employing a septal AP.
During entrainment of AVRT that uses the fast
AVN pathway as the antegrade limb, the pacing
CL may encroach upon a fast AV node pathway
refractoriness so that the stimulated orthodromic
wavefront may be forced to use a slow AV node
pathway. The AH interval on the first return beat
would be considerably prolonged in such a case.
This would prolong the PPI-TCL difference not
because of decremental conduction in the AV node
but because of a “jump” to the slow AVN pathway
during entrainment.10
The SA-VA Difference
During AVNRT the ventricle and atrium are
activated in parallel, while during entrainment
of AVNRT by VOP, their activation is in series.
In contrast, both during orthodromic AVRT and
during entrainment of orthodromic AVRT by
VOP, the ventricle and atrium are activated
in series. Accordingly, the difference between
the VA interval during entrainment and SVT
should be longer for AVNRT than for AVRT
(Fig. 8). The VA interval during entrainment
is measured from the pacing stimulus, so it
is called the SA interval. SA-VA differences
<85 ms are consistent with AVRT (Fig. 5) while
SA-VA differences >85 ms are consistent with
AVNRT.8
SA-VA differences have tended to di-
chotomize patients with AVNRT and AVRT less
well than PPI-TCL and cPPI-TCL differences
when VOP is performed from or near the RV
apex.8,9 While the SA-VA difference is not subject
to decremental conduction slowing through the
AV node during the A-H response, the SA-VA
difference could be relatively long (close to or
>85 ms) if the pacing site is far from the operative
AP (for instance, in the case of entrainment of
orthodromic AVRT using a left-sided AP by pacing
from the RVA) or if the AP has decremental
conduction properties (as might be encountered
during a long RP interval SVT).

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 VEENHUYZEN, ET AL.
Figure 8. Quantitative features of entrainment of SVT
by VOP. A, left panel: tachycardia circuit in orthodromic
AVRT (shown here using a right-sided accessory
pathway). The VA interval will be the time from initial
ventricular activation (breakout from the His-Purkinje
system, marked “V”) to earliest atrial activation (atrial
breakout from the accessory pathway, marked “A”). A,
right panel: last beat of VOP, with an apical pacing site
close to the circuit. The stimulus-to-atrial (SA) interval
will be similar to the VA interval since the impulse is
travelling over the same route in each. Note that during
SVT and VOP, the atrium and ventricle are activated
in series. The postpacing interval (PPI, time from the
last paced stimulus to the return electrogram at that
site) will also approximate the tachycardia cycle length
(TCL). Thus the PPI-TCL and SA-VA differences will
be relatively short. B, left panel: tachycardia circuit in
typical AVNRT. The VA interval during SVT is short
since the two chambers are activated in parallel. B,
right panel: last beat of VOP. The SA interval will be
longer than the VA interval during tachycardia since
activation of V and A is forced to occur in series. The PPI
will also be longer than the TCL since the impulse must
travel retrogradely up the conduction system, complete
one revolution of the AVNRT circuit, then conduct
antegradely again to the ventricular pacing site. Thus,
PPI-TCL and SA-VA will be relatively long. See text for
details.
The Importance of the Pacing Site with Respect
to the cPPI-TCL and SA-VA Differences
Compared to apical ventricular pacing sites,
pacing sites close to the AV groove should be
closer to an AP that operates in a conventional
AVRT circuit (if close to the region with early atrial
activation), yet farther from AV nodal circuits
778 June 2011
Figure 9. Influence of pacing site on PPI-TCL and SA-
VA differences. Panel A: in orthodromic AVRT (shown
here using a left free-wall accessory pathway), an
impulse from an RV apical pacing site (square wave
1) may have a larger distance to travel to enter the
tachycardia circuit (solid arrow), compared to a basal
site close to the site of earliest atrial activation (square
wave 2). The latter site should thus give shorter PPI-TCL
and SA-VA differences. Panel B: in contrast, in AVNRT
the apical site is “electrically closer” to the circuit than
a basal site, since in the latter case the impulse must
first travel through ventricular myocardium (grey arrow)
before entering the distal arborizations of the Purkinje
system. In the case of the PPI, it must also travel this
distance a second time to get back to the pacing site.
Thus, in AVNRT a basal pacing site will cause PPI-TCL
and SA-VA differences to be greater.
(because of the extra distance required for a
basal pacing stimulus to reach the more apical
arborization that appears to be the usual input to
the His-Purkinje network) (Fig. 9). Accordingly,
compared to apical pacing sites, basal pacing
sites would be expected to (1) increase the cPPI-
TCL and SA-VA differences for a given AVNRT
circuit and (2) decrease the SA-VA difference for a
given AVRT circuit. Basal pacing sites should also
decrease the cPPI-TCL difference for a given AVRT
circuit to the extent that the basal site, being closer
to the operative AP, may be closer to the circuit
(Fig. 9). These hypotheses have been born out
by a prospective study where, interestingly, the
discriminatory value for the cPPI-TCL difference
(110 ms) and the SA-VA difference (85 ms)
remained essentially unchanged (110 ms and
80 ms, respectively), but the spread between the
highest values in AVRT and the lowest values
in AVNRT increased significantly. In addition,
there was no overlap between these values in
cases of AVNRT and these values in cases of
AVRT, regardless of the location of the AP,
when basal VOP was performed. These results
indicate that cPPI-TCL and SA-VA differences
obtained from entrainment by VOP from basal
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 DIAGNOSTIC PACING MANEUVERS FOR SVT
Figure 10. Onset of ventricular overdrive pacing at a
CL of 280 ms during SVT with a CL of 300 ms. The
first four paced beats show progressive QRS complex
morphology fusion. The fifth paced beat is the first beat
to have fixed QRS complex morphology as determined
by studying all 12 leads at the onset of pacing (not
shown here). Thus, the transition zone begins with the
first pacing stimulus and ends with the fifth paced beat.
Note that the atrial CL is accelerated to the pacing
CL in the transition zone after the second paced beat,
which is fused. The arrows indicate a fixed stimulus-
atrial (SA) interval, which is also established in the
transition zone. If the diagnosis were AVNRT, one
would not expect the atrial CL to be perturbed or a
fixed SA interval to be established until one or more
beats after the transition zone. As we will discuss in
Part two of this review, the second pacing stimulus
results in a His-refractory ventricular premature beat (it
must be His-refractory since the QRS complex is fused,
indicating that the stimulated antidromic wavefront
collided with the orthodromic wavefront from the
previous beat in ventricular myocardium after it had
to exit the His-Purkinje network) that preexcites the
atrium by 20 ms without a change in the atrial acti-
vation sequence, indicating a diagnosis of orthodromic
AVRT.
PACE, Vol. 34 June 2011
sites better dichotomize AVNRT circuits from
AVRT circuits.4 As discussed earlier, basal pacing
sites close to the earliest atrial activation are
also most likely to permit the identification of
fusion (Fig. 6). Compared to RV apical pacing
sites, basal ventricular pacing sites are not as easy
to access with stability and without inadvertent
atrial or His bundle capture. Accordingly, we
reserve VOP from basal sites for those instances
when VOP from the RV apex results in an
A-H response with concealed entrainment and
borderline or questionable cPPI-TCL and/or SA-
VA differences.
Differential Entrainment
Based on the results of apex versus base
pacing (to be discussed in detail in Part two of
this review) by Martinez-Alday et al.,11 we hypoth-
esized that the SA-VA and PPI-TCL differences
after entrainment of AVNRT by basal VOP ought
to be at least 10 and 20 ms longer, respectively,
than after apical VOP. These differences should be
specific for AVNRT provided that long and similar
pacing CLs are employed at both sites to avoid
any increases that might be due to decremental
conduction slowing during VOP. We coined the
term “differential entrainment”12 to describe this
phenomenon.
Our colleagues at the University of Western
Ontario provided further proof of this concept.13
Apical VOP was performed with the RV catheter
advanced as far out to the RV apex as possible.
Basal VOP was performed by advancing a steerable
ablation catheter just beyond and superior to
the His bundle where inadvertent atrial and
His bundle capture could be reliably avoided.
The differential cPPI-TCL values and differential
SA-VA (which they called the differential VA)
interval values were defined as those values
obtained after VOP from the RV apex subtracted
from those values obtained after VOP from the
RV base. The differential VA interval could be
calculated even in cases where VOP consistently
terminated the SVT if VOP did accelerate
the atria to the pacing CL prior to termination (see
number 2 below). All patients with differential
VA and differential cPPI-TCL values >20 and
30 ms, respectively, had AVNRT, while all those
who did not had AVRT. Differential entrainment
performed in this way has the strength of
not requiring knowledge of the site of earliest
atrial activation, which might be particularly
valuable if a coronary sinus (CS) catheter is
not routinely used, or if the CS cannot be
cannulated.
779
 VEENHUYZEN, ET AL.

Figure 11. A supraventricular tachycardia with a long RP interval and earliest atrial activation along the mitral
annulus. Overdrive posterobasal left ventricular pacing is initiated about half way through the tracing. The second
pacing stimulus captures enough ventricular myocardium to result in a fusion beat. Note that the QRS complex
morphology associated with the second pacing stimulus is partly that of the QRS complex morphology of the
native tachycardia (compare to the QRS complex morphology of the preceding beats) and partly that of the QRS
complex morphology of a fully paced beat (compare to the QRS complex morphology of the subsequent paced beats).
Importantly, the second pacing stimulus is followed by abrupt VA block, which terminates the SVT. Ventricular pacing
with 1:1 VA conduction ensues. The atrial CL was perturbed (termination with abrupt VA block) in the transition
zone. As we will discuss in Part two of this review, the second pacing stimulus results in a His-refractory ventricular
premature beat (it must be His-refractory since the QRS complex is fused indicating that the stimulated antidromic
wavefront collided with the orthodromic wavefront from the previous beat in ventricular myocardium after it had
to exit the His-Purkinje network) that terminates the SVT without conduction to the atrium. If one only studied the
end of this overdrive pacing train and found that SVT had stopped, one would miss this information, indicating a
diagnosis of orthodromic AVRT (in this case, employing a slowly conducting left free-wall accessory pathway).

What if the Response to VOP Is Not
Interpretable?
Three responses to VOP, while often consid-
ered uninterpretable, may still provide important
diagnostic information.
1. The atria are not accelerated to the
pacing CL: As already discussed, repeated failure
to accelerate atrial activation to the ventricular
pacing CL suggests, but does not prove, that the
SVT is an AT.
2. The atria are accelerated to the pacing
CL, but SVT fails to continue after VOP stops.
In this situation, the reason that the SVT stops
is because the VOP CL has encroached upon the
antegrade refractory period of the AVN, so that
the last retrogradely conducted atrial wavefront
cannot echo back to the ventricles to produce an
AH response after VOP. Often, this problem can
be overcome by shortening the refractory period
of the AVN by intravenous isoproterenol. If this
problem cannot be overcome, the response can
still be helpful diagnostically, particularly when
it is part of differential entrainment as discussed
above. (In this instance, the term “differential
entrainment” is inappropriate, since the SVT
cannot be said to be entrained if VOP results in
its termination.)
Recently, three retrospective studies have
reported that resetting of the timing of atrial
activation (usually advancement; less commonly

780 June 2011 PACE, Vol. 34

 DIAGNOSTIC PACING MANEUVERS FOR SVT

Figure 12. A proposed flow chart for the use of ventricular overdrive pacing in the diagnosis of
SVT. * = closest to the site of earliest atrial activation.

delay or tachycardia termination without atrial
activation) during the early portion of VOP can
differentiate AVNRT (typical or atypical) from
AVRT (regardless of AP location) with a very
high degree of sensitivity and specificity.14–16
When VOP is initiated, there is usually a gradual
change from the tachycardia QRS morphology,
through a transition zone of varying degrees of
fusion, to a final stable paced QRS complex
morphology (which may be either fully paced
or represent stable fusion) (Figs. 10 and 11).
Definition of the first stable QRS morphology beat
is central to this discriminator and should use
all 12 surface electrocardiogram leads. In these
studies, the positive predictive value of resetting
of the timing of atrial activation either before
or at the time of the first beat showing final
paced QRS morphology for AVRT and the positive
predictive value of resetting of the timing of atrial
activation after the first beat showing final paced
QRS morphology for AVNRT both exceed 90%.
In AVRT, VOP impulses will reach the atria as
soon as the ventricular paced impulses reach the
AP and traverse it. In AVNRT, VOP impulses will
not reach the atria until the ventricular paced
impulses reach the input to the distal His-Purkinje
system and traverse the His-Purkinje system
and the AVN retrogradely. This discriminator

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 VEENHUYZEN, ET AL.
between AVRT and AVNRT is attractive be-
cause it does not require that the tachycardia
continue after termination of VOP. Accordingly,
prospective studies of this discriminator seem
warranted.
Potential pitfalls should be kept in mind,
including variable TCLs, pacing at a CL shorter
than 40 ms less than TCL (where the paced
wavefront could penetrate the His bundle and
AV node and perturb the atrial CL during AT
or AVNRT in fewer beats), decremental APs
(where the paced wavefront could take more
beats to perturb the atrial CL in AVRT), the
presence of bystander APs (which could provide
a route to readily perturb the atrial CL during
AT or AVNRT), and difficulties in identifying
the first paced beat with a stable QRS complex
morphology, for which interobserver agreement
appears to be around 80%.16 For the same reasons
discussed above, one would expect the diagnostic
yield of findings at the beginning of VOP to be
improved by basal VOP close to the earliest atrial
activation in challenging or borderline cases. That
is, one would expect that the atrial CL would be
perturbed earlier in the transition zone for cases
of AVRT, and even longer after the transition zone
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for cases of AVNRT, if VOP were performed at
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Conclusion
VOP during sustained, stable SVT is quick
and easy to perform. Because it is qualitatively
and quantitatively information rich, it can provide
a diagnosis of SVT mechanism in a majority of
cases. Basal VOP and differential entrainment can
be useful in cases where the results of VOP from
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14. Dandamudi G, Mokabberi R, Assal C, Das MK, Oren J, Storm
R, Vijayaraman P, et al. A novel approach to differentiating
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PACE, Vol. 34
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