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ARRHYTHMIAS IN
CHILDREN:
Diagnosis And
Treatment
Jassin M. Jouria, MD
Dr. Jassin M. Jouria is a medical doctor,
professor of academic medicine, and
medical author. He graduated from Ross
University School of Medicine and has completed his clinical clerkship training in
various teaching hospitals throughout New York, including King’s County Hospital
Center and Brookdale Medical Center, among others. Dr. Jouria has passed all
USMLE medical board exams, and has served as a test prep tutor and instructor for
Kaplan. He has developed several medical courses and curricula for a variety of
educational institutions. Dr. Jouria has also served on multiple levels in the academic
field including faculty member and Department Chair. Dr. Jouria continues to serves
as a Subject Matter Expert for several continuing education organizations covering
multiple basic medical sciences. He has also developed several continuing medical
education courses covering various topics in clinical medicine. Recently, Dr. Jouria
has been contracted by the University of Miami/Jackson Memorial Hospital’s
Department of Surgery to develop an e-module training series for trauma patient
management. Dr. Jouria is currently authoring an academic textbook on Human
Anatomy & Physiology.
ABSTRACT
The prevalence and spectrum of arrhythmias change with age. As a
consequence, treating arrhythmias in children has its unique
challenges. The child’s age, as well as the age of onset of arrhythmia,
history of heart symptoms or failure, and electrocardiography testing
must all be considered when making a diagnosis. Although not a
common occurrence in children, life-threatening arrhythmias need to
be identified and appropriately treated to prevent serious outcomes.
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Continuing Nursing Education Course Planners
William A. Cook, PhD, Director, Douglas Lawrence, MA, Webmaster,
Susan DePasquale, MSN, FPMHNP-BC, Lead Nurse Planner
Policy Statement
This activity has been planned and implemented in accordance with
the policies of NurseCe4Less.com and the continuing nursing education
requirements of the American Nurses Credentialing Center's
Commission on Accreditation for registered nurses. It is the policy of
NurseCe4Less.com to ensure objectivity, transparency, and best
practice in clinical education for all continuing nursing education (CNE)
activities.
Continuing Education Credit Designation
This educational activity is credited for 4.5 hours. Nurses may only
claim credit commensurate with the credit awarded for completion of
this course activity.
Pharmacology content is 1 hour.
Statement of Learning Need
There are unique challenges associated with arrhythmias in children
and the treatment options for childhood arrhythmia. This information
is needed to guide the healthcare professional who is treating
children with arrhythmia.
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Course Purpose
To provide nurses with knowledge of pediatric arrhythmias, including
its recognition and treatment options.
Target Audience
Advanced Practice Registered Nurses and Registered Nurses
(Interdisciplinary Health Team Members, including Vocational Nurses
and Medical Assistants may obtain a Certificate of Completion)
Course Author & Planning Team Conflict of Interest Disclosures
Jassin M. Jouria, MD, William S. Cook, PhD, Douglas Lawrence, MA,
Susan DePasquale, MSN, FPMHNP-BC – all have no disclosures
Acknowledgement of Commercial Support
There is no commercial support for this course.
Activity Review Information
Reviewed by Susan DePasquale, MSN, FPMHNP-BC
Release Date: 8/10/2016
Termination Date: 8/10/2019
Please take time to complete a self-assessment of knowledge, on
page 4, sample questions before reading the article.
Opportunity to complete a self-assessment of knowledge learned will
be provided at the end of the course.
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1.
Any electrical activity not initiated by the SA node is
considered
a.
b.
c.
d.
a depolarization event.
an atrioventricular (AV) impulse.
an arrhythmia.
a repolarization event.
2. Electrical stimulation of a myocardial cell results in
a.
b.
c.
d.
a slow outward leak of sodium.
depolarization.
a slow outward leak of potassium.
All of the above
3. True or False: Some arrhythmias are so common as to be
considered as almost normal variants.
a. True
b. False
4. The conduction system in the ventricles is more elaborate
than that in the atria because
a.
b.
c.
d.
the muscle mass is larger.
of the location of the bundle of His.
the superior vena cava enters through the ventricles.
of fiber stretch.
5. Normally, the _________________, located where the
superior vena cava meets the right atrium, has the most
rapid intrinsic rate (60 to 100 bpm).
a.
b.
c.
d.
atria via
atrioventricular (AV) node
coronary sinus
sinoatrial (SA) node
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Introduction
An arrhythmia is an abnormality of cardiac rhythm. The prevalence
and spectrum of arrhythmias change with age. As a consequence,
treating arrhythmias in children has its unique challenges. While
abnormal heart rates in children are often not a cause of concern,
children with an abnormal heart rhythm, including consideration of
the child’s age, age of onset of arrhythmia, history (palpitations,
heart failure, syncope, etc.), and the electrocardiogram (ECG)
findings must all be factored into a health professional’s diagnosis. It
is absolutely vital that a clinician be able to recognize when an
arrhythmia has the potential to become serious or life threatening,
and to identify appropriate treatment options. This course will provide
an understanding of the mechanics of arrhythmias, and it will discuss
the unique challenges associated with arrhythmias in children and the
treatment options. This information will help healthcare professionals
to communicate with their young patient and the patient’s parents or
guardians to determine the right course of action.
Cardiac Electrophysiology
The majority of myocardial cells share the same basic cellular
electrophysiologic properties that allow contraction when a
transmembrane action potential develops. The electrical system of
the heart consists of intrinsic pacemakers and conduction tissues.
This section reviews normal cardiac rhythm in anatomic terms and
highlights normal cardiac electrophysiology as a necessary basis for
recognizing abnormal conditions as they may occur in children.
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Normal Cellular Electrophysiology
Fully polarized cells have a resting membrane potential of -90 mV.
This resting membrane potential exists because of the electrical
gradient created by differences in extracellular and intracellular ion
concentrations. Specifically, the sodium–potassium pump primarily
controls sodium and potassium concentrations. This pump tries to
maintain intracellular sodium concentrations at 5 to 15 mEq/L and
intracellular potassium concentrations at 135 to 140 mEq/L. In
comparison, the extracellular sodium concentration is normally 135 to
142 mEq/L and extracellular potassium 3 to 5 mEq/L.2
Electrical stimulation of a myocardial cell results in depolarization.
Depolarization is initiated by a slow inward leak of sodium. When the
transmembrane potential reaches approximately -60 mV, the fast
sodium channel opens, actively transporting sodium across the cell
membrane and resulting in rapid cellular depolarization to
approximately +20 mV. This is represented by phase 0 of the action
potential and the QRS complex on a surface electrocardiogram (ECG).
After the rapid membrane depolarization, the sodium channel closes
and a complex exchange of sodium, calcium, and potassium occurs
during the plateau phases 1 and 2 of the action potential.
The dominant feature during the plateau phases of the action
potential is movement of calcium ions into the intracellular space via
L-type calcium channels. This feature differentiates myocardial cells
from nerve tissue and starts the excitation–contraction cascade of the
cell by initiating the release of intracellular calcium stores from the
sarcoplasmic reticulum. Phase 3 of the action potential is dominated
by repolarization of the cell membrane by outward movement of
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potassium ions. The rate of fall of phase 3 and its depth determine
membrane responsiveness to stimulation. Tissues may depolarize
only after reaching a particular level of repolarization called the
‘‘threshold potential,’’ at least -50 to -55 mV for normal Purkinje
fibers. This level of repolarization therefore determines the absolute
refractory period (ARP). The ARP varies in length depending primarily
on the action potential duration (APD). Phase 4 is the resting
membrane potential that results from a combination of ionic currents,
primarily the slow inward sodium current.3
Normal Cardiac Conduction
The electrical system of the heart consists of intrinsic pacemakers
and conduction tissues. It is convenient to conceptualize the
progression of normal cardiac rhythm in anatomic terms. The rate of
electrical firing of the heart depends on the most rapid pacemaker.
Spontaneous electrical firing or automaticity can occur anywhere in
the heart under certain conditions. Normally, the sinoatrial (SA)
node, located where the superior vena cava meets the right atrium,
has the most rapid intrinsic rate (60 to 100 bpm). Therefore, any
electrical activity not initiated by the SA node is considered an
arrhythmia. Consequently, most arrhythmias are labeled by the
anatomic location and rate.
Sinoatrial node firing initiates atrial contraction. The electrical impulse
is conducted through the atria via the internodal tracts to the
atrioventricular (AV) node near the coronary sinus, between the two
atria. The AV node has pacemaker properties but normally
coordinates atrial and ventricular contraction. The AV node normally
limits excessively rapid atrial rates from activating the ventricles.
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The conduction system in the ventricles is more elaborate than that
in the atria because the muscle mass is larger. Rapid and effective
excitation is critical because the ventricles contribute the most to
cardiac output. Fibers leaving the AV node are called the bundle of
His. They separate into the bundle branches, which traverse the
septum between the ventricles. Conduction between the AV node and
the bundle of His is measured by the P-R interval. The final
conducting components of the ventricles are the Purkinje fibers,
which emanate from the bundle branches to stimulate the ventricular
cardiac muscle to contract. The QRS complex measures
depolarization of the ventricles. The Q-T interval reflects both
ventricular depolarization and repolarization.
Electrical Anatomy of the Normal Heart
The atrial muscle and ventricular muscle are separated by insulation
of the fibrous mitral and tricuspid valve rings, and normally the only
connection between them is via the His bundle. All cardiac myocytes
are capable of electrical conduction and have intrinsic pacemaker
activity. Each tissue has a conduction velocity and a refractory
period, both of which vary with changes in heart rate and influences
such as autonomic tone, circulating catecholamines, etc. The
conduction velocities of various parts of the heart vary.8
Cardiac Conduction
The cardiac conduction system consists of specialized fast conducting
tissue through which the electric activity of the heart spreads from
the atria to the ventricles.
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The characteristics of the different parts of the conduction system are
a result of the different characteristics of the individual myocytes. On
a larger level, function is controlled predominantly by the autonomic
nervous system (both vagal and sympathetic nerve system). The
sinus node and atrioventricular node are especially responsive to the
autonomic nerve system. The ganglionic plexus, a conglomeration of
both vagal and sympathetic nerves, form the intrinsic cardiac nerve
system and innervate through a network of nerve fibers in the atria
and ventricles. The vagal nerve and sympathetic nerve system are
both continually active in the heart, but vagal activity dominates the
tonic background stimulation of the autonomic nerve system.
Moreover, the heart is more susceptible to vagal stimulation.
Vagal stimulation provokes a rapid response and the effect dissipates
swiftly in contrast to sympathetic stimulation, which has a slow onset
and offset. Vagal stimulation results in a reduction in sinus node
activation frequency and prolongs AV nodal conduction. These effects
can occur simultaneously or independent of each other. Sympathetic
stimulation exerts reverse effects, accelerating the sinus node firing
frequency and improving AV nodal conduction. The autonomic nerve
system has a small effect on cardiomyocytes. Vagal stimulation tends
to prolong the refractory period and decrease the myocardial
contractility. Sympathetic stimulation has the opposite effect on the
cardiac tissue. The physiological modulation of cardiac conduction is
vital to adaptation of the heart to rest and exercise. However, the
autonomic nervous system can contribute as a modifier and is certain
to facilitate the occurrence of certain arrhythmias.9
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Sinus Node
The sinus node is a densely innervated area located in the right
atrium, which is supplied by the right (55%-60%) or circumflex
(40%-45%) coronary artery. It is a small structure of 10-20 mm long
and 2-3 mm wide and contains a diversity of cells. These include
pacemaker cells, which are discharged synchronously due to mutual
entrainment. This results in an activation wave front triggering the
rest of the atrium.
Atrium
The impulse formed in the sinus node is conducted through the
atrium to the AV-node. Evidence indicates three preferential
conduction pathways. The pathways show preferential conduction due
to their anatomical structure, rather than specialized conduction
properties. The three pathways are: the anterior internodal pathway,
the middle internodal tract, and the posterior internodal pathway. The
anterior internodal pathway connects to the anterior interatrial band,
also known as the Bachmann bundle. This bundle of muscular tissue
conducts the sinus wave front from the right to the left atrium.
AV Node
The connection between atria and ventricles is facilitated through the
AV node, lying in the right atrial myocardium and a penetrating part,
the bundle of His. The AV node acts as a gatekeeper, regulating
impulse conduction from the atrium to the ventricle. Additionally, due
to the phase 4 diastolic depolarization it can exhibit impulse
formation. The AV node is supplied in most cases (85%-90%) by the
right coronary artery or in the remaining cases the circumflex artery.
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Bundle of His
Connecting the distal AV node and the proximal bundle branches, the
bundle of His is supplied by both the posterior and anterior
descending coronary arteries. The central fibrous body and
membranous septum between the atria and the ventricles enclose it.
The location and blood supply protect the bundle of His from external
influences.
Bundle Branches
From the bundle of His, the right bundle branch continues to the right
ventricular apex. The left bundle branch splits off and divides into to
two fascicular branches. Commonly, the left bundle branch consists of
an anterior fascicle, which activates the anterosuperior portion of the
left ventricle, and the thicker and more protected posterior fascicle,
which activates the inferoposterior part of the left ventricle.
Ventricle
The ventricle is activated through the dense network of Purkinje
fibers originating from the bundle branches. They penetrate the
myocardium and are the starting point of the ventricular activation.
The left ventricular areas first excited are the anterior and posterior
paraseptal wall and the central left surface of the interventricular
septum. The last part of the left ventricle to be activated is the
posterobasal area. Septal activation starts in the middle third of the
left side of the interventricular septum, and at the lower third at the
junction of the septum and posterior wall. Activation of the right
ventricle starts near the anterior papillary muscle 5 to 10 milliseconds
after onset of the left ventricle.10
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Normal Heart Rate In Children
The normal average heart rate of children is higher than that of
adults. A heart rate of 60 to 100 bpm when resting is considered
normal for adults. The variation in heart rates of children is greater
with heart rates varying from 60 bpm (when they are asleep) to 220
bpm (when they are active physically in strenuous activities).6
Age
Normal Range (Average)
bpm
< 1 day
93-154 (123)
1-2 days
91-159 (123)
3-6 days
91-166 (129)
1-3 weeks
107-182 (148)
1-2 months
121-179 (149)
3-5 months
106-186 (141)
6-11 months
109-169 (134)
1-2 years
89-151 (119)
3-4 years
73-137 (108)
5-7 years
65-133 (100)
8-11 years
62-130 (91)
12-15 years
80-119 (85)
> 16 years
60-100
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Cardiac Arrhythmias
An arrhythmia is any abnormality in the rate, regularity, or site of
origin of an electrical impulse. Arrhythmia includes a disturbance in
conduction that disrupts the normal sequence of activation in the
atria or ventricles. Arrhythmias have varying degrees of severity and
significance based on site of origin, symptoms, frequency, and
duration; and, they can be due to a variety of reasons, such as
structural abnormalities, electrolyte abnormalities, metabolic
derangements, genetic mutations, and drug toxicity. This section
provides an overview of cardiac arrhythmias in terms of pathogenesis
and clinical presentation.
Overview of Arrhythmias
Arrhythmias are relatively common in the pediatric cardiac intensive
care unit. One study revealed 59% of neonates and 79% of older
children have arrhythmias within 24 hours of surgery. An arrhythmia
is any abnormality in the rate, regularity, or site of origin or a
disturbance in conduction that disrupts the normal sequence of
activation in the atria or ventricles.
Arrhythmias differ in their population frequency, anatomical
substrate, physiological mechanism, etiology, natural history,
prognostic significance, and response to treatment. As is emphasized
throughout, it is important to gain as much information as possible
about the substrate and mechanism of an arrhythmia to be able to
predict the natural history and to define the prognosis and response
to treatment.1 A basic knowledge of the cardiac action potential and
cardiac conduction system facilitates understanding of cardiac
arrhythmias. The effects and side effects of anti-arrhythmic drugs are
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depended on the influence of ion channels involved in the generation
and/or perpetuation of the cardiac action potential. These
physiological dynamics are explained further below.3,7
The cardiac action potential is a result of ions flowing through
different ion channels. Ion channels are passages for ions (mainly
Na+, K+, Ca2+ and Cl-) that facilitate movement through the cell
membrane. Changes in the structure of these channels can open,
inactivate or close these channels and thereby control the flow of ions
into and out of the myocytes. Due to differences in the type and
structure of ion channels, the various parts of the heart have slightly
different action potential characteristics.
Ion channels are mostly a passive passageway where movement of
ions is caused by the electrochemical gradient. In addition to these
passive ion channels a few active trigger-dependent channels exist
that open or close in response to certain stimuli (for instance
acetylcholine or ATP). The changes in the membrane potential due to
the movement of ions produce an action potential, which lasts only a
few hundreds of milliseconds. Disorders in single channels can lead to
arrhythmias, as seen in the later section on primary arrhythmias. The
action potential is propagated throughout the myocardium by the
depolarization of the immediate environment of the cells and through
intracellular coupling with gap-junctions.
During the depolarization, sodium ions (Na+) stream into the
cytoplasm of the cell followed by an influx of calcium (Ca2+) ions
(both from the inside (sarcoplasmatic reticulum) and outside of the
cell). These Ca2+ ions cause the actual muscular contraction by
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coupling with the muscle fibers. During repolarization the cell returns
to the resting membrane potential, due to the passive efflux of K+.
The (ventricular) action potential can be divided in five phases, which
are listed below in detail.
Phase 0: Rapid Depolarization
Rapid depolarization is started once the membrane potential reaches
a certain threshold (about -70 to -60 mV). This produces activation of
sodium channels and a rapid influx of Na+ and a corresponding rapid
upstroke of the action potential. At higher potentials (-40 to -30)
Ca2+ influx participates in the upstroke. In the sinus node and AV
node a slower upstroke can be observed. This is because the slower
acting Ca2+ ion channels mainly mediate the rapid depolarization in
these cells. The slower activation produces a slower upstroke.
Phase 1: Early Rapid Repolarization
Immediately following rapid depolarization, the inactivation of the
Na+ channel (INa) and subsequent activation of the outward
K+ channel (Ito) and the Na+/Ca2+ exchanger (INa,Ca), which
exchanges 3 Na+ for 1 Ca2+, produces an early rapid repolarization.
Due to the limited role of the Na+ channel in the upstroke of sinus
node and AV node cells and the subsequent slower depolarization,
this rapid repolarization is not visible in their action potentials.
Phase 2: Plateau
The plateau phase represents an equal influx and efflux of ions in or
out of the cell producing a stable membrane potential. This plateau
phase is predominantly observed in the ventricular action potential.
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The inward movement of Ca2+ through the open L-type Ca2+ channels
(ICa-L) and the exchange of Na+ for internal Ca2+ by the
Na+/Ca2+ exchanger (INa,Ca) are responsible for the influx of ions
during the plateau phase. The efflux of ions is the result of outward
current carried by K+ (IKur and
Ks).
Phase 3: Final Rapid Repolarization
Final repolarization is mainly caused by inactivation of Ca2+ channels,
reducing the influx of positive ions. Furthermore repolarizing
K+ currents (delayed rectifier current IKs and IKr and inwardly
rectifying current IK1 and IK,Ach) are activated which increase efflux of
positive K+ ions. This results in a repolarization to the resting
membrane potential.
Phase 4: Resting membrane potential
During phase 4 of the action potential intracellular and extracellular
concentrations of ions are restored. Depending on cell type the
resting membrane potential is between -50 to -95 mV. Sinus node
and AV nodal cells have a higher resting membrane potential (-50 to
-60 mV and -60 to -70 respectively) in comparison with atrial and
ventricular cardiomyocytes (-80 to -90 mV). Sinus node cells and AV
nodal cells (and to a lesser degree Purkinje fiber cells) have a special
voltage dependent channel If, the funny current. Furthermore they
lack IK1, a K+ ion channel that maintains the resting membrane
potential in atrial and ventricular tissue. The If channel causes a slow
depolarization in diastole, called the phase 4 diastolic depolarization,
which results in normal automaticity. The frequency the sinus node
discharges is regulated by the autonomous nerve system, and due to
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the relative high firing frequency (60-80 beats per minute) the sinus
node dominates other potential pacemaker sites.
Arrhythmogenesis
In general, arrhythmia mechanisms have been described as
abnormalities in electrical development, electrical conduction, or a
combination of both. Abnormalities in electrical development arise
from irregular automaticity or triggered activity from the SA node or
other sites producing ectopic beats. Causes of irregular automaticity
include hypoxia, electrolyte abnormalities, fiber stretch,
catecholamine excess, ischemia, and edema. All of these factors
increase the slope of phase 4 depolarization, resulting in heightened
automaticity. Triggered activity usually develops due to transient
membrane depolarization during or immediately after repolarization.
These early and delayed afterdepolarizations can occur with
oscillations in the plateau phase of the action potential, leading to a
second depolarization before the first is completed. Hypoxia, fiber
stretch, catecholamines, high PCO2, and digitalis overdose can lead to
triggered activity.4
Reentry and conduction block are the most common electrical
conduction abnormalities associated with arrhythmogenesis. Reentry
describes a concept of infinite impulse propagation by continued
activation of previously refractory tissue. Reentry depends on
different conduction velocities along adjacent myocardial fibers, with
one fiber containing an area of unidirectional conduction block. This
allows continued excitation in a repetitive manner. This circus rhythm
may develop as areas of infarcted tissue block or delayed conduction.
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A single circuit of the fibers may induce a premature contraction,
whereas continuous cycling of impulses might produce sustained
tachycardia. This process may occur in both atrial and ventricular
tissue. Conduction block occurs when the normal conduction pathway
is blocked and the impulse either expires or conducts through an
alternative inappropriate route to depolarize the myocardium.5
Mechanisms of Arrhythmia
Structural abnormalities or electric changes in the cardiomyocytes
can impede impulse formation or change cardiac propagation,
therefore facilitating arrhythmias. Arrhythmogenic mechanisms can
arise in single cells (automaticity, triggered activity), but other
mechanisms require multiple cells for arrhythmia induction (reentry). Briefly highlighted is the pathophysiological mechanisms of
the main causes of arrhythmia.2,11

Abnormal Automaticity
The mechanism of abnormal automaticity is similar to the
normal automaticity of sinus node cells. Abnormal automaticity
can be caused by changes in the cell ion channel characteristics
due to drugs (digoxin) or changes in the electrotonic
environment (myocardial infarction). Abnormal automaticity
can result from an increase of normal automaticity in non-sinus
node cells or a truly abnormal automaticity in cells that don't
exhibit a phase 4 diastolic depolarization.
An important phenomenon in (both normal and abnormal)
automaticity is overdrive suppression. In overdrive suppression
the automaticity of cells is reduced after a period of high
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frequency excitation. The cellular mechanism responsible for
this effect is an increased activity of the Na+, K+ pump (INa, K)
which results in an increased efflux of Na+, thereby inducing a
hyperpolarization.

Triggered Activity
Triggered activity is depolarization of a cell triggered by a
preceding activation. Due to early or delayed
afterdepolarizations the membrane potential depolarizes and,
when reaching a threshold potential, activates the cell. These
afterdepolarizations are depolarizations of the membrane
potential initiated by the preceding action potential. Depending
on the phase of the action potential in which they arise, they
are defined as early or late afterdepolarizations.
A disturbance of the balance in influx and efflux of ions during
the plateau phase (phase 2 or 3) of the action potential is
responsible for the early afterdepolarizations. Multiple ion
currents can be involved in the formation of early
afterdepolarizations depending on the triggering mechanism.
Early afterdepolarizations can develop in cells with an increased
duration of the repolarization phase of the action potential, as
the plateau phase is prolonged. The prolonged repolarization
might reactivate the Ca2+ channels that have recovered from
activation at the beginning of the repolarization. Otherwise
disparity in action potential duration of surrounding myocytes
can destabilize the plateau phase through adjacent depolarizing
currents.
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Delayed afterdepolarizations occur after the cell has recovered
after completion of repolarization. In delayed
afterdepolarization an abnormal Ca2+ handling of the cell is
responsible for the afterdepolarizations due to release of
Ca2+ from the storage of Ca2+ in the sarcoplasmatic reticulum.
The accumulation of Ca2+ increases membrane potential and
depolarizes the cell until it reaches a certain threshold, thereby
creating an action potential. A high heart rate can result in the
accumulation of intracellular Ca2+ and induce delayed
afterdepolarizations.11
Disorders of Impulse Conduction
The disorders of impulse conduction generally involve the rate of and
re-entry circuits or pathways in the heart.

Conduction block
Conduction block or conduction delay is a frequent cause of
bradyarrhythmias, especially if the conduction block is located
in the cardiac conduction system. However, tachyarrhythmias
can also result from conduction block when this block produces
a re-entrant circuit. Conduction block can develop in different
(pathophysiological) conditions or can be iatrogenic
(medication, surgery).

Re-entry
Re-entry or circus movement is a multicellular mechanism of
arrhythmia. Important criteria for the development of re-entry
are a circular pathway with an area in this circle of
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unidirectional block and a trigger to induce the re-entry
movement. Re-entry can arise when an impulse enters the
circuit, follows the circular pathway and is conducted through a
unidirectional (slow conducting) pathway. Whilst the signal is in
this pathway the surrounding myocardium repolarizes. If the
surrounding myocardium has recovered from the refractory
state, the impulse that exits the area of unidirectional block can
reactivate this recovered myocardium. This process can repeat
itself and thus form the basis of a re-entry tachycardia. Slow
conduction and/or a short refractory period facilitate re-entry.
The reason of unidirectional block can be anatomical (atrial
flutter, AV node reentrant tachycardia (AVNRT), AV reentrant
tachycardia (AVRT) or functional (as with myocardial ischemia),
or a combination of both.
Epidemiology of Arrhythmias
Some arrhythmias are more
common than others but there are
almost no data on the population
prevalence of these conditions.
However, the prevalence and
spectrum of arrhythmias change
with age. Faced with a new patient
with an arrhythmia, diagnosis is
based mainly on the child’s age,
the age of onset of arrhythmia, the
history (palpitations, heart failure,
syncope, etc.), and the ECG
findings, but should also take into account the prevalence of different
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arrhythmias (in other words, a common arrhythmia is often a more
likely diagnosis than a rare one).
Probably fewer than half of new tachycardias present in the first year
of life. By far the most common tachycardia presenting in early
infancy is orthodromic AV reentry. Most of these infants have a
normal ECG in sinus rhythm but some show ventricular preexcitation. Other neonatal tachycardias are much less common and
include atrial flutter, permanent junctional reciprocating tachycardia,
atrial tachycardia, and ventricular tachycardia.12
The most common tachycardia in childhood is also orthodromic AV reentry tachycardia, although AV nodal re-entry tachycardia becomes
progressively more common after the age of 5 years. Less common
tachycardias in this age group are antidromic AV re-entry,
atriofascicular re-entry, ventricular tachycardias, and atrial
tachycardias.5
Arrhythmias presenting with palpitations include most of the common
types of supraventricular tachycardia and a few cases of ventricular
tachycardia. Many children with palpitations do not have an
arrhythmia and a detailed first-hand history is essential before
assessing the likelihood of an arrhythmia and the necessity of further
investigation. Similarly, very few children with chest pain have
arrhythmias (or indeed any cardiac abnormality) and only a few with
syncope have an arrhythmia. Again it all depends on the history.
Incessant tachycardias presenting with heart failure or apparent
cardiomyopathy include focal atrial tachycardia, permanent junctional
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reciprocating tachycardia, incessant idiopathic infant ventricular
tachycardia, and orthodromic atrioventricular re-entry tachycardia.13
Arrhythmias presenting with syncope include complete AV block,
atrial fibrillation in Wolff–Parkinson–White (WPW) syndrome,
sinoatrial disease, and ventricular tachycardia, especially in long QT
syndrome, catecholaminergic ventricular tachycardia or late after
cardiac surgery.
Some arrhythmias are so common as to be considered as almost
normal variants. They include atrial premature beats, ventricular
premature beats, and transient nocturnal Wenckebach AV block.
Arrhythmias are relatively common in the pediatric cardiac intensive
care unit. One study revealed 59% of neonates and 79% of older
children have arrhythmias within 24 hrs. of surgery. Of these
arrhythmias, junctional ectopic tachycardia (JET) was seen in 9% of
neonates and 5% of older children. Ventricular tachycardia was found
in 3% of neonates and 15% of older children.14
In terms of specific arrhythmias,
sinus tachycardia is the most
frequently seen arrhythmia, with
supraventricular tachycardia being
the next most common, followed
by sinus bradycardia. Reentrant
tachycardia is common in infants
and children with congenital heart
disease (CHD). Some arrhythmias
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in the early post operative period like premature atrial contraction’s
(PAC’s) and premature ventricular beats (bigeminy) are usually
transient and well tolerated. Others like junctional ectopic tachycardia
(JET) and atrial flutter may cause significant hemodynamic instability
and compromise or even sudden cardiac death.
Primary arrhythmias occur in children without structural heart
disease, although they may be secondary to ion channel diseases
that are still being elucidated. Risk factors that predispose children
for secondary arrhythmias include congenital cardiac malformations,
surgical repair and scarring, long cardiopulmonary bypass times, or
exposure to chronic hemodynamic stress.
Electrolyte and acid-base imbalance and the use of vasoactive drugs
also predispose children to arrhythmias. Inflammation or carditis seen
in diseases such as acquired heart diseases like Kawasaki disease,
rheumatic fever and myocarditis may produce arrhythmogenic foci.
Conditions of ventricular volume overloading, valvular regurgitation,
congestive heart failure and pulmonary hypertension are other
secondary reasons.
Regardless of the cause of the arrhythmia, there are certain common
signs, symptoms and treatment options that are ultimately based on
the rhythm more than on the etiology with certain very important
exceptions. Symptoms may vary depending upon age and include
feeding intolerance, lethargy, irritability, pallor, diaphoresis, syncope,
fatigue or palpitations.3,8
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Mechanisms of tachyarrhythmias can be enhanced automaticity with
triggered foci or enhanced conduction with the presence of reentrant
circuits. Similarly, bradycardia can result from suppressed
automaticity or suppressed conduction, where normal conduction is
delayed or blocked. Understanding the mechanism informs the
optimal treatment choice.
Types of Arrhythmias
The following tables provide a general overview of the different types
of arrhythmias.2,7,15,16 Sections of this course later on will provide
more detailed information on the most common types.
CARDIAC
ARRHYTHMIA
Sick sinus
syndrome (SSS)/
Tachy-Brady
Syndrome
CHARACTERISTICS
Sinoatrial (SA) node becomes dysfunctional and is no
longer a reliable pacemaker, most commonly manifested as
bradycardia, although there can also be tachycardia. When
the sinus rate is slower than another potential pacemaker
in the heart, it may no longer be the dominant pacemaker.
SSS can also cause an alternating bradycardia and
tachycardia. A number of rhythms result including sinus
bradycardia, sinus arrest and junctional rhythm, and
ectopic atrial and nodal rhythms.
The term SSS includes SA node dysfunction plus symptoms
of dizziness, syncope or sudden cardiac death.
Bradycardias
Often caused by hypoxia, vagal tone, hypothyroidism,
cardiac surgery, endocarditis and myocarditis,
hyperkalemia, sleep, hypothermia, sedation and
anesthesia.
Sinus bradycardia: Sinus node slower than normal for age
related normal values.
Slow junctional escape rhythm/nodal rhythm: Spontaneous
depolarization of the AV node. The sinus node has either
failed to fire or is slower than the AV node. Rates 50-80
beats/min in children less than 3 yrs. and 40-60 beats/min
for children older than 3yrs. Can be common after atrial
surgery and are usually transient.
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Ventricular escape rhythm or ideoventricular rhythm: Origin
of impulse is from the ventricle and presents with rates
slower than from the AV node. QRS have wide complex
morphology. This is a secondary phenomenon vs. a primary
arrhythmia and occurs when the sinus node and/or the AV
node are dysfunctional. An example of this is complete
heart block with a ventricular escape rhythm. The ventricle
itself is working well, and the escape rhythm is a symptom
of another problem.
Premature
Beats/ExtraSystoles
Premature atrial, junctional and ventricular ectopic beats
are common and may occur in patterns of bigeminy,
trigeminy, quadrageminy or couplets. These are generally
benign.
Wandering Atrial
Pacemaker
Shifting of the pacemaker site from the SA node to
alternate sites in the atria and junction (AV node). P-wave
configuration changes as the site changes.
Supraventricular
Tachycardias
(SVT) SVT is
used as a
collective term
Originates above the bundle of His. Reentrant circuits
generally have an abrupt onset and termination, i.e., are
paroxysmal.
Sinus tachycardia: Sinus node is faster than age-related
normal values due to enhanced automaticity. Usually due to
fever, pain, anxiety, anemia, medications, hypovolemia or
in the presence of increased catecholamines.
While not generally an indication of conduction system
pathology, sinus tachycardia may be an important indicator
of significant cardiovascular compromise.
Reentrant tachycardias: Reentrant tachyarrhythmias
require the presence of two possible conduction pathways
with different conduction and refractory properties. The
tachycardia uses both pathways; one as an antegrade limb
and one as a retrograde limb of the reentry circuit.
a) Within the atria: atrial flutter, atrial fibrillation; intraatrial reentrant tachycardia (IART) atrial flutter- or
incisional tachycardia represents macroreentry within the
atrial muscle and may be slower than atrial flutter.
b) Atrioventricular reentrant tachycardias include:
- atrioventricular reentrant tachycardia (AVRT):
commonly associated with Wolff- Parkinson-White.
Accessory pathway present allowing impulses that entered
via the AV node to enter the atria
- atrioventricular nodal reentry tachycardia (AVNRT):
uses a “slow-fast AV nodal pathway”. Antegrade conduction
limb is the slow pathway and retrograde limb fast one.
Simulation of the atria by the retrograde pathway produces
inverted p- waves. Concurrent stimulation of the ventricles.
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- permanent junctional reciprocating tachyarrhythmia
(PJRT). These are reentrant circuits in which one limb
includes the AV node.
Wolff-Parkinson-White Syndrome (WPW): Baseline resting
ECG is characterized by a short PR interval, wide QRS and
delta wave which is a manifestation of the accessory on
sinus rhythm. WPW is marked by the delta wave on the
resting ECG. Atrial flutter or atrial fibrillation in the
presence of this type of accessory connection can result in
VF.
The QRS complex in SVT is wide if there’s aberrant
conduction, in which the antegrade limb is the accessory
connection. If the AV node is the antegrade limb, the QRS
is a narrow complex.
Automatic tachycardia – AET and JET: local enhanced
automatic focus of certain cardiac myocytes in the atria or
AV node. AET and JET are non-reciprocating tachycardias
that originate from a single focus unlike reentrant rhythms.
AET/JET are seen more commonly in neonates and usually
observed within the first several days after
cardiopulmonary bypass. They are refractory arrhythmias
that are relatively resistant to treatment.
The goal is rate control and restoring AV synchrony. These
are often transient arrhythmias lasting 24-72 hours. Rapid
rates lead to early contraction of the atria against closed AV
valves resulting in cannon A waves on hemodynamic
monitoring lines (CV, RA, and LA).
AET - When this occurs at an ectopic site within the atria, it
is called atrial ectopic tachycardia. AET occurs as a result of
irritation of tissues during cardiac surgery, with placement
of intracardiac lines, application of sutures, or cutting
tissue. Any reason for dilated atria, cardiomyopathy or
diseased AV valves, ventricular dysfunction can result in
this rhythm disorder.
Rates are usually above 170-180 beats/min and beyond
200 beats/min. A block at the AV node can cause AV
dissociation, further contributing to hemodynamic instability
in addition to the rapid atrial rate. The rhythm may be
variable, and may be interspersed with periods of sinus
rhythm. The rate can ramp up or slow down over minutes
in contrast to the sudden onset and offset of SVT.
JET - When the ectopic focus initiates at or near the AV
node then the arrhythmia is junctional ectopic tachycardia.
JET is usually caused by surgery around the AV node and
rates often range between 160 beats/min to as high as 280
beats/min.
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Characteristics include inverted P- waves in lead II and an
R-P interval, which is short or absent. Primarily seen post
re-warming from cardiopulmonary bypass and within 3
days of the surgery.
Ventricular
tachycardia (VT)
Three or more consecutive ventricular complexes are by
definition VT. Wide QRS complex morphology and a
different QRS morphology than the usual QRS waveform
characterize VT. Morphology may be monomorphic
(uniform), polymorphic (multiform); or Torsades de Pointes
where the points seem to twist around the isoelectric line.
Often associated with structural heart disease, particularly
late (years) after repair. Other common clinical situations in
which one might see VT include dilated and hypertrophic
cardiomyopathy, metabolic alterations including severe
hypoxia, acidosis, hyper/hypokalemia, and drug toxicity
such as cocaine, digoxin, and tri-cyclic antidepressants.
Other conditions include myocarditis and long Q-T
syndrome. Whenever VT occurs in a pediatric patient one
must also consider ischemia or infarction. Patients may
present hemodynamically stable or in cardiac arrest.
Ventricular
Fibrillation (VF)
Completely uncoordinated depolarization of heart muscle
mass resulting in inability to maintain any global excitation
contraction coupling. The myocardium fails to squeeze and
cardiac arrest occurs.
1st Degree Heart
Block
Slowed conduction through the AV node resulting in
prolonged duration of PR interval.
2nd Degree
Heart Block
(Mobitz I,
Wenckebach)
Intermittent block of conduction of atrial beats to the
ventricle resulting in dropped QRS complexes. Progressive
lengthening of the PR interval until a QRS is dropped and
the cycle starts again with a shorter PR interval that
progressively lengthens.
2nd Degree
Heart Block
(Mobitz II;
Classical type)
Patterned dropping of QRS complex with a fixed ratio of
atrial depolarizations (P waves) to conducted beats with a
consistent PR interval throughout. It is higher risk than
Mobitz I. Intermittent block of conduction of some beats to
the ventricle without progressive prolongation of the PR
interval. Potentially may progress to complete heart block.
Related to His bundle or bundle branch dysfunction.
3rd Degree Heart
Block/ Complete
Heart Block
Complete block of AV node resulting in AV dissociation
between atrial and ventricular events. No relationship
between the P waves and QRS complexes.
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Specific Categories of Cardiac Arrhythmias
As noted earlier, there are many reasons for arrhythmias. Increased
end diastolic pressures resulting in atrial or ventricular stretch,
valvular dysfunction, tumors, multiple surgeries, scarring and
ischemia all play a significant role in arrhythmia generation. Cardiac
swelling, pro-arrhythmic drugs, acid/base and electrolyte imbalance
are also frequent etiologies of rhythm issues.
Neonatal Arrhythmias
Common arrhythmias in neonates with structurally normal hearts are
premature atrial contractions (PAC’s), atrial flutter, atrioventricular
reentry tachycardia (AVRT), permanent junctional reciprocating
tachycardia (PJRT), ventricular tachycardia, and heart block. Neonatal
heart block is associated with maternal autoimmune disease, i.e.,
systemic lupus.
Post-operative Arrhythmias
Early post-operative arrhythmias usually seen are sinus tachycardia,
sinus bradycardia, SVT, JET, complete AV block, and less frequently
ventricular tachycardia. Post-operative arrhythmias result from
manipulation or injury of the conduction system. The site of surgical
repair may increase the risk of certain types of arrhythmias observed.
Late post operative arrhythmias such as atrial flutter, and/or intraatrial reentrant tachycardia are seen months to years after surgery.
These arrhythmias are observed more often with Fontan, Mustard,
Senning and tetralogy of Fallot repairs. These tachyarrhythmias can
result in poor ventricular function and decreased quality of life.
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Common late post operative arrhythmias include atrial tachycardia,
which may be seen in 50% of Fontan patients and tend to recur after
a period of time. Arrhythmias associated with specific congenital
cardiac malformations are highlighted in this section.4,28,17
Aortic Arch with VSD
Severe Aortic Stenosis/
Aortic Valve Surgery
JET
Myocardial ischemia from severe left ventricular
outflow obstruction, LV hypertrophy and strain
resulting in ventricular arrhythmias.
Conduction abnormalities and complete heart block
may be seen post surgical resection of sub-aortic
obstructive tissue.
Although remote to the conduction system,
junctional tachycardia may occur.
Prone to VT.
Atrial Septal Defect
(ASD)
Sinus node dysfunction and transient atrial
arrhythmias, atrial flutter, atrial fibrillation,
ventricular tachycardias.
Atrioventricular Septal
Defect (AVSD)
Transient and permanent sinus node dysfunction,
supraventricular arrhythmias; JET; AV block; and
VT. Grosse-Wortmann, et al., found that complete
AV block was more common post operative repair
of complete AVSD.
Congenitally Corrected
Transposition of the
Great Arteries (cc-TGA/
L-TGA)
Accessory pathways; AV Block: 2nd & 3rd degree;
ventricular ectopy. Congenital AV block may
preexist due to intrinsic structural malformation.
Cor–Triatriatum
Sinus bradycardia, atrial tachyarrhythmias, AV
conduction disturbances
D-Transposition of the
Great Arteries (D-TGA)
Sinus bradycardia, sinoatrial block, junctional
rhythm, JET, premature atrial contractions, Mobitz
1, VT. Prone to VT if repaired with atrial level
switch procedures, Senning or Mustard.
Late complications of arrhythmias in the Jatene
arterial switch procedure are rare. Late
complications of atrial switch (Senning/Mustard)
are that greater than 50% of patients have serious
arrhythmias.
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Ebstein’s Anomaly of
the Tricuspid Valve
Common to have rhythm disturbances related to
atrial and ventricular dilatation and conduction
disturbances: accessory pathways; WPW and VT,
SVT, atrial fibrillation, atrial flutter; 1st degree
heart block and rarely 3rd degree heart block.
Congenital accessory pathways such as WPW may
preexist due to intrinsic structural malformation.
Heart Transplant
Intraatrial reentrant tachycardia, AET. Sinus
bradycardia, AV block in a small percentage of
children. Supraventricular and ventricular
arrhythmias are relatively uncommon and may
indicate rejection.
Pulmonary Atresia with
Intact Ventricular
Septum
Pulmonary Atresia with
a VSD
Single Ventricle Hypoplastic Left Heart
Syndrome (HLHS)
Single Ventricle –
Bidirectional
Cavopulmonary (Glenn)
Connection
Single Ventricle –
Fontan
Rare rhythm disturbances observed. Ventricular
arrhythmias if coronary sinusoids with ischemia.
Tetralogy of Fallot
(TOF)
Total Anomalous
Pulmonary Venous
Return (TAPVR)
Truncus Arteriosus
Tricuspid Atresia
Ventricular Septal
Defect (VSD)
Sometimes AV conduction abnormalities observed.
Atrial arrhythmias.
Transient sinus node dysfunction.
Sinus node dysfunction, atrial reentrant
tachycardia: atrial flutter, atrial
fibrillation, intra-atrial tachycardia, VT. Early or late
SVT, junctional rhythm, accelerated junctional
rhythm and VT.
Sinus node dysfunction, supraventricular
tachycardias – atrial flutter, accelerated junctional
rhythm, JET, AV blocks, VT. Right bundle branch
block (RBBB). Prone to VT due to the volume
loading on the RV causing RV dilation, failure, and
increased right sided pressures. Predisposes
patient to SCD.
Atrial arrhythmias, JET, sinus bradycardia, AV
conduction disturbances.
AV conduction disturbances; ventricular
arrhythmias due to the right ventriculotomy.
Supraventricular arrhythmias; atrial ectopy, flutter,
fibrillation.
Junctional rhythm, accelerated junctional rhythm,
JET, VT (Grosse-Wortmann, 2010), AV conduction
block.
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Inherited Cardiomyopathies
Genetic predisposition to cardiac arrhythmias with an increased risk
of sudden cardiac death are reviewed in the section below.1,7
CARDIOMYOPATHIES
PATHOPHYSIOLOGY
CARDIAC
ARRHYTHMIAS
VT, SCD.
Hypertrophic
Cardiomyopathy (HCM)
Hypertrophic myocardium
with asymmetric septal
hypertrophy.
Dilated Cardiomyopathy
(DCM)
Dilated poorly contractile
ventricles.
SVT, VT, SCD.
Arrhythmogenic Right
Ventricular (RV)
Cardiomyopathy
(ARVC) or Dysplasia
A form of dilated
cardiomyopathy.
Fibrofatty replacement of
the RV wall myocytes and
patchy areas of fibrosis
with progressive RV
dysfunction and
enlargement.
RV tachyarrhythmias
with variable response
to beta-blockers and to
catheter ablation.
Channelopathies – Electrical Myopathies:8,36
CARDIOMYOPATHIES
Long QT Syndrome
(LQTS)
PATHOPHYSIOLOGY
Identified by prolonged
QT interval corrected for
heart rate (QTc). QT
interval greater than 0.46
seconds, with upper
normal limit of 0.44
seconds.
CARDIAC
ARRHYTHMIAS
High risk of bursts of
VT such as runs of
Torsades de Pointes,
progressing to VF and
SCD. May present with
syncope, seizures or
SCD.
Acquired or congenital;
can be secondary due to
drugs, i.e., amiodarone,
procainamide, sotolol,
tricyclic antidepressants
and/or electrolyte
imbalance (hypokalemia,
hypomagnesemia).
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Catecholaminergic
Polymorphic Ventricular
Tachycardia (CPVT)
Polymorphic ventricular
tachycardia. CPVT is
initiated by stimulation of
the adrenergic receptors
from stress, emotion or
exertion/physical
activity; found in normal
hearts with normal
coronary arteries and
normal ECG’s.
VT, ventricular
fibrillation, and SCD.
Brugada Syndrome
(BrS)
Autosomal dominant
genetic In 20% of cases,
mutations in the sodium
channel are thought to
be causative.
History of ventricular
arrhythmias –
ventricular fibrillation,
syncope and SCD.
Marked by RBBB and
striking ST elevation in
V1-V3. ECG
manifestation and
arrhythmias most likely
during times of fever.
PATHOPHYSIOLOGY
CARDIAC
Inflammatory Disease:8
ACQUIRED
ARRHYTHMIAS
Myocarditis
Viral myocarditis is a cell
mediated immunologic
reaction. Myocardium
may have lymphocyte
infiltration, necrosis and
scarring. Myocarditis may
lead to cardiomegaly and
congestive heart failure,
hemodynamic
compromise, shock and
death. Cells undergo
lymphocyte infiltration,
necrosis and scarring.
Risk SCD from VT and
AV block.
Clinical Evaluation Of The Pediatric Patient
The following components of clinical assessment are necessary when
a health provider approaches the pediatric patient to evaluate for a
cardiac arrhythmia.
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Review of Family History
Family history should be reviewed, such as heart disease, death at
young age, sudden death, and seizures. Additionally, neonatal
history, child’s personal history of syncope, palpitations, racing heart
beat, seizures, exercise intolerance, family, feeding intolerance; and,
genetics, congenital cardiac malformations, diagnostic investigations,
previous surgical repair and post-surgical anatomy should be pursued
in the history taking. The provider should inquire about events
preceding rhythm disturbance.
Clinical Assessment
Irritability, feeding intolerance, respiratory distress, tachycardia or
bradycardia for age, irregular heart rate/pulse, decreased capillary
refill time, lethargy, congestive heart failure, decreased level of
consciousness, syncope, absent pulses/cardiac arrest should be
assessed. The clinician needs to be familiar with normal heart rate for
different ages. Infants generally have heart rates greater than 80
beats/min and less than 170 beats/min. Children usually have heart
rates greater than 60 beats/min and less than 140 beats/min. Heart
rates above these ranges are concerning and warrant further
assessment. Consider the appropriate heart rate response for
physiology.
Cardiac assessment includes auscultation of heart sounds for
murmurs, extra heart sounds, abnormal activity of the precordium
palpation for heaves and thrills, assessment of perfusion, pulses,
capillary refill time, blood pressure and assessment of vital signs.
Cutaneous saturation or pulse oxymetry is part of the
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cardiorespiratory assessment and should be assessed. Identify
tolerance of the arrhythmia through assessment of clinical symptoms.
Profound hemodynamic effects may result from loss of AV synchrony
such as JET, AET or AV block, heart rate that is too slow or too fast,
VT or VF. This is worse in the context of preexisting myocardial
dysfunction or palliated physiology. A rapid heart rate results in
decreased diastolic and coronary artery filling times.18
Diagnostic Evaluation
This section outlines diagnostic tests that may be considered in order
to ensure an accurate diagnosis and impact of arrhythmia.12

Recording baseline pre-operative and post-operative rhythm strips
is optimal. Any Abnormal ECG’s should be compared to baseline.

Document the rhythm disturbance by a 12 or 15 lead pediatric
electrocardiogram. Pediatric 15 Lead ECG includes right-sided
leads V4R, V5R, V6R. This can be invaluable in accurate
identification of the type of arrhythmia.

The patient should be monitored
continuously. A Holter
electrocardiogram (usually 24 hour
ambulatory) may be of value in
identification of the arrhythmia
events.
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
Perform an atrial electrocardiogram using the atrial pacing wire in
post cardiac surgical patients, where P waves cannot be clearly
identified.

It can be helpful to capture electrical evidence of termination of
the tachycardia on a 15 lead ECG or rhythm strip.

Test blood levels of potassium, calcium and magnesium; and,
thyroid function tests, complete blood count, and toxicology
screen.

Electrolyte imbalances are often associated with rhythm
disturbances. If suspicious of myocarditis or with worsening
cardiac function check viral etiologies.

Cardiac enzymes, such as troponin levels and CPK-MB are markers
of myocardial injury.

A chest X-ray may demonstrate enlargement of the heart.

Echocardiogram (ECHO) provides a qualitative and quantitative
evaluation of cardiac function to rule out underlying structural
heart disease, thrombus formation and ventricular dysfunction. A
quantitative value of ejection fraction can be reported.

Use of pharmacological agents such as adenosine and
procainamide can assist with diagnosis of arrhythmias.
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
Exercise testing may be used to provoke and diagnose
arrhythmias and associated symptoms.

A catecholamine challenge or transoesophageal pacing can also be
used to provoke arrhythmias in a controlled environment.

Invasive electrophysiology studies with cardiac catheterization
help to identify ectopic foci and accessory pathways, which can be
mapped and ablated.
12-lead ECG
The ECG is conventionally recorded at
a speed of 25 mm/s and at a
calibration of 1 cm = 1 mV. A
standard 12-lead ECG includes three
standard (bipolar) limb leads – I, II,
and III – three augmented unipolar
limb leads – aVR, aVL, and aVF – and
six unipolar chest leads – V1–V6. Accurate positioning of the leads
(especially the chest leads) is important. V1 and V2 are in the fourth
intercostal space, V4 is in the fifth intercostal space in the
midclavicular line, V5 is in the anterior axillary line, and V6 in the
midaxillary line, both these last two horizontal to V4.
Routine evaluation of an ECG involves assessment of the heart rate,
heart rhythm, and QRS axis, then the P waves, QRS complexes, T
waves, and measurement of the PR, QRS, and QT intervals. Many
modern ECG machines automatically measure and display many of
these variables. The measurements are usually accurate and reliable
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but a machine-derived interpretation of the ECG should be treated
with some caution, even if produced by a pediatric algorithm. The
machine often distinguishes between normality and abnormality fairly
accurately (assuming that the age of the patient is entered into the
algorithm) but analysis of the type of arrhythmia is often unreliable.
Whenever possible, a 12-lead ECG recording in sinus rhythm and
during symptoms should be obtained in children with suspected or
proven arrhythmia.18
Rhythm Strips
Rhythm strips are most useful in documenting changes in rhythm in
response to interventions such as adenosine administration, but they
should not be seen as an alternative to recording a 12-lead ECG.
Rhythm strips usually contain three leads but, on some machines,
there may be six, twelve, or only one. The leads selected vary. Leads
I, aVF, and V1 are a good combination but others may be preferred
after examining the 12-lead ECG.19
Holter Monitoring/Ambulatory ECG Recording
Holter monitoring, or ambulatory ECG recording, has become a
standard test in the investigation and follow-up of children with
suspected or proven arrhythmias. It is well tolerated and particularly
useful in children with fairly frequent symptoms, suggesting that
there is a reasonable chance of recording the ECG during symptoms.
It is also valuable in assessing response to treatment in children with
incessant tachycardias, congenital long QT syndrome, etc.20
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ECG Event Recorders
Event recorders are carried by children or their parents but are not
necessarily worn all the time. They can be used in loop mode (where
they are worn constantly and a button is pressed during symptoms to
make a record of the ECG) or event mode (when the recorder is
applied and a recording made when symptoms occur).21
Exercise ECG
Treadmill or bicycle exercise ECG recording is sometimes helpful in
investigation of arrhythmias but is useful in providing reassurance for
children and their families in the presence of exercise-related
symptoms thought not to be due to arrhythmia. Exercise-induced
arrhythmias are unusual but are sometimes seen in AV re-entry. The
exercise test is very helpful in suspected catecholaminergic
polymorphic ventricular tachycardia.
Implanted Loop Recorder
In children with worrying syncope but no proven diagnosis, an
implanted loop recorder may be very helpful. The device has a 3-year
battery and is inserted subcutaneously in the left axilla or on the left
anterior chest wall. It works in loop mode and can be programmed to
store recordings of arrhythmias, which have rates below or above
preset limits. Children or their parents or teachers using an external
activating device can also trigger a recording. The yield from this type
of recorder depends on the selectivity of the physician but it can be
most useful in children with infrequent major syncope.
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Transesophageal Electrophysiology Study
The transesophageal electrophysiology study is not widely employed
in pediatric practice because of its limited physical acceptability. It
involves (per oral or per nasal) positioning of a pacing wire in the
esophagus behind the left atrium. Pacing in this position can usually
capture the atria but requires a higher output stimulator than a
normal pacing box. Transesophageal pacing can be used in neonates
to overdrive atrial flutter or atrioventricular tachycardia, but its use in
older children is limited by discomfort and it often requires general
anesthesia. It has been advocated for investigation of children with
symptoms of palpitation, elucidation of arrhythmia mechanism if
tachycardia is documented on ambulatory ECG monitoring, and “risk
assessment” in asymptomatic children with a Wolff–Parkinson–White
pattern on the ECG. It is perhaps more widely used in some European
countries than in the U.K., the U.S., or elsewhere.22
Tilt Test
A head-up tilt test is sometimes used for investigation of children
older than 6 years with recurrent syncope or presyncope. Protocols
vary but all involve the child lying horizontal for 15–20 min before
being passively tilted to an angle of 60–80 for up to 45 min or until
the development of symptoms. The ECG and blood pressure are
recorded continuously. Fainting or a feeling of faintness is usually
accompanied by bradycardia and hypotension, and the child is rapidly
returned to the horizontal. Less commonly there is a hypotensive
response without bradycardia. The most unusual response is
cardioinhibitory with bradycardia or asystole before syncope.8
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A “positive” test response with passive tilting is observed in 40–50%
of children with a good history suggesting neurally mediated syncope.
The sensitivity is increased by infusion of isoprenaline (isoproterenol)
but specificity is reduced. False positives and false negatives limit the
usefulness of the test, but it can be helpful in management of
syncope.2
Common Treatments
The need for treatment of arrhythmias depends on the symptoms and
the seriousness of the arrhythmia. Treatment is directed at causes. If
necessary, direct antiarrhythmic therapy, including antiarrhythmic
drugs, cardioversion-defibrillation, implantable cardioverterdefibrillators (ICDs), pacemakers (and a special form of
pacing, cardiac resynchronization therapy), or a combination, is used.
Drugs for Arrhythmias
Antiarrhythmic drugs comprise many different drug classes and have
several different mechanisms of action. Furthermore, some classes
and even some specific drugs within a class are effective with only
certain types of arrhythmias. Therefore, attempts have been made to
classify the different antiarrhythmic drugs so by mechanism.
Although different classification schemes have been proposed, the
first scheme (Vaughan-Williams) is still the one that most physicians
use when speaking of antiarrhythmic drugs.
The following list shows the Vaughan-Williams classification and the
basic mechanism of action associated with each class. Note that Class
I drugs are further broken down into subclasses because of subtle,
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yet important differences in their effects on action potentials. Most
antiarrhythmic drugs are grouped into 4 main classes (Vaughan
Williams classification) based on their dominant cellular
electrophysiologic effect.38
Class I Drugs
Class I drugs are subdivided into subclasses a, b, and c. Class I drugs
are sodium channel blockers (membrane-stabilizing drugs) that block
fast sodium channels, slowing conduction in fast-channel tissues
(working atrial and ventricular myocytes, His-Purkinje system).
Class II Drugs
Class II drugs are beta-blockers, which affect predominantly slowchannel tissues (sinoatrial [SA] and atrioventricular [AV] nodes),
where they decrease rate of automaticity, slow conduction velocity,
and prolong refractoriness.
Class III Drugs
Class III drugs are primarily potassium channel blockers, which
prolong action potential duration and refractoriness in slow- and fastchannel tissues.
Class IV Drugs
Class IV drugs are the nondihydropyridine calcium channel blockers,
which depress calcium-dependent action potentials in slow-channel
tissues and thus decrease the rate of automaticity, slow conduction
velocity, and prolong refractoriness.
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Digoxin and adenosine are not included in the Vaughan Williams
classification. Digoxin shortens atrial and ventricular refractory
periods and is vagotonic, thereby prolonging AV nodal conduction and
AV nodal refractory periods. Adenosine slows or blocks AV nodal
conduction and can terminate tachyarrhythmias that rely upon AV
nodal conduction for their perpetuation.
The Vaughan-Williams classification has severe limitations. When
initially conceived, there were relatively few antiarrhythmic drugs and
our understanding of their mechanisms was rudimentary at best. Now
with many more antiarrhythmic drugs, and with a much greater yet
still incomplete understanding of drug mechanisms, this classification
system breaks down especially for the Class I and III drugs.
Many of these drugs have mechanisms of action that are shared with
drugs found the other classes. For example, amiodarone, a Class III
antiarrhythmic, also has sodium and calcium-channel blocking
actions. Many of the Class I compounds also affect potassium
channels. Some of these drugs, it could be argued, could fit in just as
well as a different class than the one that they may be assigned. For
this reason, different sources of information may classify some
antiarrhythmic drugs differently than other sources.78,79
The drugs that make up the different classes differ in their efficacy
(and sometimes safety) for different types of arrhythmias.
The following table provides an overview of drug classes and
associated arrhythmias. Antiarrhythmic agents that are not included
in the Vaughan-Williams scheme are also shown in the table.24
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Condition
Sinus tachycardia
Atrial fibrillation/flutter
Drug
Class II, IV
treatment
Ventricular rate control is
III, IV
important goal; anticoagulation is
digitalis
required
Class IA, IC, II,
supraventricular
III, IV
tachycardia
adenosine
AV block
Atropine
Ventricular tachycardia
Class I, II, III
complexes
Other underlying causes may need
Class IA, IC, II,
Paroxysmal
Premature ventricular
Comments
Class II, IV
magnesium
sulfate
Acute reversal
PVCs are often benign and do not
require treatment
Class IB
Digitalis toxicity
magnesium
sulfate
Class I Antiarrhythmic Drugs
Sodium channel blockers (membrane-stabilizing drugs) block fast
sodium channels, slowing conduction in fast-channel tissues (working
atrial and ventricular myocytes, His-Purkinje system). In the ECG,
this effect may be reflected as widening of the P wave, widening of
the QRS complex, prolongation of the PR interval, or a combination.
Class I drugs are subdivided based on the kinetics of the sodium
channel effects:
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
Class Ib drugs have fast kinetics.

Class Ic drugs have slow kinetics.

Class Ia drugs have intermediate kinetics.
The kinetics of sodium channel blockade determine the heart rates at
which their electrophysiologic effects become manifest. Because class
Ib drugs have fast kinetics, they express their electrophysiologic
effects only at fast heart rates. Thus, an ECG obtained during normal
rhythm at normal rates usually shows no evidence of fast-channel
tissue conduction slowing. Class Ib drugs are not very potent
antiarrhythmics and have minimal effects on atrial tissue. Because
class Ic drugs have slow kinetics, they express their
electrophysiologic effects at all heart rates. Thus, an ECG obtained
during normal rhythm at normal heart rates usually shows fastchannel tissue conduction slowing.
Class Ic drugs are more potent antiarrhythmics. Because class Ia
drugs have intermediate kinetics, their fast-channel tissue conduction
slowing effects may or may not be evident on an ECG obtained during
normal rhythm at normal rates. Class Ia drugs also block repolarizing
potassium channels, prolonging the refractory periods of fast-channel
tissues. On the ECG, this effect is reflected as QT-interval
prolongation even at normal rates. Class Ib drugs and class Ic drugs
do not block potassium channels directly.62,79 The kinetics of sodium
channel blockade determine the heart rates at which their
electrophysiologic effects become manifest.
The primary indications are supraventricular tachycardia (SVT) for
class Ia and Ic drugs and ventricular tachycardia (VTs) for all class I
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drugs. Adverse effects of class I drugs include proarrhythmia, a drugrelated arrhythmia worse than the arrhythmia being treated, which is
the most worrisome adverse effect.
All class I drugs may worsen VTs. Class I drugs also tend to depress
ventricular contractility. Because these adverse effects are more
likely to occur in patients with a structural heart disorder, class I
drugs are not generally recommended for such patients. Thus, these
drugs are usually used only in patients who do not have a structural
heart disorder or in patients who have a structural heart disorder but
who have no other therapeutic alternatives. There are other adverse
effects of class I drugs that are specific to the subclass or individual
drug.14,17,78,80
Class Ia Antiarrhythmic Drugs
Class Ia drugs have kinetics that are intermediate between the fast
kinetics of class Ib and the slow kinetics of class Ic. Their fastchannel tissue conduction slowing effects may or may not be evident
on an ECG obtained during normal rhythm at normal rates. Class Ia
drugs block repolarizing potassium channels, prolonging the
refractory periods of fast-channel tissues. On the ECG, this effect is
reflected as QT-interval prolongation even at normal rates.61
Class Ia drugs are used for suppression of atrial premature beats
(APB), ventricular premature beats (VPB), supraventricular and
ventricular tachycardias, atrial fibrillation (AF), atrial flutter, and
ventricular fibrillation. The primary indications are supraventricular
and ventricular tachycardias. Class Ia drugs may cause torsades de
pointes ventricular tachycardia. Class Ia drugs may organize and slow
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atrial tachyarrhythmias enough to permit 1:1 AV conduction with
marked acceleration of the ventricular response rate.62
Class Ib Antiarrhythmic Drugs
Class Ib drugs have fast kinetics; they express their
electrophysiologic effects only at fast heart rates. Thus, an ECG
obtained during normal rhythm at normal rates usually shows no
evidence of fast-channel tissue conduction slowing. Class Ib drugs are
not very potent antiarrhythmics and have minimal effects on atrial
tissue. Class Ib drugs do not block potassium channels directly. Class
Ib drugs are used for the suppression of ventricular arrhythmias
(ventricular premature beats, ventricular tachycardia, ventricular
fibrillation).38
Class Ic Antiarrhythmic Drugs
Class Ic drugs have slow kinetics; they express their
electrophysiologic effects at all heart rates. Thus, an ECG obtained
during normal rhythm at normal heart rates usually shows fastchannel tissue conduction slowing. Class Ic drugs are more potent
antiarrhythmics than either class Ia or class Ib drugs. Class Ic drugs
do not block potassium channels directly.
Class Ic drugs may organize and slow atrial tachyarrhythmias enough
to permit 1:1 AV conduction with marked acceleration of the
ventricular response rate. Class Ic drugs are used for suppression of
atrial and ventricular premature beats, supraventricular and
ventricular tachycardias, atrial fibrillation, atrial flutter, and
ventricular fibrillation.
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Class II Antiarrhythmic Drugs
Class II antiarrhythmic drugs are beta-blockers, which affect
predominantly slow-channel tissues (SA and AV nodes), where they
decrease rate of automaticity, slow conduction velocity, and prolong
refractoriness. Thus, heart rate is slowed, the PR interval is
lengthened, and the AV node transmits rapid atrial depolarizations at
a lower frequency.68
Class II drugs are used primarily to treat SVTs, including sinus
tachycardia, AV nodal reentry, AF, and atrial flutter. These drugs are
also used to treat VTs to raise the threshold for ventricular fibrillation
(VF) and reduce the ventricular proarrhythmic effects of betaadrenoceptor stimulation.80 Beta-blockers are generally well
tolerated; adverse effects include lassitude, sleep disturbance, and GI
upset. These drugs are contraindicated in patients with asthma.
Class III Antiarrhythmic Drugs
Class III drugs are membrane stabilizing drugs, primarily potassium
channel blockers, which prolong action potential duration and
refractoriness in slow- and fast-channel tissues. Thus, the capacity of
all cardiac tissues to transmit impulses at high frequencies is
reduced, but conduction velocity is not significantly affected. Because
the action potential is prolonged, rate of automaticity is reduced. The
predominant effect on the ECG is QT-interval prolongation. These
drugs are used to treat SVTs and VTs. Class III drugs have a risk of
ventricular proarrhythmia, particularly torsades de pointes VT and are
not used in patients with torsades de pointes VT.61,82
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Class IV Antiarrhythmic Drugs
Class IV drugs are the nondihydropyridine calcium channel blockers,
which depress calcium-dependent action potentials in slow-channel
tissues and thus decrease the rate of automaticity, slow conduction
velocity, and prolong refractoriness. Heart rate is slowed, the PR
interval is lengthened, and the AV node transmits rapid atrial
depolarizations at a lower frequency. These drugs are used primarily
to treat SVTs. They may also be used to slow rapid atrial fibrillation
or atrial flutter. One form of VT (left septal or Belhassen VT) can be
treated with verapamil.30
The following table provides specific information about each drug
used to treat arrhythmias in children.17,24,30,54,79,80
Amiodarone
Life-threatening arrhythmias (tablet):
Amiodarone is intended for use only in patients with indicated life-threatening
arrhythmias because its use is accompanied by substantial toxicity.
Potentially fatal toxicities (tablet):
Amiodarone has several potentially fatal toxicities, the most important of
which is pulmonary toxicity (hypersensitivity pneumonitis or
interstitial/alveolar pneumonitis) that has resulted in clinically manifest
disease at rates as high as 10% to 17% in some series of patients with
ventricular arrhythmias given doses of approximately 400 mg/day, and as
abnormal diffusion capacity without symptoms in a much higher percentage
of patients. Pulmonary toxicity has been fatal approximately 10% of the time.
Liver injury is common with amiodarone, but is usually mild and evidenced
only by abnormal liver enzymes. However, overt liver disease can occur and
has been fatal in a few cases.
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Like other antiarrhythmics, amiodarone can exacerbate the arrhythmia (e.g.,
by making the arrhythmia less well tolerated or more difficult to reverse).
This has occurred in 2% to 5% of patients in various series, and significant
heart block or sinus bradycardia has been seen in 2% to 5%. In most cases,
all of these events should be manageable in the proper clinical setting.
Although the frequency of such proarrhythmic events does not appear greater
with amiodarone than with many other agents used in this population, the
effects are prolonged when they occur.
High-risk patients (tablet):
Even in patients at high risk of arrhythmic death in whom the toxicity of
amiodarone is an acceptable risk, amiodarone poses major management
problems that could be life-threatening in a population at risk of sudden
death; therefore, make every effort to utilize alternative agents first.
The difficulty of using amiodarone effectively and safely poses a significant
risk to patients. Patients with the indicated arrhythmias must be hospitalized
while the loading dose of amiodarone is given, and a response generally
requires at least 1 week, usually 2 weeks or more. Because absorption and
elimination are variable, maintenance dose selection is difficult, and it is not
unusual to require dosage decrease or discontinuation of treatment. In a
retrospective survey of 192 patients with ventricular tachyarrhythmias, 84
patients required dose reduction and 18 required at least temporary
discontinuation because of adverse reactions, and several series have
reported 15% to 20% overall frequencies of discontinuation because of
adverse reactions.
The time at which a previously controlled life-threatening arrhythmia will
recur after discontinuation or dose adjustment is unpredictable, ranging from
weeks to months. The patient is obviously at great risk during this time and
may need prolonged hospitalization. Attempts to substitute other
antiarrhythmic agents when amiodarone must be stopped will be made
difficult by the gradually, but unpredictably, changing amiodarone body
burden. A similar problem exists when amiodarone is not effective; it still
poses the risk of an interaction with whatever subsequent treatment is tried.
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Brand Names:

Cordarone

Nexterone

Pacerone
Pharmacologic Category

Antiarrhythmic Agent, Class III
Dosage:

Pulseless VT or VF (PALS dosing): Infants, Children, and Adolescents IV, I.O.: 5 mg/kg (maximum: 300 mg per dose) rapid bolus; may
repeat twice up to a maximum total dose of 15 mg/kg during acute
treatment (PALS 2010).

Perfusing tachycardias (PALS dosing): Infants, Children, and
Adolescents - IV, I.O.: Loading dose: 5 mg/kg (maximum: 300 mg per
dose) over 20 to 60 minutes; may repeat twice up to maximum total
dose of 15 mg/kg during acute treatment (PALS 2010).
Nadolol
Exacerbation of ischemic heart disease following abrupt withdrawal:
Hypersensitivity to catecholamines has been observed in patients withdrawn
from beta-blocker therapy; exacerbation of angina and, in some cases,
myocardial infarction have occurred after abrupt discontinuation of such
therapy. When discontinuing nadolol administered long term, particularly in
patients with ischemic heart disease, gradually reduce the dosage over a
period of 1 to 2 weeks and carefully monitor the patient.
If angina markedly worsens or acute coronary insufficiency develops,
reinstitute nadolol administration promptly, at least temporarily, and take
other measures appropriate for the management of unstable angina. Warn
patients against interruption or discontinuation of therapy without the health
care provider's advice. Because coronary artery disease is common and may
be unrecognized, it may be prudent not to discontinue nadolol therapy
abruptly, even in patients treated only for hypertension.
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Brand Names:

Corgard
Pharmacologic Category

Antianginal Agent

Antihypertensive

Beta-Blocker, Nonselective
Sotalol
Proarrhythmic effects:
To minimize the risk of induced arrhythmia, patients initiated or reinitiated on
sotalol or sotalol AF and patients who are converted from IV to oral
administration should be placed for a minimum of 3 days (on their
maintenance dose) in a facility that can provide cardiac resuscitation,
continuous electrocardiographic (ECG) monitoring, and calculations of
creatinine clearance (CrCl).
Sotalol injection and oral solution (Sotylize):
Sotalol can cause life threatening ventricular tachycardia associated with QT
interval prolongation. Do not initiate sotalol therapy if the baseline QTc is
longer than 450 msec. If the QT interval prolongs to 500 msec or greater, the
dose must be reduced, the interval between doses prolonged, the duration of
the infusion prolonged (sotalol injection), or the drug discontinued.
Adjust the dosing interval based on CrCl.
Renal impairment:
Calculate CrCl prior to dosing.
Product interchange:
Do not substitute sotalol for sotalol AF because of significant differences in
labeling (i.e., patient package insert, dosing administration, safety
information).
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Brand Names:

Betapace

Betapace AF

Sorine

Sotylize
Pharmacologic Category

Antiarrhythmic Agent, Class II

Antiarrhythmic Agent, Class III

Beta-Blocker, Nonselective
Dosing:
Baseline QTc interval and creatinine clearance must be determined prior to
initiation. If CrCl ≤60 mL/minute, dosing interval adjustment is
necessary. Sotalol should be initiated and doses increased in a hospital for at
least 3 days with facilities for cardiac rhythm monitoring and assessment.
Proarrhythmic events can occur after initiation of therapy and with each
upward dosage adjustment. (Note: Dosing per manufacturer, based on
pediatric pharmacokinetic data; wait at least 36 hours between dosage
adjustments to allow monitoring of QTc intervals).
Atrial fibrillation/flutter (symptomatic): Oral: Betapace AF, Sotylize Infants and Children ≤2 years: Dosage should be adjusted (decreased) by
plotting of the child's age on a logarithmic scale; see graph or refer to
manufacturer's package labeling.
Children >2 years and Adolescents: Initial: 90 mg/m2/day in 3 divided doses;
may be incrementally increased to a maximum of 180 mg/m 2/day
Ventricular arrhythmias: Oral: Betapace, Sorine, Sotylize Infants and Children ≤2 years: Dosage should be adjusted (decreased) by
plotting of the child's age on a logarithmic scale; see graph or refer to
manufacturer's package labeling.
Children >2 years and Adolescents: Initial: 90 mg/m2/day in 3 divided doses;
may be incrementally increased to a maximum of 180 mg/m 2/day.
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Adenosine
Brand Names:

Adenocard

Adenoscan
Pharmacologic Category

Antiarrhythmic Agent, Miscellaneous

Diagnostic Agent
Dosing:
Rapid IV push (over 1 to 2 seconds) via peripheral line, followed by a normal
saline flush.
Paroxysmal supraventricular tachycardia (Adenocard): Infants and
Children - IV:
Manufacturer's labeling:
Children <50 kg: Initial: 0.05 to 0.1 mg/kg (maximum initial dose: 6 mg). If
conversion of PSVT does not occur within 1 to 2 minutes, may increase dose
by 0.05 to 0.1 mg/kg. May repeat until sinus rhythm is established or to a
maximum single dose of 0.3 mg/kg or 12 mg. Follow each dose with normal
saline flush.
Children ≥50 kg: Refer to adult dosing.
Pediatric advanced life support: Treatment of SVT: IV, I.O.: Initial: 0.1 mg/kg
(maximum initial dose: 6 mg); if not effective within 1 to 2 minutes,
administer 0.2 mg/kg (maximum single dose: 12 mg). Follow each dose with
≥5 mL normal saline flush.
Diltiazem
Brand Names:

Cardizem

Cardizem CD

Cardizem LA
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
Cartia XT

Dilacor XR [DSC]

Dilt-CD [DSC]

Dilt-XR

Diltiazem CD

Diltiazem HCl CD [DSC]

Diltzac [DSC]

Matzim LA

Taztia XT

Tiazac
Pharmacologic Category

Antianginal Agent

Antiarrhythmic Agent, Class IV

Antihypertensive

Calcium Channel Blocker

Calcium Channel Blocker, Nondihydropyridine
Dosing:
Children: Minimal information available; some centers use the following:
Hypertension (off-label use): Oral: Initial: 1.5-2 mg/kg/day in 3 divided
doses (maximum: 6 mg/kg/day, up to 360 mg daily). Adolescents Angina: Oral:
Capsule, extended release:
Dilacor XR, Dilt-XR: Initial: 120 mg once daily; titrate over 7 to 14 days;
usual dose range - 120 to 320 mg daily: maximum: 480 mg daily.
Cardizem CD, Cartia XT: Initial: 120 to 180 mg once daily; titrate over 7 to
14 days; usual dose range: 120 to 320 mg daily; maximum: 480 mg daily.
Tiazac, Taztia XT: Initial: 120 to 180 mg once daily; titrate over 7 to 14 days;
usual dose range - 120 to 320 mg daily; maximum: 540 mg daily.
Tablet, extended release (Cardizem LA, Matzim LA, Tiazac XC [Canadian
product]): 180 mg once daily; may increase at 7- to 14-day intervals; usual
dose range: 120 to 320 mg/day; maximum: 360 mg daily.
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Tablet, immediate release (Cardizem): Usual starting dose: 30 mg 4 times
daily; titrate dose gradually at 1- to 2-day intervals; usual dose range: 120 to
320 mg daily in 4 divided doses.
Hypertension: Oral:
Capsule, extended release (once-daily dosing):
Cardizem CD, Cartia XT: Initial: 180 to 240 mg once daily; dose adjustment
may be made after 14 days; usual dose range: 240 to 360 mg daily;
maximum: 480 mg daily
Dilacor XR, Dilt-XR: Initial: 180 to 240 mg once daily; dose adjustment may
be made after 14 days; usual dose range: 240 to 360 mg daily; maximum:
540 mg daily.
Tiazac, Taztia XT: Initial: 120 to 240 mg once daily; dose adjustment may be
made after 14 days; usual dose range: 240 to 360 mg daily; maximum: 540
mg daily.
Capsule, extended release (twice-daily dosing): Initial: 60 to 120 mg twice
daily; dose adjustment may be made after 14 days; usual range: 240 to 360
mg daily.
Note: Diltiazem is available as a generic intended for either once- or twicedaily dosing, depending on the formulation; verify appropriate extended
release capsule formulation is administered.
Tablet, extended release (Cardizem LA, Matzim LA, Tiazac XC [Canadian
product]): Initial: 180 to 240 mg once daily; dose adjustment may be made
after 14 days; usual dose range: 240-360 mg daily; maximum: 540 mg daily.
Atrial fibrillation, atrial flutter, PSVT:
Initial IV bolus dose: 0.25 mg/kg actual body weight over 2 minutes (average
adult dose: 20 mg); ACLS guideline recommends 15 to 20 mg.
Repeat bolus dose (may be administered after 15 minutes if the response is
inadequate): 0.35 mg/kg actual body weight over 2 minutes (average adult
dose: 25 mg); ACLS guideline recommends 20 to 25 mg.
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Continuous infusion (infusions >24 hours or infusion rates >15 mg/hour are
not recommended): Initial infusion rate of 10 mg/hour; rate may be
increased in 5 mg/hour increments up to 15 mg/hour as needed; some
patients may respond to an initial rate of 5 mg/hour.
If diltiazem injection is administered by continuous infusion for >24 hours,
the possibility of decreased diltiazem clearance, prolonged elimination halflife, and increased diltiazem and/or diltiazem metabolite plasma
concentrations should be considered.
Atrial fibrillation (rate control) (off-label use): Oral: Extended release
(capsule or tablet): Usual maintenance dose: 120 to 360 mg once daily.
Conversion from IV diltiazem to oral diltiazem:
Oral dose (mg daily) is approximately equal to [rate (mg/hour) x 3 + 3] x 10.
3 mg/hour = 120 mg daily
5 mg/hour = 180 mg daily
7 mg/hour = 240 mg daily
11 mg/hour = 360 mg daily
Atenolol
Advise patients with coronary artery disease who are being treated with
atenolol against abrupt discontinuation of therapy. Severe exacerbation of
angina and the occurrence of myocardial infarction (MI) and ventricular
arrhythmias have been reported in patients with angina following the abrupt
discontinuation of therapy with beta-blockers. The last 2 complications may
occur with or without preceding exacerbation of the angina pectoris. As with
other beta-blockers, when discontinuation of atenolol is planned, observe the
patient carefully and advise the patient to limit physical activity to a
minimum. If the angina worsens or acute coronary insufficiency develops, it is
recommended that atenolol be promptly reinstituted, at least temporarily.
Because coronary artery disease is common and may be unrecognized, it may
be prudent not to discontinue atenolol therapy abruptly, even in patients
treated only for hypertension.
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Brand Names:

Tenormin
Pharmacologic Category

Antianginal Agent

Antihypertensive

Beta-Blocker, Beta-1 Selective
Dosing:
Hypertension: Oral: Children: 0.5 to 1 mg/kg/dose given daily; range of 0.5
to 1.5 mg/kg/day; maximum dose: 2 mg/kg/day up to 100 mg/day.
Esmolol
Brand Names:

Brevibloc

Brevibloc in NaCl
Pharmacologic Category

Antiarrhythmic Agent, Class II

Antihypertensive

Beta-Blocker, Beta-1 Selective
Dosing:
Intraoperative and postoperative tachycardia and/or hypertension:
Immediate control: Initial IV bolus: 1 mg/kg over 30 seconds, followed by a
150 mcg/kg/minute infusion, if necessary. Adjust infusion rate as needed to
maintain desired heart rate and/or blood pressure (up to 300 mcg/kg/minute)
Gradual control: Initial bolus: 0.5 mg/kg over 1 minute, followed by a 50
mcg/kg/minute infusion for 4 minutes. Infusion may be continued at 50
mcg/kg/minute or, if the response is inadequate, titrated upward in 50
mcg/kg/minute increments (increased no more frequently than every 4
minutes) to a maximum of 300 mcg/kg/minute; may administer an optional
loading dose equal to the initial bolus (0.5 mg/kg over 1 minute) prior to each
increase in infusion rate.
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For control of tachycardia, doses >200 mcg/kg/minute provide minimal
additional effect. For control of postoperative hypertension, as many as onethird of patients may require higher doses (250-300 mcg/kg/minute) to
control blood pressure; the safety of doses >300 mcg/kg/minute has not
been studied.
Supraventricular tachycardia (SVT) or noncompensatory sinus
tachycardia: IV Loading dose (optional): 0.5 mg/kg over 1 minute; follow
with a 50 mcg/kg/minute infusion for 4 minutes; response to this initial
infusion rate may be a rough indication of the responsiveness of the
ventricular rate.
Infusion may be continued at 50 mcg/kg/minute or, if the response is
inadequate, titrated upward in 50 mcg/kg/minute increments (increased no
more frequently than every 4 minutes) to a maximum of 200 mcg/kg/minute.
To achieve more rapid response, following the initial loading dose and 50
mcg/kg/minute infusion, rebolus with a second 0.5 mg/kg loading dose over 1
minute, and increase the maintenance infusion to 100 mcg/kg/minute for 4
minutes. If necessary, a third (and final) 0.5 mg/kg loading dose may be
administered, prior to increasing to an infusion rate of 150 mcg/kg/minute.
After 4 minutes of the 150 mcg/kg/minute infusion, the infusion rate may be
increased to a maximum rate of 200 mcg/kg/minute (without a bolus dose).
(Note: If a loading dose is not administered, a continuous infusion at a fixed
dose reaches steady-state in ~30 minutes. In general, the usual effective
dose is 50-200 mcg/kg/minute; doses as low as 25 mcg/kg/minute may be
adequate. Maintenance infusions may be continued for up to 48 hours).
Acute coronary syndromes (when relative contraindications to betablockade exist; off-label use): IV: 0.5 mg/kg over 1 minute; follow with a
50 mcg/kg/minute infusion; if tolerated and response inadequate, may titrate
upward in 50 mcg/kg/minute increments every 5-15 minutes to a maximum
of 300 mcg/kg/minute (Mitchell, 2002); an additional bolus (0.5 mg/kg over 1
minute) may be administered prior to each increase in infusion rate.
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Electroconvulsive therapy (off-label use): 1 mg/kg administered IV, 1
minute prior to induction of anesthesia.
Intubation (off-label use): 1-2 mg/kg IV given 1.5-3 minutes prior to
intubation.
Thyrotoxicosis or thyroid storm (off-label use): 50-100 mcg/kg/minute
IV.
Digoxin
Brand Names:

Digitek

Digox

Lanoxin

Lanoxin Pediatric
Pharmacologic Category

Antiarrhythmic Agent, Miscellaneous

Cardiac Glycoside
Dosing:
Preterm infant
• Total digitalizing dose:
– Oral: 20-30 mcg/kg
– IV or IM: 15-25 mcg/kg
• Daily maintenance dose:
– Oral: 5-7.5 mcg/kg
– IV or IM: 4-6 mcg/kg
Full-term infant:
• Total digitalizing dose:
– Oral: 25-35 mcg/kg
– IV or IM: 20-30 mcg/kg
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• Daily maintenance dose:
– Oral: 6-10 mcg/kg; and, IV or IM: 5-8 mcg/kg
1 month to 2 years:
• Total digitalizing dose:
– Oral: 35-60 mcg/kg
– IV or IM: 30-50 mcg/kg
• Daily maintenance dose:
– Oral: 10-15 mcg/kg
– IV or IM: 7.5-12 mcg/kg
2-5 years:
• Total digitalizing dose:
– Oral: 30-40 mcg/kg
– IV or IM: 25-35 mcg/kg
• Daily maintenance dose:
– Oral: 7.5-10 mcg/kg
– IV or IM: 6-9 mcg/kg
5-10 years:
• Total digitalizing dose:
– Oral: 20-35 mcg/kg
– IV or IM: 15-30 mcg/kg
• Daily maintenance dose:
– Oral: 5-10 mcg/kg
– IV or IM: 4-8 mcg/kg
>10 years:
• Total digitalizing dose:
– Oral: 10-15 mcg/kg
– IV or IM: 8-12 mcg/kg
• Daily maintenance dose:
– Oral: 2.5-5 mcg/kg
– IV or IM: 2-3 mcg/kg
Heart failure: A lower serum digoxin concentration may be adequate to treat
heart failure (compared to cardiac arrhythmias); consider doses at the lower
end of the recommended range for treatment of heart failure; a digitalizing
dose (loading dose) may not be necessary when treating heart failure.
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Based on lean body weight and normal renal function for age. Decrease dose
in patients with decreased renal function; digitalizing dose often not
recommended in infants and children.
Do not give full total digitalizing dose (TDD) at once. Give one-half of the total
digitalizing dose (TDD) in the initial dose, then give one-quarter of the TDD in
each of two subsequent doses at 6- to 8-hour intervals. Obtain ECG 6 hours
after each dose to assess potential toxicity.
Divided every 12 hours in infants and children <10 years of age. Give once
daily to children >10 years of age and adults. IM not preferred due to severe
injection site pain. If IM route is necessary, administer as deep injection
followed by massage of injection site.
Metoprolol
ALERT: US Boxed Warning
Ischemic heart disease
Following abrupt cessation of therapy with certain beta-blocking agents,
exacerbations of angina pectoris and, in some cases, myocardial infarction
(MI) have occurred. When discontinuing chronically administered metoprolol,
particularly in patients with ischemic heart disease, gradually reduce the
dosage over a period of 1 to 2 weeks and carefully monitor the patient. If
angina markedly worsens or acute coronary insufficiency develops, reinstate
metoprolol administration promptly, at least temporarily, and take other
measures appropriate for the management of unstable angina. Warn patients
against interruption or discontinuation of therapy without their health care
provider's advice. Because coronary artery disease is common and may be
unrecognized, it may be prudent not to discontinue metoprolol therapy
abruptly, even in patients treated only for hypertension.
Brand Names:

Lopressor

Toprol XL
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Pharmacologic Category

Antianginal Agent

Antihypertensive

Beta-Blocker, Beta-1 Selective
Dosing:
Hypertension: Oral:
Immediate release tablet (metoprolol tartrate): Children: 1 to 17 years:
Initial: 1 to 2 mg/kg/day; maximum 6 mg/kg/day (≤200 mg daily);
administer in 2 divided doses.
Extended release tablet (metoprolol succinate): Children ≥6 years: Initial: 1
mg/kg once daily (maximum initial dose: 50 mg daily). Adjust dose based on
patient response (maximum: 2 mg/kg/day or 200 mg daily).
Use: Labeled Indications
Immediate-release tablets (metoprolol tartrate): Treatment of angina
pectoris, hypertension, or hemodynamically-stable acute myocardial
infarction.
Extended-release tablets (metoprolol succinate): Treatment of angina
pectoris or hypertension; to reduce mortality/hospitalization in patients with
heart failure (HF) (stable NYHA Class II or III) already receiving ACE
inhibitors, diuretics, and/or digoxin.
Injectable (metoprolol tartrate): Treatment of hemodynamically-stable
acute myocardial infarction when used in conjunction with metoprolol oral
maintenance therapy.
Acute coronary syndromes (i.e., myocardial infarction, unstable angina):
According to the ACCF/AHA 2013 guidelines for the management of STelevation myocardial infarction (STEMI) and the guidelines for the
management of unstable angina/non-STEMI, oral beta-blockers should be
initiated within the first 24 hours unless the patient has signs of heart failure,
evidence of a low-output state, an increased risk for cardiogenic shock, or
other contraindications.
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Intravenous use should be reserved for those patients who have refractory
hypertension or ongoing ischemia.
Heart failure: The ACCF/AHA 2013 heart failure guidelines recommend the
use of 1 of 3 beta blockers (i.e., bisoprolol, carvedilol, or extended-release
metoprolol succinate) for all patients with recent or remote history of MI or
ACS and reduced ejection fraction (rEF) to reduce mortality, for all patients
with rEF to prevent symptomatic HF (even if no history of MI), and for all
patients with current or prior symptoms of HF with reduced ejection fraction
(HFrEF), unless contraindicated, to reduce morbidity and mortality.
Chronic kidney disease (CKD) and hypertension: Regardless of race or
diabetes status, the use of an ACE inhibitor (ACEI) or angiotensin receptor
blocker (ARB) as initial therapy is recommended to improve kidney outcomes.
In the general nonblack population (without CKD) including those with
diabetes, initial antihypertensive treatment should consist of a thiazide-type
diuretic, calcium channel blocker, ACEI, or ARB. In the general black
population (without CKD) including those with diabetes, initial
antihypertensive treatment should consist of a thiazide-type diuretic or a
calcium channel blocker instead of an ACEI or ARB.
Coronary artery disease (CAD) and hypertension: The American Heart
Association, American College of Cardiology and American Society of
Hypertension (AHA/ACC/ASH) 2015 scientific statement for the treatment of
hypertension in patients with coronary artery disease (CAD) recommends the
use of a beta blocker as part of a regimen in patients with hypertension and
chronic stable angina with a history of prior MI.
A BP target of <140/90 mm Hg is reasonable for the secondary prevention of
cardiovascular events.
A lower target BP (<130/80 mm Hg) may be appropriate in some individuals
with CAD, previous MI, stroke or transient ischemic attack, or CAD risk
equivalents.
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Acebutolol
Brand Names:

Sectral
Pharmacologic Category

Antiarrhythmic Agent, Class II

Antihypertensive

Beta-Blocker With Intrinsic Sympathomimetic Activity

Beta-Blocker, Beta-1 Selective
Dosing:
Angina, ventricular arrhythmia: Oral: 400 mg/day in 2 divided doses;
maintenance: 600 to 1200 mg/day in divided doses; maximum: 1200 mg/day
Hypertension: Oral: Initial: 400 mg in 1 to 2 divided doses; optimal response
usually seen at 400 to 800 mg daily (larger doses may be divided) although
some patients may respond to as little as 200 mg daily; usual dose range:
200 to 400 mg daily; maximum dose: 1200 mg in 2 divided doses
Chronic stable angina (off-label use): Oral: Usual dose: 400 to 1200
mg/day in 2 divided doses; low doses (i.e., 400 mg/day) may also be given
as once daily.
Use: Labeled Indications
Treatment of hypertension; management of ventricular arrhythmias
The 2014 guideline for the management of high blood pressure in adults
(Eighth Joint National Committee, JNC 8; James, 2013) recommends initiation
of pharmacologic treatment to lower blood pressure for the following patients:
• Patients ≥60 years of age with systolic blood pressure (SBP) ≥150 mm Hg
or diastolic blood pressure (DBP) ≥90 mm Hg. Goal of therapy is SBP <150
mm Hg and DBP <90 mm Hg.
• Patients <60 years of age with SBP ≥140 mm Hg or DBP ≥90 mm Hg. Goal
of therapy is SBP <140 mm Hg and DBP <90 mm Hg.
• Patients ≥18 years of age with diabetes and SBP ≥140 mm Hg or DBP ≥90
mm Hg. Goal of therapy is SBP <140 mm Hg and DBP <90 mm Hg.
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• Patients ≥18 years of age with chronic kidney disease (CKD) and SBP ≥140
mm Hg or DBP ≥90 mm Hg. Goal of therapy is SBP <140 mm Hg and DBP
<90 mm Hg.
In patients with CKD, regardless of race or diabetes status, the use of an ACE
inhibitor (ACEI) or angiotensin receptor blocker (ARB) as initial therapy is
recommended to improve kidney outcomes. In the general nonblack
population (without CKD), including those with diabetes, initial
antihypertensive treatment should consist of a thiazide-type diuretic, calcium
channel blocker, ACEI, or ARB. In the general black population (without CKD),
including those with diabetes, initial antihypertensive treatment should
consist of a thiazide-type diuretic or a calcium channel blocker instead of an
ACEI or ARB.
Bisoprolol
Brand Names:

Zebeta
Pharmacologic Category

Antihypertensive

Beta-Blocker, Beta-1 Selective
Dosing: Adult
Hypertension: Oral: Initial: 2.5 to 5 mg once daily; may be increased to 10
mg and then up to 20 mg once daily, if necessary; usual dose range: 5 to 10
mg once daily.
Atrial fibrillation (rate control) (off-label use): Usual maintenance dose:
2.5 to 10 mg once daily.
Heart failure (off-label use): Oral: Initial: 1.25 mg once daily; maximum
dose: 10 mg once daily. (Note: Initiate only in stable patients or hospitalized
patients after volume status has been optimized and IV diuretics,
vasodilators, and inotropic agents have all been successfully discontinued).
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Caution should be used when initiating in patients who required inotropes
during their hospital course. Increase dose gradually and monitor for
congestive signs and symptoms of HF making every effort to achieve target
dose shown to be effective
Use: Labeled Indications
Hypertension: Treatment of hypertension, alone or in combination with
other agents
Hypertension: The 2014 guideline for the management of high blood pressure
in adults (Eighth Joint National Committee [JNC 8]) recommends initiation of
pharmacologic treatment to lower blood pressure for the following patients:
• Patients ≥60 years of age, with systolic blood pressure (SBP) ≥150 mm Hg
or diastolic blood pressure (DBP) ≥90 mm Hg. Goal of therapy is SBP <150
mm Hg and DBP <90 mm Hg.
• Patients <60 years of age, with SBP ≥140 mm Hg or DBP ≥90 mm Hg. Goal
of therapy is SBP <140 mm Hg and DBP <90 mm Hg.
• Patients ≥18 years of age with diabetes, with SBP ≥140 mm Hg or DBP ≥90
mm Hg. Goal of therapy is SBP <140 mm Hg and DBP <90 mm Hg.
• Patients ≥18 years of age with chronic kidney disease (CKD), with SBP
≥140 mm Hg or DBP ≥90 mm Hg. Goal of therapy is SBP <140 mm Hg and
DBP <90 mm Hg.
Chronic kidney disease (CKD) and hypertension: Regardless of race or
diabetes status, the use of an ACE inhibitor (ACEI) or angiotensin receptor
blocker (ARB) as initial therapy is recommended to improve kidney outcomes.
In the general nonblack population (without CKD) including those with
diabetes, initial antihypertensive treatment should consist of a thiazide-type
diuretic, calcium channel blocker, ACEI, or ARB. In the general black
population (without CKD) including those with diabetes, initial
antihypertensive treatment should consist of a thiazide-type diuretic or a
calcium channel blocker instead of an ACEI or ARB.
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Coronary artery disease (CAD) and hypertension: The American Heart
Association, American College of Cardiology and American Society of
Hypertension 2015 scientific statement for the treatment of hypertension in
patients with coronary artery disease (CAD) recommends the use of a beta
blocker as part of a regimen in patients with hypertension and chronic stable
angina with a history of prior MI.
A BP target of <140/90 mm Hg is reasonable for the secondary prevention of
cardiovascular events. A lower target BP (<130/80 mm Hg) may be
appropriate in some individuals with CAD, previous MI, stroke or transient
ischemic attack, or CAD risk equivalents.
Carvedilol
Brand Names:

Coreg

Coreg CR
Pharmacologic Category

Antihypertensive

Beta-Blocker With Alpha-Blocking Activity
Dosing: Adult
Reduce dosage if heart rate drops to <55 beats/minute.
Hypertension: Oral:
Immediate release: 6.25 mg twice daily; if tolerated, dose should be
maintained for 1 to 2 weeks, then increased to 12.5 mg twice daily. If
necessary, dosage may be increased to a maximum of 25 mg twice daily after
1 to 2 weeks. Usual dosage range: 6.25 to 25 mg twice daily.
Extended release: Initial: 20 mg once daily, if tolerated, dose should be
maintained for 1 to 2 weeks then increased to 40 mg once daily if necessary;
if this dose is tolerated, maintain for 1 to 2 weeks then, if necessary, increase
to 80 mg once daily; maximum dose: 80 mg once daily.
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Heart failure: Oral:
(Note: Initiate only in stable patients or hospitalized patients after volume
status has been optimized and IV diuretics, vasodilators, and inotropic agents
have all been successfully discontinued. Caution should be used when
initiating in patients who required inotropes during their hospital course.
Increase dose gradually and monitor for congestive signs and symptoms of
HF making every effort to achieve target dose shown to be effective).
Immediate release: 3.125 mg twice daily for 2 weeks; if this dose is
tolerated, may increase to 6.25 mg twice daily. Double the dose every 2
weeks to the highest dose tolerated by patient. (Prior to initiating therapy,
other heart failure medications should be stabilized and fluid retention
minimized).
Maximum recommended dose:
Mild-to-moderate heart failure <85 kg: 25 mg twice daily
>85 kg: 50 mg twice daily
Severe heart failure: 25 mg twice daily.
Extended release: Initial: 10 mg once daily for 2 weeks; if the dose is
tolerated, increase dose to 20 mg, 40 mg, and 80 mg over successive
intervals of at least 2 weeks. Maintain on lower dose if higher dose is not
tolerated. (Note: The 2013 ACCF/AHA heart failure guidelines recommend a
maximum dose of 80 mg once daily).
Left ventricular dysfunction following MI: Oral: (Note: Should be
initiated only after patient is hemodynamically stable and fluid retention has
been minimized).
Immediate release: Initial 3.125 to 6.25 mg twice daily; increase dosage
incrementally (i.e., from 6.25 to 12.5 mg twice daily) at intervals of 3 to 10
days, based on tolerance, to a target dose of 25 mg twice daily. (Note: The
2013 ACCF/AHA heart failure guidelines recommend a maximum dose of 50
mg twice daily).
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Extended release: Initial: Extended release: Initial: 10 to 20 mg once daily;
increase dosage incrementally at intervals of 3 to 10 days, based on
tolerance, to a target dose of 80 mg once daily.
Angina pectoris (off-label use): Oral: Immediate release: 25 to 50 mg
twice daily.
Atrial fibrillation (rate control) (off-label use): Usual maintenance dose:
3.125 to 25 mg twice daily. In patients with heart failure, the initial dose of
3.125 mg twice daily may be increased at 2-week intervals to a target dose of
25 mg twice daily (50 mg twice daily for patients weighing >85 kg).
Conversion from immediate release to extended release (Coreg CR):
Current dose immediate release tablets 3.125 mg twice daily: Convert to
extended release capsules 10 mg once daily.
Current dose immediate release tablets 6.25 mg twice daily: Convert to
extended release capsules 20 mg once daily.
Current dose immediate release tablets 12.5 mg twice daily: Convert to
extended release capsules 40 mg once daily.
Current dose immediate release tablets 25 mg twice daily: Convert to
extended release capsules 80 mg once daily.
Use: Labeled Indications
Hypertension: Management of hypertension.
The 2014 guideline for the management of high blood pressure in adults
recommends initiation of pharmacologic treatment to lower blood pressure for
the following patients:
• Patients ≥60 years of age, with systolic blood pressure (SBP) ≥150 mm Hg
or diastolic blood pressure (DBP) ≥90 mm Hg. Goal of therapy is SBP <150
mm Hg and DBP <90 mm Hg.
• Patients <60 years of age, with SBP ≥140 mm Hg or DBP ≥90 mm Hg. Goal
of therapy is SBP <140 mm Hg and DBP <90 mm Hg.
• Patients ≥18 years of age with diabetes, with SBP ≥140 mm Hg or DBP ≥90
mm Hg. Goal of therapy is SBP <140 mm Hg and DBP <90 mm Hg.
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• Patients ≥18 years of age with chronic kidney disease (CKD), with SBP
≥140 mm Hg or DBP ≥90 mm Hg. Goal of therapy is SBP <140 mm Hg and
DBP <90 mm Hg.
In patients with CKD, regardless of race or diabetes status, the use of an ACE
inhibitor (ACEI) or angiotensin receptor blocker (ARB) as initial therapy is
recommended to improve kidney outcomes. In the general non-black
population (without CKD) including those with diabetes, initial
antihypertensive treatment should consist of a thiazide-type diuretic, calcium
channel blocker, ACEI, or ARB. In the general black population (without CKD)
including those with diabetes, initial antihypertensive treatment should
consist of a thiazide-type diuretic or a calcium channel blocker instead of an
ACEI or ARB.
Heart failure: Mild to severe chronic heart failure of ischemic or
cardiomyopathic origin (usually in addition to standard therapy, i.e., diuretics,
ACE inhibitors). The ACCF/AHA 2013 heart failure guidelines recommend the
use of 1 of the 3 beta blockers (i.e., bisoprolol, carvedilol, or extendedrelease metoprolol succinate) for all patients with recent or remote history of
MI or ACS and reduced ejection fraction (rEF) to reduce mortality, for all
patients with rEF to prevent symptomatic HF (even if no history of MI), and
for all patients with current or prior symptoms of HF with reduced ejection
fraction (HFrEF), unless contraindicated, to reduce morbidity and mortality.
Left ventricular dysfunction following myocardial infarction (MI): Left
ventricular dysfunction following MI (clinically stable with LVEF ≤40%).
Propafenone
ALERT: US Boxed Warning
Mortality:
In the National Heart, Lung, and Blood Institute's Cardiac Arrhythmia
Suppression Trial (CAST), a long-term, multicenter, randomized, double-blind
study in patients with asymptomatic non–life-threatening ventricular
arrhythmias who had a myocardial infarction (MI) more than 6 days but less
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than 2 years previously, an increased rate of death or reversed cardiac arrest
rate (7.7%) was seen in patients treated with encainide or flecainide (class IC
antiarrhythmics) compared with that seen in patients assigned to placebo
(3%). The average duration of treatment with encainide or flecainide in this
study was 10 months.
The applicability of the CAST results to other populations (i.e., those without
recent MI) or other antiarrhythmic drugs is uncertain, but at present, it is
prudent to consider any IC antiarrhythmic to have a significant risk in patients
with structural heart disease. Given the lack of any evidence that these drugs
improve survival, generally avoid antiarrhythmic agents in patients with non–
life-threatening ventricular arrhythmias, even if the patients are experiencing
unpleasant, but not life-threatening, symptoms or signs.
Brand Names:

Rythmol

Rythmol SR
Pharmacologic Category

Antiarrhythmic Agent, Class Ic
Dosing:
Patients who exhibit significant widening of QRS complex or second- or thirddegree AV block may need dose reduction.
Atrial fibrillation (to prevent recurrence): Oral:
Extended release capsule: Initial: 225 mg every 12 hours; dosage increase
may be made at a minimum of 5-day intervals; may increase to 325 mg
every 12 hours; if further increase is necessary, may increase to 425 mg
every 12 hours
Immediate release tablet: Initial: 150 mg every 8 hours; dosage increase
may be made at minimum of 3- to 4-day intervals, may increase to 225 mg
every 8 hours; if further increase is necessary, may increase to 300 mg every
8 hours.
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Paroxysmal supraventricular tachycardia (to prevent recurrence),
ventricular arrhythmias: Oral: Immediate release tablet: Initial: 150 mg
every 8 hours (US labeling) or 300 mg every 12 hours (Canadian labeling);
dosage increase may be made at minimum of 3- to 4-day intervals, may
increase to 225 mg every 8 hours; if further increase is necessary, may
increase to 300 mg every 8 hours.
Paroxysmal atrial fibrillation, pharmacologic cardioversion (off-label
use): Oral: Immediate release tablet: Outpatient: "Pill-in-the-pocket" dose:
450 mg (weight <70 kg), 600 mg (weight ≥70 kg). May not repeat in ≤24
hours. (Note: An initial inpatient cardioversion trial should have been
successful before sending patient home on this approach. Patient must be
taking an AV nodal-blocking agent (e.g., beta-blocker, nondihydropyridine
calcium channel blocker) prior to initiation of antiarrhythmic).
Use: Labeled Indications
Treatment of life-threatening ventricular arrhythmias; to prolong the time to
recurrence of paroxysmal atrial fibrillation/flutter (PAF) or paroxysmal
supraventricular tachycardia (PSVT) in patients with disabling symptoms
without structural heart disease.
Extended release capsule: Prolong the time to recurrence of symptomatic
atrial fibrillation in patients without structural heart disease
Disopyramide
ALERT: US Boxed Warning
Mortality:
In the National Heart, Lung, and Blood Institute's Cardiac Arrhythmia
Suppression Trial (CAST), a long-term, multicenter, randomized, double-blind
study in patients with asymptomatic non-life-threatening ventricular
arrhythmias who had an MI more than 6 days but less than 2 years
previously, an excessive mortality or nonfatal cardiac arrest rate (7.7%) was
seen in patients treated with encainide or flecainide compared with that seen
in patients assigned to carefully matched placebo-treated groups (3%).
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The average duration of treatment with encainide or flecainide in this study
was 10 months.
The applicability of the CAST results to other populations (i.e., those without
recent MI) is uncertain. Considering the known proarrhythmic properties of
disopyramide and the lack of evidence of improved survival for any
antiarrhythmic drug in patients without life-threatening arrhythmias, the use
of disopyramide as well as other antiarrhythmic agents should be reserved for
patients with life-threatening ventricular arrhythmias.
Brand Names:

Norpace

Norpace CR
Pharmacologic Category

Antiarrhythmic Agent, Class Ia
Dosing:
Arrhythmias: Oral: Immediate release:
<1 year: 10 to 30 mg/kg/24 hours in 4 divided doses
1 to 4 years: 10 to 20 mg/kg/24 hours in 4 divided doses
4 to 12 years: 10 to 15 mg/kg/24 hours in 4 divided doses
12 to 18 years: 6 to 15 mg/kg/24 hours in 4 divided doses
Use: Labeled Indications
Life-threatening ventricular arrhythmias (i.e., sustained ventricular
tachycardia)
Mexiletine
ALERT: US Boxed Warning
Mortality:
In the National Heart, Lung, and Blood Institute's Cardiac Arrhythmia
Suppression Trial (CAST), a long-term, multicenter, randomized, double-blind
study in patients with asymptomatic non–life-threatening ventricular
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arrhythmias who had an myocardial infarction (MI) more than 6 days but less
than 2 years previously, an excessive mortality or nonfatal cardiac arrest rate
(7.7%) was seen in patients treated with encainide or flecainide compared
with that seen in patients assigned to carefully matched placebo-treated
groups (3%). The average duration of treatment with encainide or flecainide
in this study was 10 months.
The applicability of the CAST results to other populations (i.e., those without
recent MI) is uncertain. Considering the known proarrhythmic properties of
mexiletine and the lack of evidence of improved survival for any
antiarrhythmic drug in patients without life-threatening arrhythmias, the use
of mexiletine as well as other antiarrhythmic agents should be reserved for
patients with life-threatening ventricular arrhythmias.
Acute liver injury:
In postmarketing experience, abnormal liver function tests have been
reported, some in the first few weeks of therapy with mexiletine. Most of
these have been observed in the setting of congestive heart failure or
ischemia and their relationship to mexiletine has not been established.
Brand Names:

Novo-Mexiletine
Pharmacologic Category

Antiarrhythmic Agent, Class Ib
Dosing:
Ventricular arrhythmias (life-threatening): Oral: Initial: 200 mg every 8
hours (may load with 400 mg if necessary); adjust dose in 50 or 100 mg
increments no more frequently than every 2 to 3 days; usual dose: 200 to
300 mg every 8 hours; maximum dose: 1.2 g/day. (Note: Once controlled,
patients may be transferred to an every 12-hour dosing schedule; do not
exceed 450 mg every 12 hours with this regimen).
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Conversion:
Switching from other oral antiarrhythmics (i.e., disopyramide, quinidine
sulfate): Initiate 200 mg dose of mexiletine 6 to 12 hours after the last dose
of the former agent.
Switching from IV lidocaine: Initiate 200 mg dose of mexiletine when
lidocaine infusion is stopped.
Switching from oral procainamide: Initiate a 200 mg dose of mexiletine 3 to 6
hours after the last dose of procainamide.
Premature ventricular complex (symptomatic) suppression (off-label
use): Oral: 100 or 150 mg 3 times daily; if not controlled, may increase to
200 mg 3 times daily (Saikawa 1992; Tanabe 1991) or 100 or 200 mg 2 to 3
times daily; may progressively increase to a maximum dose of 500 mg 3
times daily.
Use: Labeled Indications
Ventricular arrhythmias: Management of life-threatening ventricular
arrhythmias. (Note: The American College of Cardiology/American Heart
Association/European Society of Cardiology (ACC/AHA/ESC) states that
mexiletine may be considered for those with long QT syndrome who present
with torsades de pointes).
Propranolol
ALERT: US Boxed Warning
Cardiac ischemia after abrupt discontinuation (Inderal LA, Inderal XL,
Innopran XL): Following abrupt discontinuation of therapy with beta-blockers,
exacerbations of angina pectoris and myocardial infarction (MI) have
occurred. When discontinuing long-term administration of propranolol,
particularly in patients with ischemic heart disease, gradually reduce the dose
over a period of 1 to 2 weeks and monitor the patient. If angina markedly
worsens or acute coronary insufficiency develops, promptly resume therapy,
at least temporarily, and take other measures appropriate for the
management of unstable angina.
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Warn patients against interruption or discontinuation of therapy without
health care provider's advice. Because coronary artery disease is common
and may be unrecognized, avoid abrupt discontinuation of propranolol
therapy, even in patients treated only for hypertension.
Brand Names:

Hemangeol

Inderal LA

Inderal XL

InnoPran XL
Pharmacologic Category

Antianginal Agent

Antiarrhythmic Agent, Class II

Antihypertensive

Beta-Blocker, Nonselective
Dosing: Pediatric
Proliferating infantile hemangioma (Hemangeol): Infants ≥2 kg:
(Note: Initiate treatment at age 5 weeks to 5 months; doses should be
administered at least 9 hours apart. Refer to product labeling for detailed
weight-based dosing tabulation).
Week 1: 0.15 mL/kg (~0.6 mg/kg) twice daily
Week 2: 0.3 mL/kg (~1.1 mg/kg) twice daily
Week 3 (maintenance): 0.4 mL/kg (~1.7 mg/kg) twice daily; maintain this
dose for 6 months.
Readjust dose periodically as the child's weight increases. Treatment may be
reinitiated if hemangiomas recur.
Hypertension (off-label use): Children and Adolescents: Oral: Immediaterelease formulations: Initial: 1 to 2 mg/kg/day divided in 2 to 3 doses/day;
titrate dose to effect; maximum dose: 4 mg/kg/day up to 640 mg/day;
sustained-release formulation may be dosed once daily.
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Thyrotoxicosis (off-label use): Adolescents: Oral: Immediate-release
formulations: 10 to 40 mg/dose every 6 to 8 hours; may also consider
administering extended or sustained release formulations.
Use: Labeled Indications
Management of hypertension; angina pectoris; pheochromocytoma; essential
tremor; supraventricular arrhythmias (such as atrial fibrillation and flutter, AV
nodal re-entrant tachycardias), ventricular tachycardias (catecholamineinduced arrhythmias, digoxin toxicity); prevention of myocardial infarction;
migraine headache prophylaxis; symptomatic treatment of obstructive
hypertrophic cardiomyopathy (formerly known as hypertrophic subaortic
stenosis); treatment of proliferating infantile hemangioma requiring systemic
therapy (Hemangeol only).
Hypertension: The 2014 guideline for the management of high blood pressure
in adults recommends initiation of pharmacologic treatment to lower blood
pressure for the following patients:
• Patients ≥60 years of age, with systolic blood pressure (SBP) ≥150 mm Hg
or diastolic blood pressure (DBP) ≥90 mm Hg. Goal of therapy is SBP <150
mm Hg and DBP <90 mm Hg.
• Patients <60 years of age, with SBP ≥140 mm Hg or DBP ≥90 mm Hg. Goal
of therapy is SBP <140 mm Hg and DBP <90 mm Hg.
• Patients ≥18 years of age with diabetes, with SBP ≥140 mm Hg or DBP ≥90
mm Hg. Goal of therapy is SBP <140 mm Hg and DBP <90 mm Hg.
• Patients ≥18 years of age with chronic kidney disease (CKD), with SBP
≥140 mm Hg or DBP ≥90 mm Hg. Goal of therapy is SBP <140 mm Hg and
DBP <90 mm Hg.
Chronic kidney disease (CKD) and hypertension: Regardless of race or
diabetes status, the use of an ACE inhibitor (ACEI) or angiotensin receptor
blocker (ARB) as initial therapy is recommended to improve kidney outcomes.
In the general nonblack population (without CKD) including those with
diabetes, initial antihypertensive treatment should consist of a thiazide-type
diuretic, calcium channel blocker, ACEI, or ARB.
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In the general black population (without CKD) including those with diabetes,
initial antihypertensive treatment should consist of a thiazide-type diuretic or
a calcium channel blocker instead of an ACEI or ARB. Beta-blockers are no
longer recommended as first-line therapy in the general patient population.
Coronary artery disease (CAD) and hypertension: The American Heart
Association, American College of Cardiology, and American Society of
Hypertension (AHA/ACC/ASH) 2015 scientific statement for the treatment of
hypertension in patients with CAD recommends the use of a beta blocker as
part of a regimen in patients with hypertension and chronic stable angina with
a history of prior MI. A BP target of <140/90 mm Hg is reasonable for the
secondary prevention of cardiovascular events. A lower target BP (<130/80
mm Hg) may be appropriate in some individuals with CAD, previous MI,
stroke or transient ischemic attack, or CAD risk equivalents (AHA/ACC/ASH)
Ibutilide
ALERT: US Boxed Warning
Life-threatening arrhythmias:
Ibutilide fumarate can cause potentially fatal arrhythmias, particularly
sustained polymorphic ventricular tachycardia usually in association with QT
prolongation (torsades de pointes), but sometimes without documented QT
prolongation. In registration studies, these arrhythmias, which require
cardioversion, occurred in 1.7% of treated patients during or within a number
of hours of using ibutilide fumarate. These arrhythmias can be reversed if
treated promptly. It is essential that ibutilide be administered in a setting of
continuous ECG monitoring and by personnel trained in identification and
treatment of acute ventricular arrhythmias, particularly polymorphic
ventricular tachycardia. Patients with atrial fibrillation of more than 2 to 3
days' duration must be adequately anticoagulated, generally at least 2 weeks.
Appropriate treatment environment:
Choice of patients: Patients with chronic atrial fibrillation have a strong
tendency to revert after conversion to sinus rhythm and treatments to
maintain sinus rhythm carry risks.
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Patients to be treated with ibutilide fumarate, therefore, should be carefully
selected such that the expected benefits of maintaining sinus rhythm
outweigh the immediate risks of ibutilide, and the risks of maintenance
therapy, and are likely to offer an advantage compared with alternative
management.
Brand Names:

Corvert
Pharmacologic Category

Antiarrhythmic Agent, Class III
Dosing:
Atrial fibrillation/flutter: IV:
<60 kg: 0.01 mg/kg over 10 minutes
≥60 kg: 1 mg over 10 minutes
(Note: Discontinue infusion if arrhythmia terminates, if sustained or
nonsustained ventricular tachycardia occurs, or if marked prolongation of
QT/QTc occurs. If the arrhythmia does not terminate within 10 minutes after
the end of the initial infusion, a second infusion of equal strength may be
infused over a 10-minute period).
Dofetilide
ALERT: US Boxed Warning
Arrhythmias:
To minimize the risk of induced arrhythmia, patients initiated or re-initiated
on dofetilide should be placed for a minimum of 3 days in a facility that can
provide calculations of creatinine clearance, continuous electrocardiographic
monitoring, and cardiac resuscitation.
Brand Names:

Tikosyn
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Pharmacologic Category

Antiarrhythmic Agent, Class III
Dosing:
(Note: CrCl and QTc (or QT interval if heart rate is <60 beats/minute) must
be determined prior to first dose. If QTc >440 msec (>500 msec in patients
with ventricular conduction abnormalities), dofetilide is contraindicated).
Atrial fibrillation/atrial flutter:
Initial: 500 mcg twice daily orally (maximum dose: 500 mcg twice daily).
Initial dosage must be adjusted in patients with estimated CrCl <60
mL/minute (see dosage adjustment in renal impairment). Dofetilide may be
initiated at lower doses than recommended based on health care provider
discretion.
Modification of dosage in response to initial dose: QTc interval should be
measured 2 to 3 hours after the initial dose. If the QTc increases to more
than 15% above baseline QTc or if the QTc is >500 msec (>550 msec in
patients with ventricular conduction abnormalities), dofetilide dose should be
reduced.
If the starting dose was 500 mcg twice daily, then reduce to 250 mcg twice
daily. If the starting dose was 250 mcg twice daily, then reduce to 125 mcg
twice daily. If the starting dose was 125 mcg twice daily, then reduce to 125
mcg once daily. If at any time after the second dose is given the QTc is >500
msec (>550 msec in patients with ventricular conduction abnormalities),
dofetilide should be discontinued.
Maintenance therapy: No further down titration of dose based on QTc is
recommended following modification of initial dose. Renal function and QTc
should be re-evaluated every 3 months or as medically warranted. If QTc
>500 msec (>550 msec in patients with ventricular conduction
abnormalities), discontinue therapy. If renal function deteriorates, adjust dose
as described in dosage adjustment in renal impairment.
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Use: Labeled Indications
Atrial fibrillation/atrial flutter: Maintenance of normal sinus rhythm in
patients with chronic atrial fibrillation/atrial flutter of longer than 1-week
duration who have been converted to normal sinus rhythm; conversion of
atrial fibrillation and atrial flutter to normal sinus rhythm.
Dronedarone
ALERT: US Boxed Warning
Increased risk of death, stroke, and heart failure:
Dronedarone is contraindicated in patients with symptomatic heart failure
with recent decompensation requiring hospitalization or New York Heart
Association (NYHA) class IV heart failure. Dronedarone doubles the risk of
death in these patients. Dronedarone is contraindicated in patients in atrial
fibrillation (AF) who will not or cannot be cardioverted into normal sinus
rhythm. In patients with permanent AF, dronedarone doubles the risk of
death, stroke, and hospitalization for heart failure.
Brand Names:

Multaq
Pharmacologic Category

Antiarrhythmic Agent, Class III
Dosing:
(Note: Prior to initiation of dronedarone, class I or III antiarrhythmics (i.e.,
amiodarone, flecainide, propafenone, quinidine, disopyramide, dofetilide,
sotalol) or drugs that are strong inhibitors of CYP3A (i.e., ketoconazole) must
be stopped).
Paroxysmal or persistent atrial fibrillation: Oral: 400 mg twice daily.
Use: Labeled Indications
Paroxysmal or persistent atrial fibrillation: To reduce the risk of
hospitalization for atrial fibrillation (AF) in patients in sinus rhythm with a
history of paroxysmal or persistent AF.
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Verapamil
Brand Names:

Calan

Calan SR

Covera-HS [DSC]

Isoptin SR

Verelan

Verelan PM
Pharmacologic Category

Antianginal Agent

Antiarrhythmic Agent, Class IV

Antihypertensive

Calcium Channel Blocker

Calcium Channel Blocker, Nondihydropyridine
Dosing:
SVT: (Note: Verapamil is no longer included in the Pediatric Advanced Life
Support (PALS) tachyarrhythmia algorithm).
Children: 1-15 years: IV: 0.1 to 0.3 mg/kg/dose over 2 minutes; maximum:
5 mg/dose, may repeat dose in 30 minutes if inadequate response; maximum
for second dose: 10 mg
Use: Labeled Indications
IV: Supraventricular tachyarrhythmia (PSVT, atrial fibrillation/flutter [rate
control])
Oral: Treatment of hypertension; angina pectoris (vasospastic, chronic stable,
unstable) (Calan, Covera-HS); supraventricular tachyarrhythmia (PSVT, atrial
fibrillation/flutter [rate control])
Acute coronary syndrome (ACS): The ACCF/AHA guidelines for the
management of unstable angina/non-ST-elevation myocardial infarction
recommend verapamil to treat hypertension or ongoing ischemia if betablocker therapy is ineffective or contraindicated and in the absence of left
ventricular dysfunction, pulmonary congestion, or AV block.
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Hypertension: The 2014 guideline for the management of high blood pressure
in adults recommends initiation of pharmacologic treatment to lower blood
pressure for the following patients:
• Patients ≥60 years of age with systolic blood pressure (SBP) ≥150 mm Hg
or diastolic blood pressure (DBP) ≥90 mm Hg. Goal of therapy is SBP <150
mm Hg and DBP <90 mm Hg.
• Patients <60 years of age with SBP ≥140 mm Hg or DBP ≥90 mm Hg. Goal
of therapy is SBP <140 mm Hg and DBP <90 mm Hg.
• Patients ≥18 years of age with diabetes with SBP ≥140 mm Hg or DBP ≥90
mm Hg. Goal of therapy is SBP <140 mm Hg and DBP <90 mm Hg.
• Patients ≥18 years of age with chronic kidney disease (CKD) with SBP ≥140
mm Hg or DBP ≥90 mm Hg. Goal of therapy is SBP <140 mm Hg and DBP
<90 mm Hg.
Chronic kidney disease (CKD) and hypertension: Regardless of race or
diabetes status, the use of an ACE inhibitor (ACEI) or angiotensin receptor
blocker (ARB) as initial therapy is recommended to improve kidney outcomes.
In the general nonblack population (without CKD) including those with
diabetes, initial antihypertensive treatment should consist of a thiazide-type
diuretic, calcium channel blocker, ACEI, or ARB. In the general black
population (without CKD) including those with diabetes, initial
antihypertensive treatment should consist of a thiazide-type diuretic or a
calcium channel blocker instead of an ACEI or ARB.
Coronary artery disease (CAD) and hypertension: The American Heart
Association, American College of Cardiology and American Society of
Hypertension (AHA/ACC/ASH) 2015 scientific statement for the treatment of
hypertension in patients with coronary artery disease (CAD) recommends that
a non-dihydropyridine CCB (verapamil, diltiazem) may be used as a substitute
for a beta blocker in patients who have an intolerance or contraindication to
beta blockers with ongoing ischemia, hypertension and chronic stable angina,
or if angina or hypertension continues to be uncontrolled while receiving
standard therapies (i.e., beta blocker). However, a non-dihydropyridine CCB
(i.e., verapamil, diltiazem) should be avoided in patients with LV dysfunction
or heart failure (with reduced ejection fraction).
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A BP target of <140/90 mm Hg is reasonable for the secondary prevention of
cardiovascular events. A lower target BP (<130/80 mm Hg) may be
appropriate in some individuals with CAD, previous MI, stroke or transient
ischemic attack, or CAD risk equivalents.
Dipyridamole
Brand Names:

Persantine
Pharmacologic Category

Antiplatelet Agent

Vasodilator
Dosing:
Adjunctive therapy for prophylaxis of thromboembolism with cardiac valve
replacement: Oral: 75 to 100 mg 4 times/day
Evaluation of coronary artery disease: IV: 0.56 mg/kg over 4 minutes;
maximum dose: 70 mg.
Following completion of dipyridamole infusion, inject radiotracer (i.e.,
thallium-201) in 3 to 5 minutes. (Note: To reverse complications and side
effects of dipyridamole, aminophylline (50 to 250 mg IV push over 30 to 60
seconds given at least 1 minute after the radiotracer injection) should be
available for urgent/emergent use).
Obesity: Dosing for patients who are obese or morbidly obese is not
established; in these patients, it is customary to use doses up to the weight
of 125 kg.
Use: Labeled Indications
Oral: Used with warfarin to decrease thrombosis in patients after artificial
heart valve replacement.
IV: Diagnostic agent in CAD.
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Cardiac Pacemakers And Defibrillators
Pacemakers sense electrical events and respond when necessary by
delivering electrical stimuli to the heart. Permanent pacemaker leads
are placed via thoracotomy or transvenously, but some temporary
emergency pacemaker leads can be placed on the chest wall.
Indications for Pacemaker Placement
Indications are numerous but generally involve symptomatic
bradycardia or high-grade atrioventricular (AV) block. Some
tachyarrhythmias may be terminated by overdrive pacing with a brief
period of pacing at a faster rate; the pacemaker is then slowed to the
desired rate. Nevertheless, ventricular tachyarrhythmias are better
treated with devices that can cardiovert and defibrillate as well as
pace (implantable cardioverter defibrillators).
Types of Pacemakers
Types of pacemakers are designated by 3 to 5 letters, representing
which cardiac chambers are paced, which chambers are sensed, how
the pacemaker responds to a sensed event (inhibits or triggers
pacing), whether it can increase heart rate during exercise (ratemodulating), and whether pacing is multisite (in both atria, both
ventricles, or more than one pacing lead in a single chamber). For
example, a VVIR pacemaker paces (V) and senses (V) events in the
ventricle, inhibits pacing in response to sensed event (I), and can
increase its rate during exercise (R).
VVI and DDD pacemakers are the devices most commonly used. They
offer equivalent survival benefits. Compared with VVI pacemakers,
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physiologic pacemakers (AAI, DDD, VDD) appear to reduce risk of
atrial fibrillation (AF) and heart failure and slightly improve quality of
life.32,183
Advances in pacemaker design include lower-energy circuitry, new
battery designs, and corticosteroid-eluting leads (which reduce pacing
threshold), all of which increase pacemaker longevity. Mode switching
refers to an automatic change in the mode of pacing in response to
sensed events (i.e., from DDDR to VVIR during AF).83,84
Complications of Pacemaker Use
Pacemakers may malfunction by oversensing or undersensing events,
failing to pace or capture, or pacing at an abnormal rate.
Tachycardias are an especially common complication. Ratemodulating pacemakers may increase stimuli in response to vibration,
muscle activity, or voltage induced by magnetic fields during MRI. In
pacemaker-mediated tachycardia, a normally functioning dualchamber pacemaker senses a ventricular premature or paced beat
transmitted to the atrium through the AV node or a retrogradeconducting accessory pathway, which triggers ventricular stimulation
in a rapid, repeating cycle.25
Additional complications associated with normally functioning devices
include cross-talk inhibition, in which sensing of the atrial pacing
impulse by the ventricular channel of a dual-chamber pacemaker
leads to inhibition of ventricular pacing, and pacemaker syndrome, in
which AV asynchrony induced by ventricular pacing causes
fluctuating, vague cerebral (i.e., light-headedness), cervical (i.e.,
neck pulsations), or respiratory (i.e., dyspnea) symptoms. Pacemaker
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syndrome is managed by restoring AV synchrony by atrial pacing
(AAI), single-lead atrial sensing ventricular pacing (VDD), or dualchamber pacing (DDD), most commonly the latter.
Environmental interference comes from electromagnetic sources such
as surgical electrocautery and MRI, although MRI may be safe when
the pacemaker generator and leads are not inside the magnet.
Cellular telephones and electronic security devices are a potential
source of interference; telephones should not be placed close to the
device but are not a problem when used normally for talking. Walking
through metal detectors does not cause pacemaker malfunction as
long as patients do not linger.
Defibrillators
Direct-Current (DC) Cardioversion-Defibrillation
A transthoracic DC shock of sufficient magnitude depolarizes the
entire myocardium, rendering the entire heart momentarily refractory
to repeat depolarization. Thereafter, the most rapid intrinsic
pacemaker, usually the sinoatrial node, reassumes control of heart
rhythm. Thus, DC cardioversion-defibrillation very effectively
terminates tachyarrhythmias that result from reentry. However, it is
less effective for terminating tachyarrhythmias that result from
automaticity because the return rhythm is likely to be the automatic
tachyarrhythmia. For tachyarrhythmias other than ventricular
fibrillation (VF), the DC shock must be synchronized to the QRS
complex (called DC cardioversion) because a shock that falls during
the vulnerable period (near the peak of the T wave) can induce VF. In
VF, synchronization of a shock to the QRS complex is neither
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necessary nor possible. A DC shock applied without synchronization
to a QRS complex is DC defibrillation.
Procedure for DC cardioversion
When DC cardioversion is elective, patients should fast for 6 to 8 h to
avoid the possibility of aspiration. Because the procedure is
frightening and painful, brief general anesthesia or IV analgesia and
sedation (i.e., fentanyl 1 mcg/kg, then midazolam 1 to 2 mg q 2 min
to a maximum of 5 mg) is necessary. Equipment and personnel to
maintain the airways must be present.
The electrodes (pads or paddles) used for cardioversion may be
placed anteroposteriorly (along the left sternal border over the 3rd
and 4th intercostal spaces and in the left infrascapular region) or
anterolaterally (between the clavicle and the 2nd intercostal space
along the right sternal border and over the 5th and 6th intercostal
spaces at the apex of the heart). After synchronization to the QRS
complex is confirmed on the monitor, a shock is given. The most
appropriate energy level varies with the tachyarrhythmia being
treated. Cardioversion efficacy increases with use of biphasic shocks,
in which the current polarity is reversed part way through the shock
waveform.85 DC cardioversion-defibrillation can also be applied
directly to the heart during a thoracotomy or through use of an
intracardiac electrode catheter; then, much lower energy levels are
required.
Complications of DC cardioversion
Complications are usually minor and include atrial and ventricular
premature beats and muscle soreness. Less commonly, but more
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likely if patients have marginal left ventricular function or multiple
shocks are used, cardioversion precipitates myocyte damage and
electromechanical dissociation.
Implantable Cardioverter-Defibrillators
Implantable cardioverter-defibrillators cardiovert or defibrillate the
heart in response to ventricular tachycardia (VT) or ventricular
fibrillation (VF). Contemporary tiered-therapy ICDs also provide
antibradycardia pacing and antitachycardia pacing (to terminate
responsive atrial or ventricular tachycardias) and store intracardiac
electrograms.
The ICDs are implanted subcutaneously or subpectorally, with
electrodes inserted transvenously into the right ventricle and
sometimes also the right atrium. A biventricular ICD also has a left
ventricular epicardial lead placed via the coronary sinus venous
system or via thoracotomy. ICDs are the preferred treatment for
patients who have had an episode of VF or hemodynamically
significant VT not due to reversible or transient conditions (i.e.,
electrolyte disturbance, antiarrhythmic drug proarrhythmia, acute
MI). ICDs may also be indicated for patients with VT or VF inducible
during an electrophysiologic study and for patients with idiopathic or
ischemic cardiomyopathy, a left ventricular ejection fraction
of < 35%, and a high risk of VT or VF. Other indications are less
clear.86
Because ICDs treat rather than prevent VT or VF, patients prone to
these arrhythmias may require both an ICD and antiarrhythmic drugs
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to reduce the number of episodes and need for uncomfortable
shocks; this approach also prolongs the life of the ICD.
Impulse generators for ICDs typically last about 5 years. ICDs may
malfunction by delivering inappropriate pacing or shocks in response
to sinus rhythm, SVTs, or nonphysiologically generated impulses (i.e.,
due to lead fracture). They also may malfunction by not delivering
appropriate pacing or shocks when needed because of factors such as
lead or impulse generator migration, undersensing, an increase in
pacing threshold due to fibrosis at the site of prior shocks, and
battery depletion.
In patients who report that the ICD has discharged but that no
associated symptoms of syncope, dyspnea, chest pain or persistent
palpitations occurred, follow up with the ICD clinic and/or the
electrophysiologist within the week is appropriate. The ICD can then
be electronically interrogated to determine the reason for discharge.
If such associated symptoms were present, or the patient received
multiple shocks, emergency department referral is indicated to look
for a treatable cause (i.e., coronary ischemia, electrolyte
abnormality) or device malfunction.87
Cardiac Resynchronization Therapy
In some patients, the normal, orderly, sequential relationship
between contraction of the cardiac chambers is disrupted (becomes
dyssynchronous). Dyssynchrony may be: 1) Atrioventricular, between
atrial and ventricular contraction, 2) Interventricular, between left
and right ventricular contraction, and 3) Intraventricular, between
different segments of left ventricular contraction.
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Patients at risk for dyssynchrony include those with: ischemic or
nonischemic dilated cardiomyopathy, prolonged QRS interval (≥ 130
msec), left ventricular end-diastolic dimension ≥ 55 mm, and left
ventricular ejection fraction ≤ 35% in sinus rhythm.
Cardiac resynchronization therapy (CRT) involves use of a pacing
system to resynchronize cardiac contraction. Such systems usually
include a right atrial lead, right ventricular lead, and left ventricular
lead. Leads may be placed transvenously or surgically via
thoracotomy. In heart failure patients with New York Heart
Association (NYHA) class II, III, and IV symptoms, CRT can reduce
hospitalization for heart failure and reduce all-cause mortality.
However, there is little to no benefit in patients with permanent atrial
fibrillation, right bundle branch block, nonspecific intraventricular
conduction delay, or only mild prolongation of QRS duration (< 150
msec).
Cardiac Ablation
If a tachyarrhythmia depends on a specific pathway or ectopic site of
automaticity, the site can be ablated by low-voltage, high-frequency
(300 to 750 MHz) electrical energy, applied through an electrode
catheter. This energy heats and necroses an area < 1 cm in diameter
and up to 1 cm deep. Before energy can be applied, the target site or
sites must be mapped during an electrophysiologic study.
Success rate is > 90% for reentrant supraventricular tachycardias
(via the atrioventricular [AV] node or an accessory pathway), focal
atrial tachycardia and flutter, and focal idiopathic ventricular
tachycardia (VT—right ventricular outflow tract, left septal, or bundle
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branch reentrant VT). Because atrial fibrillation (AF) often originates
or is maintained by an arrhythmogenic site in the pulmonary veins,
this source can be electrically isolated by ablations at the pulmonary
vein – left atrial junction or in the left atrium. Alternatively, in
patients with refractory AF and rapid ventricular rates, the AV node
may be ablated after permanent pacemaker implantation. RF ablation
is sometimes successful in patients with VT refractory to drugs
particularly when ischemic heart disease is present.58
The mortality rate of RF ablation is < 1/2000 and the procedure is
considered to be safe. Complications include valvular damage,
pulmonary vein stenosis or occlusion (if used to treat atrial
fibrillation), stroke or other embolism, cardiac perforation,
tamponade (1%), and unintended AV node ablation.40
Summary
An arrhythmia is any abnormality in the rate, regularity, or site of
origin or a disturbance in conduction that disrupts the normal
sequence of activation in the atria or ventricles. Arrhythmias can be
due to a variety of reasons, such as electrolyte abnormalities,
structural abnormalities, metabolic derangements, genetic mutations,
and drug toxicity. Arrhythmias have varying degrees of severity and
significance based on site of origin, symptoms, frequency, and
duration.
Abnormal heart rates in children are often not a cause of concern, but
it is absolutely vital that a healthcare professional be able to
recognize when an arrhythmia has the potential to become serious or
life threatening, and to identify appropriate treatment options.
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Arrhythmias may or may not present with secondary symptoms and
it often requires some investigation to determine if a cause for the
arrhythmia is present. Understanding the mechanics of arrhythmias
as well as the treatment options will ensure that you are able to
communicate with your patient and his or her parents to determine
the right course of action.
Please take time to help NurseCe4Less.com course planners evaluate
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1.
Any electrical activity not initiated by the SA node is
considered
a.
b.
c.
d.
a depolarization event.
an atrioventricular (AV) impulse.
an arrhythmia.
a repolarization event.
2. Electrical stimulation of a myocardial cell results in
a.
b.
c.
d.
a slow outward leak of sodium.
depolarization.
a slow outward leak of potassium.
All of the above
3. True or False: Some arrhythmias are so common as to be
considered as almost normal variants.
a. True
b. False
4. The conduction system in the ventricles is more elaborate
than that in the atria because
a.
b.
c.
d.
the muscle mass is larger.
of the location of the bundle of His.
the superior vena cava enters through the ventricles.
of fiber stretch.
5. Normally, the _________________, located where the
superior vena cava meets the right atrium, has the most
rapid intrinsic rate (60 to 100 bpm).
a.
b.
c.
d.
atria via
atrioventricular (AV) node
coronary sinus
sinoatrial (SA) node
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6. In general, arrhythmia mechanisms are described as
abnormalities in
a.
b.
c.
d.
electrical development.
electrical conduction.
a combination of electrical development and conduction.
All of the above
7. _________________ ions cause the actual muscular
contraction by coupling with the muscle fibers.
a.
b.
c.
d.
Potassium
Calcium
Sodium
None of the above
8. The atrial muscle and ventricular muscle are separated by
insulation of the fibrous mitral and tricuspid valve rings,
and normally the only connection between them is via
a.
b.
c.
d.
the
the
the
the
superior vena cava.
Bachmann bundle.
His bundle.
Purkinje fibers.
9. The ventricle is activated through the dense network of
_____________ originating from the bundle branches.
a.
b.
c.
d.
the Bachmann bundle
Purkinje fibers
the His bundle
the superior vena cava
10. True or False: The mechanism of abnormal automaticity is
NOT similar to the normal automaticity of sinus node
cells.
a. True
b. False
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11. Conduction block or conduction delay is a frequent cause
of ____________________, especially if the conduction
block is located in the cardiac conduction system.
a.
b.
c.
d.
bradyarrhythmias
tachyarrhythmias
depolarization
muscular contraction
12. Ion channels are passages for ions that facilitate
a.
b.
c.
d.
muscular contraction.
movement through the cell membrane.
and AV reentry.
and fiber stretch.
13. True or False: By far the most common tachycardia
presenting in early infancy is orthodromic AV reentry.
a. True
b. False
14. Depolarization is initiated by
a.
b.
c.
d.
the sodium channel closing
a slow inward leak of sodium.
an outward movement of potassium ions.
a complex exchange of sodium, calcium, and potassium.
15. The final conducting components of the ventricles are the
____________, which emanate from the bundle branches
to stimulate the ventricular cardiac muscle to contract.
a.
b.
c.
d.
bundle of His
catecholamines
Purkinje fibers
tricuspid valve rings
16. The QRS complex from an electrocardiogram measures
a.
b.
c.
d.
both ventricular depolarization and repolarization.
depolarization of the ventricles.
repolarization.
atrial activity.
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17. The conduction pathways through the atrium to the AVnode show preferential conduction due to
a.
b.
c.
d.
their connection to the Bachmann bundle.
their specialized conduction properties.
phase 4 diastolic depolarization.
their anatomical structure.
18. True or False: Conduction between the AV node and the
bundle of His is measured by the P-R interval (the time
between atrial activity and ventricular activity).
a. True
b. False
19. The anterior internodal pathway (through the atrium to
the AV-node) connects to the anterior interatrial band,
also known as
a.
b.
c.
d.
the
the
the
the
anterior internodal pathway.
Purkinje fibers.
Bachmann bundle.
His bundle.
20. The connection between atria and ventricles is facilitated
through
a.
b.
c.
d.
the
the
the
the
AV node.
sinus node.
interventricular septum.
junction with the septum.
21. The normal average heart rate of children
a.
b.
c.
d.
is higher than that of adults.
varies from 60 bpm (at rest).
varies up to 220 bpm during strenuous activities.
All of the above
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22. True or False: Many children with palpitations do not have
an arrhythmia and a detailed first-hand history is
essential before assessing the likelihood of an arrhythmia
and the necessity of further investigation.
a. True
b. False
23. When diagnosing a child with an arrhythmia, diagnosis is
based mainly on
a.
b.
c.
d.
the child’s age and the age of onset of arrhythmia.
the history (palpitations, heart failure, syncope, etc.).
the ECG findings.
All of the above
24. Infants generally have heart rates
a.
b.
c.
d.
greater
greater
greater
greater
than
than
than
than
60
60
80
80
bpm
bpm
bpm
bpm
and
and
and
and
less
less
less
less
than
than
than
than
120
140
170
220
bpm.
bpm.
bpm.
bpm.
25. Common arrhythmias in neonates with structurally
normal hearts include
a.
b.
c.
d.
sinus tachycardia.
sinus bradycardia.
atrioventricular reentry tachycardia (AVRT).
complete AV block.
26. A head-up tilt test is sometimes used for investigation of
______________ with recurrent syncope or presyncope.
a.
b.
c.
d.
infants
children older than 6 years
children between 3 and 6 years
neonates
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27. During the head-up tilt test,
a.
b.
c.
d.
blood pressure is recorded continuously.
the ECG is recorded continuously.
The patient is passively tilted to an angle of 60–80.
All of the above
28. True or False: The first scheme (Vaughan-Williams) is still
the one that most physicians use when speaking of
antiarrhythmic drugs.
a. True
b. False
29. In the Vaughan-Williams antiarrhythmic drugs
classifications, _____________ are a class I drug.
a.
b.
c.
d.
sodium channel blockers
beta-blockers
nondihydropyridine calcium channel blockers
digoxin and adenosine
30. Class Ic antiarrhythmic drugs have slow kinetics so they
express their electrophysiologic effects at _____ heart
rates.
a.
b.
c.
d.
fast
slow
intermediate
all
31. __________________________ are not included in the
Vaughan Williams classification.
a.
b.
c.
d.
Sodium channel blockers
Digoxin and adenosine
Beta-blockers
Nondihydropyridine calcium channel blockers
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32. True or False: Dronedarone is contraindicated in patients in
atrial fibrillation (AF) who will not or cannot be
cardioverted into normal sinus rhythm.
a. True
b. False
33. Class I drugs are subdivided based on the kinetics of the
sodium channel effects: Class Ia drugs have ___________
kinetics.
a.
b.
c.
d.
fast
slow
intermediate
intermittent
34. In the Vaughan-Williams antiarrhythmic drugs
classifications, _____________ are a class II drug.
a.
b.
c.
d.
sodium channel blockers
beta-blockers
nondihydropyridine calcium channel blockers
digoxin and adenosine
35. True or False: Proarrhythmia is a drug-related arrhythmia
that is worse than the arrhythmia being treated, and it is
an adverse effect of class I drugs.
a. True
b. False
36. Class Ib drugs have fast kinetics so they
a. have major effects on atrial tissue.
b. are very potent antiarrhythmics.
c. express their electrophysiologic effects only at fast heart
rates.
d. All of the above
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37. Class II drugs are contraindicated in
a.
b.
c.
d.
glaucoma patients.
older patients.
asthma patients.
patients with sinus tachycardia.
38. ______________ is intended for use only in patients with
indicated life-threatening arrhythmias because its use is
accompanied by substantial toxicity.
a.
b.
c.
d.
Nadolol
Amiodarone
Sotalol
Diltiazem
39. When discontinuing nadolol administered long-term,
particularly in patients with ischemic heart disease,
a.
b.
c.
d.
gradually reduce dose over a period of 1 to 2 days.
nadolol may not be reintroduced.
the drug should be stopped abruptly.
gradually reduce dose over a period of 1 to 2 weeks.
40. The use of an ACE inhibitor (ACEI) or angiotensin receptor
blocker (ARB) as initial therapy is recommended to
improve kidney outcomes
a.
b.
c.
d.
in non-white populations.
in non-black populations.
depending on diabetes status.
regardless of race or diabetes status.
41. True or False: It may be prudent not to discontinue nadolol
therapy abruptly in patients with possible coronary artery
disease but it is prudent in patients being treated ONLY for
hypertension.
a. True
b. False
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42. Abnormal liver function tests have been reported, some in
the first few weeks of therapy with
a.
b.
c.
d.
an ACE inhibitor (ACEI).
angiotensin receptor blocker (ARB).
mexiletine.
bisoprolol.
43. Permanent pacemaker leads are placed
a.
b.
c.
d.
via thoracotomy or transvenously.
on the chest wall.
in the diaphragm.
on the front of the breastbone.
44. Pacemakers may malfunction by
a.
b.
c.
d.
oversensing events.
undersensing events.
failing to pace or capture, or pacing at an abnormal rate.
All of the above
45. In patients with permanent atrial fibrillation (AF),
__________ doubles the risk of death, stroke, and
hospitalization for heart failure.
a.
b.
c.
d.
dofetilide
dronedarone
bisoprolol
digoxin
46. True or False: To minimize the risk of induced arrhythmia,
patients initiated or re-initiated on dofetilide should be
placed in a facility for at least 3 days for calculations of
creatinine clearance, continuous ECG monitoring, and
cardiac resuscitation.
a. True
b. False
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47. Severe exacerbation of angina and the occurrence of
myocardial infarction (MI) and ventricular arrhythmias
have been reported in patients with angina following the
abrupt discontinuation of therapy with
a.
b.
c.
d.
dofetilide
beta-blockers.
bisoprolol
digoxin
48. Class III drugs are membrane stabilizing drugs, primarily
a.
b.
c.
d.
fast-channel blockers.
beta-blockers.
calcium channel blockers.
potassium channel blockers.
49. True or False: Because class Ia drugs have intermediate
kinetics, their fast-channel tissue conduction slowing
effects WILL be evident on an ECG obtained during normal
rhythm at normal rates.
a. True
b. False
50. Class IV drugs are the nondihydropyridine
a.
b.
c.
d.
fast-channel blockers.
beta-blockers.
calcium channel blockers.
potassium channel blockers.
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CORRECT ANSWERS:
1.
Any electrical activity not initiated by the SA node is
considered
c. an arrhythmia.
2. Electrical stimulation of a myocardial cell results in
b. depolarization.
3. True or False: Some arrhythmias are so common as to be
considered as almost normal variants.
a. True
4. The conduction system in the ventricles is more elaborate
than that in the atria because
a. the muscle mass is larger.
5. Normally, the _________________, located where the
superior vena cava meets the right atrium, has the most
rapid intrinsic rate (60 to 100 bpm).
d. sinoatrial (SA) node
6. In general, arrhythmia mechanisms are described as
abnormalities in
d. All of the above
7. _________________ ions cause the actual muscular
contraction by coupling with the muscle fibers.
b. Calcium
8. The atrial muscle and ventricular muscle are separated by
insulation of the fibrous mitral and tricuspid valve rings,
and normally the only connection between them is via
c. the His bundle.
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9. The ventricle is activated through the dense network of
_____________ originating from the bundle branches.
b. Purkinje fibers
10. True or False: The mechanism of abnormal automaticity is
NOT similar to the normal automaticity of sinus node
cells.
b. False
11. Conduction block or conduction delay is a frequent cause
of ____________________, especially if the conduction
block is located in the cardiac conduction system.
a. bradyarrhythmias
12. Ion channels are passages for ions that facilitate
b. movement through the cell membrane.
13. True or False: By far the most common tachycardia
presenting in early infancy is orthodromic AV reentry.
a. True
14. Depolarization is initiated by
b. a slow inward leak of sodium.
15. The final conducting components of the ventricles are the
____________, which emanate from the bundle branches
to stimulate the ventricular cardiac muscle to contract.
c. Purkinje fibers
16. The QRS complex from an electrocardiogram measures
b. depolarization of the ventricles.
17. The conduction pathways through the atrium to the AVnode show preferential conduction due to
d. their anatomical structure.
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18. True or False: Conduction between the AV node and the
bundle of His is measured by the P-R interval (the time
between atrial activity and ventricular activity).
a. True
19. The anterior internodal pathway (through the atrium to
the AV-node) connects to the anterior interatrial band,
also known as
c. the Bachmann bundle.
20. The connection between atria and ventricles is facilitated
through
a. the AV node.
21. The normal average heart rate of children
d. All of the above
22. True or False: Many children with palpitations do not have
an arrhythmia and a detailed first-hand history is
essential before assessing the likelihood of an arrhythmia
and the necessity of further investigation.
a. True
23. When diagnosing a child with an arrhythmia, diagnosis is
based mainly on
d. All of the above
24. Infants generally have heart rates
c. greater than 80 bpm and less than 170 bpm.
25. Common arrhythmias in neonates with structurally
normal hearts include
c. atrioventricular reentry tachycardia (AVRT).
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26. A head-up tilt test is sometimes used for investigation of
______________ with recurrent syncope or presyncope.
b. children older than 6 years
27. During the head-up tilt test,
d. All of the above
28. True or False: The first scheme (Vaughan-Williams) is still
the one that most physicians use when speaking of
antiarrhythmic drugs.
a. True
29. In the Vaughan-Williams antiarrhythmic drugs
classifications, _____________ are a class I drug.
a. sodium channel blockers
30. Class Ic antiarrhythmic drugs have slow kinetics so they
express their electrophysiologic effects at _____ heart
rates.
d. all
31. Vaughan Williams classification.
b. Digoxin and adenosine
32. True or False: Dronedarone is contraindicated in patients
in atrial fibrillation (AF) who will not or cannot be
cardioverted into normal sinus rhythm.
a. True
33. Class I drugs are subdivided based on the kinetics of the
sodium channel effects: Class Ia drugs have ___________
kinetics.
c. intermediate
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34. In the Vaughan-Williams antiarrhythmic drugs
classifications, _____________ are a class II drug.
b. beta-blockers
35. True or False: Proarrhythmia is a drug-related arrhythmia
that is worse than the arrhythmia being treated, and it is
an adverse effect of class I drugs.
a. True
36. Class Ib drugs have fast kinetics so they
c. express their electrophysiologic effects only at fast heart
rates.
37. Class II drugs are contraindicated in
c. asthma patients.
38. ______________ is intended for use only in patients with
indicated life-threatening arrhythmias because its use is
accompanied by substantial toxicity.
b. Amiodarone
39. When discontinuing nadolol administered long-term,
particularly in patients with ischemic heart disease,
d. gradually reduce dose over a period of 1 to 2 weeks.
40. The use of an ACE inhibitor (ACEI) or angiotensin receptor
blocker (ARB) as initial therapy is recommended to
improve kidney outcomes
d. regardless of race or diabetes status.
41. True or False: It may be prudent not to discontinue
nadolol therapy abruptly in patients with possible
coronary artery disease but it is prudent in patients being
treated ONLY for hypertension.
b. False
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42. Abnormal liver function tests have been reported, some in
the first few weeks of therapy with
c. mexiletine.
43. Permanent pacemaker leads are placed
a. via thoracotomy or transvenously.
44. Pacemakers may malfunction by
d. All of the above
45. In patients with permanent atrial fibrillation (AF),
__________ doubles the risk of death, stroke, and
hospitalization for heart failure.
b. dronedarone
46. True or False: To minimize the risk of induced arrhythmia,
patients initiated or re-initiated on dofetilide should be
placed in a facility for at least 3 days for calculations of
creatinine clearance, continuous ECG monitoring, and
cardiac resuscitation.
a. True
47. Severe exacerbation of angina and the occurrence of
myocardial infarction (MI) and ventricular arrhythmias
have been reported in patients with angina following the
abrupt discontinuation of therapy with
b. beta-blockers.
48. Class III drugs are membrane stabilizing drugs, primarily
d. potassium channel blockers
49. True or False: Because class Ia drugs have intermediate
kinetics, their fast-channel tissue conduction slowing
effects WILL be evident on an ECG obtained during normal
rhythm at normal rates.
b. False
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50. Class IV drugs are the nondihydropyridine
c. calcium channel blockers
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