Cardiac Electrophysiology in Clinical Practice, 2nd Edition

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To my parents, Ko-En and
Linda, for teaching me that
“with diligence, nothing in the
world is too difficult,” with
much love and appreciation.
—David T. Huang
To Tyanna, Sophie, Lily, Jack,
and Ethan, whose love makes
every day better.
—Travis Prinzi
Book Introduction

In our first edition, we set out to produce an accessible EP book,

informed by the experience of attending physicians, the learning
process of EP fellows, and the day-to-day practical needs of EP
nurses and technologists. In order to accomplish this, the book
was edited by the Chief Electrophysiologist at the University of
Rochester Medical Center (David Huang, MD) and the Lead EP
Technologist (Travis Prinzi, MA, MS, CEPS) at the same institu-
tion. Contributions were made both by attending physicians and
EP Fellows working in the lab and clinic at that time.
In this new, revised edition, we’ve continued in that same
model, but we have broadened our approach to include the clinical
perspective of one of our Nurse Practitioners, Sonja Kreckel, MS,
RN, NP-C, CCDS. Most significantly, this contribution will be
seen in the added discussion on various means of ambulatory car-
diac monitoring, an aspect of EP that has grown tremendously
since the first edition.
While the foundational basics of EP remain the same, the tech-
nology to assess and treat cardiac arrhythmias has moved along at
a rapid pace, resulting in new understandings of arrhythmia cir-
cuits and how to treat them. As of the writing of this book, the EP
world is on the cusp of a potentially field-changing development
of a new treatment modality in pulsed field ablation. By the time
you are reading this book, we will likely already know far more
about it than we do at its writing. Herein lies the challenge of
producing an EP textbook. The field is advancing quickly. We
have provided here a book that focuses on the fundamentals that

vii
viii Book Introduction

will serve as an important learning tool for us all as students of

cardiac electrophysiology in labs and classrooms. We have also
pointed to advancing technology and promising developments on
the horizon wherever possible.
We also like to pay tribute to all the teachers, both personal and
virtual, who have pioneered and advanced the care of patients
with cardiac dysrhythmia to where it is today. Specifically, we
would mention and remember Drs Mark E Josephson, Hein
Wellens, and Arthur Moss for their boundless contributions.
Herein we also impart our own advice to all readers to never stop
learning while remembering the fundamentals in electrophysiol-
ogy. We are all fortunate to be involved in a medical field that has
continued to advance rapidly.
Contents

1 
Cardiac Conduction and Bradycardia������������������������  1
Mehmet K. Aktas
2 
Ambulatory Cardiac Rhythm Monitoring������������������ 15
James Gallagher and Sonja Kreckel
3 
Syncope, Tilt Table Testing, and Cardioversion���������� 31
Sarah Taylor
4 Implantable Cardiac Devices���������������������������������������� 47
Parag Patel, Erin Armenia, and Pina Spampanato
5 Diagnosis and Treatment of Supraventricular
Tachycardias������������������������������������������������������������������ 81
Spencer Rosero and Travis Prinzi
6 Wolff-Parkinson-White (WPW) Syndrome����������������103
Jeffrey M. Vinocur
7 Atrial Flutter, Typical and Atypical ����������������������������129
David T. Huang and Travis Prinzi
8  Practical Guide to Catheter Ablation of Atrial
A
Fibrillation����������������������������������������������������������������������147
Joshua Haswell, Travis Prinzi, and Burr Hall

ix
x Contents

9 V
 entricular Tachyarrhythmias��������������������������������������179
Amole Ojo, Sinan Tankut, Travis Prinzi,
and David T. Huang
10 H
 ereditary Arrhythmias������������������������������������������������219
Ido Goldenberg, Alon Barsheshet,
and David T. Huang

Index����������������������������������������������������������������������������������������255
Cardiac Conduction
and Bradycardia 1
Mehmet K. Aktas

Abstract

Bradycardia may be physiological or pathological depending

on the underlying mechanism. An understanding of cardiac
impulse formation and propagation can help provide insight in
differentiating between bradycardia that is benign and those
that are pathologic and may require implant of a permanent
pacemaker. Patients with bradycardia may present with a wide
range of symptoms including shortness of breath, activity
intolerance, fatigue, dizziness, presyncope and/or syncope. In
some patients, an electrocardiogram (ECG) and external ambu-
latory heart rhythm monitors are sufficient to document patho-
logical bradycardia. In other instances, patients may require an
insertable cardiac monitor, which can provide long-term heart
rhythm monitoring. Less often, a patient may require an elec-
trophysiology (EP) study to assess for conduction disease. In
this chapter we review common clinical presentations of bra-
dycardia and discuss the diagnostic work up of such patients.

M. K. Aktas (*)
University of Rochester Medical Center, Rochester, NY, USA
e-mail: [email protected]

© The Author(s), under exclusive license to Springer Nature 1

Switzerland AG 2023
D. T. Huang et al. (eds.), Cardiac Electrophysiology in Clinical
Practice, In Clinical Practice,
https://doi.org/10.1007/978-3-031-41479-4_1
2 M. K. Aktas

Keywords

Cardiac conduction · Bradycardia · Sinus node · AV node · His

bundle · Heart block · Cardiac anatomy · E
­ lectrocardiogram

 inus Node, Atrioventricular Node, His-Purkinje

S
System

The normal cardiac impulse originates from the sinus node

which is a small spindle-shaped structure located anteriorly in
the subepicardial region near the junction of the superior vena
cava and the right atrium [1]. Normal sinus rhythm (NSR) on an
ECG represents normal activation of the heart initiating from the
sinus node and activating the rest of the atria and ventricles.
Figure 1.1 shows a 3-dimensional electroanatomic map of the
right atrium during normal sinus rhythm. The impulse initiated
by the sinus node travels through the right atrium and propa-
gates toward the left atrium and simultaneously inferiorly to the
atrioventricular (AV) node. The sinus node is innervated by both
sympathetic and parasympathetic fibers that modulate the heart
rate accordingly [2].
The AV node is located at the apex of the triangle of Koch,
which is represented by the septal tricuspid valve annulus anteri-
orly, the coronary sinus ostium posteriorly, and the tendon of
Todaro superiorly [3]. Acting as a gateway, the AV node exhibits
decremental properties, whereby rapid stimulation of the AV node
results in progressive slowing of conduction, which helps protect
the ventricles from tachyarrhythmias starting from the atria which
could otherwise result in rapid ventricular rates [4]. From here
propagation continues inferiorly and anteriorly to the bundle of
His also known as the bundle of Tawara [5]. Once the depolariz-
ing wavefront exits the His bundle, the signal divides into the right
(activation the right ventricle) and left (activating the left ventri-
cle) bundle branches of the conduction system. The left bundle
further subdivides into the left anterior and left posterior fascicles.
Finally, the impulse disseminates throughout the ventricular myo-
cardium via Purkinje fibers.
1 Cardiac Conduction and Bradycardia 3

Fig. 1.1 Three-dimensional electroanatomic map of the right atrium during

normal sinus rhythm using Carto (Biosense-Webster). Sinus rhythm impulse
originates in the high right atrium and propagates throughout the right atrium.
Red represents earliest activation which corresponds to the location of the
sinus node. Yellow, green, teal, and blue represent respective later activation
timing relative to the sinus node impulse. SVC = superior vena cava;
IVC = inferior vena cava

Patients may present in NSR with some clues to the presence

of conduction disease on the surface ECG which may include
either a prolonged PR interval, left anterior fascicular block
(LAFB), left posterior fascicular block (LPFB), right bundle
branch block (RBBB) or left bundle branch block (LBBB). Some
patients may have more than one type of block such as first-degree
AV block (defined as a PR > 0.2 s), fascicular block (either left
anterior or left posterior), and RBBB; although the term trifas-
cicular block is used to describe this condition, it is incorrect,
since the first-degree AV block does occur in a true fascicle but
rather represents slow conduction within the atria or AV node.
4 M. K. Aktas

In patients with LBBB (both left anterior and posterior fasci-

cles are blocked) the conduction to the ventricle occurs through
the right bundle branches. Usually the remaining bundle’s con-
duction velocity is adequate to prevent symptoms. However, one
should be more suspicious of a bradyarrhythmia as an etiology of
symptoms if multiple levels of conduction block are observed on
the ECG. Of particular concern is an ECG pattern of alternating
RBBB and LBBB, as this is clear evidence of infra-nodal conduc-
tion disease. These patients should undergo pacemaker placement
without the need for invasive electrophysiology testing as they are
at high risk for the development of complete heart block [6].
Each region of cardiac tissue has automaticity, meaning it is
capable of spontaneously generating an impulse [7]. However,
automaticity within the sinus node establishes a hierarchy of
pacemaker function whereby the spontaneous discharge rate of
the sinus node exceeds the spontaneous discharge rate of other
automatic sites, rendering these sites depressed and latent. When
there is failure of impulse generation within the atria, AV nodal
automaticity is no longer suppressed, and a junctional rhythm,
usually narrow complex, with a rate of 30–40 bpm is observed. If
automaticity within the AV junction fails, latent Purkinje fibers
may initiate spontaneous depolarizations with slow ventricular
rates ranging from 20–30 bpm, with a wide QRS complex.

Sinus Node Dysfunction

Sinus node dysfunction (previously referred to as sick sinus syn-

drome) is an umbrella term that refers to abnormalities in impulse
formation and propagation and includes conditions such as sinus
bradycardia, sinus pause/arrest, chronotropic incompetence, sinus
exit block, and tachy-brady syndrome where rapid periods of
atrial fibrillation terminate often into symptomatic episodes of
sinus bradycardia or sinus pauses [8]. Sinus node dysfunction is
usually a disease of the elderly and its initial presentation may
include syncope due to inadequate impulse formation and propa-
gation, resulting in cerebral hypoperfusion and collapse. Sinus
node dysfunction is the most common diagnosis in patients
requiring permanent pacemaker implant [9].
1 Cardiac Conduction and Bradycardia 5

The action potentials of both the sinus and AV node are depen-
dent on sodium “funny” currents [10]. These channels are recog-
nized as funny because they open as the cell repolarizes rather
than reaching a more positive threshold to evoke an action
­potential. The sinus node traditionally depolarizes and repolarizes
most rapidly and therefore is responsible for setting the heart rate
in the normal heart. Sympathetic (adrenaline) and parasympa-
thetic (vagal) signals from the autonomic nervous system have
strong influences on heart rate due to their primary inputs to the
sinus and AV node. Historically, a “normal” heart rate ranges from
60–100 beats per minute (bpm); however, it is not uncommon for
those with high vagal tone (well-conditioned athletes, or during
sleep) to have rates as low as 40 bpm [11]. Electrocardiograms
may show sinus bradycardia or a junctional escape rhythm (an
impulse originating from the AV node). Bradycardia in and of
itself is not problematic unless it is associated with symptoms
such as dizziness, fatigue, shortness of breath, chest pain, or syn-
cope. Placing these patients on a treadmill may reveal chrono-
tropic incompetence, which refers to the inability of the sinus
node to increase the heart rate appropriately with activity. It is
important to make the distinction between physiologic bradycar-
dia and symptomatic pathologic bradycardia to avoid unnecessary
testing or treatments which may only cause harm and or provide
little to no benefit. Furthermore, the etiology of the arrhythmia
must strongly be considered. Electrolyte imbalances, ischemia,
infection, hypoxia, vagal tone, hypothermia, hypothyroidism,
post-surgical state, as well as other causes may be transient, and
treating the underlying cause may very well resolve the cardiac
conduction disturbance. Temporary pacemakers may be consid-
ered in specific emergent situations as deemed necessary.

Atrioventricular Conduction Block

AV block can be classified as first, second, or third degree (also

known as complete heart block). Although a distinct conduction
fiber or fascicle between the sinus nodeand this His-bundle does
not exist, first degree AV block refers to a PR interval exceeding
6 M. K. Aktas

0.2 s. A long PR interval in the setting of a normal QRS duration

usually represents conduction delay within the AV node. If the
QRS duration is prolonged, the most common site of conduction
delay is still in the AV node; however, the possibility of i­ nfra-­Hisian
conduction disease needs to be considered, especially in the pres-
ence of left bundle branch block. It is important to recognize that
a normal PR interval does not itself rule out the possibility of
more advanced conduction disease. In general, first-degree AV
block is clinically well-tolerated and is not associated with an
increase in overall mortality. However, in rare cases a PR interval
exceeding 0.3 s can produce pacemaker syndrome-like symp-
toms, where atrial activation begins as ventricular systole contin-
ues, and atrial contraction occurs across closed atrio-ventricular
valves.
Second degree AV block is subdivided into Mobitz Type 1 and
Mobitz Type 2 block. Electrocardiographically, Mobitz type 1
exhibits the Wenckebach phenomenon where progressive prolon-
gation in the PR interval is seen leading up to a non-conducted P
wave. Following the non-conducted beat, conduction with a nor-
mal PR interval is usually seen. The block cycle recurs repeti-
tively with a fixed P to QRS ratio. Typically there is evidence of
grouped beating and periodicity in the conduction pattern
observed on the ECG. For example, when 3 P waves results in 2
QRS complexes this is referred to as a 3:2 Wenckebach conduc-
tion pattern. This type of block is considered physiological and
not pathologic and conduction block typically occurs within the
AV node. Mobitz Type 1 block is common in healthy individuals
and in states of high vagal innervation such as during sleep.
Second degree Mobitz 1 heart block does not require treatment
with a pacemaker.
On the other hand, Mobitz Type 2 block demonstrates a fixed
PR interval with a non-conducted P wave. On the ECG, the non-­
conducted P waves are not preceded by prolongation in the PR
interval and there is no shortening of the PR interval subsequent
to the blocked P wave. In Mobitz Type 2 the block occurs inferior
to the His bundle. Second degree Mobitz Type 2 heart block is a
pathologic finding and requires further investigation since such
patients are at risk for progression to complete heart block. In
1 Cardiac Conduction and Bradycardia 7

patients with 2:1 AV nodal conduction as shown in Fig. 1.2,

maneuvers like carotid sinus massage, which increases vagal
tone, can be useful for differentiating between Mobitz Type 1 and
Type 2 block [12]. In Mobitz Type 1 block, higher vagal input to
the AV node will increase the amount of blocked p waves.
However, in Mobitz Type 2 block, higher vagal input slows the
sinus rate which provides the diseased infra-Hisian tissue time to
recover allowing for a 1:1 AV nodal conduction (Fig. 1.3).

Fig. 1.2 12 lead electrocardiogram demonstrating 2:1 AV block. There are 2

p waves for every QRS complex as seen on the lead II rhythm strip. It is not
possible to tell where the level of block is without provocative maneuvers
such as having the patient ambulate, vagal maneuvers or administering medi-
cations which can inhibit or enhance AV node conduction

Fig. 1.3 2:1 AV block is present throughout the top telemetry strip. During
carotid sinus massage the increased vagal tone results in slowing of the sinus
node allowing for 1:1 AV nodal conduction. This is indicative of infranodal
disease and best treated with a permanent pacemaker
8 M. K. Aktas

Fig. 1.4 12 lead electrocardiogram demonstrating complete heart block.

There are p waves that march through, seen on the rhythm strip lead II with a
slow escape rhythm. The site of the escape rhythm appears to change as seen
on the rhythm strip

Complete heart block (CHB) is present when atrial activation

does not conduct to the ventricles as seen in Fig. 1.4. Complete
heart block may occur as a result of pathology within the AV node
or in infra-nodal conducting fibers. In patients with CHB often an
escape rhythm is present, either a narrow complex junctional
rhythm or a wide complex ventricular rhythm. Isorhythmic AV
dissociation may make the diagnosis of CHB more difficult as
both the atria and ventricles are conducting at the same rate.
However, with prolonged heart rhythm monitoring or with exer-
cise testing the presence of atrial and ventricular dissociation can
often be detected. Patients with complete heart block may present
with shortness of breath, activity intolerance, weakness, dizzi-
ness, presyncope, and syncope. Patients with CHB are also at risk
for ventricular tachycardia and ventricular fibrillation and there-
fore require prompt attention and treatment [13].

Electrophysiologic Testing

In some situations, it may be difficult to determine if a patient’s

symptoms are related to a bradyarrhythmia through non-invasive
testing, and an EP study may be required. An EP study allows for
1 Cardiac Conduction and Bradycardia 9

an objective measurement of the cardiac conduction system.

Catheters are placed into the heart to evaluate for dysfunction of
either impulse formation or propagation. Following percutaneous
venous access, catheters are typically advanced to the right atrium,
the coronary sinus, the bundle of His, and into the right ventricle.
These catheters have the ability to both sense electrical potentials
and pace. Spanning the catheters into each of the locations facili-
tates accurate diagnosis and location of potential conduction dis-
ease. Baseline measurements which are noted on the surface ECG
are recorded, including the PR interval, QRS duration, and QT
interval. The intracardiac catheters provide electrograms that cor-
respond to the ECG recordings. The PR interval is represented by
the activation from the atria (A) to the His bundle (H) and the
ventricular (V) signal. Of particular importance is the assessment
of the HV interval. An HV measurement greater than 100 msec is
highly abnormal and may warrant pacemaker placement.
Pacing maneuvers during an EP study also provides an objec-
tive measurement of the sinus and AV node (both antegrade and
retrograde) function. Sinus node recovery time (SNRT) is mea-
sured by pacing the atrium for 30 s at a rate faster than the intrin-
sic sinus rate to suppress sinus node automaticity [14]. The
recovery time is measured from the last pacing stimulus to the
onset of sinus node activity as recorded on the intra-cardiac
electrogram. A SNRT that is less than 1500 milliseconds (msec)
is considered normal or less than 550 msec for the corrected
SNRT (SNRT minus the sinus cycle length in msec). Patients
may also demonstrate sinus node exit block where an electrical
impulse is unable to penetrate through the perinodal tissue due
to prolonged refractory periods. This may occur either as a
Mobitz 1 or 2 block. One may see a sinus rate at 600 ms and then
the absence of a p wave at half the interval between the two con-
ducted p waves. The remainder of the sinus rhythm will be con-
sistent at 600 ms.
One can then assess the functional properties of the AV node
via pacing stimuli including the cycle length at which Wenckebach
occurs or when atrial activation blocks in the AV node and does
not conduct into the His bundle. If the block occurs after His acti-
vation, then Mobitz Type 2 block is present, which is an important
distinction from Wenckebach (Fig. 1.5). During atrial extra-­
10 M. K. Aktas

Fig. 1.5 The first sinus beat (labeled A on the His-bundle intracardiac elec-
trograms) conducts through the AV node with subsequent activation of the
His bundle (labeled H on the His-bundle electrogram) followed by ventricular
activation (labeled V on the His-bundle electrogram). The second sinus beat
conducts through the AV node to the His bundle and blocks below the His as
denoted by * on the His-bundle recording. The third sinus beat conducts sim-
ilar to the first beat (A-H-V seen on His-bundle recordings) since the infra-­
Hisian level of block had time to recover from the prior blocked beat. The last
beat is a premature atrial contraction and blocks in the AV node as there is no
His activation observed on the His-bundle recording. The second beat is con-
sidered pathological and warrants placement of a pacemaker. P = Atrial acti-
vation on the surface electrocardiogram. A = atrial activation on the
intracardiac electrogram. H=His bundle activation on the intracardiac electro-
gram. V = ventricular activation on the intracardiac electrogram

stimuli testing, Wenckebach will show AH interval ­prolongation

on the His catheter as the progressively earlier atrial premature
beats are delivered. A thorough EPS will help rule out all potential
arrhythmogenic etiologies for a patient’s clinical presentation.
Ventricular pacing can assess the presence of VA or retrograde
conduction. Activation should be concentric in the coronary sinus
catheter, activating proximally to distally. An eccentric activation
sequence can suggest an accessory pathway that may only con-
duct retrogradely. Understanding the normal functioning proper-
ties of the AV node is essential to help exclude the potential for
either brady- or tachyarrhythmias.