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ARRHYTHMIAS IN
CHILDREN:
Pharmacology
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, 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 hours. Nurses may only claim
credit commensurate with the credit awarded for completion of this
course activity.
Pharmacology content is 2 hours.
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: 8/11/2016
Termination Date: 8/11/2019
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.
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.
2.
Long QT syndrome is a genetically transmitted cardiac
arrhythmia caused by
a.
b.
c.
d.
3.
caused by electrolyte imbalance
caused by autonomic neuropathy
hereditary
drug-induced
First-line treatment of fetal atrial flutter is the
administration of the drug _________ to the mother.
a.
b.
c.
d.
5.
a self-propagating wave of electrical excitation.
caused by re-entry.
ion channel protein abnormalities.
slow conduction.
Long QT syndrome which is _______________, is
characterized by a prolonged QTc and an increased risk of
torsade de pointes.
a.
b.
c.
d.
4.
bradyarrhythmias
tachyarrhythmias
depolarization
muscular contraction
dronedarone
procainamide
digoxin
sotalol
_________ is/are considered the initial treatment of
choice for long QT syndrome.
a.
b.
c.
d.
Sodium channel blockers
procainamide
digoxin
Beta-blockers
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Introduction
Although many arrhythmias in children are treated similar to those of
adults, unique treatments for children with cardiac anomalies and
arrhythmias exist. This Part II of a two-course series on Arrythmias in
Children highlights the conditions found in children and the associated
pharmacological treatments to manage symptoms.
Tachycardias And Bradycardias
Although it is not necessary to have a deep understanding of cardiac
electrophysiology to diagnose and treat a cardiac arrhythmia, some
knowledge of the basics is helpful. Tachycardias are mostly caused by
re-entry or abnormal automaticity. A few rare types of tachycardia
are probably caused by a third mechanism, triggered activity.
Basic Mechanisms of Tachycardias
Many common tachycardias are caused by re-entry. This means that
there is a self-propagating wave of electrical excitation, which
maintains the arrhythmia. The fundamental requirements for re-entry
are that there should be: (1) an anatomical circuit, (2) a zone of slow
conduction in the circuit, and (3) a region of unidirectional block. The
best model of re-entry is an orthodromic atrioventricular (AV) reentry, i.e., Wolff–Parkinson–White syndrome. The circuit comprises
the accessory pathway, atrium, AV node, and ventricle. The slow
conduction is in the AV node and functional unidirectional block can
occur in the accessory pathway.
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Tachycardia is interrupted if one part of the circuit has a refractory
period longer than the cycle length of the tachycardia. In practice this
is most easily achieved by prolonging AV node refractoriness with
adenosine. Tachycardia will restart only if the requirements for
reinitiation are met. These include a trigger (often an atrial or
ventricular premature beat) and an appropriate balance of electrical
behavior of the various parts of the circuit. Re-entry tachycardias can
be started and stopped by pacing and it can be stopped by
cardioversion. Other examples of re-entry include AV nodal re-entry
tachycardia, atrial flutter, and some types of ventricular
tachycardia.23
Fewer tachycardias are caused by abnormal automaticity. The best
model of automaticity is sinus rhythm. Similar to sinus rhythm,
automatic (also known as ectopic) tachycardias cannot be started or
stopped by pacing and cannot be interrupted by cardioversion. In the
normal heart the sinus node has the highest spontaneous rate and,
therefore, determines the rhythm. If the sinus node fails another part
of the heart with a lower pacemaker rate, usually the AV node, will
provide an escape rhythm. Sometimes an area of the heart other
than the sinus node will have an abnormally high spontaneous rate
and will produce an automatic (or ectopic) tachycardia, overriding the
sinus node. Examples of tachycardias caused by enhanced
automaticity include atrial ectopic tachycardia (a type of focal atrial
tachycardia), junctional ectopic tachycardia, and some types of
ventricular tachycardia.24
Triggered activity is the least common tachycardia mechanism.
Depolarization is caused by a trigger – either an early
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afterdepolarization or a delayed afterdepolarization. Triggered activity
causes ventricular arrhythmias in long QT syndrome, some electrolyte
disturbances, and in some postoperative ventricular tachycardia with
myocardial injury.
Differentiation between supraventricular tachycardias (SVT) and
ventricular tachycardias (VT) can be challenging, especially in acute
emergency settings. Supraventricular tachycardias are arrhythmias in
the atria or AV-node or arrhythmias in which these structures are
involved. Supraventricular arrhythmias are relatively common and
rarely life-threatening. Ventricular tachycardias are rhythm disorders
that originate from the ventricles. Ventricular tachycardias can both
take place in the myocardial tissue and the conduction system tissue.
Basic Mechanisms of Bradycardias
Bradycardias are due to either failure of impulse generation or failure
of conduction. The most common example of failure of impulse
generation is sinoatrial disease. Abnormal sinus node function may be
due to extrinsic effects (high vagal tone) or to depressed
automaticity. Significant bradycardias are more commonly due to
second- or third-degree AV block.
Bradycardias are symptomatic heart rhythm disorders resulting from
an inappropriately low heart rhythm due to inappropriately slow
impulse formation. Bradycardias may also result from conduction
delay of the cardiac impulse in the myocardium or in the conduction
system with physiologic conditions. These two problems can lead to a
slow heart rate, a bradycardia. Generally the definition of bradycardia
is a heart rate of <60 beats per minute. However, a normal variation
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of heart rate exists. For instance, during sleep and in athletes the
heart rate can be as low as 40 beats per minute.5
Bradycardia can be caused by a variety of intrinsic and extrinsic
causes. The most common intrinsic cause is aging, but ischemic heart
disease, infiltrative diseases or surgery can also result in conduction
disorders. Medication that modifies the excitability of the heart is the
most frequent extrinsic cause. However, electrolyte and metabolic
disorders may influence the heart rate directly or indirectly.
Symptoms emanating from bradycardia result from an insufficient
capacity of the heart to supply the body with blood.25 Complaints of
palpitations, syncope or heart failure may result from
bradyarrhythmias, but often there are vague symptoms like
dizziness, exercise intolerance or fatigue may be more prominent. A
causal relation between complaints and the bradycardia should be
established and reversible causes should be identified (for instance
use of certain drugs).
A patient with a bradyarrhythmia can be completely asymptomatic.
Otherwise, patients with bradycardia may present with a diversity of
signs and symptoms. A pause in ventricular contraction > 6 seconds
often results in syncope or near syncope. More often symptoms are
nonspecific and chronic and are a result of the chronotropic
incompetence and reduced cardiac output. Symptoms like dizziness,
light-headedness or confusional states, episodes of fatigue or
muscular weakness, exercise intolerance, heart failure or palpitations
can be experienced by the patient.26
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Long Q-T Syndrome
Long QT syndrome is a genetically transmitted cardiac arrhythmia
caused by ion channel protein abnormalities. It is characterized by
electrocardiographic abnormalities and a high incidence of syncope
and sudden cardiac death. Long QT syndrome can be mistaken for
palpitations, neurocardiogenic syncope, and epilepsy. The diagnosis is
suggested when ventricular repolarization abnormalities result in
prolongation of the corrected QT interval.
Diagnostic Criteria
It is recommended to incorporate clinical and electrocardiogram
(ECG) findings in a probability-based diagnostic criterion for long QT
syndrome. The maximum score is 9, and a score of more than 3
indicates a high probability of long QT syndrome. The criteria are
outlined below.
Electrocardiogram
Electrocardiogram findings (without medications or disorders known
to affect ECG features) include the following:

QT corrected for heart rate (QTc), calculated using Bazett's
formula, of more than 480 milliseconds (ms) - 3 points

QTc of 460-470 ms - 2 points

QTc of 450 ms in male patients - 1 point

Torsade de pointes (mutually exclusive) - 2 points

T-wave alternans - 1 point

Notched T wave in 3 leads - 1 point

Low heart rate for age (i.e., resting heart rate below the second
percentile for age) - 0.5 point
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Clinical History
Clinical history includes the following:

Syncope with stress (mutually exclusive) - 2 points

Syncope without stress - 1 point

Congenital deafness - 0.5 point
Family History
Family history includes the following (the same family member
cannot be counted in both categories):

Family member with definite long QT syndrome - 1 point

Unexplained sudden cardiac death (age < 30 y) in an
immediate family member - 0.5 point
Epidemiology
The frequency of long QT syndrome is unknown (possibly about 1 per
5000 population). The condition is present in all races and ethnic
groups, although frequency may differ among these populations.
However, population-based prevalence studies are not available on
this disease at the current time. Long QT syndrome is responsible for
approximately 1000 deaths each year in the United States, most of
which occur in children and young adults.27,28
This syndrome, once diagnosed by clinical profile, has been more
clearly defined by specific genetic defects that cause ion channel
abnormalities, resulting in a syndrome that predisposes to lethal
cardiac arrhythmias. Initial studies using monophasic action
potentials have shown evidence of early afterdepolarizations (EADs)
in congenital and acquired long QT syndrome. Excessive prolongation
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of action potential results in reactivation of certain L-type calcium
channels, leading to afterdepolarizations.68
Sympathetic activity is thought to enhance the EADs, which in turn
can initiate a lethal form of ventricular arrhythmia termed torsade de
pointes. Abnormal cardiac repolarization renders the heart susceptible
to these lethal ventricular tachyarrhythmias, increasing the risk of
sudden cardiac death in patients of all ages.29
Acquired Long QT Syndrome
The acquired causes of long QT syndrome include drugs, electrolyte
imbalance, marked bradycardia, cocaine, organophosphorus
compounds, subarachnoid hemorrhage, myocardial ischemia, proteinsparing fasting, autonomic neuropathy, and human immunodeficiency
virus (HIV) disease. A prolonged QTc and an increased risk of torsade
de pointes characterize drug-induced long QT syndrome. Virtually all
drugs that prolong QTc block the rapid component of the delayed
rectifier current (Ikr). Some drugs prolong QTc in a dose-dependent
manner, whereas others do so at any dose. Most patients who
develop drug-induced torsade de pointes have underlying risk factors.
The incidence is more common in females. Drugs implicated in
causing torsade de pointes include:

Class Ia and III antiarrhythmics

Macrolide antibiotics

Pentamidine

Antimalarials

Antipsychotics

Arsenic trioxide

Methadone
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The prognosis for patients with long QT syndrome who have been
treated with beta-blockers (and other therapeutic measures, if
needed) is satisfactory. Fortunately, episodes of torsade de pointes
are usually self-terminating in patients with long QT syndrome; only
about 4-5% of cardiac events are fatal. Patients at high risk (i.e.,
those with aborted cardiac arrest or recurrent cardiac events despite
beta-blocker therapy) have a markedly increased risk of sudden
death. These patients should be treated with an implantable
cardioverter-defibrillator device (ICD), which will lead to a good
prognosis.
In a study of adolescent patients with clinically suspected long QT
syndrome, Hobbs et al., found that the timing and frequency of
syncope, QTc prolongation, and gender were predictive of risk for
aborted cardiac arrest and sudden cardiac death during adolescence.
Neurologic deficits after aborted cardiac arrest may complicate the
clinical course even after successful resuscitation.
Treatment
Treatment of long QT syndrome depends on the relative risk of
sudden cardiac death, which is increased with longer QT durations, a
history of prior cardiac events, and a family history of sudden cardiac
death. Short-term treatment of long QT syndrome is aimed at
preventing recurrences of torsade de pointes and includes
intravenous (IV) magnesium and potassium administration,
temporary cardiac pacing, withdrawal of the offending agent,
correction of electrolyte imbalance, and, rarely, IV isoproterenol
administration.14
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Long-term treatment is aimed at reducing the QT interval duration
and preventing torsade de pointes and sudden death. Beta-blockers
are considered the initial treatment of choice, with ICD therapy
warranted in high-risk patients. In patients with frequent ICD shocks
or in those at a high risk for sudden cardiac death in whom ICD
placement cannot be performed, cardiac pacing, left cardiac
sympathetic denervation, or both may be indicated.
Lifestyle modification to avoid triggers for malignant cardiac
arrhythmias should be made to treat symptoms and reduce mortality
in patients with long QT syndrome.
Inpatient Care
Inpatient care of long QT syndrome is in most cases related to
emergencies or procedures such as ICD implantations. In certain
situations; however, telemetry monitoring and observations may be
necessary. Asymptomatic patients rarely need inpatient care.
Outpatient Care
Outpatient care is provided by a pediatric cardiologist or an
electrophysiologist. Regular monitoring is mandatory in these
patients.
Deterrence or Prevention
Trigger avoidance, antiadrenergic therapy, and ICDs can be used to
prevent future cardiac events.
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Consultations
A pediatric cardiologist or electrophysiologist should be immediately
involved. A social counseling team should be involved to facilitate
patient and family evaluations.
Medications
In patients who had suffered syncope in the previous two years,
beta-blocker treatment was associated with a 64% risk reduction for
aborted cardiac arrest and sudden cardiac death during adolescence.
However, there seems to be variation in the efficacy in preventing
cardiac events among the different classes of beta-blockers, and
metoprolol seems to have the greatest risk of recurrent cardiac
events.2
The data favor treating asymptomatic patients, who are younger than
40 years at the time of diagnosis, with beta-adrenergic blockers.
Sodium channel blockers are promising agents under investigation.
Risk of cardiac events increases during pregnancy and the
postpartum period. Because of this increased risk, pregnant women
with long QT syndrome should be treated with beta-blockers.
Physicians should be aware that high doses of beta blockade in the
second and third trimesters may cause neonatal bradycardia at birth.
Propranolol and nadolol are the preferred beta-blockers during
pregnancy.30
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Class Summary
These agents currently represent the first-choice therapy in patients
with symptomatic long QT syndrome unless specific contraindications
are present. Patients with long QT syndrome who are unable to take
beta-blockers may require an ICD (implantable cardioverterdefibrillator) as first-line therapy.31

Propranolol (Inderal, InnoPran XL)
Propranolol reduces the effect of sympathetic stimulation on the
heart. It decreases conduction through the atrioventricular (AV)
node and has negative chronotropic and inotropic effects. A
cardiologist should be consulted because dosing practice varies
and is individualized in patients with long QT syndrome. Patients
with asthma should use cardioselective beta-blockers. Patients
with long QT syndrome who are unable to take beta-blockers may
require an ICD as first-line therapy.

Nadolol (Corgard)
Nadolol is frequently prescribed because of its long-term effect. It
reduces the effect of sympathetic stimulation on the heart.
Nadolol decreases conduction through the AV node and has
negative chronotropic and inotropic effects. A cardiologist should
be consulted because dosing practice varies and is individualized
in patients with long QT syndrome. Patients with asthma should
use cardioselective beta-blockers. Patients with long QT syndrome
who are unable to take beta-blockers may require an ICD as firstline therapy.
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
Metoprolol (Lopressor, Toprol XL)
Metoprolol is a selective beta1-adrenergic receptor blocker that
decreases the automaticity of contractions. During IV
administration, carefully monitoring the blood pressure, heart
rate, and ECG is needed. A cardiologist should be consulted
because dosing varies and is individualized in patients with long
QT syndrome. Patients with long QT syndrome who cannot take
beta-blockers may require an ICD as first-line therapy.

Atenolol (Tenormin)
Atenolol selectively blocks beta1-receptors, with little or no effect
on beta2 types. A cardiologist should be consulted because dosing
varies and is individualized in patients with long QT syndrome.
Patients with long QT syndrome who cannot take beta-blockers
may require an ICD as first-line therapy.
Premature Atrial Contraction And
Premature Ventricular Contraction
Premature Atrial Contractions
Premature Atrial Contractions (PACs) are amongst the most common
forms of arrhythmias. It is due to the premature discharge of an
electrical impulse in the atrium, causing a premature
contraction. Therefore, it is named "premature atrial contraction," or
PAC. A PAC is premature, because the beat occurs earlier than the
next regular beat should have occurred.32
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Symptoms of PACs
Most often, patients with PACs complain of palpitations. However,
rather than reporting sustained racing heartbeat, they usually
describe "missing" or "skipping" of the heartbeat. Some patients even
feel that the heart has "stopped" while others describe a sensation of
"flip-flop." This is due to the fact that the PAC comes too early
(prematurely) in the cardiac cycle to have resulted in an effective
pulse or heartbeat. Therefore, no heartbeat is felt until the next
regularly timed heartbeat occurs after a pause (so-called
compensatory pause). Incidentally, the beat after the PAC usually
occurs with stronger contraction than usual and can be associated
with an urge to cough. Symptoms of PACs are virtually
indistinguishable from those of PVCs as the physiological effects are
identical.
Causes of PACs

Stress

Stimulants

o
Caffeine
o
Tobacco
o
Alcohol
Underlying Heart Disease
o
Hypertension
o
Valve disorder
o
Previous myocardial infarct

Abnormal blood levels of magnesium and/or potassium

Digitalis toxicity
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In the majority of cases, PACs occur in normal healthy individuals
without any evidence of heart disease. Stress or stimulants such as
tea, coffee, or alcohol can increase the frequency of PACs, which can
also occur in both children and adolescents where the use of
substances or caffeine addiction may already be a concern. In the
minority of cases, PACs can be a sign of underlying heart condition in
the atrium associated with hypertension or valvular condition.
Consequences of PACs
The great majority of PACs is completely benign and requires little if
any treatment at all. As mentioned above, in rare cases, PACs may
be the only sign of underlying heart conditions and these should be
ruled out with appropriate evaluations. However, PACs may change
into atrial flutter, atrial fibrillation, or supraventricular tachycardia.11
Diagnosis
Evaluation is similar as with any patient first seen for palpitations and
arrhythmias and includes blood tests, EKGs, as well as
echocardiograms.
Treatment of PACs
As most PACs are benign, treatment is optional and is usually geared
toward alleviation of symptoms. Medications such as beta-blockers or
calcium blockers are often used but with mixed result. After ruling out
severe underlying heart conditions, the most important treatment in
these cases is to reassure the patient and teach the patient coping
mechanisms.32
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Premature Ventricular Contractions (PVCs)
Premature ventricular contractions (PVCs) are extra, abnormal
heartbeats that begin in the ventricles, or lower pumping chambers,
and disrupt the regular heart rhythm, sometimes causing an
individual to feel a skipped beat or palpitations. Premature ventricular
contractions are very common and usually harmless. Premature
ventricular contractions are also called premature ventricular
complexes, ventricular premature beats and extrasystoles.33
Symptoms, Causes and Diagnosis of PVCs
Symptoms of PVCs include a fluttering or flip-flop feeling in the chest,
pounding or jumping heart rate, skipped beats and palpitations, or an
increased awareness of one’s heartbeat. The heart’s normal, or sinus,
rhythm is controlled by a natural pacemaker, the sinus node, which
creates electrical impulses that travel across the atria to the
ventricles, causing them to contract and pump blood out to the lungs
and body in what is known as normal sinus rhythm.
Premature ventricular contractions occur when ventricle contractions
beat sooner than the next expected regular heartbeat, often
interrupting the normal order of pumping. The extra beat is followed
by a stronger heartbeat, which creates the feeling of a skipped beat
or a flutter. These extra beats are usually less effective in pumping
blood throughout the body. Premature ventricular contractions can be
caused or triggered by heart diseases or scarring which can interfere
with the normal electrical impulses.33
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Prevention and Treatment
Patients should be encouraged to report any symptoms of PVCs so
the provider can determine if there is an underlying cause that needs
to be treated, such as other rhythm problems, serious heart
problems, anxiety, anemia or infections. Patients should also report
any symptoms like dizziness or fainting.
Many of the causes of PVCs can be managed, such as mineral and
chemical imbalances in the body, medications, alcohol, damage to
the heart muscle from heart disease or high blood pressure, elevated
levels of adrenaline (which could be caused by caffeine, exercise, or
anxiety). Premature ventricular contractions can also be trigged by
low blood oxygen, which could happen if the patient has chronic
obstructive pulmonary disease (COPD) or pneumonia.
In people with healthy hearts, occasional PVCs are harmless and
usually resolve on their own without treatment; however, in patients
with heart problems such as heart failure or heart disease, PVC’s may
be a sign of a more dangerous heart rhythm to come.33,34
Arterial Flutter
Atrial flutter is an electrocardiographic descriptor used both
specifically and nonspecifically to describe various atrial tachycardias.
The term was originally applied to adults with regular atrial
depolarizations at a rate of 260-340 beats per minute (bpm).
Historically, the diagnosis of atrial flutter was restricted to those
patients whose surface electrocardiogram (ECG) revealed the classic
appearance of "flutter waves." This sharp demarcation is used less
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frequently in the current era, where the more electrophysiologically
descriptive "atrial reentry tachycardia" is used instead.35
Atrial flutter is infrequent in children without congenital heart disease.
In these patients with otherwise normal cardiac anatomy atrial
reentry tachycardias are observed mostly during fetal life in late
pregnancy, and during adolescence. In the fetus, atrial flutter is
defined as a rapid regular atrial rate of 300-600 bpm accompanied by
variable degrees of atrioventricular (AV) conduction block, resulting in
slower ventricular rates.11 During this type of tachycardia, the atrial
rate is so rapid that normal AV nodes usually display a
physiologic second-degree block, with a resultant 2:1 conduction
ratio.
In individuals with AV nodal disease or increased vagal tone, or when
certain drugs are used, higher degrees of AV block may develop, such
as 3:1 or higher. In individuals with accessory AV nodal pathways, a
1:1 conduction ratio may occur through the accessory pathway with
resultant ventricular rates of 260-340 bpm, which can cause sudden
death. A 1:1 conduction ratio may also occur when the atrial rate is
relatively slow (i.e., < 340 bpm) during atrial flutter or when
physiologic processes facilitate AV nodal conduction, such that a rapid
ventricular response can still result in sudden death.36 Patients who
have undergone Mustard, Senning, or Fontan operations are more
prone to developing this arrhythmia because of atrial scars from
surgery and right atrial enlargement, such as after the classic Fontan
operation. Similarly, patients who have undergone surgical repair of
an atrial septal defect, total anomalous pulmonary venous
connection, and tetralogy of Fallot may later develop atrial flutter.
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Individuals with muscular dystrophies such as Emery-Dreifuss and
myotonic dystrophy may also develop atrial flutter, as well as those
with dilated, restrictive, and hypertrophic cardiomyopathies.
Treatment of children with atrial flutter depends on the age of
presentation and baseline cardiac anatomy. Fetal atrial flutter is
usually treated with oral maternal antiarrhythmics without need for
further intervention if ventricular function is acceptable and if there is
no placental edema. Once the baby is born, it usually responds well
to oral antiarrhythmics until it resolves. In the other age groups and
in patients with baseline abnormal cardiac anatomy or surgical scars,
it usually recurs. In general, treatment may involve medication,
cardiac pacing, cardioversion, radiofrequency catheter ablation, or
surgical procedures. Drug therapy of atrial flutter in children can be
classified under the three broad headings of ventricular rate control,
acute conversion, and chronic suppression.
Atrial flutter is a reentrant arrhythmia circuit confined to the atrial
chambers. As a rule, atrial flutter originates in the right atrium,
whereas atrial fibrillation, which is more frequent in adults, originates
in the left atrium.
A flutter circuit typically surrounds an anatomical or functional barrier
and includes a zone of slow conduction (or conduction over an
extended circuit) and an area of unidirectional block, as required for
reentry of all types. Frequently, a premature beat blocks one limb of
the circuit and is sufficiently delayed in the other limb (while
traversing around the anatomical or functional barrier) to allow for
recovery from refractoriness in the first limb.37
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The reentrant circuits that occur in children with atrial flutter after
congenital heart disease surgery are believed to involve abnormal
atrial tissue that has been subject to chronic cyanosis, inflammation
secondary to surgery, scarring, and increased wall stress in cases of
enlarged atria. Such circuits may encircle anatomical barriers such as
atriotomy scars or surgical anastomoses, and they may use areas of
slow conduction along baffle limbs and other sites of injury in addition
to the tricuspid valve–coronary sinus isthmus.
Sinus node dysfunction with bradycardia is generally present in many
of these patients, years after surgery. This is a contributing factor for
development and maintenance of atrial flutter. Atrial flutter circuits in
children with congenital heart disease are typically more variable
than those in adults. For the most part, atrial flutter circuits in adults
are confined to the tricuspid valve–coronary sinus isthmus (or
isthmus-dependent flutter). In the fetus, atrial flutter occurs mainly
during the third trimester. The atrium is believed to reach a critical
mass to support an intra-atrial macroreentry circuit at about 27-30
weeks of gestation.5
Most fetuses and neonates with atrial flutter have structurally normal
hearts. However, when atrial flutter is detected in a fetus, structural
cardiac anomalies such as Ebstein’s anomaly of the tricuspid valve
and AV septal defects should be ruled out because of a higher
incidence of such defects in these cases.38 Neonatal atrial flutter is
usually a self-limiting illness, requiring only conversion of the rhythm
with esophageal atrial pacing or cardioversion. Incisional reentrant
atrial tachycardia following complex atrial surgery in the repair of
congenital heart disease may occur early in the postoperative period.
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This event is predictive of the occurrence of late postoperative flutter.
The prevalence of atrial flutter in several classes of postoperative
patients increases with the duration of follow-up care.
Some newborns and young children have associated conditions or
anomalies that may predispose them to atrial flutter. Atrial septal
aneurysms appear to be associated with sustained atrial arrhythmias
in newborns. Restrictive cardiomyopathies are also associated with
refractory atrial flutter. In Costello syndrome, the dysmorphic
appearance is also associated with a dysrhythmia characterized as
chaotic atrial tachycardia, and this dysrhythmia may include long
episodes of atrial flutter.
The fetus with atrial flutter may have significant morbidity and be at
risk for mortality. According to one review, hydrops fetalis developed
in as many as 40% of fetuses with atrial flutter. The mortality rate in
these fetuses was 8%. Mortality in newborns with atrial flutter is
uncommon. Most patients remain in sinus rhythm following their
initial conversion, and the need for antiarrhythmic prophylaxis in
these patients during infancy is debated.6
Atrial flutter is not uncommon in the immediate postoperative period
after congenital heart surgery. Surgery-induced inflammation of the
pericardium, scarring, and volume overload may trigger atrial flutter.
Case reports have linked atrial flutter to ingestion of herbal medicines
and certain foods. These episodes did not recur after avoidance of the
triggers.
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Atrial flutter and atrial fibrillation have been related to obesity,
alcohol consumption, and hyperthyroidism. One study reported that
in adults, diabetes mellitus is a strong independent risk factor for
development of atrial flutter and atrial fibrillation. Morbidity and
mortality in patients with atrial flutter largely depend on the following
factors:

Age at presentation

Cardiac anatomy (normal anatomy vs. congenital heart
disease)

Integrity and anatomy of the myocardial conduction system
(normal sinus node versus sinus node dysfunction; AV block
versus normal AV node, with or without accessory pathways)

Ventricular function

Prompt recognition of the arrhythmia and initiation of adequate
therapy
In patients with postoperative atrial flutter that develops late
following repair of congenital heart disease, the severity of
presentation depends on the atrial flutter rate, conduction ratio, and
presence of ventricular dysfunction. In patients who have undergone
the Mustard procedure, Holter recordings incidentally capturing
episodes of sudden fatality confirm that rapidly conducted atrial
flutter is the dysrhythmia most frequently responsible for these
fatalities.39
In contrast, patients who have undergone the Fontan procedure
rarely die suddenly but frequently present with symptomatic atrial
flutter. A relatively slower atrial flutter rate, a higher degree of AV
conduction block, or both may cause this.
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Prolonged episodes of atrial flutter in
asymptomatic or mildly symptomatic
patients may be associated with
development of atrial thrombi and,
although rarely in the congenital heart
disease population, the possibility of
thromboembolic events. When women
with heart disease and arrhythmias
reach childbearing age, arrhythmias can recur during pregnancy.
These arrhythmias significantly increase the risk for the mother and
fetus.
Treatment
In children with atrial flutter, medical care should be broadly directed
at the following:

Ensuring hemodynamic stability before, during, and after
conversion to sinus rhythm

Minimizing influences favoring initiation or maintenance of atrial
arrhythmias (i.e., electrolyte disturbances, pericardial effusion,
indwelling atrial lines or catheters)

Excluding or managing complications (i.e., ventricular
dysfunction, thromboembolic phenomena)

Restoring
Drug therapy may be indicated in some children with atrial flutter. In
these cases, drug therapy can be classified under the 3 broad
headings of ventricular rate control, acute conversion, and chronic
suppression.
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Thrombosis and thromboembolic events are recognized complications
in patients with atrial flutter, particularly in the setting of repaired
congenital heart disease. Patients who have thrombi identified on
transesophageal echocardiography or have a history of chronic atrial
flutter (>2 week duration) should be treated with a period of
anticoagulation (2 - 4 week), if hemodynamically and
symptomatically tolerated, before undergoing direct current (DC)
cardioversion or other conversion of their rhythm.
According to a legal precedent, patients with Mustard repair of
transposition of the great vessels and sick sinus syndrome should not
receive quinidine without a previously implanted pacemaker.
However, quinidine is now recognized to have a detrimental adverse
effect profile in general, and it is essentially no longer used in the
treatment of rhythm disorders following congenital heart disease.
Disagreement surrounds whether this recommendation should be
extrapolated to other antiarrhythmics and other forms of repaired
congenital heart disease.
Programmable Stimulation
Pace-termination of atrial flutter is best performed with a
programmable stimulator that is capable of sensing atrial
electrograms and delivering single, double, or multiple extrastimuli at
adequate output and individually programmable cycle lengths down
to 100 milliseconds. Short discrete ramps or bursts of atrial stimuli
are the most likely to produce a type I conversion of atrial flutter
(immediate conversion to sinus rhythm), particularly if they can be
delivered in or near the flutter circuit. If such a device is unavailable,
a pacemaker capable of burst pacing at a specified rate may be used.
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If pacing is performed via an esophageal electrode, the device should
be capable of delivering stimuli at pulse widths of 9.9-20 milliseconds
and outputs of 10-26 mA. Patients who are treated with atrial
antitachycardia pacing should undergo testing to confirm that their
device is effective and not proarrhythmic.75
Cardioversion
R-wave synchronized cardioversion is the mainstay of therapy in
patients who are unstable or if other therapies have failed. In
patients who are stable and have chronic atrial flutter, perform
cardioversion only after documentation of freedom from intracardiac
thrombi or following a 2-week course of anticoagulation.
Cardioversion may be performed at increasing doses of 0.5, 1, 2, and
4 J/kg. Newer biphasic waveform defibrillators may allow for lower
energy applications.
Ideally, defibrillator paddles or pads should be placed in an
anteroposterior configuration, with the apex paddle located over the
mid sternum and the base paddle between the scapulae. An
anesthesiologist usually administers a brief general anesthetic, except
in truly emergent circumstances that mandate immediate
cardioversion. Hemodynamic instability requires immediate
cardioversion as described above. However, patients who are
relatively stable may be allowed to remain in flutter while careful
consideration of possible interventions is undertaken. The patient
should rest in a supine position without undue excitement or
agitation. Consider digoxin if not already in use because it frequently
increases the conduction ratio and decreases the ventricular rate.
However, this effect usually takes many hours.
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Medications with the potential to slow the atrial rate without affecting
the atrioventricular (AV) node should be used with caution because
the conduction ratio often decreases to 1:1 AV association. This may
result in a rapid ventricular rate and hemodynamic compromise.
Avoid adrenergic and atropinic agents during sedation or anesthesia
for cardioversion. Ketamine is relatively contraindicated. Such agents
may result in rapid 1:1 AV conduction, with resultant hemodynamic
compromise. On the other hand, insufficient sedation during
attempted esophageal overdrive pacing or a failed cardioversion may
result in patient distress and 1:1 AV conduction ratio.
Radiofrequency Catheter Ablation
Currently, radiofrequency catheter ablation appears to be somewhat
effective in treating postoperative intra-atrial reentrant tachycardia in
children. Because the flutter circuits and critical isthmuses are quite
variable in these patients, mapping of flutter circuits may be
enhanced by 3-dimensional electroanatomical display systems,
identification of split potentials, and demonstration of concealed
entrainment during pacing.40
Surgical Correction of Atrial Flutter
In patients with atrial flutter, surgical care may include one of the
following procedures:

Correction of hemodynamic lesions that could be causing atrial
volume loading

Specifically placed atrial incisions or cryoablation
prophylactically to prevent atrial flutter

Empiric or map-directed lesions to eliminate documented atrial
flutter and its circuits
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These surgeries include various modifications and updates to maze
procedures and modifications of the Mustard and Fontan procedures.
One study reported that a right-sided maze procedure in patients
with atrial flutter or fibrillation undergoing congenital heart disease
repair significantly reduced arrhythmia recurrence at a mean of 2.7
years after surgery.
Activity Restriction
Aggressive strategies to convert atrial flutter and maintain sinus
rhythm should be pursued in children. In rare cases of resistant
chronic atrial flutter when only rate control can be accomplished,
patients should avoid competitive sports. Also restrict the activities of
patients likely to develop rapid conduction of intermittent acute
episodes of flutter.41
Deterrence/Prevention of Atrial Flutter
Atrial stretch, surgical scarring, and sinus node dysfunction all appear
to play important roles in the development of atrial flutter in patients
with congenital heart disease. The development of new surgical
techniques to avoid atrial suture lines or dilatation and to
prophylactically interrupt potential conduction isthmuses within the
atria may reduce the frequency of this disorder in future surgical
cohorts of patients with congenital heart disease. Efforts directed at
sparing the sinus node during surgery, coupled with more aggressive
pacing strategies in patients with sinus node dysfunction, could also
play an important role in prevention of atrial flutter.
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Medication
Drug therapy of atrial flutter in children can be classified under the 3
broad headings of ventricular rate control, acute conversion, and
chronic suppression. This section summarizes the treatment for all
three headings.35,42
Digoxin is relatively safe for preventing rapid conduction of atrial
flutter via the atrioventricular (AV) node to the ventricles, and some
evidence indicates that this reduces symptomatology during flutter.
Nevertheless, digoxin is unlikely to be particularly effective in the
acute conversion or prevention of atrial flutter recurrence. It is devoid
of negative inotropic effects (as is amiodarone) and is useful to
control ventricular rate when using propafenone, flecainide, or
procainamide.
Intravenous procainamide has been used with variable success to
effect acute conversion of atrial flutter to sinus rhythm. Procainamide
infusion should be preceded by digitalization to prevent
procainamide-induced acceleration of AV node conduction to the
ventricles.
The Vaughan Williams class III agents ibutilide and dofetilide may be
used for acute conversion of atrial flutter and fibrillation. Both are
more effective than other medications in converting atrial flutter, but
their use is associated with QT prolongation with a nontrivial risk of
induction of torsade de pointes polymorphic ventricular tachycardia.
Clinical experience in adults is limited, and efficacy, dosing, and
safety in children have not been established.
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A more recent drug, dronedarone, a less-lipophilic amiodarone
analog, has been shown to prevent recurrence of atrial flutter and
atrial fibrillation in adult patients, according to several multicenter
trials. However, it increases mortality in patients with decompensated
heart failure and therefore should be avoided in such cases. Safety
and efficacy of this drug have not been confirmed in patients younger
than 18 years.
Fetal atrial flutter is the second most common intrauterine
tachyarrhythmia. Treatment is aimed at controlling ventricular rate
and, thus, avoiding hydrops fetalis. First-line treatment is digoxin
administered to the mother, which provides a conversion rate to
sinus rhythm of 45-52%. In addition, its positive inotropic effect may
be beneficial.
Sotalol has also been used in numerous cases with success. Maternal
drug levels were not reliable predictors of successful therapy.
Flecainide alone or in combination with digoxin is used as second-line
treatment. Fetal atrial flutter in a structurally normal heart seldom
recurs after conversion before or after birth, and postnatal
suppressive antiarrhythmic therapy may not be necessary. Flutter in
patients with repaired or palliated structural congenital lesions is
more likely to recur, and long-term antiarrhythmic therapy aimed at
flutter suppression is often instituted after the first or the second
flutter episode.
Vaughan Williams class Ic (i.e., flecainide, propafenone) or class III
(i.e., sotalol, amiodarone) agents have been prescribed with variable
success. Some authors have cautioned against use of flecainide in
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this setting, but the data are equivocal. Combinations of agents
occasionally succeed after failure of single-agent therapy. Use of
antiarrhythmic agents other than digoxin for the long-term
suppression of atrial flutter in sinus node disease (a frequent
coexisting finding) is particularly controversial. In patients with atrial
flutter who have had the Mustard procedure, treatment with quinidine
was associated with case reports of sudden death. This resulted in
the recommendation of antibradycardia pacing initiation before
antiarrhythmic drug therapy in these patients. This recommendation
has gradually broadened to encompass other antiarrhythmic agents
in patients with other types of repaired congenital heart disease.
Diltiazem can provide rapid, consistent, and safe temporary
ventricular rate control in children.
Antibradycardia pacing may be directly advantageous in flutter
suppression by reducing the frequency of flutter-inducing pauses and
premature beats. It also provides a safety factor for more aggressive
antiflutter drug therapy.
Class Summary
These agents alter the electrophysiologic mechanisms responsible for
arrhythmia.
Digoxin (Lanoxin)
Digoxin is a cardiac glycoside with direct inotropic effects in addition
to indirect effects on the cardiovascular system. It acts directly on
cardiac muscle, increasing myocardial systolic contractions. Its
indirect actions result in increased carotid sinus nerve activity and
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enhanced sympathetic withdrawal for any given increase in mean
arterial pressure.
Procainamide
Procainamide is a class Ia antiarrhythmic used for premature
ventricular contractions (PVCs). It increases the refractory period of
the atria and ventricles. Myocardiac excitability is reduced by increase
in threshold for excitation and inhibition of ectopic pacemaker
activity.
Propafenone (Rythmol, Rythmol SR)
Propafenone treats life-threatening arrhythmias. It may work by
reducing spontaneous automaticity and prolonging the refractory
period.
Amiodarone (Cordarone, Pacerone)
Amiodarone may inhibit AV conduction and sinus node function. It
prolongs the action potential and refractory period in myocardium
and inhibits adrenergic stimulation. Before administration, control
ventricular rate and congestive heart failure (if present) with digoxin.
Diltiazem (Cardizem, Tiazac, Dilacor XR)
Diltiazem is an AV nodal blocking agent. It is administered IV
temporarily (i.e., < 24 hours) until definitive treatment can be
initiated.
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Flecainide (Tambocor)
This agent treats life-threatening ventricular arrhythmias. It causes a
prolongation of refractory periods and decreases action potential
without affecting duration. Flecainide blocks sodium channels,
producing a dose-related decrease in intracardiac conduction in all
parts of the heart with greatest effect on the His-Purkinje system (HV conduction). Effects on AV nodal conduction time and intra-atrial
conduction times, although present, are less pronounced than on
ventricular conduction velocity.
Sotalol (Betapace, Betapace AF, Sorine)
Sotalol is a class III antiarrhythmic agent that blocks potassium
channels, prolongs action potential duration, and lengthens the QT
interval. It is a non–cardiac selective beta-adrenergic blocker.
Ibutilide (Corvert)
This newer class III antiarrhythmic agent may work by increasing
action potential duration, thereby changing atrial cycle length
variability. Mean time to conversion is 30 minutes. Two-thirds of
patients who convert are in sinus rhythm at 24 hours. Ventricular
arrhythmias may occur, mostly PVCs; and, torsade de pointes is a
rare complication.
Dofetilide (Tikosyn)
Recently approved by the FDA for maintenance of sinus rhythm,
dofetilide increases monophasic action potential duration, primarily
because of delayed repolarization. It terminates induced reentrant
tachyarrhythmias (i.e., atrial fibrillation/flutter, ventricular
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tachycardia) and prevents their reinduction. It does not affect cardiac
output, cardiac index, stroke volume index, or systemic vascular
resistance in patients with ventricular tachycardia, mild-to-moderate
CHF, angina, and either normal or reduced LVEF. There is no
evidence of a negative inotropic effect.
Dronedarone (Multaq)
Dronedarone is a benzofuran derivative indicated to reduce the risk of
cardiovascular hospitalization in patients with paroxysmal or
persistent atrial fibrillation (AF) or atrial flutter (AFL), with a recent
episode of AF/AFL. It is not effective in patients with permanent atrial
fibrillation. It may cause bradycardia and QT prolongation.
Dronedarone is contraindicated in patients with NYHA class IV heart
failure or NYHA class II and class III heart failure who had a recent
decompensation. Safety and efficacy of this drug have not been
confirmed in patients younger than 18 years.
Sinus Tachycardia
Sinus tachycardia is sinus rhythm with a rate of > 100 bpm. Sinus
tachycardia is an example of a supraventricular rhythm. In sinus
tachycardia the sinus node fires between 100 and 180 beats per
minute, faster than normal. The maximal heart rate decreases with
age from around 200 bpm to 140 bpm. The maximal heart rate can
be estimated by subtracting the age in years from 210. Sinus
tachycardia normally has a gradual start and ending. Most often sinus
tachycardia is caused by an increase in the body's demand for
oxygen, such as during exercise, stress, infection, blood loss and
hyperthyroidism. It can also express an effort of the heart to
compensate for a reduced stroke volume, as occurs during
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cardiomyopathy. The maximal heart rate is considered to be 220/min
minus the age (or more precisely 207-0.7xAge. However, this is often
exceeded during vigorous exercise and has a large inter-individual
variation.43
Appropriate sinus tachycardia can result from:

Exercise

Anxiety

Alcohol/caffeine use

Drugs (i.e., beta-agonists like dobutamine)
Inappropriate sinus tachycardia can result from:

Fever

Hypotension

Hypoxia

Congestive heart failure

Bleeding

Anemia

Hyperthyroidism

Cardiomyopathy (with reduced left ventricular function and
compensatory tachycardia)

Myocarditis
Inappropriate sinus tachycardia is rare and characterized by
tachycardia at rest and exaggerated acceleration of the heart during
physiologic stress. The mechanism leading to an exaggerated
response of the sinus node to minimal physiologic stress is
incompletely understood.44
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Supraventricular Tachycardia
Supraventricular tachycardia (SVT) is the most common tachycardia
in children. Also known as PSVT (paroxysmal supraventricular
tachycardia) and PAT (paroxysmal atrial tachycardia), the condition is
not considered a serious life threat for young children. The upper and
lower heart chambers are involved in the quick heart rate induced by
this condition. Doctors only call for treatment if the tachycardia
episodes are either too common or too prolonged. Treatments often
prove effective with the symptoms stopping after the first six to
twelve months of treatment.
Newborns and Infants
Supraventricular tachycardia can occur in children of all ages. The
condition is capable of affecting newborns and young infants who
have completely normal hearts. Among infants, an episode of SVT
can take the heart rate to over 220 bpm. Infants become sleepier and
more fussy than normal during an episode of SVT and start to
breathe very quickly too. Early diagnosis and treatment of the
episode is necessary to restore normalcy. Once the episode is
controlled, the infant is given medications to stop any further
recurrences. It is possible that a baby’s heart beats quicker than
normal while in the womb. If the condition is diagnosed at such a
point, the mother is given medications, which would slow down the
heart rate of the child.45
Older Children
In children who are slightly grown up, SVT is accompanied with
symptoms like general weakness, pain in the stomach, palpitations,
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nausea, dizziness and a slight discomfort in the chest region. Children
can be taught to control their heart rate with a technique known as
Valsalva maneuver. In this technique, the child simply needs to close
the mouth and the nose and then make an effort to breathe out.46
As compared to newborns and
infants, children who are older
often suffer from greater number
of tachycardia episodes. This is
why older children need to be
tested more often and need to be
treated for longer periods.
Neither the episodes nor the tests
and treatments should stop the
children from living a normal life.
Children with SVT may need to visit the doctor more often than usual
but the child’s life should not be otherwise affected by SVT.47
Treatments
The treatment of SVT consists of two phases. The first phase involves
steps taken in order to stop or control the current attack of
tachycardia while the second phase involves steps to prevent any
further recurrence. A few easy procedures can prove very effective in
ending a given episode of tachycardia. One such procedure is the use
of intravenous medications. Catheters (very thin and flexible tubes)
can also be used for stopping SVT. In this treatment, the catheter
needs to be passed from the nostril to the child’s esophagus and then
a very minute current is passed through the catheter in order to
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control the SVT. A low intensity electrical shock to the wall of the
child’s test is another way of controlling SVT.48
Treatments to ensure that there is no recurrence of another episode
depend entirely on the age of the child. While children above the age
of three do not need to be admitted for the purpose, infants are often
kept at the hospital with tests done in order to consistently monitor
the effectiveness of the treatment.47
Wolff-Parkinson-White Syndrome
Wolff-Parkinson-White (WPW) syndrome is defined as a congenital
condition involving abnormal conductive cardiac tissue between the
atria and the ventricles that provides a pathway for a reentrant
tachycardia circuit, in association with supraventricular tachycardia
(SVT).
The clinical manifestations of WPW syndrome reflect the associated
tachyarrhythmia episodes, rather than the anomalous ventricular
excitation per se. They may have their onset at any time from
childhood to middle age, and they can vary in severity from mild
chest discomfort or palpitations with or without syncope to severe
cardiopulmonary compromise and cardiac arrest. Thus, presentation
varies by patient age.49
Infants may present with the following:

Tachypnea

Irritability

Pallor

Intolerance of feedings
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
Evidence of congestive heart failure if the episode has been
untreated for several hours

A history of not behaving as usual for 1-2 days

An intercurrent febrile illness may be present
A verbal child with WPW syndrome usually reports the following:

Chest pain

Palpitations

Breathing difficulty
Older patients can usually describe the following:

Sudden onset of a pounding heartbeat

Pulse that is regular and “too rapid to count”

Typically, a concomitant reduction in their tolerance for activity
Physical findings include the following:

Normal cardiac examination findings in the vast majority of
cases

During tachycardic episodes, the patient may be cool,
diaphoretic, and hypotensive

Crackles in the lungs from pulmonary vascular congestion
(during or following an SVT episode)

Many young patients may present with resting tachycardia on
examination, with only minimal symptoms (i.e., palpitations,
weakness, mild dizziness) despite exceedingly fast heart rates
Clinical features of associated cardiac defects may be present, such
as the following:

Cardiomyopathy
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
Ebstein’s anomaly

Hypertrophic cardiomyopathy (AMPK mutation)
Routine blood studies may be needed to help rule out noncardiac
conditions triggering tachycardia. These may include the following:50

Complete blood count

Chemistry panel, with renal function studies and electrolytes

Liver function tests

Thyroid panel

Drug screening
The diagnosis of WPW syndrome is typically made with a 12-lead
electrocardiogram (ECG) and sometimes with ambulatory monitoring
(i.e., telemetry, Holter monitoring). SVT is best diagnosed by
documenting a 12-lead ECG during tachycardia, although it is often
diagnosed with a monitoring strip or even recorder. The index of
suspicion is based on the history, and rarely, physical examination
(Ebstein’s anomaly or hypertrophic cardiomyopathy [HOCM]).
Although the ECG morphology varies widely, the classic ECG features
are as follows:

A shortened PR interval (typically <120 ms in a teenager or
adult)

A slurring and slow rise of the initial upstroke of the QRS
complex (delta wave)

A widened QRS complex (total duration >0.12 seconds)

ST segment–T wave (repolarization) changes, generally
directed opposite the major delta wave and QRS complex,
reflecting altered depolarization
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Echocardiography is needed for the following:

Evaluation of left ventricular (LV) function, septal thickness,
and wall motion abnormalities

Excluding cardiomyopathy and an associated congenital heart
defect (i.e., HOCM, Ebstein’s anomaly, L-transposition of the
great vessels)
Stress testing is ancillary and may be used for the following:

To reproduce a transient paroxysmal SVT, which is triggered by
exercise

To document the relationship of exercise to the onset of
tachycardia

To evaluate the efficacy of antiarrhythmic drug therapy (class
Ic antiarrhythmic medications and effects on antegrade
preexcitation)
To determine whether consistent or intermittent preexcitation is
present at different sinus (heart) rates. Electrophysiologic studies
(EPS) can be used in patients with WPW syndrome to determine the
following:50

The mechanism of the clinical tachycardia

The electrophysiologic properties (i.e., conduction capability,
refractory periods) of the accessory pathway and the normal
atrioventricular (AV) nodal and His Purkinje conduction system

The number and locations of accessory pathways (necessary for
catheter ablation)

The response to pharmacologic or ablation therapy
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Once identified and appropriately treated, Wolff-Parkinson-White
(WPW) syndrome is associated with an excellent prognosis, including
the potential for permanent cure through radiofrequency (RF)
catheter ablation.
Asymptomatic patients with only preexcitation on electrocardiography
(ECG) generally have a very good prognosis. Many develop
symptomatic arrhythmias over time, which can be prevented with
prophylactic electrophysiologic studies (EPS) and RF catheter
ablation. Patients with a family history of sudden cardiac death (SCD)
or significant symptoms of tachyarrhythmias or cardiac arrest have
worse prognoses. However, once definitive therapy is performed,
including curative ablation, the prognosis is once again excellent.
Noninvasive risk stratification (i.e., Holter monitoring, exercise stress
test) can be useful if abrupt and complete loss of preexcitation occurs
with exercise or procainamide infusion. However, this is not an
absolute predictor for the absence of arrhythmic episodes. The
2012 Pediatric and Congenital Electrophysiology Society (PACES) and
the Heart Rhythm Society (HRS) guidelines indicate that more
invasive EPS should be considered when the absolute loss of manifest
preexcitation cannot be clearly demonstrated. The recommendations
include the following:51

Measurement of the shortest preexcited RR interval during
induced atrial fibrillation (AF)

Determination of the number and location of accessory
pathways (APs)

Evaluation of the anterograde and retrograde features of the
APs and atrioventricular (AV) node
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
Assessment at multiple cycle lengths of the effective refractory
period of the APs and the ventricle
In 2017 three new expert consensus statements are planned that will
update the 2012 – 2014 practice statements on: 1) Catheter and
Surgical Ablation of Atrial Fibrillation (recommendations for patient
selection, procedural techniques, patient management and follow-up,
definitions, endpoints, and research trial design) 2) MRI and Radiation
Exposure in Patients with IEDs (safety considerations and
management of IED patients requiring imaging, as well as indications
and considerations for MRI-conditional IEDs, as well as protocols and
programming for MRI imaging in patients with IEDs), and 3) IED Lead
Management and Extraction (definitions, identification and
management of lead failure, recalls and advisories, indications for lead
extraction, periprocedural patient management, facility and operator
training considerations, data management, registries and trial design).
Morbidity and Mortality
Mortality in WPW syndrome is rare and is related to SCD. The
incidence of SCD in WPW syndrome is approximately 1 in 100
symptomatic cases when followed for up to 15 years. Although
relatively uncommon, SCD may be the initial presentation in as many
as 4.5% of cases.52
Even in patients with asymptomatic WPW, the risk of SCD is
increased above that of the general population. Medical therapy with
agents such as digoxin may increase this risk if the patient has AF or
atrial flutter by favoring atrial-to-ventricular conduction over the
bypass tract rather than the AV node. The risk in asymptomatic
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patients is low and can be reduced further with prophylactic catheter
ablation of the accessory pathway (EPS and RF ablation).
Other factors that appear to influence the risk of SCD are the
presence of multiple bypass tracts, short accessory pathway (AP)
refractory periods (<240 ms), AF and atrial flutter, or a family history
of premature sudden death. SCD is unusual without preceding
symptoms.
The cause of SCD in WPW syndrome is rapid conduction of AF to the
ventricles via the AP, resulting in ventricular fibrillation (VF). AF
develops in one-fifth to one-third of patients with WPW syndrome;
the reasons for this and the effects of AP ablation on its development
are unclear. However, a study hypothesized that two mechanisms are
involved in the pathogenesis of AF in patients with WPW syndrome:
one is related to the AP that predisposes the atria to fibrillation, and
the other is independent from the AP and is related to increased atrial
vulnerability present in these individuals. Notably, AF may still occur
and be symptomatic in some patients after successful ablation of the
bypass tract, but AF does not then carry the same associated risk of
SCD.
In a study that evaluated the long-term (median 6.9 y) natural
history of WPW in adult patients treated with (n = 872) and without
catheter ablation (n = 1461) compared to a control group (n =
111,75), Bunch et al., found similarly low death rates but higher
incident AF risk in patients with WPW versus the control group. The
risk of long-term mortality was higher in those who did not undergo
ablation compared to the group treated with ablation, whereas the
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risk of incident AF was higher in the ablation group. Thus, ablation
did not reduce the risk of AF. According to the literature, risk factors
for the development of AF in the setting of WPW syndrome include
advancing age (two peak ages for AF occurrence are recognized, one
at 30 years and the other at 50 years), male sex, and prior history of
syncope. Certain factors increase the likelihood of VF, including
rapidly conducting APs and multiple pathways. Cases have also been
reported in association with esophageal studies, digoxin, and
verapamil. A few reports document spontaneous VF in WPW
syndrome, and supraventricular tachycardia (SVT) may degenerate
into AF, thus leading to VF; however, both scenarios are rare in
pediatric patients.49,52,53
Morbidity may be related to rapid near syncope or syncopal
arrhythmias. Even when syncope is absent, the arrhythmia episodes
may be highly symptomatic. In most patients, the SVT is well
tolerated and is not life-threatening. However, the potential for
syncope, hemodynamically compromising rhythms, or sudden death
may prevent patients with WPW syndrome from participating in
competitive sports or hazardous occupations until the substrate is
definitively addressed and cured by a catheter ablation procedure.
Complications
Complications include the following:

Tachyarrhythmia

Palpitations

Dizziness or syncope

Sudden cardiac death
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
Complications of drug therapy (i.e., proarrhythmia, organ
toxicity)

Complications associated with invasive procedures and surgery

Recurrence
Treatment of Wolff-Parkinson-White (WPW)-associated arrhythmias is
directed at the underlying cause (through the use of radiofrequency
(RF) ablation of the accessory pathway (AP), antiarrhythmic drugs in
adults to slow AP conduction in certain situations, for example,
Mahaim or atriofascicular pathway-mediated supraventricular
tachycardia (SVT); typically, atrioventricular (AV) nodal-conduction
blocking medications are avoided in the acute setting of WPW, or AV
nodal blocking medications to slow AV nodal conduction. For adult
patients, it also addresses the triggers that perpetuate the
dysrhythmia, which include coronary heart disease, ischemia,
cardiomyopathy, pericarditis, electrolyte disturbances, thyroid
disease, and anemia.
Treatment must be individualized for each patient and should include
individual risk assessment. Appropriate therapy for WPW syndrome is
based on the likely prognosis and on the degree of symptoms the
patient experiences. Specific subspecialty consultations are often
needed and may include a cardiovascular specialist (adult or pediatric
cardiologist) and/or an electrophysiologist (arrhythmia specialist)
with expertise in invasive studies.54
Despite the importance of risk stratification with electrophysiologic
study (EPS) to assess the risk of sudden cardiac death (SCD), few
reliable noninvasive markers are known. The adult literature has
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focused on preexcited RR intervals in atrial fibrillation (AF) as an
indicator of the ability to rapidly conduct. In a series of 60 pediatric
patients, a preexcited RR interval of less than 220 ms identified
patients at high risk for cardiac arrest. Thus, if an AP can conduct 4
impulses per second, it can be considered a high-risk pathway.50
Ambulatory monitoring and treadmill testing can provide additional
noninvasive information if the preexcitation disappears suddenly at a
discrete heart rate. However, care should be exercised in the
interpretation of these noninvasive test results. Invasive risk
assessment with subsequent RF ablation should be performed in
patients who present with syncope or aborted SCD.
The two main treatment approaches to WPW syndrome are (1)
pharmacotherapy and (2) EPS with RF catheter ablation. An
electrophysiologic study with ablation is the first-line treatment for
symptomatic WPW syndrome and for patients with high-risk
occupations. It has replaced surgical treatment and most drug
treatments. Radiofrequency ablation used in conjunction with
cryoablation for septal APs and APs near small coronary arteries has
had high success rates with low risk.55
Drug therapy can be useful in some instances, such as in patients
who refuse RF ablation and in temporizing patients with a higher risk
of ablation-related complications (i.e., AV block with pacing
requirement for anteroseptal or midseptal pathways). Medical therapy
may also be appropriate in pregnant women until radiation exposure
is safe.
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In choosing drug therapy, keep in mind that class Ic and class III
antiarrhythmic medications will slow AP conduction, facilitating
blockage of SVT. If the patient has a history of AF or atrial flutter, an
AV nodal blocking medication should also be used.
2012 PACES/HRS Guidelines
The 2012 Pediatric and Congenital Electrophysiology Society (PACES)
and the Heart Rhythm Society (HRS) guidelines include the following
management recommendations in asymptomatic patients aged 8-21
years with WPW:51

For those with a shortest preexcited RR interval (SPERRI) of
250 ms or less in AF, consider catheter ablation and factor in
the associated procedural risk factors on the basis of the AP
anatomic site.

Consider catheter ablation also for those with concomitant (1)
structural heart disease, regardless of the anterograde AP
features, or (2) ventricular dysfunction due to dyssynchronous
contractions, regardless of the anterograde bypass tract
characteristics.

Previously asymptomatic patients who develop cardiovascular
(CV) symptoms should be considered symptomatic and thus
potential candidates for catheter ablation.

For those with a SPERRI longer than 250 ms in AF, consider
deferring catheter ablation.

Consider administration of attention-deficit/hyperactivity
disorder (ADHD) medications; if ADHD are used, closely
monitor patients for CV symptoms.
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2014 PACES/HRS Guidelines
The 2014 PACES/HRS recommendations for preoperative EPS in
adults with congenital heart disease (CHD) for the identification and
mapping of arrhythmias that may be managed with surgical ablation
or incisional lesion sets includes (1) a history of unexplained syncope
or sustained ventricular tachycardia that is not due to a correctable
predisposing etiology; (2) documented SVT, not including AF; or (3)
ventricular preexcitation. However, preoperative EPS is not
recommended (1) in adults with simple forms of CHD, asymptomatic
patients (i.e., no history of palpitations, no arrhythmia symptoms),
and no significant documented arrhythmia on noninvasive studies; as
well as (2) in adults with CHD and AF in the absence of a triggering
supraventricular arrhythmia.51
Initial Management
Patients who present in cardiac arrest or with hemodynamic
compromise require management of the ABCs (A-Airway, BBreathing, C-Circulation), as is standard; this includes having a
defibrillator available and providing appropriate monitoring. Once the
patient is determined to be experiencing a dysrhythmia, directcurrent (DC) cardioversion is indicated.
In a stable patient, various vagal maneuvers may be attempted. A
bag of ice slurry to the face is very effective in infants. Older children
may be able to perform a Valsalva maneuver. Creative alternatives
abound, such as having a patient blow with a thumb in the mouth.
Unilateral carotid sinus massage may also be attempted. Ocular
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compression should not be performed, because it has been
associated with retinal injury.
When conservative measures fail, intravenous (IV) access is
necessary. Adenosine is the first-line agent and is effective in
approximately 90% of reentrant narrow-complex tachycardias.
Adenosine must be administered as a rapid bolus because of its short
half-life. Most instances of adenosine failure in this setting are caused
by inadequate administration of the drug. A defibrillator must be
available in the event that new dysrhythmias emerge, particularly
postadenosine atrial fibrillation (AF).
Procainamide and esmolol are available for use in resistant cases but
should only be administered by physicians familiar with these
medications. Verapamil should not be administered to patients
younger than 1 year of age because of risk of severe hypotension,
severe bradycardia, or heart failure in this population of patients; this
drug has also been reported to accelerate the ventricular rate in AF,
leading to rapid conduction that results in ventricular fibrillation (VF).
Treatment of WPW associated arrhythmias comprises the following
pharmacology and non-pharmacology recommendations.49-56

Radiofrequency ablation of the accessory pathway

Antiarrhythmic drugs to slow accessory pathway conduction

AV nodal blocking medications (in adult patients) to slow AV
nodal conduction in certain situations (i.e., Mahaim or
atriofascicular pathway-mediated SVT; typically, AV nodeconduction blocking medications are avoided in the acute
setting of WPW)
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
For WPW patients (adult), address the triggers that perpetuate
the dysrhythmia, which include coronary heart disease (CAD),
ischemia, cardiomyopathy, pericarditis, electrolyte
disturbances, thyroid disease, and anemia.
Termination of Acute Episodes
Narrow-complex AV reentrant tachycardia (AVRT) and AV nodal
reentrant tachycardia (AVNRT) are treated by blocking AV node
conduction with the following:

Vagal maneuvers (i.e., Valsalva maneuver, carotid sinus
massage, splashing cold water or ice water on the face)

Adults: IV adenosine 6-12 mg via a large-bore line (the drug
has a very short half-life)

Adults: IV verapamil 5-10 mg or diltiazem 10 mg

Pediatric patients: Adenosine and verapamil or diltiazem are
dosed on the basis of weight.
Atrial flutter/fibrillation or wide-complex tachycardia is treated as
follows:

IV procainamide or amiodarone if wide-complex tachycardia is
present, ventricular tachycardia (VT) cannot be excluded, and
the patient is stable hemodynamically.

Ibutilide
The initial treatment of choice for hemodynamically unstable
tachycardia is direct-current synchronized electrical cardioversion,
biphasic, as follows:

A level of 100 J (monophasic or lower biphasic) initially.
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
If necessary, a second shock with higher energy (200 J or 360
J).
Radiofrequency Ablation
Radiofrequency ablation is indicated in the following patients:

Patients with symptomatic AVRT

Patients with AF or other atrial tachyarrhythmias that have
rapid ventricular response via an accessory pathway
(preexcited AF)

Patients with AVRT or AF with rapid ventricular rates found
incidentally during EPS for unrelated dysrhythmia, if the
shortest preexcited RR interval during AF is less than 250 ms

Asymptomatic patients with ventricular preexcitation whose
livelihood, profession, insurability, or mental well-being may be
influenced by unpredictable tachyarrhythmias or in whom such
tachyarrhythmias would endanger the public safety

Patients with WPW and a family history of sudden cardiac death
Surgical Treatment
Radiofrequency catheter ablation has virtually eliminated surgical
open heart treatments in the vast majority of WPW patients, with the
following exceptions:

Patients in whom RF catheter ablation (with repeated attempts)
fails

Patients undergoing concomitant cardiac surgery (possible
exception)

Patients with other tachycardias with multiple foci who require
surgical intervention (very rare)
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Long-term Antiarrhythmic Therapy
Oral medication is the mainstay of therapy in patients not undergoing
radiofrequency ablation, although the response to long-term
antiarrhythmic therapy for the prevention of further episodes of
tachycardia in patients with WPW syndrome remains quite variable
and unpredictable. Choices include the following:49,50-52,54

Class Ic drugs (i.e., flecainide, propafenone), typically used
with an AV nodal blocking agent in low doses to avoid atrial
flutter with a 1:1 conduction

Class III drugs (i.e., amiodarone, sotalol), although these are
less effective for altering accessory pathway conduction
properties

In pregnancy, sotalol (class B) or flecainide (class C)
Pharmacologic Therapy
Antiarrhythmic drugs act on the atrioventricular (AV) node,
myocardial tissue, or the accessory pathways (APs). They work by
increasing either conduction velocity or the refractory period
(prolonging action potential duration) or by prolonging the conduction
time through an AP to prevent perpetuation of an atrioventricular
(AV) reciprocating tachycardia. They may also act to reduce the
ventricular response to atrial fibrillation (AF) or atrial flutter.
Agents Acting on the Atrioventricular Node
Verapamil and diltiazem (calcium channel blockers), metoprolol and
atenolol (beta-blockers), and digitalis all prolong conduction time and
refractoriness in the atrioventricular (AV) node.
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Verapamil and metoprolol do not affect conduction in the AV bypass
tract (may slow Mahaim fibers or atriofascicular pathway conduction).
Intravenous (IV) verapamil can speed up the ventricular response in
patients with Wolff-Parkinson-White (WPW) syndrome who have AF.
Verapamil is not recommended as a sole agent in patients with WPW
syndrome.
Digitalis shortens refractoriness in the myocardium and in the bypass
tract. Thus, it may accelerate the ventricular response in the setting
of AF in a patient with WPW syndrome. It should generally be
avoided.
Adenosine causes profound changes in AV nodal conduction leading
to transient AV block and typically does not affect the accessory
pathway conduction. Adenosine should not be used in this setting and
could induce ventricular fibrillation (VF).
Digoxin is contraindicated in patients with WPW syndrome, although
it may play some role in children only. Some deaths from WPW
syndrome have been associated with digoxin use.49,50,51,57
Class Ia drugs (i.e., quinidine) and class Ic drugs (i.e., flecainide,
propafenone) slow conduction velocity in the AP and prolong the AP
refractory period in the bypass tract.
Amiodarone, dofetilide, and sotalol prolong refractoriness in
myocardial tissue, including AV bypass tracts. Procainamide is no
longer available in an oral formulation and is typically only used
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during electrophysiologic studies (EPS) or in the emergency
department (ED) or cardiac intensive care unit (ICU) setting.
Radiofrequency Ablation
In radiofrequency (RF) ablation, platinum-tipped 3.5- to 8-mm
steerable multielectrode catheters are advanced via the femoral
artery or vein to locate and ablate the accessory pathway (AP) by
delivering thermal RF energy. APs at all the sites in the heart and in
persons of all age groups can be ablated successfully. In addition, RF
ablation of the AP in patients with frequent AP-mediated tachycardia
improved left ventricular systolic and diastolic functions.
Electrophysiology study (EPS) with RF ablation is now the treatment
of choice for most adults and many children with symptomatic WolffParkinson-White (WPW) syndrome, as well as many asymptomatic
patients. This approach has largely supplanted surgical and directcurrent (DC) modalities because it is more efficacious, safe, and costeffective. With successful EPS and RF ablation, patients are usually
cured of the disease and are not at risk for further tachyarrhythmias
related to the AP. Note that RF ablation with fluoroscopy includes
increased radiation exposure. Fluoroscopic-free imaging modalities
(i.e., three-dimensional electroanatomic mapping, ultrasonography)
reduce radiation exposure, but they have not yet supplanted
fluoroscopy.40,58
Although current guidelines do not always recommend routine EPS in
patients with asymptomatic WPW syndrome, especially in children
who are younger than 12 years, others strongly advocate the need
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for at least an intraesophageal study to assess the risk for sudden
cardiac death (SCD).
Patients with Ebstein’s anomaly should be evaluated for multiple APs.
During EPS and RF ablation, all such pathways should be recognized
and treated.
Patients presenting with tachyarrhythmic symptoms who do not opt
for RF ablation may require drug therapy to prevent further
episodes.40
Indications:
Radiofrequency ablation is indicated in the following patients:

Patients with symptomatic atrioventricular reentrant
tachycardia (AVRT)

Patients with atrial fibrillation (AF) or other atrial
tachyarrhythmias that have rapid ventricular response via an
AP (preexcited AF)

Patients with AVRT or AF with rapid ventricular rates found
incidentally during EPS for unrelated dysrhythmia, if the
shortest preexcited RR interval during AF is less than 250 ms

Asymptomatic patients with ventricular preexcitation whose
livelihood, profession, insurability, or mental well-being may be
influenced by unpredictable tachyarrhythmias or in whom such
tachyarrhythmias would endanger the public safety

Patients with WPW and a family history of SCD
Asymptomatic patients who have a low-risk pathway and no
supraventricular tachycardia (SVT) can be monitored expectantly, or
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they may undergo RF ablation to prevent any possibilities of SCD and
prevent late onset of SVT. In addition, there is an associated rise in
incidence of atrial fibrillation in patients with WPW, which may be
reduced with prophylactic RF ablation of the accessory pathway.
Symptomatic individuals with orthodromic tachycardia should
undergo risk assessment and should be offered therapy according to
their symptoms. Radiofrequency ablation can be curative and carried
out with a high degree of success, a low complication rate, and a low
recurrence rate. Symptomatic individuals with antidromic tachycardia
(i.e., antegrade conduction through the AP) should be offered
ablation.
Identification of accessory pathway and selection of ablation site
requires the following: First, perform EPS (1) to determine that the
AP is part of the tachycardia reentrant circuit and (2) to locate the
optimal site for ablation. Accessory pathways may be located in the
left or right free wall or septum of the heart. In approximately 5-10%
of patients, multiple pathways are present.
The ventricular insertion site is indicated by the earliest onset of the
ventricular electrogram in relation to the delta wave during sinus
rhythm or atrial pacing. The region of the shortest VA interval
indicates the atrial insertion site during orthodromic tachycardia (i.e.,
AVRT) or ventricular pacing. Mechanical trauma during mapping,
“bump mapping,” often may occur at the site of pathway insertion
and signals a potential effective ablation site.44
During EPS, direct recordings of the AP potential indicate the optimal
site for ablation, followed by areas of AV or ventriculoatrial (VA)
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fusion. Successful ablation sites show stable fluoroscopic and
electrical features. During orthodromic AVRT, the time between the
ventricular and atrial potentials is short and an AP potential may be
observed. Temperatures of at least 50°C are required for permanent
elimination of AP conduction. Often, a single RF ablation will cure the
patient. The RF ablation creates a conduction block that can be seen
on intracardiac electrography (i.e., during EPS) between the atrial
activation and the AP potential.34
Effectiveness and Safety of Ablation
Success rates for RF catheter ablation exceed 90%. Anteroseptal or
midseptal pathways have lower success rates due to difficulty
achieving a safe lesion formation near the AV node and His bundle. In
experienced operators’ hands, the success rate should still exceed
90%, but may come with a 5-10% rate of AV block, usually leading
to permanent pacemaker implantation.59
Posteroseptal pathways are expected to have a more than 90%
success rate as well, with little risk of injury to the AV node in
experienced hands. Occasionally, during ablation of the slow pathway
of the AV node for AVNRT, a right posteroseptal pathway may also be
ablated, as they are typically in close proximity.
Radiofrequency catheter ablation is relatively safe, with a
complication rate of approximately 1% in most centers. A threecatheter ablation technique appears to be similarly successful and
safe as, but involves less cost than, the standard five-catheter
approach for mapping and ablation of SVTs in pediatric patients with
WPW and left-sided AP. Adverse consequences include bleeding
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complications, pericardial effusion, chest pain, stroke, myocardial
infarction, and AV node block.60
Surgical Care
Surgical open-heart procedures were more common before
radiofrequency (RF) ablation was developed. Now, RF catheter
ablation has virtually eliminated surgical open heart treatments in the
vast majority of patients, with the following exceptions:

Patients in whom RF catheter ablation (with repeated attempts)
fails

Patients undergoing concomitant cardiac surgery (i.e., for
structural heart disease) (possible exception)

Patients with other tachycardias with multiple foci who require
surgical intervention (very rare)
Long-Term Antiarrhythmic Therapy
Long-term oral medication is the mainstay of therapy in patients not
undergoing radiofrequency (RF) ablation. Response to long-term
antiarrhythmic therapy for the prevention of further episodes of
tachycardia in patients with Wolff-Parkinson-White (WPW) syndrome
remains quite variable and unpredictable. Some drugs may
paradoxically make the reciprocating tachycardia more frequent.
Class Ic drugs (i.e., flecainide, propafenone) are typically used with
an atrioventricular (AV) nodal blocking agent in low doses to avoid
atrial flutter with a 1:1 conduction. Class III drugs (i.e., amiodarone,
sotalol) are also reasonable choices, although these agents are less
effective for altering accessory pathway conduction properties. Class
Ic drugs should not be given if the patient has structural heart
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disease (coronary artery disease, myocardial infarction, congestive
heart failure, left ventricular hypertrophy). Class Ic drugs are
typically used with an AV nodal blocking agent.61
The best, long-term plan is not to use drugs at all. All patients who
have symptomatic WPW syndrome should be referred for
electrophysiologic studies (EPS) and considered for ablation, which
has a very high cure rate and a low complication rate. Patients who
have asymptomatic accessory pathways (APs) with short refractory
periods (< 240 ms) are poor candidates for medical therapy and are
best treated with ablation as well.61-63
Medication
Emergency treatment in Wolff-Parkinson-White (WPW) patients with
hemodynamic instability is directed toward converting the rhythm to
sinus through a brief episode of atrioventricular (AV) block.
Adenosine is the drug of choice for immediate conversion of narrowcomplex supraventricular tachycardia (SVT) but should not be used
for preexcited atrial fibrillation (AF). Esmolol has also been used with
some success.13
Beta-blockers are probably the medications most commonly used to
treat SVT in the presence of preexcitation. They are moderately
effective and have frequent, but rarely life-threatening, adverse
effects (except in the presence of reactive airway disease). Their
efficacy in reducing the risk of accelerated conduction of AF in WPW
patients is unclear. More potent medications (i.e., flecainide,
propafenone, sotalol, or amiodarone) may have more effect on
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accessory pathway (AP) conduction or refractoriness than betablockers and are preferred by some.
The use of digoxin or verapamil for long-term therapy appears to be
contraindicated for many patients with WPW syndrome, because
these medications may enhance antegrade conduction through the AP
by increasing the refractory period in the AV node. In addition,
digoxin may shorten the refractory period of the AP, further
enhancing its antegrade conduction.
Antiarrhythmic Agents
Antiarrhythmic agents alter the electrophysiologic mechanisms
responsible for dysrhythmia, prolonging the refractory period of the
conduction tissue, the AP, or both.

Adenosine (Adenocard, Adenoscan)
Adenosine slows conduction time through the AV node. It can
interrupt atrioventricular reentrant tachycardia (AVRT) by
blocking conduction in the AV node to restore normal sinus
rhythm in paroxysmal supraventricular tachycardia (PSVT),
including PSVT associated with WPW syndrome. It should not
be given to patients with preexcitation unless by a cardiac
electrophysiologist.

Verapamil (Verelan, Calan)
Verapamil interrupts reentry at the AV node and restores
normal sinus rhythm in patients with PSVT. It is used for shortterm treatment only in children older than 2 years. It is not
intended for long-term treatment, because of a shortened
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refractory period. It should not be used in children younger
than 2 years, because of severe hypotension.

Digoxin (Lanoxin)
Digoxin has direct inotropic effects in addition to indirect effects
on the cardiovascular system. However, it may shorten the
refractory period. Most deaths in WPW have been associated
with digoxin use.

Procainamide
Procainamide is a class Ia antiarrhythmic. It increases the
refractory period of atria, ventricles, and APs. It is excellent in
preexcited AF or atrial flutter.

Quinidine
Quinidine maintains normal heart rhythm and converts AF or
atrial flutter. It is not recommended as a first-line drug for
WPW syndrome.

Amiodarone (Cordarone, Pacerone)
Amiodarone may inhibit AV conduction and sinus node function.
It prolongs the action potential and refractory period in
myocardium and inhibits adrenergic stimulation.

Sotalol (Betapace, Sorine)
Sotalol is a class III antiarrhythmic agent that blocks potassium
channels, prolongs action potential duration, and lengthens the
QT interval. It is a noncardiac selective beta-adrenergic blocker.
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
Diltiazem (Cardizem, Dilacor, Cartia XT, Tiazac)
Diltiazem slows AV nodal conduction.

Ibutilide (Corvert)
Ibutilide is a class III antiarrhythmic agent that may work by
increasing action potential duration, thereby changing atrial
cycle length variability. Mean time to conversion is 30 minutes.
Two-thirds of patients who converted were in sinus rhythm at
24 hours. Ventricular arrhythmias occurred in 9.6% of patients
and were mostly premature ventricular complexes (PVCs). The
incidence of torsades de pointes was less than 2%.

Dofetilide (Tikosyn)
Dofetilide increases monophasic action potential duration,
primarily through delayed repolarization. It terminates induced
reentrant tachyarrhythmias (i.e., AF, atrial flutter, ventricular
tachycardia (VT)) and prevents their reinduction. No data are
available on its use in WPW syndrome.

Flecainide (Tambocor)
Flecainide blocks sodium channels, producing dose-related
decreases in intracardiac conduction in all parts of heart. It has
its greatest effect on the His-Purkinje system (HV conduction).
Effects on AV nodal conduction time and intra-atrial conduction
times, though present, are less pronounced than those on
ventricular conduction velocity. Flecainide is indicated for the
treatment of paroxysmal AF or atrial flutter associated with
disabling symptoms and PSVT, including AV nodal reentrant
tachycardia (AVNRT), AVRT, and other SVTs of unspecified
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mechanism associated with disabling symptoms in patients
without structural heart disease. It is also indicated for
prevention of documented life-threatening ventricular
arrhythmias, such as sustained VT. It is not recommended in
less severe ventricular arrhythmias, even if patients are
symptomatic.

Propafenone (Rythmol)
Propafenone shortens the upstroke velocity (phase 0) of a
monophasic action potential. It reduces the fast inward current
carried by sodium ions in Purkinje fibers and, to a lesser extent,
myocardial fibers. It may increase the diastolic excitability
threshold and prolong the effective refractory period (ERP). It
reduces spontaneous automaticity and depresses triggered
activity.
Propafenone is indicated for treatment of documented lifethreatening ventricular arrhythmias, such as sustained VT. It
appears to be effective in the treatment of SVTs, including AF
and atrial flutter. It is not recommended in patients with less
severe ventricular arrhythmias, even if they are symptomatic.

Esmolol (Brevibloc)
Esmolol is an ultra–short-acting agent that selectively blocks
beta1-receptors, with little or no effect on beta2-receptor
types. It is excellent for patients at risk of complications from
beta-blockade, particularly those with reactive airway disease,
mild-to-moderate left ventricular dysfunction, and/or peripheral
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vascular disease. Its short half-life of 8 minutes allows for
titration to desired effect and quick discontinuation if needed.

Propranolol (Inderal LA, InnoPran XL)
Propranolol is a class II antiarrhythmic nonselective betaadrenergic receptor blocker with membrane-stabilizing activity
that decreases automaticity of contractions.

Atenolol (Tenormin)
Atenolol selectively blocks beta1-receptors with little or no
effect on beta 2 types.
Ventricular Tachycardia
Ventricular tachycardia is defined as three or more consecutive beats
of ventricular origin at a rate >100 bpm. Ventricular tachycardia is
called sustained VT if it continues for at least 30 seconds or causes
hemodynamic compromise requiring termination within 30 seconds.
Ventricular tachycardia lasting for <30 seconds and not causing
hemodynamic compromise is classified as nonsustained VT (NSVT).
Ventricular tachycardia is categorized as monomorphic if all the
ventricular complexes are similar. Polymorphic VT has changing QRS
morphology, as opposed to monomorphic VT with constant QRS
morphology. Torsades de pointes is a type of polymorphic VT with
QRS complexes of changing amplitude that appear to twist around
the isoelectric line. Bidirectional VT is a specific type of VT seen in
certain conditions (i.e., digoxin toxicity) and has alternating QRS axis
in the consecutive beats.63
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Ventricular tachycardia/fibrillation has multiple etiologies. They can
be classified into the following sections:13,64
Structural Heart Disease
Patients with structural heart disease are at a risk of developing VAs.
These can be broadly grouped as below.
Ischemic Heart Disease
Ventricular arrhythmias (VAs) can be seen in patients with acute as
well as chronic ischemic heart disease. Acute coronary syndrome with
ongoing myocardial ischemia and acute myocardial infarction
predispose the patients to VAs including PVCs, NSVT, and more
malignant VT and ventricular fibrillation. Patients with chronic
coronary artery disease (CAD) and with a history of myocardial
infarction leading to myocardial scar are predisposed to scar-related
VT, which is usually monomorphic. PVC and other forms of VA
associated with acute ischemia are likely to be polymorphic.
Nonischemic Cardiomyopathy
Various forms of nonischemic cardiomyopathy have the propensity to
develop VAs. These include idiopathic dilated, hypertrophic, and
arrhythmogenic right ventricular cardiomyopathy (ARVC).
Infiltrative Cardiac Diseases and Myocarditis
Cardiac involvement with sarcoidosis is another cause of VA
encountered in clinical practice. Various forms of myocarditis also
have the potential of causing VAs, which at times may be clinically
unstable.
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Ventricular Arrhythmias without Structural Heart Disease
Many of these arrhythmias are considered to be owing to some defect
in the handling of ions responsible for various phases of
depolarization and repolarization of cardiac myocytes and conducting
tissue of the heart. The exact molecular basis is not clear in some of
these, which are categorized as idiopathic. Specific conditions in this
group are as below.

Brugada syndrome:
This is a distinct syndrome seen frequently in south-east Asians,
characterized by idiopathic ventricular fibrillation with presence of
right bundle branch block (RBBB) pattern with ST-segment
elevation in right precordial leads on baseline ECG. Mutation in
the Na+channel gene has been seen in many of the families with
Brugada syndrome.

Catecholaminergic polymorphic ventricular tachycardia:
This is a rare form of inherited polymorphic VT caused by a
mutation in the genes encoding ryanodine receptor and
calsequestrin involved in handling calcium ion in the cells.

Long QT syndromes:
These are a group of inherited syndromes caused by mutation in
ion channels regulating the repolarization of myocytes, which lead
to prolongation of the QT interval. These cause a specific form of
VT, torsades de pointes, with characteristic ECG pattern. The
acquired form of long QT syndrome is caused by certain drugs.
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
Idiopathic ventricular tachycardias:
These are focal monomorphic VTs originating in the outflow tracts
or left ventricular septum. These can be subcategorized into
outflow tract tachycardia (RV outflow tract being a commoner site
of origin than LV outflow tract), fascicular (originating in the left
ventricular side of the interventricular septum), and rare RV
inflow tachycardia. These probably have multiple mechanisms
including reentry (fascicular VT) and triggered activity (outflow
tract tachycardias and fascicular VT).

Reversible noncardiac etiologies:
VAs can be caused by certain factors leading to abnormal
excitability of the myocardium.
 Electrolyte abnormalities such as hypokalemia and
hypomagnesemia can precipitate VAs.
 Intracardiac leads may occasionally cause irritation of the
myocardium initiating VAs.
 Physiological stress in general can lead to a
hyperadrenergic state predisposing to VAs. This may be a
causative factor in patients admitted to the intensive care
unit. Hypoxia, hypotension, and other physiological stress
factors may be causative.
 Drugs: Other causes of VT are pro-arrhythmic
medications. A high degree of suspicion should be
exercised for this etiology in evaluating a patient’s having
VT, especially in patients admitted in the hospital on
multiple medications. Certain drug interactions causing
elevation of the serum level of pro-arrhythmic drugs
should be kept in mind in these situations. Electrolyte
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abnormality can augment the pro-arrhythmic potential of
a drug, for example, hypokalemia in patients on digoxin
increases its arrhythmogenic potential.
These reversible factors can lead to VAs on its own, but
they are even more likely to cause these arrhythmias in
the presence of cardiac substrate abnormalities such as
cardiomyopathy and ischemic heart disease. As can be
seen, some of these have correctable factors and should
be an important focus of management in these patients.
Treatment of Ventricular Tachycardia
Therapy may not be needed in asymptomatic patients whose VT
patterns suggest a low risk of sudden death. Symptoms or a clinically
significant short-term risk of SCD frequently warrants admission for
evaluation and consideration of therapeutic options.65
Initial therapy for ventricular fibrillation is immediate, unsynchronized
direct current (DC) defibrillation. Data suggest that a brief (i.e., 90 s)
period of chest compressions may improve survival when ventricular
fibrillation is witnessed, but immediate defibrillation is the therapy of
choice. Time should not be wasted on other aspects of resuscitation
before initial defibrillation, unless defibrillation is unavailable. It’s
important to identify and target potential substrates for arrhythmiaspecific therapy.
Optimal inpatient management is performed with secure vascular
access and continuous cardiac monitoring. In the ideal case, cardiac
monitoring systems are connected to a central monitoring station in a
cardiac care unit or ICU. Simple bedside monitors with high-rate and
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low-rate alarms are inadequate to monitor patients with the potential
for unstable VA. For unstable patients, simultaneous evaluation and
therapy should be conducted. For hemodynamically stable patients,
evaluation is followed by serial drug therapy. Diagnostic or
therapeutic catheterization also may be performed.
Pharmacologic Therapy
Although antiarrhythmic drug therapy can suppress spontaneous
arrhythmia and although it may help individual patients, some of
these medications have resulted in increased mortality rates in
selected adult and pediatric patients. Mortality rates typically increase
when the overall risk of the arrhythmia is less than the proarrhythmia
risk of the drug. Estimates of both are problematic in pediatric
patients.
Although digoxin is approved for use in infants, it lacks specific
antiarrhythmic properties that aid in the control of most ventricular
arrhythmias. All other agents, despite the current use, are not
approved for use in young children.
Antiarrhythmic drug therapy is further complicated because no single
drug is ideal in all settings. Beta-blockade, with intravenous
(IV) esmolol or any of the oral (PO) preparations, is a good initial
choice for nearly all forms of VA. In addition, it has few absolute
contraindications in the treatment of serious arrhythmia. Other
medications have important limitations. Many are negative inotropes
and all have important drug and metabolic interactions. Use
of verapamil in children younger than 1 year is associated with
infrequent episodes of cardiovascular collapse and
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death. Procainamide is an excellent choice for incessant reentrant VA
in many settings, but it may exacerbate long QT syndrome
(LQTS).30,66
Oral agents in Vaughn-Williams class I-A (i.e., quinidine,
procainamide), class I-C (i.e., flecainide, propafenone), or class III
(i.e., sotalol, amiodarone) can cause ventricular proarrhythmia and
suppress clinical arrhythmia while increasing mortality rates in
selected populations.67
Amiodarone is generally reserved for potentially life-threatening VA.
Both IV and oral amiodarone may have important noncardiac adverse
effects. Make therapeutic decisions carefully after consulting with an
experienced pediatric cardiologist (electrophysiologist).
Intravenous amiodarone in infants and young children deserves
particular attention. The medication’s broad efficacy and ready
availability has increased its popularity in managing sustained
arrhythmias in the ICU and emergency setting. A prospective tiered
dose pediatric trial showed good efficacy but a nearly 50% incidence
of major adverse events.
Neonates may have relatively frequent episodes of nonsustained
ventricular tachycardia or, more precisely, accelerated idioventricular
rhythm (AIVR). Although thorough noninvasive evaluation with
monitoring and echocardiography is warranted, the risk of mortality is
probably zero. Similarly, the risks associated with many forms of VA
are quite low in the patient without cardiomyopathy or a probable
ion-channel defect. In both of these settings, avoiding therapy with
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potentially risky drugs and then choosing an agent that is more
effective at decreasing arrhythmias on ambulatory monitoring may be
important.
Beta-blockers
Propranolol, atenolol, nadolol, and esmolol are the beta-blockers
most frequently used to manage VA. They appear to be particularly
effective in treating patients with VA, LQTS, or HCM. Other agents
may be useful; sotalol, propafenone, and amiodarone have betablocking properties. Beta-blockers have not been associated with
ventricular proarrhythmia; this is a major advantage of this class
compared with other agents, particularly class I and III agents. Base
the choice between beta-blockers on the duration of action,
selectivity, and preparation.68
Class I Antiarrhythmics
This class of agents has complex actions. The drugs primarily block
sodium channels, decreasing conduction velocity (QRS widening).
Only IV procainamide and lidocaine are presented here. Quinidine,
the initial drug in this class, is associated with excessive ventricular
proarrhythmia in most patient groups.
Propafenone, disopyramide, flecainide, and other agents may have a
role in long-term therapy in some patients. Some children, and adults
with ischemic heart disease have increased mortality rates while
taking these medications despite apparent control of their
arrhythmia. Interesting data suggest that flecainide may offer specific
therapy for some patients with CPVT.24
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Surgical Treatment
Selected patients require highly individualized interventional
procedures, such as the following:63

Excisional biopsy

Implantable cardioverter/defibrillators

Radiofrequency catheter ablation or cryoablation

Left cervical sympathectomy

Myocardial tumor resection
Incessant VT is sometimes secondary to focal lipoid cardiomyopathy,
isolated fibromas, or hamartomas. In selected patients, surgical
excision may be both diagnostic and therapeutic.69
Implantable cardioverter-defibrillators (ICDs) have revolutionized the
care of individuals with high-risk VT after myocardial infarction.
Implantable cardioverter-defibrillators are increasingly used in highrisk pediatric patients. Transvenous systems have been used in
patients who weigh as little as 20 kg. In highly selective situations,
toddlers and large infants have received epicardial systems implanted
through a sternotomy. Creative, hybrid approaches are further
increasing clinicians' willingness to use ICDs in young patients.65
Both catheter-directed radiofrequency ablation and intraoperative
resection or cryoablation of VT foci have been successful with
monomorphic VTs; however, their use is unproved for patients with
polymorphic VT. Unlike supraventricular arrhythmias, for which
catheter ablation has a more than 95% success rate, VT ablation in
pediatric patients and in patients with CHD has a success rate of
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about 60%. Both a lack of arrhythmia and proximity to the bundle of
His limit the ability to provide effective therapy.
For many years, left cervical sympathectomy was performed for
refractory long QT syndrome. The use of video-assisted/minimally
invasive techniques has increased the use of this therapy for patients
with long QT, CPVT, and recurrent symptomatic arrhythmias. Often
this is subsequent to ICD placement.70
Consultations
Primary care physicians may certainly observe patients with
infrequent asymptomatic premature ventricular contractions (PVCs),
often with a 24-hour Holter evaluation, to confirm the frequency and
severity of arrhythmia. For most other patients with VA more
complex than this, prompt referral and direct communication with a
pediatric cardiologist is indicated. Referral facilitates appropriate
testing and decision making about evaluating the patient on an
inpatient or outpatient basis.71
The patterns and relative risks of arrhythmia in adult and pediatric
patients differ substantially. Whenever feasible, a cardiologist with
specific training and expertise in pediatric heart disease should
evaluate the patient. Expedite referral when any of the following
indications are present:69

Symptoms of syncope or apparent heart failure

Family history of premature death or seizures

History or physical suggesting structural heart disease or heart
failure

Arrhythmia triggered by medications
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
Arrhythmia triggered by recreational drugs

Nonsustained or sustained VT

History of cardiac surgery or known heart disease, even if it is
apparently repaired
Diet
Diet is rarely is a factor in VA. Diuretic use or abuse, anorexia, or
chronic diarrhea can induce hypokalemia, which exacerbates VA.
Primary or dietary rickets rarely produces sufficient hypocalcemia to
cause QT prolongation and a risk of arrhythmia.62
Sick Sinus Syndrome
Sick sinus syndrome results from intrinsic disease of the sinus node.
Some individuals with this syndrome also have underlying disease of
other portions of the conduction system, particularly the AV node.
Manifestations of the sick sinus syndrome are symptomatic sinus
bradycardia, sinus pauses or arrest, chronotropic incompetence, and
tachy–bradycardia syndrome.74
Sinus Bradycardia
Sinus bradycardia is defined as a sinus rhythm with a rate <60 bpm.
Sinus bradycardia is most frequently caused by an increase in vagal
tone or a reduction in sympathetic tone (and thus a physiologic
change). Sinus bradycardia occurs in normal children and adults,
particularly during sleep when rates of 30 bpm and pauses of up to 2
seconds are not uncommon. It may also be seen in the absence of
heart disease in the following settings:34
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
At rest, in 25% to 35% of asymptomatic individuals under 25
years of age

In well-conditioned athletes

In some elderly patients
As a result, sinus bradycardia is very common at night. When sinus
bradycardia results from increased vagal tone, slowing of impulse
conduction through the atrioventricular node also results in PR
interval prolongation. There is no prognostic significance to sinus
bradycardia in otherwise healthy subjects.35
Pathophysiologic Sinus Bradycardia
Sinus bradycardia can be the result of pathophysiologic condition
including intrinsic disease of the sinus node (“sick sinus”) and several
extrinsic causes, manifested as a decrease in spontaneous
automaticity and the impulse generation rate.
Exaggerated Vagal Activity
Vasovagal responses may be associated with a profound bradycardia
owing to heightened parasympathetic activity and sympathetic
withdrawal on the sinus node. The combination of the slow heart rate
and an associated decline in peripheral vascular resistance is often
sufficient to produce presyncope or syncope.
There are a variety of stimuli for vagal activation. These include
pressure on the carotid sinus, as may occur with a tight collar or with
the impact of the stream of water in a shower, vomiting, or coughing;
and, valsalva maneuver when straining at stool, sudden exposure of
the face to cold water, and prolonged standing through a Bezold–
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Jarisch reflex. Hypervagotonia can also result in chronic (i.e.,
nonepisodic) resting sinus bradycardia. This is the primary
mechanism of resting bradycardia in well-trained athletes. Junctional
bradycardia and Mobitz type I AV block can also be seen in this
setting.
Increased Intracranial Pressure
Increased intracranial pressure should be excluded when sinus
bradycardia occurs in a patient with neurologic dysfunction.
Acute Myocardial Infarction (AMI)
Sinus bradycardia occurs in 15% to 25% of patients with AMI,
particularly those affecting the inferior wall as the right coronary
artery supplies the sinus node in approximately 60% of people.
Increased vagal activity is primarily responsible, and the bradycardia
is typically transient.
Obstructive Sleep Apnea
Individuals with obstructive sleep apnea frequently have sinus
bradycardia and sinus pauses during apneic episodes. Therapies to
improve the apnea frequently alleviate the bradycardia.
Medication
A number of drugs can depress the sinus node and slow the heart
rate. These include parasympathomimetic agents, sympatholytic
drugs (ß-blockers, reserpine, guanethidine, methyldopa, and
clonidine), cimetidine, digitalis, calcium channel blockers, amiodarone
and other antiarrhythmic drugs, and lithium.
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Other Causes
Other causes of sinus bradycardia include hypothyroidism,
hypothermia, and severe prolonged hypoxia. Infectious agents
associated with relative sinus bradycardia include Chagas’ disease,
legionella, psittacosis, Q fever, typhoid fever, typhus, babesiosis,
malaria, leptospirosis, yellow fever, dengue fever, viral hemorrhagic
fevers, trichinosis, and Rocky Mountain Spotted fever.
Sinus Pause Or Sinus Arrest
Sinus pause or sinus arrest is the result of intermittent failure of
sinus node impulse generation. Sinus pause or arrest may be owing
to intrinsic sinus node disease and dysfunction or from drugs that
directly or indirectly (through the autonomic nervous system) depress
sinus node activity. On the surface ECG, a sinus pause or arrest is
manifest as a long PP cycle length that is longer than the P-P interval
of the underlying sinus rhythm but less than two P-P intervals. There
is no relationship between the cycle length of the pause and that of
the intrinsic sinus rhythm. This occurs in intrinsic sinus node disease
or in the setting of vagal stimulation such as respiratory lavage in an
intubated patient in intensive care unit.
Sinoatrial Exit Block
Sinoatrial (SA) exit block most commonly arises from a change in the
electrophysiologic characteristics of the tissue surrounding the sinus
node resulting in an inability to respond to or conduct an impulse
from the sinus node into the atrium. This can be owing to drugs,
disease, or increased vagal activity. SA nodal exit block is classified
as the first degree, second degree, and third degree.75
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
First degree SA nodal exit block reflects a slowing of impulse
exit but there is still 1:1 conduction. This abnormality cannot be
recognized on the surface ECG.

Second degree SA nodal exit block has two types. Type I
(Wenckebach type) is characterized by progressively decreasing
P-P intervals prior to a pause caused by a dropped P wave; the
pause has a duration that is less than two P-P cycles. The
mechanisms of progressive shortening of P-P interval are
Wenckebach phenomenon between sinus node to atrium. In
type II exit block, the P-P output is an arithmetic multiple of
the presumed sinus pacemaker input (i.e., 2:1, 3:1, 4:1).
Therefore the P-P cycle length surrounding the pause is a
multiple of the normal P-P interval.

Third degree SA nodal exit block prevents pacemaker impulses
from reaching the right atrium, giving the appearance of sinus
arrest (i.e., no P waves).
Tachycardia–Bradycardia Syndrome
This form of the syndrome is most often characterized by bursts of an
atrial tachyarrhythmia (usually atrial fibrillation), which terminate
spontaneously and are followed by long offset pauses and symptoms.
The pause is often long, and there may be no junctional escape
rhythm because of associated AV nodal disease. The tachy–
bradycardia syndrome is the result of overdrive suppression of the
sinus node by the atrial arrhythmia.
After arrhythmia termination, there is a variable delay before the
sinus node recovers and again generates an impulse because of sinus
node dysfunction. Catheter ablation of atrial arrhythmia sometimes
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cures the arrhythmia. Symptomatic patients, who are not a candidate
for catheter ablation, receive permanent pacemakers for bradycardia,
and tachycardia is treated by calcium or ß-blockers.
Chronotropic Incompetence
Chronotropic incompetence is defined as the inability to accelerate
sinus rate appropriate to the level of exercise. This definition includes
inability to reach 70th to 80th percentile of maximum predicted heart
rate, delayed peak of heart rate (heart rate peaks during recovery
period after the exercise), early peaking of heart rate (prior to the
peak exercise), fluctuations of heart rate during exercise or inability
to reach a heart rate of 100 to 120 bpm. The heart rate response to
exercise also depends on several factors such as deconditioning, drug
therapy, and comorbidities.
Major Causes of Bradycardia
Intrinsic
Idiopathic degeneration (aging)
Extrinsic
Autonomically mediated syndromes
Infarction or ischemia

Neurocardiac syncope
Infiltrative diseases

Carotid-sinus

Sarcoidosis

Amyloidosis

Situational disturbances

Hemochromatosis

Coughing

Micturition
Collagen vascular diseases
hypersensitivity

Systemic lupus erythematosus

Defecation

Rheumatoid arthritis

Vomiting

Scleroderma

Myotonic muscular dystrophy
Surgical trauma

Valve replacement
Drugs

ß-Adrenergic blockers

Calcium-channel blockers

Clonidine
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
Correction of congenital heart

Digoxin
disease

Antiarrhythmic agents

Heart transplantation
Hypothyroidism

Familial diseases
Hypothermia
Infectious diseases
Neurologic disorders

Chagas’ disease

Endocarditis
Electrolyte imbalances

Hypokalemia

Hyperkalemia
Atrioventricular (AV) Block
Atrioventricular (AV) block is partial or complete interruption of
impulse transmission from the atria to the ventricles. The most
common cause is idiopathic fibrosis and sclerosis of the conduction
system. Diagnosis is by ECG; symptoms and treatment depend on
degree of block, but treatment, when necessary, usually involves
pacing.
The most common causes of AV block are listed below.

Idiopathic fibrosis and sclerosis of the conduction system
(about 50% of patients)

Ischemic heart disease (40%)
The remaining cases of AV block are caused by

Drugs (i.e., beta-blockers, calcium channel
blockers, digoxin, amiodarone)

Increased vagal tone

Valvulopathy

Congenital heart, genetic, or other disorders
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AV block may be partial or complete. First-degree and second-degree
blocks are partial. Third degree blocks are complete. For 1st-degree
block, conduction is slowed without skipped beats. All normal P waves
are followed by QRS complexes, but the PR interval is longer than
normal (> 0.2 sec). For 3rd-degree block, there is no relationship
between P waves and QRS complexes, and the P wave rate is greater
than the QRS rate.
First-degree AV Block
All normal P waves are followed by QRS complexes, but the PR
interval is longer than normal (> 0.20 sec). First-degree AV block
may be physiologic in younger patients with high vagal tone and in
well-trained athletes. First-degree AV block is rarely symptomatic and
no treatment is required, but further investigation may be indicated
when it accompanies another heart disorder or appears to be caused
by drugs.169
Second-degree AV Block
Some normal P waves are followed by QRS complexes, but some are
not. The following outlines the types that exist:

Mobitz type I 2nd-degree AV block
In Mobitz type I 2nd-degree AV block, the PR interval
progressively lengthens with each beat until the atrial impulse
is not conducted and the QRS complex is dropped (Wenckebach
phenomenon); AV nodal conduction resumes with the next
beat, and the sequence is repeated Mobitz type I 2nd-degree
AV block may be physiologic in younger and more athletic
patients.
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The block occurs at the AV node in about 75% of patients with
a narrow QRS complex and at infranodal sites (His bundle,
bundle branches, or fascicles) in the rest. If the block becomes
complete, a reliable junctional escape rhythm typically
develops. Treatment is therefore unnecessary unless the block
causes symptomatic bradycardia and transient or reversible
causes have been excluded. Treatment is pacemaker insertion,
which may also benefit asymptomatic patients with Mobitz type
I 2nd-degree AV block at infranodal sites detected by
electrophysiologic studies done for other reasons.

Mobitz type II 2nd-degree AV block
In Mobitz type II 2nd-degree AV block, the PR interval remains
constant. Beats are intermittently nonconducted and QRS
complexes dropped, usually in a repeating cycle of every 3rd
(3:1 block) or 4th (4:1 block) P wave. Mobitz type II 2nddegree AV block is always pathologic; the block occurs at the
His bundle in 20% of patients and in the bundle branches in the
rest. Patients may be asymptomatic or experience lightheadedness, presyncope, and syncope, depending on the ratio
of conducted to blocked beats. Patients are at risk of
developing symptomatic high-grade or complete AV block, in
which the escape rhythm is likely to be ventricular and thus too
slow and unreliable to maintain systemic perfusion; therefore,
a pacemaker is indicated.

High-grade 2nd-degree AV block
In high-grade 2nd-degree AV block, every 2nd (or more) P
wave is blocked.
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The distinction between Mobitz type I and Mobitz type II block is
difficult to make because 2 P waves are never conducted in a row.
Risk of complete AV block is difficult to predict, and a pacemaker is
indicated. Patients with any form of 2nd-degree AV block and a
structural heart disorder should be considered candidates
for permanent pacing unless there is a transient or reversible cause.
Third-degree AV Block
Heart block is complete. There is no electrical communication
between the atria and ventricles and no relationship between P waves
and QRS complexes (AV dissociation). Cardiac function is maintained
by an escape junctional or ventricular pacemaker. Escape rhythms
originating above the bifurcation of the His bundle produce narrow
QRS complexes, relatively rapid (> 40 beats/min) and reliable heart
rates, and mild symptoms (i.e., fatigue, postural light-headedness,
effort intolerance). Escape rhythms originating below the bifurcation
produce wider QRS complexes, slower and unreliable heart rates, and
more severe symptoms (i.e., presyncope, syncope, heart failure).
Signs include those of AV dissociation, such as cannon a waves, BP
fluctuations, and changes in loudness of the 1st heart sound (S1).
Risk of asystole-related syncope and sudden death is greater if low
escape rhythms are present.
Most patients require a pacemaker. If antiarrhythmic drugs cause the
block, stopping the drug may be effective, although temporary pacing
may be needed. A block caused by acute inferior MI usually reflects
AV nodal dysfunction and may respond to atropine or resolve
spontaneously over several days. A block caused by anterior MI
usually reflects extensive myocardial necrosis involving the His-
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Purkinje system and requires immediate transvenous pacemaker
insertion with interim external pacing as necessary. Spontaneous
resolution may occur but warrants evaluation of AV nodal and
infranodal conduction (i.e., electrophysiologic study, exercise testing,
24-h ECG).
Most patients with congenital 3rd-degree AV block have a junctional
escape rhythm that maintains a reasonable rate, but they require a
permanent pacemaker before they reach middle age. Less commonly,
patients with congenital AV block have a slow escape rhythm and
require a permanent pacemaker at a young age, perhaps even during
infancy.76
Treatment
Depending on the type and severity of the arrhythmia, and the
results of various tests including the electrophysiology study, there
are several treatment options.38,77
Medications
Certain anti-arrhythmic drugs change the electrical signals in the
heart and help prevent abnormal sites from starting irregular or rapid
heart rhythms.
Follow-up Electrophysiology Study
To make sure the medication is working properly after two or more
days in the hospital, the patient may be brought back to the
laboratory for a follow-up study. The goal is to find the drug that
works best for you.
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Implantable Device (Pacemaker)
All implantable devices or pacemakers work on "demand" and are
used to treat slow heart rhythms. They are small devices that are
implanted beneath the skin below the collarbone and connected to a
pace wire(s) positioned inside the heart via a vein; this delivers a
small electrical impulse to stimulate the heart to beat when it is going
too slow.
Catheter Ablation
As mentioned previously, with this technique, radiofrequency catheter
ablation destroys or disrupts parts of the electrical pathways causing
the arrhythmias, providing relief for patients who may not have
responded well to medications, or who would rather not or can't take
medications. Catheter ablation involves threading a tiny metal-tipped
wire catheter through a vein or artery in the leg and into the heart.
Fluoroscopy, which allows cardiologists to view on a monitor the
catheter moving through the vessel, provides a road map. Other
catheters, usually inserted through the neck, contain electrical
sensors to help find the area causing short-circuits. The metal-tipped
catheter is then maneuvered to each problem site and radiofrequency
waves — the same energy used for radio and television transmission
— gently burn away each unwanted strand of tissue.
Clinicians should also know that when catheter ablation was first
tried, direct current shocks were used, but researchers later
developed the use of radiofrequency waves — a more precise form of
energy. With radiofrequency catheter ablation, patients usually leave
the hospital in one day, compared to open heart surgery, which
requires a week stay and months of recovery.
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For conditions like Wolff-Parkinson-White syndrome, in which a hairthin strand of tissue creates an extra electrical pathway between the
upper and lower chambers of the heart, radiofrequency ablation
offers a cure. It has become the treatment of choice for patients with
that disorder who do not respond well to drug therapy or who have a
propensity for rapid heart rates. Even in blocks that can be controlled
with drugs, the procedure has been shown to be cost effective
because it eliminates medication failures that require hospitalization.
While studies have shown that catheter ablation is more cost effective
than drug therapy or surgery, patients who undergo the procedure
also experience remarkable improvement in quality of life. A recent
study of nearly 400 ablation patients with dangerously rapid heart
rates — nearly a third of whom were considered candidates for open
heart surgery — found that one month after the procedure 98 percent
required no medication and 95 percent reported that their overall
health had markedly improved. It was also found that there was
improvement in the patients' ability to exercise and take on physical
activities, as well as other daily functions.
Internal Cardioversion
Internal cardioversion for conversion of atrial fibrillation and atrial
flutter to a normal sinus rhythm was developed at UCSF Medical
Center in 1991. Internal cardioversion is low energy electrical shock
(1 to 10 joules) delivered internally in the heart through two
catheters inserted in a vein in the groin and a small electrode pad
applied to the chest. This procedure is performed in the
electrophysiology lab by an electrophysiologist. During the internal
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cardioversion, short-acting sedatives are given to make the patient
sleepy.
Currently, atrial flutter is successfully "cured" by radiofrequency
catheter ablation; but treatment to restore atrial fibrillation to sinus
rhythm has been the traditional use of medications and external
cardioversion. External cardioversion is delivery of high energy
shocks of 50 to 300 joules through two defibrillator pads attached to
the chest. In some cases, external cardioversion has failed because
the electrical current has to first travel through chest muscle and
skeletal structures before reaching the heart. Internal cardioversion
has been performed when medications and external cardioversion
have failed to restore a patient's rhythm back to a normal sinus
rhythm.
The success rate of converting a patient from atrial fibrillation to
normal sinus rhythm with internal cardioversion has been 95 percent.
The less time a patient is in atrial fibrillation, the easier it is to
cardiovert back to a normal rhythm, but even patients with longstanding chronic atrial fibrillation can be converted successfully to a
normal rhythm through internal cardioversion. With internal
cardioversion, our electrophysiology team was successful in
converting a patient who had been in chronic atrial fibrillation for
eight years.
Implantable Cardioverter Defibrillator
An implantable cardioverter defibrillator is a device for people who
are prone to life-threatening rapid heart rhythms. It is slightly larger
than a pacemaker and usually is implanted beneath the skin below
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the collarbone. It is connected to a defibrillation/pace wire(s)
positioned inside the heart via a vein. It has the capability of
delivering an electric shock to the heart when it determines the heart
rate is too fast. It also is capable of pacing or stimulating the heart
when it is going too slow.
Biventricular Pacemaker
The U.S. Food and Drug Administration (FDA) recently approved the
first of a new type of pacemaker that paces both ventricles of the
heart to coordinate their contractions and improve their pumping
ability. According to the test results presented to the FDA, cardiac
resynchronization therapy (CRT):
 Increases the amount of daily activities patient can perform
without the symptoms of heart failure
 Extends the exercise capacity of heart failure patients as
measured by the distance they can walk in 6 minutes
 Improves the overall quality of life as judged by standard
measurements
 Promotes changes in heart anatomy to improve cardiac function
 Reduces the number of days patients spend in the hospital and
the total number of hospitalizations
CRT devices work by pacing both the left and right ventricles
simultaneously, which results in resynchronizing the muscle
contractions and improving the efficiency of the weakened heart. In
the normal heart, the electrical conduction system delivers electrical
impulses to the left ventricle in a highly organized pattern of
contractions that pump blood out of the ventricle very efficiently. In
systolic heart failure caused by an enlarged heart (dilated
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cardiomyopathy), this electrical coordination is lost. Uncoordinated
heart muscle function leads to inefficient ejection of blood from the
ventricles.
Summary
Antiarrhythmic drug therapy and non-pharmacological treatment of
arrhythmia, such as ablation, can be effective in children. More recent
guidelines and consensus statements on the treatment of arrhythmias
in children have been reviewed here. Although the rate of children
reported to have arrhythmias is small, helpful criteria and
recommendations exist for clinicians in health centers or practices
where expertise on pediatric cardiac conditions is not available. Helpful
resources through the Pediatric and Congenital Electrophysiology
Society (PACES) are readily available online for clinicians at all levels
of care. It is important for clinicians to recognize that arrhythmias in
children differ from those diagnosed in adults and to treat appropriate
to the guidelines and refer to cardiology specialists as a child’s
condition may warrant, ensuring the cause and correctly selecting
pharmacological and other treatments for a cardiac arrhythmia. Drug
side-effect and combination treatment may be needed, which further
necessitates ongoing collaboration with a cardiology specialist for safe
monitoring of the patient during and after treatment.
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1.
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.
2.
Long QT syndrome is a genetically transmitted cardiac
arrhythmia caused by
a.
b.
c.
d.
3.
caused by electrolyte imbalance
caused by autonomic neuropathy
hereditary
drug-induced
First-line treatment of fetal atrial flutter is the
administration of the drug _________ to the mother.
a.
b.
c.
d.
5.
a self-propagating wave of electrical excitation.
caused by re-entry.
ion channel protein abnormalities.
slow conduction.
Long QT syndrome which is _______________, is
characterized by a prolonged QTc and an increased risk of
torsade de pointes.
a.
b.
c.
d.
4.
bradyarrhythmias
tachyarrhythmias
depolarization
muscular contraction
dronedarone
procainamide
digoxin
sotalol
_________ is/are considered the initial treatment of
choice for long QT syndrome.
a.
b.
c.
d.
Sodium channel blockers
procainamide
digoxin
Beta-blockers
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6.
______________________ are the preferred betablockers during pregnancy.
a.
b.
c.
d.
7.
Propranolol and nadolol
Metoprolol and atenolol
Procainamide and digoxin
Bisoprolol and acebutolol
True or False: Symptoms of premature atrial contractions
(PACs) are virtually indistinguishable from those of
premature ventricular contractions (PVCs) as the
physiological effects are identical.
a. True
b. False
8.
Patients with long QT syndrome who cannot take betablockers may require _________________ as first-line
therapy.
a.
b.
c.
d.
9.
sodium channel blockers
metoprolol or atenolol
an implantable cardioverter-defibrillator
a class II antiarrhythmic drugs
Most premature atrial contractions (PACs) are benign, so
after ruling out severe underlying heart conditions, the
important treatment is
a.
b.
c.
d.
to
to
to
to
prescribe calcium blockers.
reassure the patient and teach coping mechanisms.
prescribe beta-blockers.
prescribe amiodarone.
10. Most patients who develop drug-induced torsade de
pointes
a.
b.
c.
d.
will experience episodes from then on.
do not have underlying risk factors.
are more often men.
are more often women.
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11. Causes of premature atrial contractions (PACs) include
a.
b.
c.
d.
stress.
stimulants (i.e., caffeine)
abnormal blood levels of magnesium and/or potassium.
All of the above
12. The heart’s normal rhythm is controlled by a natural
pacemaker, ______________, which creates electrical
impulses that travel across the atria to the ventricles.
a.
b.
c.
d.
the
the
the
the
atrioventricular node
internodal tract
sinus node
coronary sinus
13. In fetal or young patients with otherwise normal cardiac
anatomy, atrial reentry tachycardias are mostly
a.
b.
c.
d.
observed during adolescence.
observed during fetal life in late pregnancy.
observed after adolescence.
Answers a., and b., above
14. In the fetus, atrial flutter is defined as a rapid regular
atrial rate of ________ accompanied by variable degrees
of atrioventricular (AV) conduction block, resulting in
slower ventricular rates.
a.
b.
c.
d.
300-600 bpm
200 bpm
200-400 bpm
250 bpm
15. Fetal atrial flutter is usually treated with ____________
without need for further intervention if ventricular
function is acceptable and if there is no placental edema.
a.
b.
c.
d.
cardiac pacing
oral maternal antiarrhythmics
cardioversion
radiofrequency catheter ablation
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16. True or False: Atrial flutter circuits in children with
congenital heart disease are typically less variable than
those in adults.
a. True
b. False
17. Patients who are treated with atrial antitachycardia
pacing should undergo testing to confirm that their
device is effective and
a.
b.
c.
d.
free from excitement.
biphasic.
not proarrhythmic.
patient should avoid competitive sports.
18. Atrial stretch, surgical scarring, and sinus node
dysfunction all appear to play important roles in the
development of atrial flutter in patients with
a.
b.
c.
d.
congenital heart disease.
arrhythmia.
torsade de pointes.
stress.
19. ___________________ has been used with variable
success to effect acute conversion of atrial flutter to
sinus rhythm.
a.
b.
c.
d.
Digoxin
Amiodarone
Flecainide
Intravenous procainamide
20. A more recent drug, dronedarone, a less-lipophilic
amiodarone analog, has been shown to prevent
recurrence of atrial flutter and atrial fibrillation
a.
b.
c.
d.
in
in
in
in
adult patients.
patients younger than 18 years.
patients with decompensated heart failure.
fetal patients.
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21. ___________ is a cardiac glycoside with direct inotropic
effects in addition to indirect effects on the
cardiovascular system.
a.
b.
c.
d.
Procainamide
Dronedarone
Amiodarone
Digoxin
22. Which of the following is a class III antiarrhythmic agent
that blocks potassium channels, prolongs action
potential duration, and lengthens the QT interval?
a.
b.
c.
d.
Procainamide
Propafenone
Sotalol
Digoxin
23. True or False: Sinus tachycardia is sinus rhythm with a
rate of > 100 bpm.
a. True
b. False
24. Most often sinus tachycardia is caused by an increase in
the body's demand for
a.
b.
c.
d.
potassium.
oxygen.
calcium.
Vitamin D.
25. Supraventricular Tachycardia (SVT) is the most common
tachycardia
a.
b.
c.
d.
in
in
in
in
elderly patients.
post-adolescents.
women.
children.
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26. Once identified and appropriately treated, WolffParkinson-White (WPW) syndrome is associated with an
excellent prognosis, including the potential for
permanent cure through
a.
b.
c.
d.
procainamide infusion.
radiofrequency (RF) catheter ablation.
cardiac pacing.
cardioversion.
27. True or False: Verapamil (a calcium channel blocker) IS
recommended as a sole agent in patients with WolffParkinson-White WPW syndrome.
a. True
b. False
28. Once a patient who presents in cardiac arrest or with
hemodynamic compromise is determined to be
experiencing a dysrhythmia, _________________ is
indicated.
a.
b.
c.
d.
radiofrequency (RF) catheter ablation
direct-current (DC) cardioversion
cardiac pacing
an implantable cardioverter-defibrillator
29. In a stable patient with dysrhythmia, various vagal
maneuvers may be attempted: for infants the following
is very effectivea.
b.
c.
d.
ocular compression.
blowing with his thumb in his mouth.
a bag of ice slurry to the face.
using a defibrillator.
30. When conservative measures fail in a patient with
dysrhythmia, intravenous (IV) ________ is the first-line
agent.
a.
b.
c.
d.
adenosine
procainamide
esmolol
verapamil
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31. ______________ should not be administered to patients
younger than 1 year because of risk of severe
hypotension, severe bradycardia, or heart failure in this
population of patients.
a.
b.
c.
d.
adenosine
procainamide
esmolol
Verapamil
32. True or False: Surgical open-heart procedures were more
common before radiofrequency (RF) catheter ablation
but now RF ablation has virtually eliminated open-heart
procedures in the vast majority of patients, with a few
exceptions.
a. True
b. False
33. Which of the following beta-blockers prolongs
conduction time and refractoriness in the atrioventricular
(AV) node?
a.
b.
c.
d.
Verapamil
Metoprolol
Diltiazem
Digoxin
34. ____________ is contraindicated in patients with WolffParkinson-White WPW syndrome.
a.
b.
c.
d.
Verapamil
Metoprolol
Diltiazem
Digoxin
35. Accessory pathways (Aps) at all the sites in the heart
and in persons __________________ can be ablated
successfully.
a.
b.
c.
d.
of all age groups
over six years of age
who are adults
with asymptomatic Wolff-Parkinson-White (WPW) syndrome.
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36. True or False: Procainamide is no longer available in an
oral formulation and is typically only used during
electrophysiologic studies (EPS) or in the emergency
department (ED) or cardiac intensive care unit (ICU)
setting.
a. True
b. False
37. Success rates for radiofrequency (RF) catheter ablation
a.
b.
c.
d.
is about 40%.
is 60%.
exceed 90%.
is 50-50.
38. Radiofrequency (RF) catheter ablation is relatively safe,
with a complication rate of approximately ___ in most
centers.
a.
b.
c.
d.
10%
1%
12%
5%
39. Long-term ________________ is the mainstay of
therapy in patients not undergoing radiofrequency (RF)
ablation.
a.
b.
c.
d.
cardiac pacing
use of implantable cardioverter-defibrillator
oral medication
exercise and breathing programs
40. True or False: Beta-blockers are probably the
medications most commonly used to treat SVT in the
presence of preexcitation.
a. True
b. False
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Correct Answers:
1.
Conduction block or conduction delay is a frequent cause
of ____________________, especially if the conduction
block is located in the cardiac conduction system.
a. bradyarrhythmias
2.
Long QT syndrome is a genetically transmitted cardiac
arrhythmia caused by
c. ion channel protein abnormalities.
3.
Long QT syndrome which is _______________, is
characterized by a prolonged QTc and an increased risk of
torsade de pointes.
d. drug-induced
4.
First-line treatment of fetal atrial flutter is the
administration of the drug _________ to the mother.
c. digoxin
5.
_________ is/are considered the initial treatment of
choice for long QT syndrome.
d. Beta-blockers
6.
______________________ are the preferred betablockers during pregnancy.
a. Propranolol and nadolol
7.
True or False: Symptoms of premature atrial contractions
(PACs) are virtually indistinguishable from those of
premature ventricular contractions (PVCs) as the
physiological effects are identical.
a. True
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8.
Patients with long QT syndrome who cannot take betablockers may require _________________ as first-line
therapy.
c. an implantable cardioverter-defibrillator
9.
Most premature atrial contractions (PACs) are benign, so
after ruling out severe underlying heart conditions, the
important treatment is
b. to reassure the patient and teach coping mechanisms.
10. Most patients who develop drug-induced torsade de
pointes
d. are more often women.
11. Causes of premature atrial contractions (PACs) include
d. All of the above
12. The heart’s normal rhythm is controlled by a natural
pacemaker, ______________, which creates electrical
impulses that travel across the atria to the ventricles.
c. the sinus node
13. In fetal or young patients with otherwise normal cardiac
anatomy, atrial reentry tachycardias are mostly
d. Answers a., and b., above
14. In the fetus, atrial flutter is defined as a rapid regular
atrial rate of ________ accompanied by variable degrees
of atrioventricular (AV) conduction block, resulting in
slower ventricular rates.
a. 300-600 bpm
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15. Fetal atrial flutter is usually treated with ____________
without need for further intervention if ventricular
function is acceptable and if there is no placental edema.
b. oral maternal antiarrhythmics
16. True or False: Atrial flutter circuits in children with
congenital heart disease are typically less variable than
those in adults.
b. False
17. Patients who are treated with atrial antitachycardia
pacing should undergo testing to confirm that their
device is effective and
c. not proarrhythmic.
18. Atrial stretch, surgical scarring, and sinus node
dysfunction all appear to play important roles in the
development of atrial flutter in patients with
a. congenital heart disease.
19. ___________________ has been used with variable
success to effect acute conversion of atrial flutter to sinus
rhythm.
d. Intravenous procainamide
20. A more recent drug, dronedarone, a less-lipophilic
amiodarone analog, has been shown to prevent
recurrence of atrial flutter and atrial fibrillation
a. in adult patients.
21. ___________ is a cardiac glycoside with direct inotropic
effects in addition to indirect effects on the cardiovascular
system.
d. Digoxin
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22. Which of the following is a class III antiarrhythmic agent
that blocks potassium channels, prolongs action potential
duration, and lengthens the QT interval?
c. Sotalol
23. True or False: Sinus tachycardia is sinus rhythm with a
rate of > 100 bpm.
a. True
24. Most often sinus tachycardia is caused by an increase in
the body's demand for
b. oxygen.
25. Supraventricular Tachycardia (SVT) is the most common
tachycardia
d. in children.
26. Once identified and appropriately treated, WolffParkinson-White (WPW) syndrome is associated with an
excellent prognosis, including the potential for permanent
cure through
b. radiofrequency (RF) catheter ablation.
27. True or False: Verapamil (a calcium channel blocker) IS
recommended as a sole agent in patients with WolffParkinson-White WPW syndrome.
b. False
28. Once a patient who presents in cardiac arrest or with
hemodynamic compromise is determined to be
experiencing a dysrhythmia, _________________ is
indicated.
b. direct-current (DC) cardioversion
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29. In a stable patient with dysrhythmia, various vagal
maneuvers may be attempted: for infants the following is
very effectivec. a bag of ice slurry to the face.
30. When conservative measures fail in a patient with
dysrhythmia, intravenous (IV) ________ is the first-line
agent.
a. adenosine
31. ______________ should not be administered to patients
younger than 1 year because of risk of severe
hypotension, severe bradycardia, or heart failure in this
population of patients.
d. Verapamil
32. True or False: Surgical open-heart procedures were more
common before radiofrequency (RF) catheter ablation but
now RF ablation has virtually eliminated open-heart
procedures in the vast majority of patients, with a few
exceptions.
a. True
33. Which of the following beta-blockers prolongs conduction
time and refractoriness in the atrioventricular (AV) node?
b. Metoprolol
34. ____________ is contraindicated in patients with WolffParkinson-White WPW syndrome.
d. Digoxin
35. Accessory pathways (Aps) at all the sites in the heart and
in persons __________________ can be ablated
successfully.
a. of all age groups
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36. True or False: Procainamide is no longer available in an
oral formulation and is typically only used during
electrophysiologic studies (EPS) or in the emergency
department (ED) or cardiac intensive care unit (ICU)
setting.
a. True
37. Success rates for radiofrequency (RF) catheter ablation
c. exceed 90%.
38. Radiofrequency (RF) catheter ablation is relatively safe,
with a complication rate of approximately ___ in most
centers.
b. 1%
39. Long-term ________________ is the mainstay of therapy
in patients not undergoing radiofrequency (RF) ablation.
c. oral medication
40. True or False: Beta-blockers are probably the medications
most commonly used to treat SVT in the presence of
preexcitation.
a. True
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The reference section of in-text citations include published works
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