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Following the bestselling Cardiac Electrophysiology: A Visual Guide for Nurses, Techs,
and Fellows, this book builds upon the basic concepts of electrophysiology introduced in
the first volume and guides the reader to a more in-depth understanding of cardiac
developing the knowledge and skills required to practice clinical cardiac electrophysiology.
for Nurses, Techs, and Fellows is an invaluable resource, providing superb guidance in
ISBN: 978-1-935395-97-3
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3 9 5 973
Cardiac Electrophysiology 2
observations and unknowns, followed by annotated tracings and discussions that emphasize
Cardiac
Electrophysiology 2
An ADVANCED Visual Guide
for Nurses, Techs, and Fellows
Paul D. Purves l George J. Klein
Peter Leong-Sit l Raymond Yee
Allan C. Skanes l Lorne J. Gula
Jaimie Manlucu
Cardiac Electrophysiology 2
Cardiac Electrophysiology 2
Minneapolis, Minnesota
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ISBN: 978-1-935395-97-3
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eISBN: 978-1-935395-18-8
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iv
Contents
About the Authors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . vii
Foreword . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ix
Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xi
Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xiii
Glossary and Abbreviations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xv
1. Physiology . . . . . . . . . . . . . . . . . . . 1
1.1
Common Pitfalls
1.2
Heart Block
1.3
Proximal Delay
1.4
Aberrancy
1.5
Normalization
1.6
2 . AVNRT . . . . . . . . . . . . . . . . . . . . . . . . 59
2.1
Signal ID
60
2.2
Pathways
64
2.3
Initiation
2.4
Reset
22
2.5
Cool Initiation
Bundle Reset
30
2.6
Block to A
1.7
Differentiation
34
2.7
Bundle Blocks
1.8
Concealment
2.8
Echoes?
88
1.9
Concealment 2
2.9
Atypical
92
6
10
18
40
46
50
54
68
72
76
80
84
96
100
continues
Contents
continued
3. AVRT . . . . . . . . . . . . . . . . . . . . . . . . . 105
3.1
Subtle
106
3.2
Pacing Site
3.3
AP Revealed
3.4
ERPs
3.5
VA?
3.6
ERPs?
3.7
His Pacing
3.8
Narrow QRS
3.9
Narrow QRS 2
110
114
118
4.1
Differential Pacing
4.2
Proof of?
4.3
Re-do
172
176
180
122
126
130
134
138
142
146
150
154
vi
4 . AF . . . . . . . . . . . . . . . . . . . . . . . . . . . 171
158
162
166
5.1
Tachycardias
186
5.2
Tachycardias 2
190
5.3
Tachycardias 3
194
5.4
VT
5.5
Substrate for?
5.6
12-lead Diagnosis
5.7
Break
198
202
206
214
Case 1
220
6.2
Case 2
240
6.3
Case 3
248
Professor of Medicine
Division of Cardiology
Western University
Professor of Medicine
Division of Cardiology
Division of Cardiology
Western University
Western University
Division of Cardiology
Division of Cardiology
Western University
Western University
Professor of Medicine
Director, Arrhythmia Service
Division of Cardiology
Western University
London, Ontario, Canada
vii
Foreword
The process of moving beyond basic EP concepts and applying
environment.
and hope that you find it helpful as you move on to the next level.
Jaimie Manlucu
Western University
ix
Preface
Cardiac Electrophysiology 2 : An Advanced Visual Guide for
with arrows and other clues that highlight the key aspects of the
The ca ses a re designed to guide you towa rds a more in- depth
Enjoy!
xi
Acknowledgements
This second book would not have happened without the ongoing
xiii
atrial
AP
Ashman phenomenon
than the AV node) between the atria and ventricles. Accessory pathways
by a relatively short R-R, the Q R S associated with the short R-R often has
may conduct:
long-shorting the bundle branches. The right bundle branch has had
therefore blocks.
Action potential
AEGM
AF
atrial electrogram
A-H interval
Anisotropy
AT
atrioventricular
Referring to the total transit time from the atria to the ventricles.
AVCS
AVNRT
AVRT
Bipolar
xv
Bundle of His
Depolarization
Carto
Digitization
CFEs
Contralateral
CTI
Coronary sinus
Cavotricuspid isthmus
Decapolar
Decrement
of depolarization.
Delta wave
ECG
Electrocardiogram
Echo
Electrogram
Entrainment
that structure.
CS
Duo-deca
Electrophysiology
Effective refractory period. By definition it is the longest S1S 2 that
fails to conduct. Most of the time we are looking for the E R P of the AV
node or an accessory pathway. With a very tight S1S 2 (600, 200), you may
reach the E R P of the myocardium itself (seen as no capture of the S2).
Escape rhythm
S A node.
Far-field
accessory pathway.
electrograms.
xvi
FP
pathway.
FRP
Jump
Junctional
AV node.
the ventricle, it is the shortest V1-V2 achievable from any S1S 2 input,
meaning that no latency has yet to occur.
LA
Left atrial
LAA
LAO
His
Lasso
Gap
The tissue connecting the distal AV node with the proximal bundle
branches.
His-Purkinje system
ventricles that includes the His bundle, left and right bundle branches,
and the Purkinje network.
HRA
H-V interval
Infrahisian
Ipsilateral
Latency
discussing AVNRT.
LRA
LV
Mobitz type I
xvii
MRA
ms
millisecond; ms
Peel back
that lasts only a few hours. May be used with any tachycardia lasting
millisecond; msec
msec.
NC
Paroxysmal
Mid-right atrium
Persistent
or longer.
Orthodromic
Posteroseptal
of a tachycardia circuit.
Preexcitation
PR interval
PAC
PS
PV
Pulmonary vein
P-A interval
His (para = beside or next to). A pacing maneuver used to determine the
presence or absence of an anteroseptal accessory pathway.
xviii
PVC
P wave
QRS
The timing between the onset of the P wave and the onset
Radiofrequency
RVA
S1
S2
S3
SA
Sinoatrial node
SP
Ventriculoatrial
V-A
Referring to the total transit time from the ventricles to the atria.
VEGM
Ventricular electrogram
VERP
T wave
Unipolar
Right ventricle/ventricular
Spontaneous normalization
VF
Ventricular fibrillation
VT
Ventricular tachycardia
Wenkebach
atria) occurs.
SVT
Wobble
Supraventricular tachycardia
per minute.
between the atria and the ventricles (or between the ventricle and the
activation.
Tachycardia
electrical stimulation.
RV
Transseptal conduction
Refractory
RBBB
TCL
a tachycardia.
WPW
Wolff - Parkinson-White
xix
Notes
Cardiac Electrophysiology 2
CHAPTER 1
OUTLI N E
1.1
1.2
1.3
1.4
1.5
1.6
Common Pitfalls
Heart Block
Proximal Delay
Aberrancy
18
Normalization
Bundle Reset
1.7
1.8
10
22
30
1.9
PHYSIOLOGY
Differentiation
Concealment
Concealment 2
40
34
46
50
54
CHAPTER 1.1
PHYSIOLOGY
CHAPTER 1.1
PHYSIOLOGY
Discussion
In this example, the R V apical ( R VA ) catheter is positioned at the
basal septum, where it can often record a right bundle potential.
This should not be confused with a His potential.
Mistaking the right bundle potential for a His electrogram would
underestimate the tr ue H-V inter va l, leading to the er roneous
conclusion that an accessory pathway ( A P ) is present. A normal
H-V interval is approximately 35 to 45 ms.
In this particular case, mistaking the right bundle potential for a
His electrogram would lead to an H-V of 10 ms, falsely suggesting
that the patient is preexcited. This is clearly not the case since
there is no manifest preexcitation on the surface E C G .
In this tracing, when the H-V is properly measured using the His
catheter electrograms, it is within the normal range.
CHAPTER 1. 2
PHYSIOLOGY
CHAPTER 1. 2
PHYSIOLOGY
Discussion
This figure demonstrates the presence of Mobitz Type II seconddegree hear t block. As mentioned, this is usually indicative of
distal conduction system disease.
T he i nt r a c a r d i a c ele c t r og r a m s s how r e g u l a r a t r i a l p a c i n g
with intermittent block to the ventricles while displaying a His
electrogram (white arrow). Lack of conduction below the His is
indicative of the presence of conduction disease below the AV node.
T h i s m a ke s A-V conduct ion u n rel iable a nd of t en prog re s se s
unpredictably to complete heart block. Therefore, these patients
are usually referred for pacemaker implantation.
CHAPTER 1.3
PHYSIOLOGY
10
Figure 1
11
Figure 2
12
CHAPTER 1.3
PHYSIOLOGY
Discussion
Figure 2 uses calipers to highlight 80 ms of latency (local
continues
13
Figure 3
14
CHAPTER 1.3
PHYSIOLOGY
continues
15
Figure 4
16
CHAPTER 1.3
PHYSIOLOGY
17
CHAPTER 1.4
PHYSIOLOGY
1.4 Aberrancy
Both of these tracings demonstrate AV nodal reentrant
tachycardia (AV NRT ) with aberrant conduction. Discussion
of AV NRT will be covered in a subsequent chapter. These figures
focus on the physiology of aberrant conduction.
18
Figure 1
19
Figure 2
20
CHAPTER 1.4
PHYSIOLOGY
Discussion
In both tracings, AV N R T is initiated with atrial extra-stimulus
pacing. We see development of a typical left bundle branch block
( L B B B ) i n Figure 1, a nd a t y pica l r ig ht bu nd le bra nch block
( R B B B ) in Figure 2 .
These bundle branch blocks develop due to a sudden shortening
of the tachycardia cycle length, which catches one of the bundle
branches (most commonly the right bundle) still in its refractory
period. This is commonly referred to as a rate-related bundle
branch block or Phase III block. This is a functional block and is a
normal phenomenon.
The bundle branch block usually spontaneously resolves due to
a phenomenon referred to as peeling back of refractoriness, a
process by which the refractor y period of the bundle shor tens
a nd conduction velocity is enha nced in response to increa sed
heart rate.
See Chapter 1.5 for further clarification.
21
CHAPTER 1.5
PHYSIOLOGY
1.5 Normalization
Previously in Section 4, we discussed the reasons for aberrant
conduction. However, aberrant conduction may spontaneously
normalize. Please consider the reasons why this may occur.
22
23
Figure 1
24
CHAPTER 1.5
PHYSIOLOGY
Discussion
S p o nt a ne ou s no r m a l i z a t io n of t he Q R S o c c u r s d u e t o t he
progressive shor tening of the refractor y periods of the bundle
branches, as well as enhanced conduction velocity in response to
an increase in heart rate and/or catecholamine levels.
As mentioned previously, this is a form of functional block and
is a normal physiological phenomenon. In this example, a R B B B
spontaneously resolves. Note the intermediate Q R S morphology
just before complete normalization.
I n Figure 1, t he i n itia l R B B B occu r s qu ite prox i ma l ly i n t he
bundle. The wave of depolarization continues to conduct down
the left bundle, through the interventricular septum and retrograde
up the right bundle. The collision point between the antegrade and
retrograde waves is quite proximal in the right bundle.
continues
25
Figure 2
26
CHAPTER 1.5
PHYSIOLOGY
continues
27
Figure 3
28
CHAPTER 1.5
PHYSIOLOGY
When the collision occurs distal to the insertion site of the right
bundle, the Q R S normalizes ( Figure 3).
[Presented as movie in digital version.]
29
CHAPTER 1.6
PHYSIOLOGY
30
31
32
CHAPTER 1.6
PHYSIOLOGY
Discussion
In this tracing, we see a Q R S tra nsition from a L B B B patter n
to a nor ma l na r row Q R S mor pholog y fol low i ng a vent r icu la r
extrasystole (or premature ventricular contraction ( P VC )) from
the R VA catheter.
The right ventricular P VC resolves the L B B B by preexciting both
bundle branches. This shortens their refractory periods and also
a llows them more time to recover before the nex t beat of the
AV NRT tachycardia arrives.
33
CHAPTER 1.7
PHYSIOLOGY
1.7 Differentiation
This is a nice example of a very common observation. The
question to be answered is, How do you differentiate between
2 AV nodal echoes versus 2 junctional beats?
34
Figure 1
35
Figure 2
36
CHAPTER 1.7
PHYSIOLOGY
Discussion
Figure 1 : Following an atrial extra-stimulus ( S1 S 2 ), there is a
37
Figure 3
38
CHAPTER 1.7
PHYSIOLOGY
39
CHAPTER 1.8
PHYSIOLOGY
1.8 Concealment
This figure nicely demonstrates the concept
of concealed conduction.
40
41
42
CHAPTER 1.8
PHYSIOLOGY
Discussion
The first beat in this tracing shows a normally conducted sinus
beat, followed by a junctional beat (with the His deflection being
first), and then a sinus beat conducted with a long A - H interval.
The prolonged A - H interval on the third beat is due to concealed
ret rog r a de conduct ion i nt o t he AV node f rom t he preced i ng
ju nct iona l beat . T h i s mea n s t hat t he wave of depola r i zat ion
generated by the ju nctiona l beat retrogradely penetrated the
AV node ( just as an extra-stimulus would), causing the AV node
continues
43
Figure 3
44
CHAPTER 1.8
PHYSIOLOGY
45
CHAPTER 1.9
PHYSIOLOGY
1.9 Concealment 2
This figure nicely demonstrates the concept of concealed
conduction into an accessory pathway.
46
Figure 1
47
Figure 2
48
CHAPTER 1.9
PHYSIOLOGY
Discussion
Draw your attention to the last 2 beats on Figure 1 (# 6 and #7).
Based on the short A-V interval and presence of a delta wave on the
the Q R S #5 is narrow.
49
CHAPTER 1.10
PHYSIOLOGY
50
51
52
CHAPTER 1.10
PHYSIOLOGY
Discussion
The P R inter val associated with this first sinus beat is physiologically too short to conduct down the AV node. Therefore, beat
#3 must be a junctional beat that occurred at the same time as the
sinus beat. The oncoming sinus wave of depolarization could not
conduct through the AV node since the junction and ventricles have
already been depolarized and are therefore refractory.
This is an example of a junctional escape beat. This occurred due
to overdrive suppression of the sinus node from programmed atrial
extra-stimulus pacing. Recovery of the sinoatrial ( S A ) node from
this overdrive suppression was long enough to allow the junctional
escape rhythm to take over.
53
CHAPTER 1.11
PHYSIOLOGY
54
Figure 1
55
Figure 2
56
CHAPTER 1.11
PHYSIOLOGY
Discussion
Notice also that the intracardiac electrograms show that the His
V electrogram occurs before the local ventricular electrogram
recorded at the R VA catheter. This suggests that the ventr icle
is bei ng activated at t he ba se before t he R V apex (where t he
His-Purkinje a nd r ight bundles activate the ventr icle). This is
intracardiac evidence of preexcitation.
In Figure 2 , the arrow points to a His deflection that occurs after
the local His V electrogram. Why does this happen?
Reca ll that, u nless the patient is in AV reentra nt tachyca rdia
(AV RT ) (either orthodromic or antidromic), there is always fusion
of conduction between the AV node and the A P. Therefore, as the
atrial extra-stimulus pacing is delivered earlier and earlier, the
AV node will progressively decrement, but the A P usually will
not. Therefore, the A-V interval will remain constant, but the A - H
interval will continue to prolong. The local His bundle electrogram
may eventually be seen after the local His V electrogram.
57
Notes
Cardiac Electrophysiology 2
CHAPTER 2
OUTLI N E
2.1
2.2
2.3
2.4
2.5
2.6
Signal ID
Pathways
Initiation
Reset
72
60
64
2.8
68
Cool Initiation
Block to A
2.7
80
2.9
76
AVNRT
Bundle Blocks
Echoes?
Atypical
88
92
84
96
100
59
CHAPTER 2.1
AVNRT
2.1 Signal ID
The first step in analyzing any tracing involves identifying the
atrial (A), ventricular (V), and His bundle (H) electrograms
( E G M ) where appropriate. In some tachycardias, this
identification may be difficult.
60
61
62
CHAPTER 2.1
AVNRT
Discussion
This tracing shows atrial extra-stimulus testing with the last of the
S1 drive train and the S2 displayed. The S2 generated an AV nodal
63
CHAPTER 2.2
AVNRT
2.2 Pathways
During any electrophysiology study for AV NRT, we identify
the number of antegrade and retrograde AV nodal pathways
by observing how many distinct populations of A - H and V- A
intervals occur. How many pathways do you see in this tracing?
64
65
66
CHAPTER 2.2
AVNRT
Discussion
In this tracing, extra-stimulus testing elicited 3 out of the 4 AV
nodal pathways; 2 in the antegrade direction and 1 in the retrograde
direction.
1. The S1 s conduct to the His via an antegrade fast pathway
with a short A - H interval.
2. The S2 conducts to the His via an antegrade slow pathway as
evidenced by the much longer A - H interval.
3. Following the fourth Q R S , retrograde conduction up an AV
nodal slow pathway results in a retrograde A with a long
V-A interval.
Ashmans phenomenon.
67
CHAPTER 2.3
AVNRT
2.3 Initiation
During a diagnostic study, utilizing S1S 2 extra-stimulus pacing
may result in some surprising tachycardias. This is a very
unexpected result of ventricular extra-stimulus testing!
68
69
70
CHAPTER 2.3
AVNRT
Discussion
With the S2, ventricular activation propagates to the atria via a
nodal slow pathway to the His bundle and back up the retrograde
We have initiated 2:1 AVNRT. This illustrates nicely that AVNRT can
71
CHAPTER 2.4
AVNRT
2.4 Reset
Similar to the previous tracing, we have ongoing 2:1 AV NRT.
Is it possible to convert 2:1 AV NRT into 1:1 AV NRT ? Can you
explain the mechanism by which this may be accomplished?
72
73
74
CHAPTER 2.4
AVNRT
Discussion
The insertion of the paced ventricular beat (equivalent to a P VC )
advanced or reset the refractory period of the His-Purkinje tissue
below the AV N RT reentrant circuit. This results in the next and
every subsequent AV NRT beat finding the His no longer refractory.
Consequently, this converts the previous 2:1 A-V relationship into
a 1:1 A-V relationship.
In response to an increase in hear t rate, gradual shor tening of
the refractor y per iod of the His-Purkinje tissue a nd enha nced
conduction velocity, will often result in spontaneous resolution
of the 2 :1 A-V block. This is sometimes (somewhat colloquially)
referred to as peel back.
See Chapter 3, Section 12 for another example of spontaneous
normalization.
75
CHAPTER 2.5
AVNRT
76
77
78
CHAPTER 2.5
AVNRT
Discussion
Q R S #4 is the interesting beat. A sinus beat has occurred (the A
79
CHAPTER 2.6
AVNRT
2.6 Block to A
As we have seen in previous tracings, AV NRT does not require
the ventricles or the atria to sustain its reentrant circuit.
What is the unusual observation in this tracing?
80
81
82
CHAPTER 2.6
AVNRT
Discussion
The previous tracings in sections 3 and 4 demonstrated block to
the ventricle.
This tracing demonstrates block to the atrium proving that the
AVNRT circuit does not require the atr ium for ma intena nce of
83
CHAPTER 2.7
AVNRT
84
85
86
CHAPTER 2.7
AVNRT
Discussion
The first 2 cycles show ongoing AV NRT with a 2:1 A-V relationship
87
CHAPTER 2.8
AVNRT
2.8 Echoes?
This is an exercise in methodically explaining the mechanism
of each beat, one at a time. Differences in tachycardia
mechanisms and their initiation can be quite subtle leading to
misinterpretation.
88
89
90
CHAPTER 2.8
AVNRT
Discussion
The S2-initiated A conducted to the ventricles via the antegrade
AV nodal slow pathway. The first arrow points to where the His
91
CHAPTER 2.9
AVNRT
2.9 Atypical
What have we initiated and how was it initiated?
92
93
94
CHAPTER 2.9
AVNRT
Discussion
W hat we have here is a long V - A t achyca rd ia i nduced du r i ng
Following the S2, we see a PAC (earliest A at the H R A ). It conducts to the ventricles via an antegrade AV nodal slow pathway
followed by another A which is earliest at the His channel. This
sequence then repeats itself.
The most likely explanation is that the A conducted antegradely
down the AV nodal slow pathway, then conducted retrogradely back
up another retrograde AV nodal slow pathway (long V- A interval).
On subsequent beats, the antegrade limb of the circuit is an AV
nodal fast pathway.
95
CHAPTER 2.10
AVNRT
96
97
98
CHAPTER 2.10
AVNRT
Discussion
Earlier in this E P study, we demonstrated single AV nodal echo
beats initiated by atrial S2s but no tachycardia was inducible. So
an S 3 was added. There are 3 possible effects of the S 3 :
1. The S 3 -induced A wavefront could conduct over an even
slower antegrade AV nodal pathway and initiate AVNRT.
2. The S 3 -induced A wavefront could conceal antegradely into
the AV nodal fast pathway, rendering it refractory and thus
preventing any retrograde fast pathway echo beats.
3. The S 3 -induced A wavefront renders the atrial myocardium
adjacent to the retrograde limb of the circuit refractory thus
blocking the initiation of AVNRT. This option is functionally
the same as option #2 above.
When we removed the S 3 , the single AV nodal echo beat returned thus
proving option #2 above. The S 3 must have antegradely penetrated
the retrograde limb of the AVNRT circuit rendering it refractory
and thus blocking the echo.
99
CHAPTER 2.11
AVNRT
10 0
101
10 2
CHAPTER 2.11
AVNRT
Discussion
The tachycardia ter minated simultaneous with deliver y of the
single paced A ( PAC equivalent). Measuring the V-V intervals on
the right ventricular apex (RVA ) channel before and after the PAC ,
reveals that the paced PAC terminated the tachycardia without
advancing the next V! There are 2 possible explanations for this:
Scenario 1: This is junctional rhythm (not AV NRT ). If this is true,
10 3
Notes
Cardiac Electrophysiology 2
CHAPTER 3
OUTLI N E
3.1
3.2
3.3
3.4
3.5
3.6
3.7
3.8
Subtle
106
Pacing Site
3.9
AP Revealed
ERPs
VA?
118
110
114
122
ERPs?
126
His Pacing
Narrow QRS
AVRT
Narrow QRS 2
138
146
130
134
150
142
154
158
162
166
10 5
CHAPTER 3.1
AVRT
3.1 Subtle
Changes during pacing maneuvers can be quite subtle, requiring
focus and concentration. Explain the atrial activation sequence
associated with each paced ventricular beat.
10 6
10 7
10 8
CHAPTER 3.1
AVRT
Discussion
Q R S #1 and # 2 have a central atrial activation sequence (His
now follows the proximal C S 9-10. Since C S 9-10 has not moved
and is now second in the atrial activation sequence this suggests
conduction over a posteroseptal A P although conduction over a
slow AV nodal pathway is also possible.
In Q R S #8, 9, 10, the distal C S 1-2 is now earliest (eccentric atrial
activation) indicating conduction over a left lateral A P.
This patient did indeed have 2 accessory pathways, a posteroseptal
and a left lateral.
10 9
CHAPTER 3.2
AVRT
110
111
112
CHAPTER 3.2
AVRT
Discussion
During atrial extra-stimulus pacing from the H R A , there was no
evidence of preexcitation. This can be due to:
1. The A P conducts retrograde only.
2. Right atrial pacing favors AV nodal conduction over that of a
distant left lateral A P. A normal, short A-V conduction time
may result in the ventricles being depolarized before the atrial
impulse can get to the A P. Ventricular pacing (not shown here)
confirmed a left lateral A P.
There were no A P echoes dur ing H R A extra-stimulus testing.
However, we did induce A P echoes while pacing from C S 3-4. Why?
Pacing from the H R A depolarizes the lateral left atrium relatively
late, such that a wave of depolarization tr ying to return to the
left atrium via a left lateral A P will find the atrial insertion site
refractory.
However, pacing the atrium closer to the atrial insertion site of
the A P (in this case C S 3-4) allows the atrial insertion site more
time to recover excitability. This allows the retrograde wave of
depolarization coming from the A P to depolarization of the left
atrium generating an echo beat.
113
CHAPTER 3.3
AVRT
3.3 AP Revealed
The term concealed conduction is used since one does not
see this conduction directly on the E C G or E G M signals
but infers that it must be there by other observations that are
difficult to explain otherwise. This is an example of
concealed retrograde penetration of the AV node as an
explanation for the E C G observations.
114
115
116
CHAPTER 3.3
AVRT
Discussion
The first beat is slightly preexcited with a delta wave best appreciated in leads I and II. This suggests that the ventricle is being
depol a r i zed i n it i a l ly over a n A P (i.e., delt a wave) a nd t hen
predominately over the normal A-V conduction system.
The second cycle is a premature ventricular contraction ( P VC )
created by catheter manipulation.
The third cycle is aga in different, a little broader a nd more
preexcited. This is compatible with more of the ventricle being
activated by the accessor y pathway and less by the normal A-V
conduction system.
This is most compatible with concealed retrograde conduction
into the AV node by the P VC , which impedes or blocks AV nodal
conduction and thus allows the A P to predominately depolarize
the ventricle.
117
CHAPTER 3.4
AVRT
3.4 ERPs
There are several key observations in this tracing.
118
119
12 0
CHAPTER 3.4
AVRT
Discussion
1. Arrows 1 and 2 are highlighting the relationship between
the RVA V and the His V. With normal conduction over the
AV node and R BBB , the RVA is activated well before the His
121
CHAPTER 3.5
AVRT
3.5 VA?
An interesting question during ventricular pacing with eccentric
atrial activation via an accessory pathway is: Is there V-A
conduction over the AV node? Does this tracing help determine
if retrograde conduction over the normal A-V conduction system
will be present following successful ablation of the A P ?
12 2
12 3
12 4
CHAPTER 3.5
AVRT
Discussion
Wit h t he vent r icu la r ex t ra - st i mu lus (S2), at r ia l act ivat ion is
conduction to occur.
12 5
CHAPTER 3.6
AVRT
3.6 ERPs?
This tracing indicates 3 levels of block! Can you find them?
12 6
12 7
12 8
CHAPTER 3.6
AVRT
Discussion
Ventricular depolarization following the S1 demonstrates eccentric
retrograde atrial conduction (distal C S 1-2 early) indicating conduction over a left lateral A P. There is no atrial activity following
the ventricular extra-stimulus (S2). This is indication of conduction
block over the A P. Thats one.
In addition, this also means that there is no retrograde conduction
over the normal AV conduction system. Thats two.
Finally, we see a retrograde His (arrow) well after the ventricular
electrogram ( V EGM ) on the distal His channel. The retrograde His
usually appears ver y early at the onset of ventricular depolarization. This marked delay suggests that retrograde block in the
right bundle branch occurred, necessitating transseptal conduction
and entry to the His via the left bundle branch. Thats three.
12 9
CHAPTER 3.7
AVRT
13 0
131
13 2
CHAPTER 3.7
AVRT
Discussion
The first 2 beats display a narrow-complex Q R S that is virtually
but not entirely normal. This suggests capture of the His bundle
and the ventricular myocardium ad jacent to it simultaneously.
The stimulator output was 20 mA and 2 ms wide. Take note of the
Stim-A time.
The third and four th beats are wide Q R S complexes indicating
loss of His bundle capture and capture of local myocardium only.
The stimulator output was 2 mA and 2 ms wide. Again, take note
of the Stim-A time.
The difference in Stim-A time between the wide-complex Q R S s and
the narrow-complex Q R S s is 10 ms. This indicates the presence of
a septal A P.
A d i f ference i n Sti m-A ti me g reater t ha n 50 ms i nd icates t he
absence of a septal A P at the cycle length tested. It is not, strictly
speaking, a nodal response, as commonly described, since it can
be seen with accessory pathways distant from the septal region.
13 3
CHAPTER 3.8
AVRT
13 4
13 5
13 6
CHAPTER 3.8
AVRT
Discussion
The first intracardiac signal in the narrow second beat is a His
def lection, indicating an extrasystole from the His region. This
is commonly obser ved during His catheter placement. Since the
junctional focus is below the insertion site of the A P, there will be
no preexcitation.
The junctional extrasystole in general may conduct to the atrium
over: 1) either; 2) both; or 3) neither of the AV node and the A P.
In this instance, there is retrograde conduction but there is not
enough information in this tracing to make this distinction.
13 7
CHAPTER 3.9
AVRT
13 8
13 9
14 0
CHAPTER 3.9
AVRT
Discussion
The preexcited first cycle is during sinus rhythm. The first paced
beat wa s tig htly coupled to t he preced i ng si nus beat a nd t he
interval between the preceding atrial depolarization and the one
related to the atrial extra-stimulus was less than the E R P of the
accessory. Conduction therefore proceeds exclusively over the AV
node generating a narrow-complex Q R S . The A-H interval of these
normal beats is quite long and thus consistent with an AV nodal
slow pathway.
The remaining beats remain narrow most likely because the pacing
cycle length is shorter (faster rate) than the refractory period of
the accessory pathway. This could be ascertained by knowing the
E R P of the A P as determined during the rest of the study.
141
CHAPTER 3.10
AVRT
14 2
14 3
14 4
CHAPTER 3.10
AVRT
Discussion
During induction of S V T by atrial extra-stimulus pacing, as in this
example, antegrade delay is usually related to an A-H prolongation
because of the decremental properties of the AV node. In this
example, the bulk of the delay is related to an H-V prolongation.
Usually, H-V prolongation or block is not generally seen because
prolon ga t ion of A- H conduc t ion prevent s t he a t t a i n ment of
sufficiently shor t H-H inter vals to cause delay or block. In this
example, minimal delay in the A-H interval allowed the attainment
of a sufficiently short H-H interval to prolong the H-V interval. This
is rarely seen as the initiator of AV RT.
A follow-up question is : Will the obser ved R B B B affect the V-A
interval? The answer is No, because the right bundle system is not
involved in the tachycardia circuit. This is known as contralateral
bundle branch block.
The circuit includes the left lateral A P, the atrium between the
A P and the AV node, the AV node and His bundle, the left bundle
14 5
CHAPTER 3.11
AVRT
14 6
147
14 8
CHAPTER 3.11
AVRT
Discussion
The ventricular extra-stimulus results in a P VC that interrupts the
tachycardia. It arrives at a time when the His bundle has already
been depolarized (i.e., a His refractory P VC ). This P VC breaks
the tachycardia without getting to the atrium!
Breaking the tachycardia from the ventricle without conduction to
the atrium rules out AT regardless of how premature the P VC is.
A His refractor y P VC that advances the next A is proof of the
ex istence of a n A P . It does not prove that the A P is a n active
participant in the tachycardia circuit. However, a His refractory
P V C that breaks the tachyca rd ia w ithout getting to the A is
14 9
CHAPTER 3.12
AVRT
15 0
151
15 2
CHAPTER 3.12
AVRT
Discussion
The first 3 cycles demonstrate a L B B B patter n, which spontaneously nor ma lizes at the four th cycle. Compa re the V-A time
dur ing the L B B B cycles a nd the nor ma l Q R S cycles (2 yel l ow
ar rows). Note that the V-A time during L B B B is longer than the
V-A time during the normal Q R S cycles.
This indicates that the left bundle branch must be involved in
the circuit.
L BBB makes the circuit longer than with a normal Q R S (and hence
increasing V-A time). With L BBB , the circuit must return to the leftsided A P via the right bundle branch and transseptal conduction,
a much longer distance than if it were getting to the pathway via
the left bundle branch system. This is known as ipsilateral bundle
branch block.
We refer to the transition from a L BB B pattern to a normal Q R S as
spontaneous normalization.
Sponta neous nor ma lization of the Q R S most likely occurs by
mu ltiple mecha n isms, but may occu r because the lef t bu nd le
system (as well as the right) respond to increases in heart rate and
increasing sympathetic tone with shortening its E R P and enhanced
conduction velocity, allowing resumption of conduction through
the left bundle system.
15 3
CHAPTER 3.13
AVRT
15 4
15 5
15 6
CHAPTER 3.13
AVRT
Discussion
T he at r i a l S1 ( f ir st a r r o w) conduc t s t o t he vent r icle s w it h
maximum ventricular preexcitation over a left lateral A P (the V EGM
at the lateral LV, C S 1-2, is earliest and the Q R S morphology is wide
and compatible with exclusive accessor y pathway conduction).
The S2 produces an identical Q R S (third one) but now results in
an atrial echo preceded by a retrograde His def lection ( first
small arrow). The retrograde H is probably delayed and visible
because of retrograde L BBB related to prematurity, which requires
the impulse to return to the normal AV conduction via the distal
R B B B (a longer circuit).
15 7
CHAPTER 3.14
AVRT
15 8
15 9
16 0
CHAPTER 3.14
AVRT
Discussion
The first cycle is preceded by a His bundle electrogra m but is
and the right-axis deviation with R BBB pattern are consistent with
a left-sided A P ).
161
CHAPTER 3.15
AVRT
16 2
16 3
16 4
CHAPTER 3.15
AVRT
Discussion
T he t a chyca rd ia i n t h i s ca se st a r t s l i ke t hat i n t he prev iou s
to R B B to AV node to atrium).
by, and explained by, shortening of the V-A inter val (horizontal
16 5
CHAPTER 3.16
AVRT
16 6
16 7
16 8
CHAPTER 3.16
AVRT
Discussion
The tracing begins with ongoing orthodromic AV RT with L B B B
aberrancy over a left-sided A P. Atrial activation is eccentric and
earliest at C S 1-2. The surface E C G demonstrates a L B B B pattern
with normalization of the Q R S complex on the final beat coincident
with termination of tachycardia. This suggests that maintenance
of L B B B (ipsilateral B B B ) is important to the tachycardia circuit.
In the presence of L B B B , the wave front of activation during this
tachycardia travels antegradely down the AV node, down the right
bundle, through the septum to the LV and retrogradely up the A P
to the atrium.
W h e n L B B B r e c o v e r s (r e fe r t o C h a p t e r 1, S e c t i o n 5 ) , t h e
tachycardia circuit becomes smaller. The ventricular component is
now from the distal left bundle to the left A P. The resulting abrupt
shortening of the time of arrival of activation to the A P encroaches
on the refractory period of the A P, which now fails to conduct to
the atrium and tachycardia terminates.
[See movie in digital edition.]
16 9
Notes
Cardiac Electrophysiology 2
CHAPTER 4
OUTLI N E
4.1
4.2
4.3
Differential Pacing
Proof of?
Re-do
176
AF
172
180
17 1
CHAPTER 4.1
AF
17 2
17 3
174
CHAPTER 4.1
AF
Discussion
In this example, the magenta ar row points to the electrograms
in question (LA vs. P V ) on the Lasso catheter. The yellow arrow
points to far-field ventricular potentials.
Beats 1 a nd 2 a re recorded dur ing C S pacing. Beats 3 to 5 a re
recorded during pacing from the ablation catheter placed in the
left atrial appendage ( L A A ). Notice that during L A A pacing, the
electrograms identified with the magenta arrow, have been pulled
in toward the pacing stimulus. This demonstrates that the source
of these electrograms is far-field from the pacing site and not
the pulmonary veins. If the electrograms had been near-field P V
potentials, upon switching to L A A pacing, they would have stayed
late or would not have been pulled in.
This principle can test the source of electrograms recorded from
any of the pulmonary veins.
175
CHAPTER 4.2
AF
17 6
17 7
17 8
CHAPTER 4.2
AF
Discussion
Note that these activations do not per tu rb the ongoi ng si nus
rhy th m. In essence, they a re independent of the sur face E C G
P waves, independent of the ablation catheter electrograms and
17 9
CHAPTER 4.3
AF
4.3 Re-do
During the healing phase following P V isolation, some of the P V
encircling lesions can recover resulting in gaps in the ablation
circle and thus electrical reconnection of the pulmonary veins.
Commonly, this occurs at 1 to 3 sites per vein or pair of veins.
A repeat procedure attempts to map and ablate the gaps in the
previous circle rather than redoing the entire circle.
18 0
181
18 2
CHAPTER 4.3
AF
Discussion
In this tracing, the circular mapping catheter (blue signals) shows
near-field electrograms in A 9 -10 to A 1 9 - 2 0 strongly suggesting
reconnection of the P V . Activation of the near-field signals shows
earliest activity at A 9 -10 (green arrow) suggesting these poles are
nearest the gap. Also notice that the local electrogram at A 9 -10 is
long and fractionated indicative of a zone of slow conduction (see
expanded view).
T he ablation cat heter, nea r electrode A 9 - 1 0 , shows a si m i la r
electrogram with fractionated continuous activity from the early
L A signal (proximal ablation, yellow line) to the near-field P V
potential (A 9 -10 , magenta line).
Ablation at this site quickly re-isolated the P V .
18 3
Notes
Cardiac Electrophysiology 2
CHAPTER 5
TH E U N E X P E C TE D
OUTLI N E
5.1
5.2
5.3
5.4
5.5
5.6
5.7
Tachycardias
Tachycardias 2
Tachycardias 3
VT
198
Substrate for?
186
190
194
202
12-lead Diagnosis
Break
214
206
18 5
CHAPTER 5.1
THE UNEXPECTED
5.1 Tachycardias
To terminate a tachycardia, we often overdrive pace the
tachycardia from the ventricle, as in this example. Occasionally,
unexpected and somewhat surprising results occur.
18 6
18 7
18 8
CHAPTER 5.1
THE UNEXPECTED
Discussion
The first 3 beats in this tracing demonstrate AV R T using a left
lateral A P. Note the eccentric atrial activation pattern with earliest
A i n t he d ist a l C S 3 - 4. A shor t 5 -beat ventr icu la r bu r st wa s
delivered in an attempt to terminate the tachycardia. However,
sinus rhythm was not restored!
Following the ventricular burst, the tachycardia continues, but
it ha s a shor ter cycle leng t h a nd a d i f ferent at r ia l act ivat ion
sequence. The atrial activation sequence is central (earliest A in
the proximal coronary sinus (C S )) with a constant V-A time of zero.
These findings are compatible with AV NRT !
Dual AV nodal physiology is relatively common and can coexist
in patients w ith AV R T . In fact, some patients w ith AV R T have
tachyca rdia only when the AV noda l slow pathway is used for
initiation and maintenance of the AV R T . Once the A P has been
ablated, it would not be unexpected to initiate AV NRT.
Note: On the surface E C G , with the initiation of AV NRT, a R B B B
pat ter n developed a nd wa s ma i nta i ned. Ex pla i n t he possible
mechanisms responsible for the bundle branch block, how it may
be maintained and what maneuver may be able to normalize the
bundle branch block. These questions were answered earlier in
this book.
18 9
CHAPTER 5.2
THE UNEXPECTED
5.2 Tachycardias 2
During the course of an E P study, routine
maneuvers occasionally lead to unexpected results.
What has this single P VC done?
19 0
Figure 1
191
Figure 2
19 2
CHAPTER 5.2
THE UNEXPECTED
Discussion
At the beginning of this tracing, the tachycardia has an eccentric
atrial activation pattern consistent with orthodromic AV RT using
a left lateral A P. Following the stimulated P VC , the tachycardia
converts to an AV NRT with a central atrial activation!
Try to explain the mechanism of how this transition occurred.
Figure 2 gives you a hint. During AV RT, the tachycardia circuit
19 3
CHAPTER 5.3
THE UNEXPECTED
5.3 Tachycardias 3
This is another example of unexpected findings during
routine E P maneuvers! Review both tracings to
discover the unusual finding!
19 4
Figure 1
19 5
Figure 2
19 6
CHAPTER 5.3
THE UNEXPECTED
Discussion
F i g u r e 1 d e mo n s t r a t e s or t ho d r om ic AV R T . B y d e f i n it io n ,
is a left lateral A P.
The first S1 seen in this tracing fails to capture the atrium and is
His channel).
19 7
CHAPTER 5.4
THE UNEXPECTED
5.4 VT
This tracing demonstrates ventricular tachycardia ( V T )
initiation using ventricular extra-stimulus pacing. This is an
example of a very specific type of V T . What is it?
19 8
19 9
200
CHAPTER 5.4
THE UNEXPECTED
Discussion
There is a differential diagnosis for a wide-complex tachycardia
induced with ventricular extra-stimulus pacing including: 1) V T ; 2)
S V T with aberrancy or; 3) a tachycardia using an A P (preexcited
tachycardia).
While the exact diagnosis cannot be confirmed on this tracing
alone, the diagnosis was V T and, more specifically, bundle branch
reentry V T . Notice that there is a His catheter in place and that the
His electrograms (white arrows) have a 1:1 relationship with the
ventricular electrograms.
The ty pical features of bundle branch reentr y V T include: 1) a
typical L B B B morphology on the surface E C G ; 2) a His E G M in
a 1:1 relationship with the ventricle and; 3) a relatively long H-V
interval.
The mechanism of bundle branch reentry V T is a macro-reentrant
circuit using the His-Purkinje system.
Most commonly, the circuit involves antegrade conduction down
the r ight bu nd le (therefore a L B B B mor pholog y), tra nssepta l
myocardial conduction, followed by retrograde conduction using
the left bundle branch. The upper common pathway of this circuit
is the His bundle. Therefore, a retrograde His, in a 1:1 relationship
with the V T , is the critical diagnostic finding confirming bundle
branch reentry.
2 01
CHAPTER 5.5
THE UNEXPECTED
202
203
204
CHAPTER 5.5
THE UNEXPECTED
Discussion
This tracing demonstrates ventr icula r extra- stimulus pacing.
Notice that the 2 S1s conduct to the atria with an eccentric atrial
activation patter n using a left-lateral A P . One would correctly
assume that this patient has the substrate for orthodromic AV RT.
However, notice the response to the ventricular S2. It appears
to block and is followed by an atrial depolarization with a His
A first.
The differential diagnosis for this observation include:
1. The S 2 truly fails to conduct retrogradely to the atrium
(thus we have reached the E R P of the A P and the AV node)
and is followed by a PAC , which conducts to the ventricle.
2. The S 2 conducts to the atrium via a retrograde slow AV
nodal pathway (long yellow arrow). This is followed by
conduction antegradely via a fast pathway to the ventricle
(short yellow arrow).
The S1S 2 maneuver was repeated several times with a reproducible
result. This speaks well for scenario #2 rather than scenario #1.
T he pre sence of a n at y pica l AV noda l echo beat (ret rog ra de
conduction via the slow pathway and antegrade conduction via
the fast pathway) is an indication that the patient also has the
substrate for atypical AV NRT. In fact, this patient demonstrated
both AV RT and atypical AV NRT !
205
CHAPTER 5.6
THE UNEXPECTED
206
Figure 1
207
Figure 2
208
CHAPTER 5.6
THE UNEXPECTED
Discussion
Figure 1 shows sinus rhy thm a nd then the onset of a na r row-
continues
209
Figure 3
210
CHAPTER 5.6
THE UNEXPECTED
211
Figure 4
2 12
CHAPTER 5.6
THE UNEXPECTED
Figure 4 gives you yet another hint. The circled P VC precedes the
213
CHAPTER 5.7
THE UNEXPECTED
5.7 Break
This tracing demonstrates another example of concealed
conduction. Explain the termination of the tachycardia.
2 14
215
216
CHAPTER 5.7
THE UNEXPECTED
Discussion
The tracing begins with a 1:1 narrow-complex tachycardia with
conduction.
217
Notes
Cardiac Electrophysiology 2
CHAPTER 6
OUTLI N E
CAS E S TU D I E S
6.1
6.2
6.3
Case 1
220
Case 3
248
Case 2
240
219
CHAPTER 6.1
CASE STUDIES
6.1 Case 1
Here is a series of tracings presented in the order
that they were performed. Read through each tracing and
establish the diagnosis.
220
Figure 1
2 21
Figure 2
222
CHAPTER 6.1
CASE STUDIES
Discussion
Figure 1: During incremental V pacing, the His A delays,
223
Figure 3
224
CHAPTER 6.1
CASE STUDIES
activation sequence.
225
Figure 4
226
CHAPTER 6.1
CASE STUDIES
227
Figure 5
228
CHAPTER 6.1
CASE STUDIES
Fig u r e 5 : Descr ibe what you see compa red to t he prev iou s
229
Figure 6
230
CHAPTER 6.1
CASE STUDIES
left-lateral A P.
2 31
Figure 7
232
CHAPTER 6.1
CASE STUDIES
AVRT from the RVA catheter should indicate that the RVA catheter
233
Figure 8
234
CHAPTER 6.1
CASE STUDIES
235
Figure 9
236
CHAPTER 6.1
CASE STUDIES
237
Figure 10
238
CHAPTER 6.1
CASE STUDIES
239
CHAPTER 6.2
CASE STUDIES
6.2 Case 2
Here is a series of tracings presented in the order
that they were performed. Read through each tracing and
establish the diagnosis.
240
Figure 1
2 41
Figure 2
242
CHAPTER 6.2
CASE STUDIES
Discussion
Figure 1: Note that the His V is earlier than the R VA V. Pacing
This occurs when the pacing site has poor access to the A P.
These f irst 2 tracings demonstrate that pacing different sites
produce different amount of preexcitation depending on the pacing
sites access to the A P.
243
Figure 3
244
CHAPTER 6.2
CASE STUDIES
245
Figure 4
246
CHAPTER 6.2
CASE STUDIES
2 47
CHAPTER 6.3
CASE STUDIES
6.3 Case 3
Here is a series of tracings presented in the order that they
were performed. Read through each tracing and establish
the diagnosis.
This is a case of an E C G suggesting one possible diagnosis and
the diagnostic E P study demonstrating another.
248
Figure 1
249
Figure 2
250
CHAPTER 6.3
CASE STUDIES
Discussion
Figure 1: The 12-lead E C G suggests the possibility of a
posteroseptal A P.
Figure 2 : While catheters are being inserted, we observed this
2 51
Figure 3
252
CHAPTER 6.3
CASE STUDIES
253
Figure 4
254
CHAPTER 6.3
CASE STUDIES
255
Figure 5
256
CHAPTER 6.3
CASE STUDIES
257
Figure 6
258
CHAPTER 6.3
CASE STUDIES
Conduction to the atria was via the left lateral A P. The narrow
Q R S is due to conduction down the AV node, followed by an
echo up the A P.
259
Figure 7
260
CHAPTER 6.3
CASE STUDIES
2 61
Figure 8
262
CHAPTER 6.3
CASE STUDIES
263
Figure 9
264
CHAPTER 6.3
CASE STUDIES
265
Figure 10
266
CHAPTER 6.3
CASE STUDIES
while V pacing.
267
Figure 11
268
CHAPTER 6.3
CASE STUDIES
269
Figure 12
270
CHAPTER 6.3
CASE STUDIES
271
Notes