AVNRT
SVTs are due to:
Enhanced Impulse Formation: due to enhanced phase 4 automaticity in normal or abnormal cells or
triggered activity. Cannot be predictively initiated or terminated by electrical stimulation. The response to
overdrive pacing is overdrive suppression or no effect at all. Overdrive acceleration is typical of triggered
arrhythmias and distinguishes them from reentrant arrhythmias.
Reentry: require
-At least 2 functionally or anatomically distinct pathways that join proximally or distally to form a
closed             circuit of conduction.
-Unidirectional block in one of these pathways
-Slow conduction down the unblocked pathway allowing the previously blocked pathway to
recover                   excitability (the conduction time along the alternative pathway must exceed the refractory
period of the            initially blocked pathway.
The sine qua non of a reentrant arrhythmia is the ability to reproducibly initiate the tachycardia by timed ES.
PES can also reproducibly terminate the tachycardia.
resetting or entrainment of the tachycardia in the
presence of fusion can be demonstrated.

AVNRT 51%
Typical                 89%
Uncommon           6%
Intermediate         4%
AVRT (CBT) 38%
Fast                      88%
Slow                      12%
AT 11%
AAT                      67%       
PAT                      23%
SNRT                    10%

AVNRT
Women < 40 (median age 28). Average rates 170 bpm. In between episodes APDs and isolated atrial echo
beats. First described by Mines in 1913, demonstrated by Moe who also demonstrated ES initiation in the
rabbit.
Slowly conducting alpha pathway with a short RP
Fast conduction beta pathway with a longer RP
A-Sinus Rhythm:
down the fast Beta and produces a single QRS. Simultaneously down the slow alpha
and meets refractoriness at the lower part of the AVN.
B-APD: blocks in beta because of its long RP and proceeds slowly down the Alpha with a long PRI.
Conduction down the alpha is not slow enough to allow the Beta to recover and no echo beat is
generated.
C-Earlier APD: blocks in Beta because of its short RP, goes down the slow Alpha, slow enough to allow
Beta to recover and conduct retrogradely through it generating an Echo beat, however Alpha has still not
recovered and only a single Echo beat occurs.
D-Earlier APD: Beta is refractoy, goes down the slow alpha with a long PRI, Alpha is too slow and Beta
has had time to recover. Echo beat is produced by retrograde activation of Beta. Now Alpha has
recovered and a sustained tachycardia results.
Uncommon AVNRT (6%): rarely the Beta pathway has a shorter RP than the Alpha and the tachycardia
can be reversed conducting antegradely down the fast pathway and retrogradely up the slow pathway.
The free border of the EV
continues as the Tendon of
Todaro that runs in the
musculature of the
Eustachian Ridge. It is one of
the borders of the
Triangle
of Koch
that delineates the
location of the AVN. The
anterior border is marked by
the annulus of the septal
tricuspid leaflet. Superiorly
the Central Fibrous Body is
the landmark for the
penetrating bundle of His.
The inferior border of the
triangle is the orifice of the
CS together with the vestibule
immediately anterior to it.
RA in RAO - The vestibular
portion is the area often
targeted for ablation of the
slow pathway. The FP
corresponds to the area of
musculature close to the apex
of the TOK. The TV covers
the orifice of the CS.
CS size as a marker for
AVNRT.
A direct contrast
injection using an Amplatzer
catheter (AL2) can easily
delineate the size of the CS
Ostium. Increased distance to
the CS os could be an
indicator of different
conduction properties of the
SP.
The SP area is the base of the
TOK. The body of the compact
AVN is contained near the
apical portion of the triangle,
and the His Bundle penetrates
the CFB at the apex. Toward
the inferior portion of the
triangle there are prongs of
nodal tissue that extend
inferiorly rightward and
leftward toward the tricuspid
and mitral valves. These nodal
extensions have been
implicated in SP conduction.
Because this area also
contains the zone of
transitional cells that feed into
the compact node, this too
may have a role in SP
conduction.
Red line = Tricuspid annulus, depicted by the CS catheter in RAO and starts at
the His recording region marked by the His catheter. The Tendon of Todaro is a
very thin structure and its location is approximated by the proximal His Catheter
RAO
LAO
Mapping of the SP area can
be made by starting with large
V potential above and anterior
to the CS, followed by slow
withdrawal of the catheter and
CW rotation toward the CS os.
because the SP is located in
the endocardium there is no
need to use high energy.  
There is no clear anatomical evidence of two distinct structures. The slow pathway potentials described by
Jackman et al and Hassaguere et al are non specific electrograms that can be recorded in all people in the
posterior triangle of Koch. Most likely the electrophysiologic demonstration of dual AV nodal pathways is the result
of the influence of nonuniform anisotropy on propagation in the AV junction.
Two A-H intervals at the same Paced CL suggest dual AVN pathways.

MECHANISMS OF INITIATION OF AVNRT

Spontaneous AVNRT is almost always by an APD that is associated by a long P-R and A-H interval leading to a
tachycardia in which the atria and ventricles are activated near simultaneously. In typical AVNRT, initiation is
produced when an APD blocks in the FP and conduction proceeds antegradely over the SP and retrogradely over
the FP. In 100% of patients with a history of AVNRT the tachycardia can be induced by timed APDs over a
reproducible range of coupling intervals. In some instances catecholamines or atropine facilitate induction.  
Spontaneous
inititation of an
AVNRT by an APD
with a marked long
A-H (SP transition)
AVNRT initiated
by the second Ap
at a tighter
coupling interval
of 310 ms. AH is
longer (295 vs
105)
AVN conduction delay (A-H Jump) and not the coupling interval of APD is of prime importance in the
initiation of AVNRT (example above). This can be demonstrated by initiation of AVNRT by using the
alternative method of A pacingto produce A-H delays at longer cycle lengths than at the coupling intervals of
single ES required to produce comparable A-H delays. If you were to compare both medthods you would
notice that only after sufficient AVN conduction delay is achieved as reflected by the A-H interval that SVT is
induced.
AVN delay not the coupling interval or the PCL is the critical determinant for initiating AVNRT.
Single AVN echoes and SVT appear only during antegrade conduction down the SP and retrograde
conduction up the FP. In approximately 25% of cases one does not see either an AVN echo or SVT
immediately after block in the FP and conduction proceeds down the SP.
The echo is observed only
after a critical A-H interval is reached during a SP conduction. Typical nodal reentry is initiated by
atrial stimulation producing block in the FP with a jump to the SP only when conduction is slow
enough.

Uncommonly (3%) the jump is more evident with CS pacing and not HRA pacing. The critical AVN
delay (A-H jump) is almost always shorter when pacing from the CS.
This could be related to the fact
that the left atrial extension of the AVN is closer to the FP allowing for earlier recovery
. In ~ 1/3 of patients
the RP of the FP is shorter during CS stimulation than during HRA stim.
Because of the nonuniform
anisotropy of the AVN and the variable responses obtained it is important to ES from both the
HRA and the CS.

In order to diagnose dual pathways one must see a jump > 50 ms in A-H with a small (10 ms)
decrease in the coupling interval of the APD. Also dual pathways may manifest by different P-R or
A-H intervals during sinus rhythm or at identical pacing rates.

Double response to ES (1:2 response) is an uncommon manifestation of dual AVN pathways whereby
one stimulus produces 2 QRS complexes. Atrial ES goes down the FP and the SP in the same time and by
the time conduction through the SP has reached the HB it has recovered and able to go down to the
ventricles. In order for this to happen conduction down the SP has to be very slow so that the HPS has time
to recover to produce a second response.
AVNRT initiation by rapid A pacing. The second
impulse is marked by a "jump" in the A-H interval.
With progressive delays in the A-H interval AVNRT
is induced.
Dual pathways in response to APDs may be observed in as many as 25% of patients without SVT. Despite
the jump from fast to slow pathway, with very long A-H intervals, these patients never have an atrial echo.
One assumes the major limitation is retrograde conduction over the FP.

Multiple pathways may be observed in as many as 5% to 10% of patients. These are characterized by
multiple jumps of > 50 ms with increasingly premature AES. Such patients have AVNRTs with longer CLs and
longer ERPs and FRPs of the AVN.

Failure to demonstrate dual AVN pathways in patients with AVNRT in response to AES is usually
due to one of three factors:
1- The RPs of the SP and FP are similar.
More rapid APacing, mutiple drive CLs, multiple AES, BB, CCB
or digoxin may be required to dissociate them. An inadequate stimulation protocol is the most common cause
of failure.
2- A long atrial FRP limits the prematurity in which APDs can reach the AVN. which renders the APD
incapable of dissociating SP and FP. This problem can be overcome by either performing stimulation at a
shorter drive CL, which decreases the FRP of the atrium, allowing shorter A1-A2 coupling intervals to be
achieved and to reach the AVN. Or by the introduction of double APDs, the first of which shortens atrial
refractoriness, allowing the second to conduct to the AVN at an earlier point in time
3- Block in the FP has already occurred during basal drive. Thus conduction always proceeds over the
SP. In this case SVt will develop in the absence of a jump in AVN conduction time but will depend on
achieving sufficiently prolonged conduction over the SP to allow recovery of the FP.
Atypical Reversed AVNRT: fast/slow type
The AVN reentrant circuit is reversed, so that the FP is used for antegrade conduction and the SP for
retrograde conduction.
The ECG exhibits a long R-P interval and a short P-R interval. The apex of
the Triangle of Koch is the FP and the base is the SP. These patients do not typically have evidence of
dual AVN pathways in response to APDs or to AP. The tachycardia is initiated with APDs or AP producing
modest increases in the AH interval along the FP. Block in the SP is concealed during antegrade
stimulation because no jump occurs in A-H intervals. The only manifestation of block in the SP is the
developement of an atrial echo with a long retrograde conduction time producing a long R-P and short
P-R tachycardia. This type of tachycardia must be distinguished from a posteroseptal concealed bypass
tract with AVN like properties.
V stim can induce AVNRT in 40% of patients with typical AVNRT while A stim can induce it in 100%.
In contrast atypical AVNRT is induced as frequently from the ventricle than from the atrium. V pacing is
three times more effective than VPDs in initiating typical AVNRT. In patients with typical AVNRT retrograde
conduction is usually very good and occurs over the FP (Beta). Retrograde block to the atrium over the FP
rarely occurs in patients with typical AVNRT and when it occurs it suggests that the atrium is not required
for AVNRT.
Rapid Ventricular Pacing will produce block in the SP (concealed), conduction up the
FP with subsequent recovery of the SP in time to accept antegrade conduction over it to initiate
the ventricular echo and sustained tachycardia and produces SVT more easily than Ventricular
extrastimuli
. With VPDs the initial site of delay or block is in the HPS. Even when conduction proceeds
retrogradely through the HPS because of delay in it V1-H2 remains constant . As a result the prematurity
with which the impulse reaches the AVN remains constant.
Induction of typical AVNRT by VPDs only
succeeds in ~ 10% of cases.
Initiation of AVNRT by rapid ventricular pacing
Initiation of typical AVNRT by a VPD
Induction of typical AVNRT by a VPD with block in the atrium (successful only in 10%)
Typical AVNRT induction by VPD is successful in only 10% of cases. Specific reasons for failure include:
- Block in the HPS
-The FRP of the HPS exceeds the ERP of the SP in the retrograde direction
-The ERP of the SP is equal to that of the FP in the retrograde direction
-The antegrade SP ERP exceeds the V-paced CL, therefore unable to accept any input from the FP
-Following its engagement from the FP, there is insufficient antegrade delay in the SP to allow the FP to
recover
-Block in a final common pathway in the AVN (proximal to the SP & FP in a retrograde direction)

Pacing at shorter drive CLs might increase the % of pts in whom typical AVNRT might be
induced by V stim because of shortening of the ERP and FRP of the HPS.
Many of the problems
imposed by the HPS refractoriness can be overcome by rapid ventricular pacing, during which the AVN
is the primary site of delay. This explains why rapid pacing is more likely to longitudinally dissociate
SP&FP in the AVN than ES. The observation that V Pacing does not always induce typical AVNRT is
explained in part by the occurrence of repetitive concealment, not block, in the SP, rendering it
incapable of antegrade conduction. Block cannot be distinguished from concealment in humans.

The mechanism by which V pacing can induce AVNRT:
1-Retrograde RP of the alpha pathway (SP) > RP of beta pathway (FP). In this case, rapid V pacing or
VPDs induce typical AVNRT in the absence of demonstration of retrograde dual pathways. Retrograde
conduction proceeds up the FP without prolonged retrograde conduction. Block in the SP is manifested
(concealed) and is only inferred by initiation of the tachycardia. Thus no critical V-A or H-A interval is
required to initiate the tachycardia.
2-Interpolated VPDs can result in the production of antegrade dual pathways (=>retrograde concealed
conduction can result in antegrade block in the FP and allow slow conduction down the alpha SP. This
produces dual AVN physiology with induction of typical AVNRT. this happens less commonly than 1
3-If retrograde RP of FP>SP, VPDs or V pacing can produce retrograde dual AVN pathways. This leads
to the development of atypical uncommon AVNRT because initial block in the Beta FP results in long
retrograde conduction time through the alpha SP which is followed by antegrade conduction down the
FP.
This is a common mechanism of induction of the atypical form of AVNRT in the lab. As
noted, with atypical AVNRT, V stim is as likely to induce the tachycardia as A stim.
Occasionally VES can lead to conduction up both Slow and FP. The HA interval over the SP at the
initiation of the tachycardia is much longer than the H-A interval during the tachycardia because of
concealment into the SP by the initial conduction over the FP.
VPD going up both FP and SP giving rise to 2 A with AVNRT
AVNRT through V pacing and jump in VA
DETERMINANTS OF THE INDUCTION OF AVNRT
Although dual AVN pathways are required for AVNRT they are insufficient. The most common finding in
patients with dual AVN pathways who do not develop SV is the failure of the impulse to return up the FP
once antegrade conduction has proceeded over the SP. This could be due to 4 explanations:
1-Longitudinal dissociation of the AVN is not really present, but the pattern of conduction of
"pseudo-dual" pathways is produced by electrotonic propagation across a non homogeneous linear area
in the AVN
2-The APD that blocks in the FP produces post-depolarization refractoriness (a manifestation of
concealed conduction) resulting in the inability of the FP to recover excitability in time to be reexcited.
Conduction down the SP is insufficiently slow to allow the fast pathway to recover.
3-The FP has a long retrograde refractory period, which renders it incapable of retrograde conduction
despite slow antegrade conduction of the SP
4-There is no distal connection between the SP & FP
The most common reason for failure to induce typical AVNRT in patients with antegrade dual
pathways is that the FP is incapable of rapid retrograde conduction.
SP posteroseptal RA with slow conduction and short RP
Typical AVNRT is slow-fast. Repetitive concealment from SP to FP maintains SP conduction
Dual antegrade tachycardia: every P wave conducts down the SP and FP simultaneously. For each p there are 2
QRS. For this to happen you need to have 2 conditions present
          -AH
SP - AHFP>300 ms
          -H
SP-HFP interval > HPS ERP


-APDs: Jump > 50 ms in A-H with a small (10 ms) decrease in the coupling interval of the APD
(A1A2 defines the antegrade FP ERP)
-VPDs: prolongation of VA interval accompanied by a switch from a midline anteroseptal atrial activation earliest
from along the anteroseptum (His A earlies = FP) to a midline earliest in the posteroseptum (CS 9-10 A earliest)
If single APDs do not result in block in the FP or if block does occur but does not result in
sufficient AVN delay to initiate AVNRT then repeated stim at shorter drive CL which increase AVN
refractoriness and prolong conduction of both FP and SP, or the use of double ES, or APacing,
frequently produce the block or delay requried to initiate SVT. 85% of patients exhibit dual AVN
pathways in response to a single HRA ES. by adding the previously mentioned methods +/-
isoproterenol or atropin increases this number to 95% of patients with AVNRT.
LAO - Abl catheter on lip of CS with nice movement back&forth. Catheter in CS Os then CCW
out. Tip of abl cath should be below CS Os. Keep CW to keep it steady on septum and insure
good contact.
RAO - Parallel to his
Start with V Pacing: midline concentric VA conduction, VAWB, VA decrement, HA in retrograde
A Pacing: decrement, AVNWB, jump, echo, AVNRT
Mullins sheath: cut shorter for AVNT, give it a parallel superior direction, cut 1" for flutter
TCL
AH>HA
VH jump: block in RB, goes up contralateral septum, up LB, engage HB then AVN, and
increase in VH time
VA increase secondary to VH or HA?
Sometimes dual AVN physiology is seen caused by VA jump, with the earliest A in the posterior
septum (Prox CS) going up the SP

-V stim: look for VA decrement, retrograde WB, His before CS
-VPDs: decrement jump: change in retrograde activation with CS before His, sometimes you
could see the retrograde His
-APDs: antegrade WB, AVNERP, AERP, FPERP
Looking for a jump, if you cannot see the His you could measure A-V
If AERP is reached before AVNERP, then say AVNERP < (previous coupling cycle)
-Induction of SVT attempt: AP, APDs (singles, doubles, triples)
-In SVT: look for H-A=V, Do his refractory VPDs, no preexcitation, H-H is the same and A-A is
not advanced
in SVT: VA short (making septal BT unlikely)
in SVT HA time is short
in SVT look at termination: VAVA
in SVT VA-HA > 100 ms
-Ablation:
RAO -> go in RV and pull back CCW
LAO -> go in CS Os and CCW out
-Post ablation:
VA conduction unchanged
measure WB if changed

HA(SVT) - VA(Pacing) > 60 ms

All of the following tachycardia characteristics can be used to differentiate junctional
tachycardia from typical slow-fast AVNRT, except:




A. Long AH interval at the time of tachycardia induction


B. VA interval < 70 msec


C. Termination of tachycardia with His refractory premature atrial complex


D. Presence of a retrograde A after last entrained beat from atrium.



Which of the following statements is incorrect pertaining to typical AVNRT?



A. Bundle branch block during tachycardia would not change AA or HH interval


B. Bundle branch block during tachycardia would only minimally change the VA time


C. Delay in lower common pathway could cause atrial electrogram to precede His-electrogram


D. During 2:1 AV block, VA interval is usually variable




Which of the following statements is incorrect? 



A. AH interval during atrial pacing (at AVNRT cycle length) > AH interval during AVNRT suggests an
upper common pathway


B. HA interval during ventricular pacing (at AVNRT cycle length) > HA interval during AVNRT suggests an
lower common pathway


C. Ventriculo-atrial wenckebach during ventricular pacing occurring at cycle length longer than the
AVNRT cycle length suggests lower common pathway


D. Atrio-ventricular wenckebach occurring at shorter cycle length than the AVNRT cycle length
suggests a presence of upper common pathway




Which of the following are not characteristics of typical AVNRT? 


A. Septal VA time < 70 msec


B. Presence of discontinuous response of A-V nodal conduction time to progressively premature atrial
complexes


C
. Bundle branch aberrancy increases VA interval > 20 msec


D. Induction of tachycardia with critical AH interval





5 Which of the following would not rule out atrial tachycardia?


A. A-V response upon cessation of ventricular overdrive pacing


B. Termination of tachycardia during burst ventricular pacing without atrial capture


C. VA time < 70 msec


D. Spontaneous cessation of tachycardia with AV block