ARRHYTHMIAS IN CHILDREN - NurseCe4Less.com · 2016-08-12 · treating arrhythmias in children has...

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ARRHYTHMIAS IN

CHILDREN:

Diagnosis And

Treatment

Jassin M. Jouria, MD

Dr. Jassin M. Jouria is a medical doctor,

professor of academic medicine, and medical author. He graduated from Ross

University School of Medicine and has completed his clinical clerkship training in

various teaching hospitals throughout New York, including King’s County Hospital Center and Brookdale Medical Center, among others. Dr. Jouria has passed all

USMLE medical board exams, and has served as a test prep tutor and instructor for Kaplan. He has developed several medical courses and curricula for a variety of

educational institutions. Dr. Jouria has also served on multiple levels in the academic field including faculty member and Department Chair. Dr. Jouria continues to serves

as a Subject Matter Expert for several continuing education organizations covering multiple basic medical sciences. He has also developed several continuing medical

education courses covering various topics in clinical medicine. Recently, Dr. Jouria has been contracted by the University of Miami/Jackson Memorial Hospital’s

Department of Surgery to develop an e-module training series for trauma patient

management. Dr. Jouria is currently authoring an academic textbook on Human Anatomy & Physiology.

ABSTRACT

The prevalence and spectrum of arrhythmias change with age. As a

consequence, treating arrhythmias in children has its unique

challenges. The child’s age, as well as the age of onset of arrhythmia,

history of heart symptoms or failure, and electrocardiography testing

must all be considered when making a diagnosis. Although not a

common occurrence in children, life-threatening arrhythmias need to

be identified and appropriately treated to prevent serious outcomes.


Continuing Nursing Education Course Planners

William A. Cook, PhD, Director, Douglas Lawrence, MA, Webmaster,

Susan DePasquale, MSN, FPMHNP-BC, Lead Nurse Planner

Policy Statement

This activity has been planned and implemented in accordance with

the policies of NurseCe4Less.com and the continuing nursing education

requirements of the American Nurses Credentialing Center's

Commission on Accreditation for registered nurses. It is the policy of

NurseCe4Less.com to ensure objectivity, transparency, and best

practice in clinical education for all continuing nursing education (CNE)

activities.

Continuing Education Credit Designation

This educational activity is credited for 4.5 hours. Nurses may only

claim credit commensurate with the credit awarded for completion of

this course activity.

Pharmacology content is 1 hour.

Statement of Learning Need

There are unique challenges associated with arrhythmias in children

and the treatment options for childhood arrhythmia. This information

is needed to guide the healthcare professional who is treating

children with arrhythmia.


Course Purpose

To provide nurses with knowledge of pediatric arrhythmias, including

its recognition and treatment options.

Target Audience

Advanced Practice Registered Nurses and Registered Nurses

(Interdisciplinary Health Team Members, including Vocational Nurses

and Medical Assistants may obtain a Certificate of Completion)

Course Author & Planning Team Conflict of Interest Disclosures

Jassin M. Jouria, MD, William S. Cook, PhD, Douglas Lawrence, MA,

Susan DePasquale, MSN, FPMHNP-BC – all have no disclosures

Acknowledgement of Commercial Support

There is no commercial support for this course.

Activity Review Information

Reviewed by Susan DePasquale, MSN, FPMHNP-BC

Release Date: 8/10/2016 Termination Date: 8/10/2019

Please take time to complete a self-assessment of knowledge, on

page 4, sample questions before reading the article.

Opportunity to complete a self-assessment of knowledge learned will

be provided at the end of the course.


1. Any electrical activity not initiated by the SA node is

considered

a. a depolarization event.

b. an atrioventricular (AV) impulse. c. an arrhythmia.

d. a repolarization event.

2. Electrical stimulation of a myocardial cell results in

a. a slow outward leak of sodium.

b. depolarization. c. a slow outward leak of potassium.

d. All of the above

3. True or False: Some arrhythmias are so common as to be

considered as almost normal variants.

a. True b. False

4. The conduction system in the ventricles is more elaborate than that in the atria because

a. the muscle mass is larger. b. of the location of the bundle of His. c. the superior vena cava enters through the ventricles.

d. of fiber stretch.

5. Normally, the _________________, located where the superior vena cava meets the right atrium, has the most

rapid intrinsic rate (60 to 100 bpm).

a. atria via

b. atrioventricular (AV) node

c. coronary sinus

d. sinoatrial (SA) node


Introduction

An arrhythmia is an abnormality of cardiac rhythm. The prevalence

and spectrum of arrhythmias change with age. As a consequence,

treating arrhythmias in children has its unique challenges. While

abnormal heart rates in children are often not a cause of concern,

children with an abnormal heart rhythm, including consideration of

the child’s age, age of onset of arrhythmia, history (palpitations,

heart failure, syncope, etc.), and the electrocardiogram (ECG)

findings must all be factored into a health professional’s diagnosis. It

is absolutely vital that a clinician be able to recognize when an

arrhythmia has the potential to become serious or life threatening,

and to identify appropriate treatment options. This course will provide

an understanding of the mechanics of arrhythmias, and it will discuss

the unique challenges associated with arrhythmias in children and the

treatment options. This information will help healthcare professionals

to communicate with their young patient and the patient’s parents or

guardians to determine the right course of action.

Cardiac Electrophysiology

The majority of myocardial cells share the same basic cellular

electrophysiologic properties that allow contraction when a

transmembrane action potential develops. The electrical system of

the heart consists of intrinsic pacemakers and conduction tissues.

This section reviews normal cardiac rhythm in anatomic terms and

highlights normal cardiac electrophysiology as a necessary basis for

recognizing abnormal conditions as they may occur in children.


Normal Cellular Electrophysiology

Fully polarized cells have a resting membrane potential of -90 mV.

This resting membrane potential exists because of the electrical

gradient created by differences in extracellular and intracellular ion

concentrations. Specifically, the sodium–potassium pump primarily

controls sodium and potassium concentrations. This pump tries to

maintain intracellular sodium concentrations at 5 to 15 mEq/L and

intracellular potassium concentrations at 135 to 140 mEq/L. In

comparison, the extracellular sodium concentration is normally 135 to

142 mEq/L and extracellular potassium 3 to 5 mEq/L.2

Electrical stimulation of a myocardial cell results in depolarization.

Depolarization is initiated by a slow inward leak of sodium. When the

transmembrane potential reaches approximately -60 mV, the fast

sodium channel opens, actively transporting sodium across the cell

membrane and resulting in rapid cellular depolarization to

approximately +20 mV. This is represented by phase 0 of the action

potential and the QRS complex on a surface electrocardiogram (ECG).

After the rapid membrane depolarization, the sodium channel closes

and a complex exchange of sodium, calcium, and potassium occurs

during the plateau phases 1 and 2 of the action potential.

The dominant feature during the plateau phases of the action

potential is movement of calcium ions into the intracellular space via

L-type calcium channels. This feature differentiates myocardial cells

from nerve tissue and starts the excitation–contraction cascade of the

cell by initiating the release of intracellular calcium stores from the

sarcoplasmic reticulum. Phase 3 of the action potential is dominated

by repolarization of the cell membrane by outward movement of


potassium ions. The rate of fall of phase 3 and its depth determine

membrane responsiveness to stimulation. Tissues may depolarize

only after reaching a particular level of repolarization called the

‘‘threshold potential,’’ at least -50 to -55 mV for normal Purkinje

fibers. This level of repolarization therefore determines the absolute

refractory period (ARP). The ARP varies in length depending primarily

on the action potential duration (APD). Phase 4 is the resting

membrane potential that results from a combination of ionic currents,

primarily the slow inward sodium current.3

Normal Cardiac Conduction

The electrical system of the heart consists of intrinsic pacemakers

and conduction tissues. It is convenient to conceptualize the

progression of normal cardiac rhythm in anatomic terms. The rate of

electrical firing of the heart depends on the most rapid pacemaker.

Spontaneous electrical firing or automaticity can occur anywhere in

the heart under certain conditions. Normally, the sinoatrial (SA)

node, located where the superior vena cava meets the right atrium,

has the most rapid intrinsic rate (60 to 100 bpm). Therefore, any

electrical activity not initiated by the SA node is considered an

arrhythmia. Consequently, most arrhythmias are labeled by the

anatomic location and rate.

Sinoatrial node firing initiates atrial contraction. The electrical impulse

is conducted through the atria via the internodal tracts to the

atrioventricular (AV) node near the coronary sinus, between the two

atria. The AV node has pacemaker properties but normally

coordinates atrial and ventricular contraction. The AV node normally

limits excessively rapid atrial rates from activating the ventricles.


The conduction system in the ventricles is more elaborate than that

in the atria because the muscle mass is larger. Rapid and effective

excitation is critical because the ventricles contribute the most to

cardiac output. Fibers leaving the AV node are called the bundle of

His. They separate into the bundle branches, which traverse the

septum between the ventricles. Conduction between the AV node and

the bundle of His is measured by the P-R interval. The final

conducting components of the ventricles are the Purkinje fibers,

which emanate from the bundle branches to stimulate the ventricular

cardiac muscle to contract. The QRS complex measures

depolarization of the ventricles. The Q-T interval reflects both

ventricular depolarization and repolarization.

Electrical Anatomy of the Normal Heart

The atrial muscle and ventricular muscle are separated by insulation

of the fibrous mitral and tricuspid valve rings, and normally the only

connection between them is via the His bundle. All cardiac myocytes

are capable of electrical conduction and have intrinsic pacemaker

activity. Each tissue has a conduction velocity and a refractory

period, both of which vary with changes in heart rate and influences

such as autonomic tone, circulating catecholamines, etc. The

conduction velocities of various parts of the heart vary.8

Cardiac Conduction

The cardiac conduction system consists of specialized fast conducting

tissue through which the electric activity of the heart spreads from

the atria to the ventricles.


The characteristics of the different parts of the conduction system are

a result of the different characteristics of the individual myocytes. On

a larger level, function is controlled predominantly by the autonomic

nervous system (both vagal and sympathetic nerve system). The

sinus node and atrioventricular node are especially responsive to the

autonomic nerve system. The ganglionic plexus, a conglomeration of

both vagal and sympathetic nerves, form the intrinsic cardiac nerve

system and innervate through a network of nerve fibers in the atria

and ventricles. The vagal nerve and sympathetic nerve system are

both continually active in the heart, but vagal activity dominates the

tonic background stimulation of the autonomic nerve system.

Moreover, the heart is more susceptible to vagal stimulation.

Vagal stimulation provokes a rapid response and the effect dissipates

swiftly in contrast to sympathetic stimulation, which has a slow onset

and offset. Vagal stimulation results in a reduction in sinus node

activation frequency and prolongs AV nodal conduction. These effects

can occur simultaneously or independent of each other. Sympathetic

stimulation exerts reverse effects, accelerating the sinus node firing

frequency and improving AV nodal conduction. The autonomic nerve

system has a small effect on cardiomyocytes. Vagal stimulation tends

to prolong the refractory period and decrease the myocardial

contractility. Sympathetic stimulation has the opposite effect on the

cardiac tissue. The physiological modulation of cardiac conduction is

vital to adaptation of the heart to rest and exercise. However, the

autonomic nervous system can contribute as a modifier and is certain

to facilitate the occurrence of certain arrhythmias.9


Sinus Node

The sinus node is a densely innervated area located in the right

atrium, which is supplied by the right (55%-60%) or circumflex

(40%-45%) coronary artery. It is a small structure of 10-20 mm long

and 2-3 mm wide and contains a diversity of cells. These include

pacemaker cells, which are discharged synchronously due to mutual

entrainment. This results in an activation wave front triggering the

rest of the atrium.

Atrium

The impulse formed in the sinus node is conducted through the

atrium to the AV-node. Evidence indicates three preferential

conduction pathways. The pathways show preferential conduction due

to their anatomical structure, rather than specialized conduction

properties. The three pathways are: the anterior internodal pathway,

the middle internodal tract, and the posterior internodal pathway. The

anterior internodal pathway connects to the anterior interatrial band,

also known as the Bachmann bundle. This bundle of muscular tissue

conducts the sinus wave front from the right to the left atrium.

AV Node

The connection between atria and ventricles is facilitated through the

AV node, lying in the right atrial myocardium and a penetrating part,

the bundle of His. The AV node acts as a gatekeeper, regulating

impulse conduction from the atrium to the ventricle. Additionally, due

to the phase 4 diastolic depolarization it can exhibit impulse

formation. The AV node is supplied in most cases (85%-90%) by the

right coronary artery or in the remaining cases the circumflex artery.


Bundle of His

Connecting the distal AV node and the proximal bundle branches, the

bundle of His is supplied by both the posterior and anterior

descending coronary arteries. The central fibrous body and

membranous septum between the atria and the ventricles enclose it.

The location and blood supply protect the bundle of His from external

influences.

Bundle Branches

From the bundle of His, the right bundle branch continues to the right

ventricular apex. The left bundle branch splits off and divides into to

two fascicular branches. Commonly, the left bundle branch consists of

an anterior fascicle, which activates the anterosuperior portion of the

left ventricle, and the thicker and more protected posterior fascicle,

which activates the inferoposterior part of the left ventricle.

Ventricle

The ventricle is activated through the dense network of Purkinje

fibers originating from the bundle branches. They penetrate the

myocardium and are the starting point of the ventricular activation.

The left ventricular areas first excited are the anterior and posterior

paraseptal wall and the central left surface of the interventricular

septum. The last part of the left ventricle to be activated is the

posterobasal area. Septal activation starts in the middle third of the

left side of the interventricular septum, and at the lower third at the

junction of the septum and posterior wall. Activation of the right

ventricle starts near the anterior papillary muscle 5 to 10 milliseconds

after onset of the left ventricle.10


Normal Heart Rate In Children

The normal average heart rate of children is higher than that of

adults. A heart rate of 60 to 100 bpm when resting is considered

normal for adults. The variation in heart rates of children is greater

with heart rates varying from 60 bpm (when they are asleep) to 220

bpm (when they are active physically in strenuous activities).6

Age

Normal Range (Average)

bpm

< 1 day 93-154 (123)

1-2 days 91-159 (123)

3-6 days 91-166 (129)

1-3 weeks 107-182 (148)

1-2 months 121-179 (149)

3-5 months 106-186 (141)

6-11 months 109-169 (134)

1-2 years 89-151 (119)

3-4 years 73-137 (108)

5-7 years 65-133 (100)

8-11 years 62-130 (91)

12-15 years 80-119 (85)

> 16 years 60-100


Cardiac Arrhythmias

An arrhythmia is any abnormality in the rate, regularity, or site of

origin of an electrical impulse. Arrhythmia includes a disturbance in

conduction that disrupts the normal sequence of activation in the

atria or ventricles. Arrhythmias have varying degrees of severity and

significance based on site of origin, symptoms, frequency, and

duration; and, they can be due to a variety of reasons, such as

structural abnormalities, electrolyte abnormalities, metabolic

derangements, genetic mutations, and drug toxicity. This section

provides an overview of cardiac arrhythmias in terms of pathogenesis

and clinical presentation.

Overview of Arrhythmias

Arrhythmias are relatively common in the pediatric cardiac intensive

care unit. One study revealed 59% of neonates and 79% of older

children have arrhythmias within 24 hours of surgery. An arrhythmia

is any abnormality in the rate, regularity, or site of origin or a

disturbance in conduction that disrupts the normal sequence of

activation in the atria or ventricles.

Arrhythmias differ in their population frequency, anatomical

substrate, physiological mechanism, etiology, natural history,

prognostic significance, and response to treatment. As is emphasized

throughout, it is important to gain as much information as possible

about the substrate and mechanism of an arrhythmia to be able to

predict the natural history and to define the prognosis and response

to treatment.1 A basic knowledge of the cardiac action potential and

cardiac conduction system facilitates understanding of cardiac

arrhythmias. The effects and side effects of anti-arrhythmic drugs are


depended on the influence of ion channels involved in the generation

and/or perpetuation of the cardiac action potential. These

physiological dynamics are explained further below.3,7

The cardiac action potential is a result of ions flowing through

different ion channels. Ion channels are passages for ions (mainly

Na+, K+, Ca2+ and Cl-) that facilitate movement through the cell

membrane. Changes in the structure of these channels can open,

inactivate or close these channels and thereby control the flow of ions

into and out of the myocytes. Due to differences in the type and

structure of ion channels, the various parts of the heart have slightly

different action potential characteristics.

Ion channels are mostly a passive passageway where movement of

ions is caused by the electrochemical gradient. In addition to these

passive ion channels a few active trigger-dependent channels exist

that open or close in response to certain stimuli (for instance

acetylcholine or ATP). The changes in the membrane potential due to

the movement of ions produce an action potential, which lasts only a

few hundreds of milliseconds. Disorders in single channels can lead to

arrhythmias, as seen in the later section on primary arrhythmias. The

action potential is propagated throughout the myocardium by the

depolarization of the immediate environment of the cells and through

intracellular coupling with gap-junctions.

During the depolarization, sodium ions (Na+) stream into the

cytoplasm of the cell followed by an influx of calcium (Ca2+) ions

(both from the inside (sarcoplasmatic reticulum) and outside of the

cell). These Ca2+ ions cause the actual muscular contraction by


coupling with the muscle fibers. During repolarization the cell returns

to the resting membrane potential, due to the passive efflux of K+.

The (ventricular) action potential can be divided in five phases, which

are listed below in detail.

Phase 0: Rapid Depolarization

Rapid depolarization is started once the membrane potential reaches

a certain threshold (about -70 to -60 mV). This produces activation of

sodium channels and a rapid influx of Na+ and a corresponding rapid

upstroke of the action potential. At higher potentials (-40 to -30)

Ca2+ influx participates in the upstroke. In the sinus node and AV

node a slower upstroke can be observed. This is because the slower

acting Ca2+ ion channels mainly mediate the rapid depolarization in

these cells. The slower activation produces a slower upstroke.

Phase 1: Early Rapid Repolarization

Immediately following rapid depolarization, the inactivation of the

Na+ channel (INa) and subsequent activation of the outward

K+ channel (Ito) and the Na+/Ca2+ exchanger (INa,Ca), which

exchanges 3 Na+ for 1 Ca2+, produces an early rapid repolarization.

Due to the limited role of the Na+ channel in the upstroke of sinus

node and AV node cells and the subsequent slower depolarization,

this rapid repolarization is not visible in their action potentials.

Phase 2: Plateau

The plateau phase represents an equal influx and efflux of ions in or

out of the cell producing a stable membrane potential. This plateau

phase is predominantly observed in the ventricular action potential.


The inward movement of Ca2+ through the open L-type Ca2+ channels

(ICa-L) and the exchange of Na+ for internal Ca2+ by the

Na+/Ca2+ exchanger (INa,Ca) are responsible for the influx of ions

during the plateau phase. The efflux of ions is the result of outward

current carried by K+ (IKur and Ks).

Phase 3: Final Rapid Repolarization

Final repolarization is mainly caused by inactivation of Ca2+ channels,

reducing the influx of positive ions. Furthermore repolarizing

K+ currents (delayed rectifier current IKs and IKr and inwardly

rectifying current IK1 and IK,Ach) are activated which increase efflux of

positive K+ ions. This results in a repolarization to the resting

membrane potential.

Phase 4: Resting membrane potential

During phase 4 of the action potential intracellular and extracellular

concentrations of ions are restored. Depending on cell type the

resting membrane potential is between -50 to -95 mV. Sinus node

and AV nodal cells have a higher resting membrane potential (-50 to

-60 mV and -60 to -70 respectively) in comparison with atrial and

ventricular cardiomyocytes (-80 to -90 mV). Sinus node cells and AV

nodal cells (and to a lesser degree Purkinje fiber cells) have a special

voltage dependent channel If, the funny current. Furthermore they

lack IK1, a K+ ion channel that maintains the resting membrane

potential in atrial and ventricular tissue. The If channel causes a slow

depolarization in diastole, called the phase 4 diastolic depolarization,

which results in normal automaticity. The frequency the sinus node

discharges is regulated by the autonomous nerve system, and due to


the relative high firing frequency (60-80 beats per minute) the sinus

node dominates other potential pacemaker sites.

Arrhythmogenesis

In general, arrhythmia mechanisms have been described as

abnormalities in electrical development, electrical conduction, or a

combination of both. Abnormalities in electrical development arise

from irregular automaticity or triggered activity from the SA node or

other sites producing ectopic beats. Causes of irregular automaticity

include hypoxia, electrolyte abnormalities, fiber stretch,

catecholamine excess, ischemia, and edema. All of these factors

increase the slope of phase 4 depolarization, resulting in heightened

automaticity. Triggered activity usually develops due to transient

membrane depolarization during or immediately after repolarization.

These early and delayed afterdepolarizations can occur with

oscillations in the plateau phase of the action potential, leading to a

second depolarization before the first is completed. Hypoxia, fiber

stretch, catecholamines, high PCO2, and digitalis overdose can lead to

triggered activity.4

Reentry and conduction block are the most common electrical

conduction abnormalities associated with arrhythmogenesis. Reentry

describes a concept of infinite impulse propagation by continued

activation of previously refractory tissue. Reentry depends on

different conduction velocities along adjacent myocardial fibers, with

one fiber containing an area of unidirectional conduction block. This

allows continued excitation in a repetitive manner. This circus rhythm

may develop as areas of infarcted tissue block or delayed conduction.


A single circuit of the fibers may induce a premature contraction,

whereas continuous cycling of impulses might produce sustained

tachycardia. This process may occur in both atrial and ventricular

tissue. Conduction block occurs when the normal conduction pathway

is blocked and the impulse either expires or conducts through an

alternative inappropriate route to depolarize the myocardium.5

Mechanisms of Arrhythmia

Structural abnormalities or electric changes in the cardiomyocytes

can impede impulse formation or change cardiac propagation,

therefore facilitating arrhythmias. Arrhythmogenic mechanisms can

arise in single cells (automaticity, triggered activity), but other

mechanisms require multiple cells for arrhythmia induction (re-

entry). Briefly highlighted is the pathophysiological mechanisms of

the main causes of arrhythmia.2,11

Abnormal Automaticity

The mechanism of abnormal automaticity is similar to the

normal automaticity of sinus node cells. Abnormal automaticity

can be caused by changes in the cell ion channel characteristics

due to drugs (digoxin) or changes in the electrotonic

environment (myocardial infarction). Abnormal automaticity

can result from an increase of normal automaticity in non-sinus

node cells or a truly abnormal automaticity in cells that don't

exhibit a phase 4 diastolic depolarization.

An important phenomenon in (both normal and abnormal)

automaticity is overdrive suppression. In overdrive suppression

the automaticity of cells is reduced after a period of high


frequency excitation. The cellular mechanism responsible for

this effect is an increased activity of the Na+, K+ pump (INa, K)

which results in an increased efflux of Na+, thereby inducing a

hyperpolarization.

Triggered Activity

Triggered activity is depolarization of a cell triggered by a

preceding activation. Due to early or delayed

afterdepolarizations the membrane potential depolarizes and,

when reaching a threshold potential, activates the cell. These

afterdepolarizations are depolarizations of the membrane

potential initiated by the preceding action potential. Depending

on the phase of the action potential in which they arise, they

are defined as early or late afterdepolarizations.

A disturbance of the balance in influx and efflux of ions during

the plateau phase (phase 2 or 3) of the action potential is

responsible for the early afterdepolarizations. Multiple ion

currents can be involved in the formation of early

afterdepolarizations depending on the triggering mechanism.

Early afterdepolarizations can develop in cells with an increased

duration of the repolarization phase of the action potential, as

the plateau phase is prolonged. The prolonged repolarization

might reactivate the Ca2+ channels that have recovered from

activation at the beginning of the repolarization. Otherwise

disparity in action potential duration of surrounding myocytes

can destabilize the plateau phase through adjacent depolarizing

currents.


Delayed afterdepolarizations occur after the cell has recovered

after completion of repolarization. In delayed

afterdepolarization an abnormal Ca2+ handling of the cell is

responsible for the afterdepolarizations due to release of

Ca2+ from the storage of Ca2+ in the sarcoplasmatic reticulum.

The accumulation of Ca2+ increases membrane potential and

depolarizes the cell until it reaches a certain threshold, thereby

creating an action potential. A high heart rate can result in the

accumulation of intracellular Ca2+ and induce delayed

afterdepolarizations.11

Disorders of Impulse Conduction

The disorders of impulse conduction generally involve the rate of and

re-entry circuits or pathways in the heart.

Conduction block

Conduction block or conduction delay is a frequent cause of

bradyarrhythmias, especially if the conduction block is located

in the cardiac conduction system. However, tachyarrhythmias

can also result from conduction block when this block produces

a re-entrant circuit. Conduction block can develop in different

(pathophysiological) conditions or can be iatrogenic

(medication, surgery).

Re-entry

Re-entry or circus movement is a multicellular mechanism of

arrhythmia. Important criteria for the development of re-entry

are a circular pathway with an area in this circle of


unidirectional block and a trigger to induce the re-entry

movement. Re-entry can arise when an impulse enters the

circuit, follows the circular pathway and is conducted through a

unidirectional (slow conducting) pathway. Whilst the signal is in

this pathway the surrounding myocardium repolarizes. If the

surrounding myocardium has recovered from the refractory

state, the impulse that exits the area of unidirectional block can

reactivate this recovered myocardium. This process can repeat

itself and thus form the basis of a re-entry tachycardia. Slow

conduction and/or a short refractory period facilitate re-entry.

The reason of unidirectional block can be anatomical (atrial

flutter, AV node reentrant tachycardia (AVNRT), AV reentrant

tachycardia (AVRT) or functional (as with myocardial ischemia),

or a combination of both.

Epidemiology of Arrhythmias

Some arrhythmias are more

common than others but there are

almost no data on the population

prevalence of these conditions.

However, the prevalence and

spectrum of arrhythmias change

with age. Faced with a new patient

with an arrhythmia, diagnosis is

based mainly on the child’s age,

the age of onset of arrhythmia, the

history (palpitations, heart failure,

syncope, etc.), and the ECG

findings, but should also take into account the prevalence of different


arrhythmias (in other words, a common arrhythmia is often a more

likely diagnosis than a rare one).

Probably fewer than half of new tachycardias present in the first year

of life. By far the most common tachycardia presenting in early

infancy is orthodromic AV reentry. Most of these infants have a

normal ECG in sinus rhythm but some show ventricular pre-

excitation. Other neonatal tachycardias are much less common and

include atrial flutter, permanent junctional reciprocating tachycardia,

atrial tachycardia, and ventricular tachycardia.12

The most common tachycardia in childhood is also orthodromic AV re-

entry tachycardia, although AV nodal re-entry tachycardia becomes

progressively more common after the age of 5 years. Less common

tachycardias in this age group are antidromic AV re-entry,

atriofascicular re-entry, ventricular tachycardias, and atrial

tachycardias.5

Arrhythmias presenting with palpitations include most of the common

types of supraventricular tachycardia and a few cases of ventricular

tachycardia. Many children with palpitations do not have an

arrhythmia and a detailed first-hand history is essential before

assessing the likelihood of an arrhythmia and the necessity of further

investigation. Similarly, very few children with chest pain have

arrhythmias (or indeed any cardiac abnormality) and only a few with

syncope have an arrhythmia. Again it all depends on the history.

Incessant tachycardias presenting with heart failure or apparent

cardiomyopathy include focal atrial tachycardia, permanent junctional


reciprocating tachycardia, incessant idiopathic infant ventricular

tachycardia, and orthodromic atrioventricular re-entry tachycardia.13

Arrhythmias presenting with syncope include complete AV block,

atrial fibrillation in Wolff–Parkinson–White (WPW) syndrome,

sinoatrial disease, and ventricular tachycardia, especially in long QT

syndrome, catecholaminergic ventricular tachycardia or late after

cardiac surgery.

Some arrhythmias are so common as to be considered as almost

normal variants. They include atrial premature beats, ventricular

premature beats, and transient nocturnal Wenckebach AV block.

Arrhythmias are relatively common in the pediatric cardiac intensive

care unit. One study revealed 59% of neonates and 79% of older

children have arrhythmias within 24 hrs. of surgery. Of these

arrhythmias, junctional ectopic tachycardia (JET) was seen in 9% of

neonates and 5% of older children. Ventricular tachycardia was found

in 3% of neonates and 15% of older children.14

In terms of specific arrhythmias,

sinus tachycardia is the most

frequently seen arrhythmia, with

supraventricular tachycardia being

the next most common, followed

by sinus bradycardia. Reentrant

tachycardia is common in infants

and children with congenital heart

disease (CHD). Some arrhythmias


in the early post operative period like premature atrial contraction’s

(PAC’s) and premature ventricular beats (bigeminy) are usually

transient and well tolerated. Others like junctional ectopic tachycardia

(JET) and atrial flutter may cause significant hemodynamic instability

and compromise or even sudden cardiac death.

Primary arrhythmias occur in children without structural heart

disease, although they may be secondary to ion channel diseases

that are still being elucidated. Risk factors that predispose children

for secondary arrhythmias include congenital cardiac malformations,

surgical repair and scarring, long cardiopulmonary bypass times, or

exposure to chronic hemodynamic stress.

Electrolyte and acid-base imbalance and the use of vasoactive drugs

also predispose children to arrhythmias. Inflammation or carditis seen

in diseases such as acquired heart diseases like Kawasaki disease,

rheumatic fever and myocarditis may produce arrhythmogenic foci.

Conditions of ventricular volume overloading, valvular regurgitation,

congestive heart failure and pulmonary hypertension are other

secondary reasons.

Regardless of the cause of the arrhythmia, there are certain common

signs, symptoms and treatment options that are ultimately based on

the rhythm more than on the etiology with certain very important

exceptions. Symptoms may vary depending upon age and include

feeding intolerance, lethargy, irritability, pallor, diaphoresis, syncope,

fatigue or palpitations.3,8


Mechanisms of tachyarrhythmias can be enhanced automaticity with

triggered foci or enhanced conduction with the presence of reentrant

circuits. Similarly, bradycardia can result from suppressed

automaticity or suppressed conduction, where normal conduction is

delayed or blocked. Understanding the mechanism informs the

optimal treatment choice.

Types of Arrhythmias

The following tables provide a general overview of the different types

of arrhythmias.2,7,15,16 Sections of this course later on will provide

more detailed information on the most common types.

CARDIAC

ARRHYTHMIA

CHARACTERISTICS

Sick sinus syndrome (SSS)/

Tachy-Brady Syndrome

Sinoatrial (SA) node becomes dysfunctional and is no longer a reliable pacemaker, most commonly manifested as

bradycardia, although there can also be tachycardia. When the sinus rate is slower than another potential pacemaker

in the heart, it may no longer be the dominant pacemaker. SSS can also cause an alternating bradycardia and

tachycardia. A number of rhythms result including sinus bradycardia, sinus arrest and junctional rhythm, and

ectopic atrial and nodal rhythms.

The term SSS includes SA node dysfunction plus symptoms

of dizziness, syncope or sudden cardiac death.

Bradycardias

Often caused by hypoxia, vagal tone, hypothyroidism,

cardiac surgery, endocarditis and myocarditis, hyperkalemia, sleep, hypothermia, sedation and

anesthesia.

Sinus bradycardia: Sinus node slower than normal for age related normal values.

Slow junctional escape rhythm/nodal rhythm: Spontaneous depolarization of the AV node. The sinus node has either

failed to fire or is slower than the AV node. Rates 50-80 beats/min in children less than 3 yrs. and 40-60 beats/min

for children older than 3yrs. Can be common after atrial surgery and are usually transient.


Ventricular escape rhythm or ideoventricular rhythm: Origin

of impulse is from the ventricle and presents with rates slower than from the AV node. QRS have wide complex

morphology. This is a secondary phenomenon vs. a primary

arrhythmia and occurs when the sinus node and/or the AV node are dysfunctional. An example of this is complete

heart block with a ventricular escape rhythm. The ventricle itself is working well, and the escape rhythm is a symptom

of another problem.

Premature

Beats/Extra- Systoles

Premature atrial, junctional and ventricular ectopic beats

are common and may occur in patterns of bigeminy, trigeminy, quadrageminy or couplets. These are generally

benign.

Wandering Atrial

Pacemaker

Shifting of the pacemaker site from the SA node to

alternate sites in the atria and junction (AV node). P-wave configuration changes as the site changes.

Supraventricular Tachycardias

(SVT) SVT is

used as a collective term

Originates above the bundle of His. Reentrant circuits generally have an abrupt onset and termination, i.e., are

paroxysmal.

Sinus tachycardia: Sinus node is faster than age-related

normal values due to enhanced automaticity. Usually due to fever, pain, anxiety, anemia, medications, hypovolemia or

in the presence of increased catecholamines.

While not generally an indication of conduction system pathology, sinus tachycardia may be an important indicator

of significant cardiovascular compromise.

Reentrant tachycardias: Reentrant tachyarrhythmias

require the presence of two possible conduction pathways with different conduction and refractory properties. The

tachycardia uses both pathways; one as an antegrade limb and one as a retrograde limb of the reentry circuit.

a) Within the atria: atrial flutter, atrial fibrillation; intra-

atrial reentrant tachycardia (IART) atrial flutter- or

incisional tachycardia represents macroreentry within the atrial muscle and may be slower than atrial flutter.

b) Atrioventricular reentrant tachycardias include:

- atrioventricular reentrant tachycardia (AVRT): commonly associated with Wolff- Parkinson-White.

Accessory pathway present allowing impulses that entered via the AV node to enter the atria

- atrioventricular nodal reentry tachycardia (AVNRT):

uses a “slow-fast AV nodal pathway”. Antegrade conduction limb is the slow pathway and retrograde limb fast one.

Simulation of the atria by the retrograde pathway produces inverted p- waves. Concurrent stimulation of the ventricles.


- permanent junctional reciprocating tachyarrhythmia

(PJRT). These are reentrant circuits in which one limb includes the AV node.

Wolff-Parkinson-White Syndrome (WPW): Baseline resting ECG is characterized by a short PR interval, wide QRS and

delta wave which is a manifestation of the accessory on sinus rhythm. WPW is marked by the delta wave on the

resting ECG. Atrial flutter or atrial fibrillation in the presence of this type of accessory connection can result in

VF.

The QRS complex in SVT is wide if there’s aberrant

conduction, in which the antegrade limb is the accessory connection. If the AV node is the antegrade limb, the QRS

is a narrow complex.

Automatic tachycardia – AET and JET: local enhanced automatic focus of certain cardiac myocytes in the atria or

AV node. AET and JET are non-reciprocating tachycardias that originate from a single focus unlike reentrant rhythms.

AET/JET are seen more commonly in neonates and usually

observed within the first several days after cardiopulmonary bypass. They are refractory arrhythmias

that are relatively resistant to treatment.

The goal is rate control and restoring AV synchrony. These are often transient arrhythmias lasting 24-72 hours. Rapid

rates lead to early contraction of the atria against closed AV valves resulting in cannon A waves on hemodynamic

monitoring lines (CV, RA, and LA).

AET - When this occurs at an ectopic site within the atria, it

is called atrial ectopic tachycardia. AET occurs as a result of irritation of tissues during cardiac surgery, with placement

of intracardiac lines, application of sutures, or cutting tissue. Any reason for dilated atria, cardiomyopathy or

diseased AV valves, ventricular dysfunction can result in this rhythm disorder.

Rates are usually above 170-180 beats/min and beyond 200 beats/min. A block at the AV node can cause AV

dissociation, further contributing to hemodynamic instability in addition to the rapid atrial rate. The rhythm may be

variable, and may be interspersed with periods of sinus rhythm. The rate can ramp up or slow down over minutes

in contrast to the sudden onset and offset of SVT.

JET - When the ectopic focus initiates at or near the AV

node then the arrhythmia is junctional ectopic tachycardia. JET is usually caused by surgery around the AV node and

rates often range between 160 beats/min to as high as 280 beats/min.


Characteristics include inverted P- waves in lead II and an

R-P interval, which is short or absent. Primarily seen post re-warming from cardiopulmonary bypass and within 3

days of the surgery.

Ventricular

tachycardia (VT)

Three or more consecutive ventricular complexes are by

definition VT. Wide QRS complex morphology and a

different QRS morphology than the usual QRS waveform characterize VT. Morphology may be monomorphic

(uniform), polymorphic (multiform); or Torsades de Pointes where the points seem to twist around the isoelectric line.

Often associated with structural heart disease, particularly

late (years) after repair. Other common clinical situations in which one might see VT include dilated and hypertrophic

cardiomyopathy, metabolic alterations including severe

hypoxia, acidosis, hyper/hypokalemia, and drug toxicity such as cocaine, digoxin, and tri-cyclic antidepressants.

Other conditions include myocarditis and long Q-T

syndrome. Whenever VT occurs in a pediatric patient one must also consider ischemia or infarction. Patients may

present hemodynamically stable or in cardiac arrest.

Ventricular

Fibrillation (VF)

Completely uncoordinated depolarization of heart muscle

mass resulting in inability to maintain any global excitation contraction coupling. The myocardium fails to squeeze and

cardiac arrest occurs.

1st Degree Heart

Block

Slowed conduction through the AV node resulting in

prolonged duration of PR interval.

2nd Degree

Heart Block

(Mobitz I, Wenckebach)

Intermittent block of conduction of atrial beats to the

ventricle resulting in dropped QRS complexes. Progressive

lengthening of the PR interval until a QRS is dropped and the cycle starts again with a shorter PR interval that

progressively lengthens.

2nd Degree

Heart Block (Mobitz II;

Classical type)

Patterned dropping of QRS complex with a fixed ratio of

atrial depolarizations (P waves) to conducted beats with a consistent PR interval throughout. It is higher risk than

Mobitz I. Intermittent block of conduction of some beats to the ventricle without progressive prolongation of the PR

interval. Potentially may progress to complete heart block. Related to His bundle or bundle branch dysfunction.

3rd Degree Heart Block/ Complete

Heart Block

Complete block of AV node resulting in AV dissociation between atrial and ventricular events. No relationship

between the P waves and QRS complexes.


Specific Categories of Cardiac Arrhythmias

As noted earlier, there are many reasons for arrhythmias. Increased

end diastolic pressures resulting in atrial or ventricular stretch,

valvular dysfunction, tumors, multiple surgeries, scarring and

ischemia all play a significant role in arrhythmia generation. Cardiac

swelling, pro-arrhythmic drugs, acid/base and electrolyte imbalance

are also frequent etiologies of rhythm issues.

Neonatal Arrhythmias

Common arrhythmias in neonates with structurally normal hearts are

premature atrial contractions (PAC’s), atrial flutter, atrioventricular

reentry tachycardia (AVRT), permanent junctional reciprocating

tachycardia (PJRT), ventricular tachycardia, and heart block. Neonatal

heart block is associated with maternal autoimmune disease, i.e.,

systemic lupus.

Post-operative Arrhythmias

Early post-operative arrhythmias usually seen are sinus tachycardia,

sinus bradycardia, SVT, JET, complete AV block, and less frequently

ventricular tachycardia. Post-operative arrhythmias result from

manipulation or injury of the conduction system. The site of surgical

repair may increase the risk of certain types of arrhythmias observed.

Late post operative arrhythmias such as atrial flutter, and/or intra-

atrial reentrant tachycardia are seen months to years after surgery.

These arrhythmias are observed more often with Fontan, Mustard,

Senning and tetralogy of Fallot repairs. These tachyarrhythmias can

result in poor ventricular function and decreased quality of life.


Common late post operative arrhythmias include atrial tachycardia,

which may be seen in 50% of Fontan patients and tend to recur after

a period of time. Arrhythmias associated with specific congenital

cardiac malformations are highlighted in this section.4,28,17

Aortic Arch with VSD JET

Severe Aortic Stenosis/ Aortic Valve Surgery

Myocardial ischemia from severe left ventricular outflow obstruction, LV hypertrophy and strain

resulting in ventricular arrhythmias.

Conduction abnormalities and complete heart block

may be seen post surgical resection of sub-aortic obstructive tissue.

Although remote to the conduction system,

junctional tachycardia may occur.

Prone to VT.

Atrial Septal Defect

(ASD)

Sinus node dysfunction and transient atrial

arrhythmias, atrial flutter, atrial fibrillation, ventricular tachycardias.

Atrioventricular Septal Defect (AVSD)

Transient and permanent sinus node dysfunction, supraventricular arrhythmias; JET; AV block; and

VT. Grosse-Wortmann, et al., found that complete

AV block was more common post operative repair of complete AVSD.

Congenitally Corrected Transposition of the

Great Arteries (cc-TGA/ L-TGA)

Accessory pathways; AV Block: 2nd & 3rd degree; ventricular ectopy. Congenital AV block may

preexist due to intrinsic structural malformation.

Cor–Triatriatum

Sinus bradycardia, atrial tachyarrhythmias, AV conduction disturbances

D-Transposition of the Great Arteries (D-TGA)

Sinus bradycardia, sinoatrial block, junctional rhythm, JET, premature atrial contractions, Mobitz

1, VT. Prone to VT if repaired with atrial level switch procedures, Senning or Mustard.

Late complications of arrhythmias in the Jatene

arterial switch procedure are rare. Late

complications of atrial switch (Senning/Mustard) are that greater than 50% of patients have serious

arrhythmias.


Ebstein’s Anomaly of

the Tricuspid Valve

Common to have rhythm disturbances related to

atrial and ventricular dilatation and conduction disturbances: accessory pathways; WPW and VT,

SVT, atrial fibrillation, atrial flutter; 1st degree

heart block and rarely 3rd degree heart block. Congenital accessory pathways such as WPW may

preexist due to intrinsic structural malformation.

Heart Transplant

Intraatrial reentrant tachycardia, AET. Sinus

bradycardia, AV block in a small percentage of children. Supraventricular and ventricular

arrhythmias are relatively uncommon and may indicate rejection.

Pulmonary Atresia with Intact Ventricular

Septum

Rare rhythm disturbances observed. Ventricular arrhythmias if coronary sinusoids with ischemia.

Pulmonary Atresia with a VSD

Sometimes AV conduction abnormalities observed.

Single Ventricle -

Hypoplastic Left Heart Syndrome (HLHS)

Atrial arrhythmias.

Single Ventricle –

Bidirectional Cavopulmonary (Glenn)

Connection

Transient sinus node dysfunction.

Single Ventricle – Fontan

Sinus node dysfunction, atrial reentrant tachycardia: atrial flutter, atrial

fibrillation, intra-atrial tachycardia, VT. Early or late SVT, junctional rhythm, accelerated junctional

rhythm and VT.

Tetralogy of Fallot (TOF)

Sinus node dysfunction, supraventricular tachycardias – atrial flutter, accelerated junctional

rhythm, JET, AV blocks, VT. Right bundle branch

block (RBBB). Prone to VT due to the volume loading on the RV causing RV dilation, failure, and

increased right sided pressures. Predisposes patient to SCD.

Total Anomalous

Pulmonary Venous Return (TAPVR)

Atrial arrhythmias, JET, sinus bradycardia, AV

conduction disturbances.

Truncus Arteriosus AV conduction disturbances; ventricular

arrhythmias due to the right ventriculotomy.

Tricuspid Atresia

Supraventricular arrhythmias; atrial ectopy, flutter, fibrillation.

Ventricular Septal

Defect (VSD)

Junctional rhythm, accelerated junctional rhythm,

JET, VT (Grosse-Wortmann, 2010), AV conduction block.


Inherited Cardiomyopathies

Genetic predisposition to cardiac arrhythmias with an increased risk

of sudden cardiac death are reviewed in the section below.1,7

CARDIOMYOPATHIES PATHOPHYSIOLOGY

CARDIAC

ARRHYTHMIAS

Hypertrophic Cardiomyopathy (HCM)

Hypertrophic myocardium with asymmetric septal

hypertrophy.

VT, SCD.

Dilated Cardiomyopathy

(DCM)

Dilated poorly contractile

ventricles.

SVT, VT, SCD.

Arrhythmogenic Right

Ventricular (RV) Cardiomyopathy

(ARVC) or Dysplasia

A form of dilated

cardiomyopathy. Fibrofatty replacement of

the RV wall myocytes and patchy areas of fibrosis

with progressive RV

dysfunction and enlargement.

RV tachyarrhythmias

with variable response to beta-blockers and to

catheter ablation.

Channelopathies – Electrical Myopathies:8,36

CARDIOMYOPATHIES PATHOPHYSIOLOGY

CARDIAC

ARRHYTHMIAS

Long QT Syndrome (LQTS)

Identified by prolonged QT interval corrected for

heart rate (QTc). QT interval greater than 0.46

seconds, with upper

normal limit of 0.44 seconds.

Acquired or congenital;

can be secondary due to drugs, i.e., amiodarone,

procainamide, sotolol, tricyclic antidepressants

and/or electrolyte

imbalance (hypokalemia, hypomagnesemia).

High risk of bursts of VT such as runs of

Torsades de Pointes, progressing to VF and

SCD. May present with

syncope, seizures or SCD.


Catecholaminergic

Polymorphic Ventricular Tachycardia (CPVT)

Polymorphic ventricular

tachycardia. CPVT is initiated by stimulation of

the adrenergic receptors

from stress, emotion or exertion/physical

activity; found in normal hearts with normal

coronary arteries and normal ECG’s.

VT, ventricular

fibrillation, and SCD.

Brugada Syndrome (BrS)

Autosomal dominant genetic In 20% of cases,

mutations in the sodium channel are thought to

be causative.

History of ventricular arrhythmias –

ventricular fibrillation, syncope and SCD.

Marked by RBBB and

striking ST elevation in V1-V3. ECG

manifestation and arrhythmias most likely

during times of fever.

Inflammatory Disease:8

ACQUIRED PATHOPHYSIOLOGY CARDIAC

ARRHYTHMIAS

Myocarditis

Viral myocarditis is a cell mediated immunologic

reaction. Myocardium may have lymphocyte

infiltration, necrosis and

scarring. Myocarditis may lead to cardiomegaly and

congestive heart failure, hemodynamic

compromise, shock and death. Cells undergo

lymphocyte infiltration, necrosis and scarring.

Risk SCD from VT and AV block.

Clinical Evaluation Of The Pediatric Patient

The following components of clinical assessment are necessary when

a health provider approaches the pediatric patient to evaluate for a

cardiac arrhythmia.


Review of Family History

Family history should be reviewed, such as heart disease, death at

young age, sudden death, and seizures. Additionally, neonatal

history, child’s personal history of syncope, palpitations, racing heart

beat, seizures, exercise intolerance, family, feeding intolerance; and,

genetics, congenital cardiac malformations, diagnostic investigations,

previous surgical repair and post-surgical anatomy should be pursued

in the history taking. The provider should inquire about events

preceding rhythm disturbance.

Clinical Assessment

Irritability, feeding intolerance, respiratory distress, tachycardia or

bradycardia for age, irregular heart rate/pulse, decreased capillary

refill time, lethargy, congestive heart failure, decreased level of

consciousness, syncope, absent pulses/cardiac arrest should be

assessed. The clinician needs to be familiar with normal heart rate for

different ages. Infants generally have heart rates greater than 80

beats/min and less than 170 beats/min. Children usually have heart

rates greater than 60 beats/min and less than 140 beats/min. Heart

rates above these ranges are concerning and warrant further

assessment. Consider the appropriate heart rate response for

physiology.

Cardiac assessment includes auscultation of heart sounds for

murmurs, extra heart sounds, abnormal activity of the precordium

palpation for heaves and thrills, assessment of perfusion, pulses,

capillary refill time, blood pressure and assessment of vital signs.

Cutaneous saturation or pulse oxymetry is part of the


cardiorespiratory assessment and should be assessed. Identify

tolerance of the arrhythmia through assessment of clinical symptoms.

Profound hemodynamic effects may result from loss of AV synchrony

such as JET, AET or AV block, heart rate that is too slow or too fast,

VT or VF. This is worse in the context of preexisting myocardial

dysfunction or palliated physiology. A rapid heart rate results in

decreased diastolic and coronary artery filling times.18

Diagnostic Evaluation

This section outlines diagnostic tests that may be considered in order

to ensure an accurate diagnosis and impact of arrhythmia.12

Recording baseline pre-operative and post-operative rhythm strips

is optimal. Any Abnormal ECG’s should be compared to baseline.

Document the rhythm disturbance by a 12 or 15 lead pediatric

electrocardiogram. Pediatric 15 Lead ECG includes right-sided

leads V4R, V5R, V6R. This can be invaluable in accurate

identification of the type of arrhythmia.

The patient should be monitored

continuously. A Holter

electrocardiogram (usually 24 hour

ambulatory) may be of value in

identification of the arrhythmia

events.


Perform an atrial electrocardiogram using the atrial pacing wire in

post cardiac surgical patients, where P waves cannot be clearly

identified.

It can be helpful to capture electrical evidence of termination of

the tachycardia on a 15 lead ECG or rhythm strip.

Test blood levels of potassium, calcium and magnesium; and,

thyroid function tests, complete blood count, and toxicology

screen.

Electrolyte imbalances are often associated with rhythm

disturbances. If suspicious of myocarditis or with worsening

cardiac function check viral etiologies.

Cardiac enzymes, such as troponin levels and CPK-MB are markers

of myocardial injury.

A chest X-ray may demonstrate enlargement of the heart.

Echocardiogram (ECHO) provides a qualitative and quantitative

evaluation of cardiac function to rule out underlying structural

heart disease, thrombus formation and ventricular dysfunction. A

quantitative value of ejection fraction can be reported.

Use of pharmacological agents such as adenosine and

procainamide can assist with diagnosis of arrhythmias.


Exercise testing may be used to provoke and diagnose

arrhythmias and associated symptoms.

A catecholamine challenge or transoesophageal pacing can also be

used to provoke arrhythmias in a controlled environment.

Invasive electrophysiology studies with cardiac catheterization

help to identify ectopic foci and accessory pathways, which can be

mapped and ablated.

12-lead ECG

The ECG is conventionally recorded at

a speed of 25 mm/s and at a

calibration of 1 cm = 1 mV. A

standard 12-lead ECG includes three

standard (bipolar) limb leads – I, II,

and III – three augmented unipolar

limb leads – aVR, aVL, and aVF – and

six unipolar chest leads – V1–V6. Accurate positioning of the leads

(especially the chest leads) is important. V1 and V2 are in the fourth

intercostal space, V4 is in the fifth intercostal space in the

midclavicular line, V5 is in the anterior axillary line, and V6 in the

midaxillary line, both these last two horizontal to V4.

Routine evaluation of an ECG involves assessment of the heart rate,

heart rhythm, and QRS axis, then the P waves, QRS complexes, T

waves, and measurement of the PR, QRS, and QT intervals. Many

modern ECG machines automatically measure and display many of

these variables. The measurements are usually accurate and reliable


but a machine-derived interpretation of the ECG should be treated

with some caution, even if produced by a pediatric algorithm. The

machine often distinguishes between normality and abnormality fairly

accurately (assuming that the age of the patient is entered into the

algorithm) but analysis of the type of arrhythmia is often unreliable.

Whenever possible, a 12-lead ECG recording in sinus rhythm and

during symptoms should be obtained in children with suspected or

proven arrhythmia.18

Rhythm Strips

Rhythm strips are most useful in documenting changes in rhythm in

response to interventions such as adenosine administration, but they

should not be seen as an alternative to recording a 12-lead ECG.

Rhythm strips usually contain three leads but, on some machines,

there may be six, twelve, or only one. The leads selected vary. Leads

I, aVF, and V1 are a good combination but others may be preferred

after examining the 12-lead ECG.19

Holter Monitoring/Ambulatory ECG Recording

Holter monitoring, or ambulatory ECG recording, has become a

standard test in the investigation and follow-up of children with

suspected or proven arrhythmias. It is well tolerated and particularly

useful in children with fairly frequent symptoms, suggesting that

there is a reasonable chance of recording the ECG during symptoms.

It is also valuable in assessing response to treatment in children with

incessant tachycardias, congenital long QT syndrome, etc.20


ECG Event Recorders

Event recorders are carried by children or their parents but are not

necessarily worn all the time. They can be used in loop mode (where

they are worn constantly and a button is pressed during symptoms to

make a record of the ECG) or event mode (when the recorder is

applied and a recording made when symptoms occur).21

Exercise ECG

Treadmill or bicycle exercise ECG recording is sometimes helpful in

investigation of arrhythmias but is useful in providing reassurance for

children and their families in the presence of exercise-related

symptoms thought not to be due to arrhythmia. Exercise-induced

arrhythmias are unusual but are sometimes seen in AV re-entry. The

exercise test is very helpful in suspected catecholaminergic

polymorphic ventricular tachycardia.

Implanted Loop Recorder

In children with worrying syncope but no proven diagnosis, an

implanted loop recorder may be very helpful. The device has a 3-year

battery and is inserted subcutaneously in the left axilla or on the left

anterior chest wall. It works in loop mode and can be programmed to

store recordings of arrhythmias, which have rates below or above

preset limits. Children or their parents or teachers using an external

activating device can also trigger a recording. The yield from this type

of recorder depends on the selectivity of the physician but it can be

most useful in children with infrequent major syncope.


Transesophageal Electrophysiology Study

The transesophageal electrophysiology study is not widely employed

in pediatric practice because of its limited physical acceptability. It

involves (per oral or per nasal) positioning of a pacing wire in the

esophagus behind the left atrium. Pacing in this position can usually

capture the atria but requires a higher output stimulator than a

normal pacing box. Transesophageal pacing can be used in neonates

to overdrive atrial flutter or atrioventricular tachycardia, but its use in

older children is limited by discomfort and it often requires general

anesthesia. It has been advocated for investigation of children with

symptoms of palpitation, elucidation of arrhythmia mechanism if

tachycardia is documented on ambulatory ECG monitoring, and “risk

assessment” in asymptomatic children with a Wolff–Parkinson–White

pattern on the ECG. It is perhaps more widely used in some European

countries than in the U.K., the U.S., or elsewhere.22

Tilt Test

A head-up tilt test is sometimes used for investigation of children

older than 6 years with recurrent syncope or presyncope. Protocols

vary but all involve the child lying horizontal for 15–20 min before

being passively tilted to an angle of 60–80 for up to 45 min or until

the development of symptoms. The ECG and blood pressure are

recorded continuously. Fainting or a feeling of faintness is usually

accompanied by bradycardia and hypotension, and the child is rapidly

returned to the horizontal. Less commonly there is a hypotensive

response without bradycardia. The most unusual response is

cardioinhibitory with bradycardia or asystole before syncope.8


A “positive” test response with passive tilting is observed in 40–50%

of children with a good history suggesting neurally mediated syncope.

The sensitivity is increased by infusion of isoprenaline (isoproterenol)

but specificity is reduced. False positives and false negatives limit the

usefulness of the test, but it can be helpful in management of

syncope.2

Common Treatments

The need for treatment of arrhythmias depends on the symptoms and

the seriousness of the arrhythmia. Treatment is directed at causes. If

necessary, direct antiarrhythmic therapy, including antiarrhythmic

drugs, cardioversion-defibrillation, implantable cardioverter-

defibrillators (ICDs), pacemakers (and a special form of

pacing, cardiac resynchronization therapy), or a combination, is used.

Drugs for Arrhythmias Antiarrhythmic drugs comprise many different drug classes and have

several different mechanisms of action. Furthermore, some classes

and even some specific drugs within a class are effective with only

certain types of arrhythmias. Therefore, attempts have been made to

classify the different antiarrhythmic drugs so by mechanism.

Although different classification schemes have been proposed, the

first scheme (Vaughan-Williams) is still the one that most physicians

use when speaking of antiarrhythmic drugs.

The following list shows the Vaughan-Williams classification and the

basic mechanism of action associated with each class. Note that Class

I drugs are further broken down into subclasses because of subtle,


yet important differences in their effects on action potentials. Most

antiarrhythmic drugs are grouped into 4 main classes (Vaughan

Williams classification) based on their dominant cellular

electrophysiologic effect.38

Class I Drugs

Class I drugs are subdivided into subclasses a, b, and c. Class I drugs

are sodium channel blockers (membrane-stabilizing drugs) that block

fast sodium channels, slowing conduction in fast-channel tissues

(working atrial and ventricular myocytes, His-Purkinje system).

Class II Drugs

Class II drugs are beta-blockers, which affect predominantly slow-

channel tissues (sinoatrial [SA] and atrioventricular [AV] nodes),

where they decrease rate of automaticity, slow conduction velocity,

and prolong refractoriness.

Class III Drugs

Class III drugs are primarily potassium channel blockers, which

prolong action potential duration and refractoriness in slow- and fast-

channel tissues.

Class IV Drugs

Class IV drugs are the nondihydropyridine calcium channel blockers,

which depress calcium-dependent action potentials in slow-channel

tissues and thus decrease the rate of automaticity, slow conduction

velocity, and prolong refractoriness.


Digoxin and adenosine are not included in the Vaughan Williams

classification. Digoxin shortens atrial and ventricular refractory

periods and is vagotonic, thereby prolonging AV nodal conduction and

AV nodal refractory periods. Adenosine slows or blocks AV nodal

conduction and can terminate tachyarrhythmias that rely upon AV

nodal conduction for their perpetuation.

The Vaughan-Williams classification has severe limitations. When

initially conceived, there were relatively few antiarrhythmic drugs and

our understanding of their mechanisms was rudimentary at best. Now

with many more antiarrhythmic drugs, and with a much greater yet

still incomplete understanding of drug mechanisms, this classification

system breaks down especially for the Class I and III drugs.

Many of these drugs have mechanisms of action that are shared with

drugs found the other classes. For example, amiodarone, a Class III

antiarrhythmic, also has sodium and calcium-channel blocking

actions. Many of the Class I compounds also affect potassium

channels. Some of these drugs, it could be argued, could fit in just as

well as a different class than the one that they may be assigned. For

this reason, different sources of information may classify some

antiarrhythmic drugs differently than other sources.78,79

The drugs that make up the different classes differ in their efficacy

(and sometimes safety) for different types of arrhythmias.

The following table provides an overview of drug classes and

associated arrhythmias. Antiarrhythmic agents that are not included

in the Vaughan-Williams scheme are also shown in the table.24


Condition Drug Comments

Sinus tachycardia Class II, IV Other underlying causes may need

treatment

Atrial fibrillation/flutter

Class IA, IC, II,

III, IV

digitalis

Ventricular rate control is

important goal; anticoagulation is

required

Paroxysmal

supraventricular

tachycardia

Class IA, IC, II,

III, IV

adenosine

AV block Atropine Acute reversal

Ventricular tachycardia Class I, II, III

Premature ventricular

complexes

Class II, IV

magnesium

sulfate

PVCs are often benign and do not

require treatment

Digitalis toxicity

Class IB

magnesium

sulfate

Class I Antiarrhythmic Drugs

Sodium channel blockers (membrane-stabilizing drugs) block fast

sodium channels, slowing conduction in fast-channel tissues (working

atrial and ventricular myocytes, His-Purkinje system). In the ECG,

this effect may be reflected as widening of the P wave, widening of

the QRS complex, prolongation of the PR interval, or a combination.

Class I drugs are subdivided based on the kinetics of the sodium

channel effects:


Class Ib drugs have fast kinetics.

Class Ic drugs have slow kinetics.

Class Ia drugs have intermediate kinetics.

The kinetics of sodium channel blockade determine the heart rates at

which their electrophysiologic effects become manifest. Because class

Ib drugs have fast kinetics, they express their electrophysiologic

effects only at fast heart rates. Thus, an ECG obtained during normal

rhythm at normal rates usually shows no evidence of fast-channel

tissue conduction slowing. Class Ib drugs are not very potent

antiarrhythmics and have minimal effects on atrial tissue. Because

class Ic drugs have slow kinetics, they express their

electrophysiologic effects at all heart rates. Thus, an ECG obtained

during normal rhythm at normal heart rates usually shows fast-

channel tissue conduction slowing.

Class Ic drugs are more potent antiarrhythmics. Because class Ia

drugs have intermediate kinetics, their fast-channel tissue conduction

slowing effects may or may not be evident on an ECG obtained during

normal rhythm at normal rates. Class Ia drugs also block repolarizing

potassium channels, prolonging the refractory periods of fast-channel

tissues. On the ECG, this effect is reflected as QT-interval

prolongation even at normal rates. Class Ib drugs and class Ic drugs

do not block potassium channels directly.62,79 The kinetics of sodium

channel blockade determine the heart rates at which their

electrophysiologic effects become manifest.

The primary indications are supraventricular tachycardia (SVT) for

class Ia and Ic drugs and ventricular tachycardia (VTs) for all class I


drugs. Adverse effects of class I drugs include proarrhythmia, a drug-

related arrhythmia worse than the arrhythmia being treated, which is

the most worrisome adverse effect.

All class I drugs may worsen VTs. Class I drugs also tend to depress

ventricular contractility. Because these adverse effects are more

likely to occur in patients with a structural heart disorder, class I

drugs are not generally recommended for such patients. Thus, these

drugs are usually used only in patients who do not have a structural

heart disorder or in patients who have a structural heart disorder but

who have no other therapeutic alternatives. There are other adverse

effects of class I drugs that are specific to the subclass or individual

drug.14,17,78,80

Class Ia Antiarrhythmic Drugs

Class Ia drugs have kinetics that are intermediate between the fast

kinetics of class Ib and the slow kinetics of class Ic. Their fast-

channel tissue conduction slowing effects may or may not be evident

on an ECG obtained during normal rhythm at normal rates. Class Ia

drugs block repolarizing potassium channels, prolonging the

refractory periods of fast-channel tissues. On the ECG, this effect is

reflected as QT-interval prolongation even at normal rates.61

Class Ia drugs are used for suppression of atrial premature beats

(APB), ventricular premature beats (VPB), supraventricular and

ventricular tachycardias, atrial fibrillation (AF), atrial flutter, and

ventricular fibrillation. The primary indications are supraventricular

and ventricular tachycardias. Class Ia drugs may cause torsades de

pointes ventricular tachycardia. Class Ia drugs may organize and slow


atrial tachyarrhythmias enough to permit 1:1 AV conduction with

marked acceleration of the ventricular response rate.62

Class Ib Antiarrhythmic Drugs

Class Ib drugs have fast kinetics; they express their

electrophysiologic effects only at fast heart rates. Thus, an ECG

obtained during normal rhythm at normal rates usually shows no

evidence of fast-channel tissue conduction slowing. Class Ib drugs are

not very potent antiarrhythmics and have minimal effects on atrial

tissue. Class Ib drugs do not block potassium channels directly. Class

Ib drugs are used for the suppression of ventricular arrhythmias

(ventricular premature beats, ventricular tachycardia, ventricular

fibrillation).38

Class Ic Antiarrhythmic Drugs

Class Ic drugs have slow kinetics; they express their

electrophysiologic effects at all heart rates. Thus, an ECG obtained

during normal rhythm at normal heart rates usually shows fast-

channel tissue conduction slowing. Class Ic drugs are more potent

antiarrhythmics than either class Ia or class Ib drugs. Class Ic drugs

do not block potassium channels directly.

Class Ic drugs may organize and slow atrial tachyarrhythmias enough

to permit 1:1 AV conduction with marked acceleration of the

ventricular response rate. Class Ic drugs are used for suppression of

atrial and ventricular premature beats, supraventricular and

ventricular tachycardias, atrial fibrillation, atrial flutter, and

ventricular fibrillation.


Class II Antiarrhythmic Drugs

Class II antiarrhythmic drugs are beta-blockers, which affect

predominantly slow-channel tissues (SA and AV nodes), where they

decrease rate of automaticity, slow conduction velocity, and prolong

refractoriness. Thus, heart rate is slowed, the PR interval is

lengthened, and the AV node transmits rapid atrial depolarizations at

a lower frequency.68

Class II drugs are used primarily to treat SVTs, including sinus

tachycardia, AV nodal reentry, AF, and atrial flutter. These drugs are

also used to treat VTs to raise the threshold for ventricular fibrillation

(VF) and reduce the ventricular proarrhythmic effects of beta-

adrenoceptor stimulation.80 Beta-blockers are generally well

tolerated; adverse effects include lassitude, sleep disturbance, and GI

upset. These drugs are contraindicated in patients with asthma.

Class III Antiarrhythmic Drugs

Class III drugs are membrane stabilizing drugs, primarily potassium

channel blockers, which prolong action potential duration and

refractoriness in slow- and fast-channel tissues. Thus, the capacity of

all cardiac tissues to transmit impulses at high frequencies is

reduced, but conduction velocity is not significantly affected. Because

the action potential is prolonged, rate of automaticity is reduced. The

predominant effect on the ECG is QT-interval prolongation. These

drugs are used to treat SVTs and VTs. Class III drugs have a risk of

ventricular proarrhythmia, particularly torsades de pointes VT and are

not used in patients with torsades de pointes VT.61,82


Class IV Antiarrhythmic Drugs

Class IV drugs are the nondihydropyridine calcium channel blockers,

which depress calcium-dependent action potentials in slow-channel

tissues and thus decrease the rate of automaticity, slow conduction

velocity, and prolong refractoriness. Heart rate is slowed, the PR

interval is lengthened, and the AV node transmits rapid atrial

depolarizations at a lower frequency. These drugs are used primarily

to treat SVTs. They may also be used to slow rapid atrial fibrillation

or atrial flutter. One form of VT (left septal or Belhassen VT) can be

treated with verapamil.30

The following table provides specific information about each drug

used to treat arrhythmias in children.17,24,30,54,79,80

Amiodarone

Life-threatening arrhythmias (tablet):

Amiodarone is intended for use only in patients with indicated life-threatening

arrhythmias because its use is accompanied by substantial toxicity.

Potentially fatal toxicities (tablet):

Amiodarone has several potentially fatal toxicities, the most important of

which is pulmonary toxicity (hypersensitivity pneumonitis or

interstitial/alveolar pneumonitis) that has resulted in clinically manifest

disease at rates as high as 10% to 17% in some series of patients with

ventricular arrhythmias given doses of approximately 400 mg/day, and as

abnormal diffusion capacity without symptoms in a much higher percentage

of patients. Pulmonary toxicity has been fatal approximately 10% of the time.

Liver injury is common with amiodarone, but is usually mild and evidenced

only by abnormal liver enzymes. However, overt liver disease can occur and

has been fatal in a few cases.


Like other antiarrhythmics, amiodarone can exacerbate the arrhythmia (e.g.,

by making the arrhythmia less well tolerated or more difficult to reverse).

This has occurred in 2% to 5% of patients in various series, and significant

heart block or sinus bradycardia has been seen in 2% to 5%. In most cases,

all of these events should be manageable in the proper clinical setting.

Although the frequency of such proarrhythmic events does not appear greater

with amiodarone than with many other agents used in this population, the

effects are prolonged when they occur.

High-risk patients (tablet):

Even in patients at high risk of arrhythmic death in whom the toxicity of

amiodarone is an acceptable risk, amiodarone poses major management

problems that could be life-threatening in a population at risk of sudden

death; therefore, make every effort to utilize alternative agents first.

The difficulty of using amiodarone effectively and safely poses a significant

risk to patients. Patients with the indicated arrhythmias must be hospitalized

while the loading dose of amiodarone is given, and a response generally

requires at least 1 week, usually 2 weeks or more. Because absorption and

elimination are variable, maintenance dose selection is difficult, and it is not

unusual to require dosage decrease or discontinuation of treatment. In a

retrospective survey of 192 patients with ventricular tachyarrhythmias, 84

patients required dose reduction and 18 required at least temporary

discontinuation because of adverse reactions, and several series have

reported 15% to 20% overall frequencies of discontinuation because of

adverse reactions.

The time at which a previously controlled life-threatening arrhythmia will

recur after discontinuation or dose adjustment is unpredictable, ranging from

weeks to months. The patient is obviously at great risk during this time and

may need prolonged hospitalization. Attempts to substitute other

antiarrhythmic agents when amiodarone must be stopped will be made

difficult by the gradually, but unpredictably, changing amiodarone body

burden. A similar problem exists when amiodarone is not effective; it still

poses the risk of an interaction with whatever subsequent treatment is tried.


Brand Names:

Cordarone

Nexterone

Pacerone

Pharmacologic Category

Antiarrhythmic Agent, Class III

Dosage:

Pulseless VT or VF (PALS dosing): Infants, Children, and Adolescents -

IV, I.O.: 5 mg/kg (maximum: 300 mg per dose) rapid bolus; may

repeat twice up to a maximum total dose of 15 mg/kg during acute

treatment (PALS 2010).

Perfusing tachycardias (PALS dosing): Infants, Children, and

Adolescents - IV, I.O.: Loading dose: 5 mg/kg (maximum: 300 mg per

dose) over 20 to 60 minutes; may repeat twice up to maximum total

dose of 15 mg/kg during acute treatment (PALS 2010).

Nadolol

Exacerbation of ischemic heart disease following abrupt withdrawal:

Hypersensitivity to catecholamines has been observed in patients withdrawn

from beta-blocker therapy; exacerbation of angina and, in some cases,

myocardial infarction have occurred after abrupt discontinuation of such

therapy. When discontinuing nadolol administered long term, particularly in

patients with ischemic heart disease, gradually reduce the dosage over a

period of 1 to 2 weeks and carefully monitor the patient.

If angina markedly worsens or acute coronary insufficiency develops,

reinstitute nadolol administration promptly, at least temporarily, and take

other measures appropriate for the management of unstable angina. Warn

patients against interruption or discontinuation of therapy without the health

care provider's advice. Because coronary artery disease is common and may

be unrecognized, it may be prudent not to discontinue nadolol therapy

abruptly, even in patients treated only for hypertension.


Brand Names:

Corgard


Antianginal Agent

Antihypertensive

Beta-Blocker, Nonselective

Sotalol

Proarrhythmic effects:

To minimize the risk of induced arrhythmia, patients initiated or reinitiated on

sotalol or sotalol AF and patients who are converted from IV to oral

administration should be placed for a minimum of 3 days (on their

maintenance dose) in a facility that can provide cardiac resuscitation,

continuous electrocardiographic (ECG) monitoring, and calculations of

creatinine clearance (CrCl).

Sotalol injection and oral solution (Sotylize):

Sotalol can cause life threatening ventricular tachycardia associated with QT

interval prolongation. Do not initiate sotalol therapy if the baseline QTc is

longer than 450 msec. If the QT interval prolongs to 500 msec or greater, the

dose must be reduced, the interval between doses prolonged, the duration of

the infusion prolonged (sotalol injection), or the drug discontinued.

Adjust the dosing interval based on CrCl.

Renal impairment:

Calculate CrCl prior to dosing.

Product interchange:

Do not substitute sotalol for sotalol AF because of significant differences in

labeling (i.e., patient package insert, dosing administration, safety

information).


Brand Names:

Betapace

Betapace AF

Sorine

Sotylize


Antiarrhythmic Agent, Class II



Dosing:

Baseline QTc interval and creatinine clearance must be determined prior to

initiation. If CrCl ≤60 mL/minute, dosing interval adjustment is

necessary. Sotalol should be initiated and doses increased in a hospital for at

least 3 days with facilities for cardiac rhythm monitoring and assessment.

Proarrhythmic events can occur after initiation of therapy and with each

upward dosage adjustment. (Note: Dosing per manufacturer, based on

pediatric pharmacokinetic data; wait at least 36 hours between dosage

adjustments to allow monitoring of QTc intervals).

Atrial fibrillation/flutter (symptomatic): Oral: Betapace AF, Sotylize -

Infants and Children ≤2 years: Dosage should be adjusted (decreased) by

plotting of the child's age on a logarithmic scale; see graph or refer to

manufacturer's package labeling.

Children >2 years and Adolescents: Initial: 90 mg/m2/day in 3 divided doses;

may be incrementally increased to a maximum of 180 mg/m2/day

Ventricular arrhythmias: Oral: Betapace, Sorine, Sotylize -

Infants and Children ≤2 years: Dosage should be adjusted (decreased) by

plotting of the child's age on a logarithmic scale; see graph or refer to

manufacturer's package labeling.

Children >2 years and Adolescents: Initial: 90 mg/m2/day in 3 divided doses;

may be incrementally increased to a maximum of 180 mg/m2/day.


Adenosine

Brand Names:

Adenocard

Adenoscan


Antiarrhythmic Agent, Miscellaneous

Diagnostic Agent

Dosing:

Rapid IV push (over 1 to 2 seconds) via peripheral line, followed by a normal

saline flush.

Paroxysmal supraventricular tachycardia (Adenocard): Infants and

Children - IV:

Manufacturer's labeling:

Children <50 kg: Initial: 0.05 to 0.1 mg/kg (maximum initial dose: 6 mg). If

conversion of PSVT does not occur within 1 to 2 minutes, may increase dose

by 0.05 to 0.1 mg/kg. May repeat until sinus rhythm is established or to a

maximum single dose of 0.3 mg/kg or 12 mg. Follow each dose with normal

saline flush.

Children ≥50 kg: Refer to adult dosing.

Pediatric advanced life support: Treatment of SVT: IV, I.O.: Initial: 0.1 mg/kg

(maximum initial dose: 6 mg); if not effective within 1 to 2 minutes,

administer 0.2 mg/kg (maximum single dose: 12 mg). Follow each dose with

≥5 mL normal saline flush.

Diltiazem

Brand Names:

Cardizem

Cardizem CD

Cardizem LA


Cartia XT

Dilacor XR [DSC]

Dilt-CD [DSC]

Dilt-XR

Diltiazem CD

Diltiazem HCl CD [DSC]

Diltzac [DSC]

Matzim LA

Taztia XT

Tiazac


Antianginal Agent

Antiarrhythmic Agent, Class IV

Antihypertensive

Calcium Channel Blocker

Calcium Channel Blocker, Nondihydropyridine

Dosing:

Children: Minimal information available; some centers use the following:

Hypertension (off-label use): Oral: Initial: 1.5-2 mg/kg/day in 3 divided

doses (maximum: 6 mg/kg/day, up to 360 mg daily). Adolescents -

Angina: Oral:

Capsule, extended release:

Dilacor XR, Dilt-XR: Initial: 120 mg once daily; titrate over 7 to 14 days;

usual dose range - 120 to 320 mg daily: maximum: 480 mg daily.

Cardizem CD, Cartia XT: Initial: 120 to 180 mg once daily; titrate over 7 to

14 days; usual dose range: 120 to 320 mg daily; maximum: 480 mg daily.

Tiazac, Taztia XT: Initial: 120 to 180 mg once daily; titrate over 7 to 14 days;

usual dose range - 120 to 320 mg daily; maximum: 540 mg daily.

Tablet, extended release (Cardizem LA, Matzim LA, Tiazac XC [Canadian

product]): 180 mg once daily; may increase at 7- to 14-day intervals; usual

dose range: 120 to 320 mg/day; maximum: 360 mg daily.


Tablet, immediate release (Cardizem): Usual starting dose: 30 mg 4 times

daily; titrate dose gradually at 1- to 2-day intervals; usual dose range: 120 to

320 mg daily in 4 divided doses.

Hypertension: Oral:

Capsule, extended release (once-daily dosing):

Cardizem CD, Cartia XT: Initial: 180 to 240 mg once daily; dose adjustment

may be made after 14 days; usual dose range: 240 to 360 mg daily;

maximum: 480 mg daily

Dilacor XR, Dilt-XR: Initial: 180 to 240 mg once daily; dose adjustment may

be made after 14 days; usual dose range: 240 to 360 mg daily; maximum:

540 mg daily.

Tiazac, Taztia XT: Initial: 120 to 240 mg once daily; dose adjustment may be

made after 14 days; usual dose range: 240 to 360 mg daily; maximum: 540

mg daily.

Capsule, extended release (twice-daily dosing): Initial: 60 to 120 mg twice

daily; dose adjustment may be made after 14 days; usual range: 240 to 360

mg daily.

Note: Diltiazem is available as a generic intended for either once- or twice-

daily dosing, depending on the formulation; verify appropriate extended

release capsule formulation is administered.

Tablet, extended release (Cardizem LA, Matzim LA, Tiazac XC [Canadian

product]): Initial: 180 to 240 mg once daily; dose adjustment may be made

after 14 days; usual dose range: 240-360 mg daily; maximum: 540 mg daily.

Atrial fibrillation, atrial flutter, PSVT:

Initial IV bolus dose: 0.25 mg/kg actual body weight over 2 minutes (average

adult dose: 20 mg); ACLS guideline recommends 15 to 20 mg.

Repeat bolus dose (may be administered after 15 minutes if the response is

inadequate): 0.35 mg/kg actual body weight over 2 minutes (average adult

dose: 25 mg); ACLS guideline recommends 20 to 25 mg.


Continuous infusion (infusions >24 hours or infusion rates >15 mg/hour are

not recommended): Initial infusion rate of 10 mg/hour; rate may be

increased in 5 mg/hour increments up to 15 mg/hour as needed; some

patients may respond to an initial rate of 5 mg/hour.

If diltiazem injection is administered by continuous infusion for >24 hours,

the possibility of decreased diltiazem clearance, prolonged elimination half-

life, and increased diltiazem and/or diltiazem metabolite plasma

concentrations should be considered.

Atrial fibrillation (rate control) (off-label use): Oral: Extended release

(capsule or tablet): Usual maintenance dose: 120 to 360 mg once daily.

Conversion from IV diltiazem to oral diltiazem:

Oral dose (mg daily) is approximately equal to [rate (mg/hour) x 3 + 3] x 10.

3 mg/hour = 120 mg daily




Atenolol

Advise patients with coronary artery disease who are being treated with

atenolol against abrupt discontinuation of therapy. Severe exacerbation of

angina and the occurrence of myocardial infarction (MI) and ventricular

arrhythmias have been reported in patients with angina following the abrupt

discontinuation of therapy with beta-blockers. The last 2 complications may

occur with or without preceding exacerbation of the angina pectoris. As with

other beta-blockers, when discontinuation of atenolol is planned, observe the

patient carefully and advise the patient to limit physical activity to a

minimum. If the angina worsens or acute coronary insufficiency develops, it is

recommended that atenolol be promptly reinstituted, at least temporarily.

Because coronary artery disease is common and may be unrecognized, it may

be prudent not to discontinue atenolol therapy abruptly, even in patients

treated only for hypertension.


Brand Names:

Tenormin


Antianginal Agent

Antihypertensive

Beta-Blocker, Beta-1 Selective

Dosing:

Hypertension: Oral: Children: 0.5 to 1 mg/kg/dose given daily; range of 0.5

to 1.5 mg/kg/day; maximum dose: 2 mg/kg/day up to 100 mg/day.

Esmolol

Brand Names:

Brevibloc

Brevibloc in NaCl



Antihypertensive


Dosing:

Intraoperative and postoperative tachycardia and/or hypertension:

Immediate control: Initial IV bolus: 1 mg/kg over 30 seconds, followed by a

150 mcg/kg/minute infusion, if necessary. Adjust infusion rate as needed to

maintain desired heart rate and/or blood pressure (up to 300 mcg/kg/minute)

Gradual control: Initial bolus: 0.5 mg/kg over 1 minute, followed by a 50

mcg/kg/minute infusion for 4 minutes. Infusion may be continued at 50

mcg/kg/minute or, if the response is inadequate, titrated upward in 50

mcg/kg/minute increments (increased no more frequently than every 4

minutes) to a maximum of 300 mcg/kg/minute; may administer an optional

loading dose equal to the initial bolus (0.5 mg/kg over 1 minute) prior to each

increase in infusion rate.


For control of tachycardia, doses >200 mcg/kg/minute provide minimal

additional effect. For control of postoperative hypertension, as many as one-

third of patients may require higher doses (250-300 mcg/kg/minute) to

control blood pressure; the safety of doses >300 mcg/kg/minute has not

been studied.

Supraventricular tachycardia (SVT) or noncompensatory sinus

tachycardia: IV Loading dose (optional): 0.5 mg/kg over 1 minute; follow

with a 50 mcg/kg/minute infusion for 4 minutes; response to this initial

infusion rate may be a rough indication of the responsiveness of the

ventricular rate.

Infusion may be continued at 50 mcg/kg/minute or, if the response is

inadequate, titrated upward in 50 mcg/kg/minute increments (increased no

more frequently than every 4 minutes) to a maximum of 200 mcg/kg/minute.

To achieve more rapid response, following the initial loading dose and 50

mcg/kg/minute infusion, rebolus with a second 0.5 mg/kg loading dose over 1

minute, and increase the maintenance infusion to 100 mcg/kg/minute for 4

minutes. If necessary, a third (and final) 0.5 mg/kg loading dose may be

administered, prior to increasing to an infusion rate of 150 mcg/kg/minute.

After 4 minutes of the 150 mcg/kg/minute infusion, the infusion rate may be

increased to a maximum rate of 200 mcg/kg/minute (without a bolus dose).

(Note: If a loading dose is not administered, a continuous infusion at a fixed

dose reaches steady-state in ~30 minutes. In general, the usual effective

dose is 50-200 mcg/kg/minute; doses as low as 25 mcg/kg/minute may be

adequate. Maintenance infusions may be continued for up to 48 hours).

Acute coronary syndromes (when relative contraindications to beta-

blockade exist; off-label use): IV: 0.5 mg/kg over 1 minute; follow with a

50 mcg/kg/minute infusion; if tolerated and response inadequate, may titrate

upward in 50 mcg/kg/minute increments every 5-15 minutes to a maximum

of 300 mcg/kg/minute (Mitchell, 2002); an additional bolus (0.5 mg/kg over 1

minute) may be administered prior to each increase in infusion rate.


Electroconvulsive therapy (off-label use): 1 mg/kg administered IV, 1

minute prior to induction of anesthesia.

Intubation (off-label use): 1-2 mg/kg IV given 1.5-3 minutes prior to

intubation.

Thyrotoxicosis or thyroid storm (off-label use): 50-100 mcg/kg/minute

IV.

Digoxin

Brand Names:

Digitek

Digox

Lanoxin

Lanoxin Pediatric


Antiarrhythmic Agent, Miscellaneous

Cardiac Glycoside

Dosing:

Preterm infant

• Total digitalizing dose:

– Oral: 20-30 mcg/kg

– IV or IM: 15-25 mcg/kg

• Daily maintenance dose:

– Oral: 5-7.5 mcg/kg


Full-term infant:






– Oral: 6-10 mcg/kg; and, IV or IM: 5-8 mcg/kg

1 month to 2 years:






– IV or IM: 7.5-12 mcg/kg

2-5 years:





– Oral: 7.5-10 mcg/kg


5-10 years:







>10 years:





– Oral: 2.5-5 mcg/kg


Heart failure: A lower serum digoxin concentration may be adequate to treat

heart failure (compared to cardiac arrhythmias); consider doses at the lower

end of the recommended range for treatment of heart failure; a digitalizing

dose (loading dose) may not be necessary when treating heart failure.


Based on lean body weight and normal renal function for age. Decrease dose

in patients with decreased renal function; digitalizing dose often not

recommended in infants and children.

Do not give full total digitalizing dose (TDD) at once. Give one-half of the total

digitalizing dose (TDD) in the initial dose, then give one-quarter of the TDD in

each of two subsequent doses at 6- to 8-hour intervals. Obtain ECG 6 hours

after each dose to assess potential toxicity.

Divided every 12 hours in infants and children <10 years of age. Give once

daily to children >10 years of age and adults. IM not preferred due to severe

injection site pain. If IM route is necessary, administer as deep injection

followed by massage of injection site.

Metoprolol

ALERT: US Boxed Warning

Ischemic heart disease

Following abrupt cessation of therapy with certain beta-blocking agents,

exacerbations of angina pectoris and, in some cases, myocardial infarction

(MI) have occurred. When discontinuing chronically administered metoprolol,

particularly in patients with ischemic heart disease, gradually reduce the

dosage over a period of 1 to 2 weeks and carefully monitor the patient. If

angina markedly worsens or acute coronary insufficiency develops, reinstate

metoprolol administration promptly, at least temporarily, and take other

measures appropriate for the management of unstable angina. Warn patients

against interruption or discontinuation of therapy without their health care

provider's advice. Because coronary artery disease is common and may be

unrecognized, it may be prudent not to discontinue metoprolol therapy

abruptly, even in patients treated only for hypertension.

Brand Names:

Lopressor

Toprol XL



Antianginal Agent

Antihypertensive


Dosing:

Hypertension: Oral:

Immediate release tablet (metoprolol tartrate): Children: 1 to 17 years:

Initial: 1 to 2 mg/kg/day; maximum 6 mg/kg/day (≤200 mg daily);

administer in 2 divided doses.

Extended release tablet (metoprolol succinate): Children ≥6 years: Initial: 1

mg/kg once daily (maximum initial dose: 50 mg daily). Adjust dose based on

patient response (maximum: 2 mg/kg/day or 200 mg daily).

Use: Labeled Indications

Immediate-release tablets (metoprolol tartrate): Treatment of angina

pectoris, hypertension, or hemodynamically-stable acute myocardial

infarction.

Extended-release tablets (metoprolol succinate): Treatment of angina

pectoris or hypertension; to reduce mortality/hospitalization in patients with

heart failure (HF) (stable NYHA Class II or III) already receiving ACE

inhibitors, diuretics, and/or digoxin.

Injectable (metoprolol tartrate): Treatment of hemodynamically-stable

acute myocardial infarction when used in conjunction with metoprolol oral

maintenance therapy.

Acute coronary syndromes (i.e., myocardial infarction, unstable angina):

According to the ACCF/AHA 2013 guidelines for the management of ST-

elevation myocardial infarction (STEMI) and the guidelines for the

management of unstable angina/non-STEMI, oral beta-blockers should be

initiated within the first 24 hours unless the patient has signs of heart failure,

evidence of a low-output state, an increased risk for cardiogenic shock, or

other contraindications.


Intravenous use should be reserved for those patients who have refractory

hypertension or ongoing ischemia.

Heart failure: The ACCF/AHA 2013 heart failure guidelines recommend the

use of 1 of 3 beta blockers (i.e., bisoprolol, carvedilol, or extended-release

metoprolol succinate) for all patients with recent or remote history of MI or

ACS and reduced ejection fraction (rEF) to reduce mortality, for all patients

with rEF to prevent symptomatic HF (even if no history of MI), and for all

patients with current or prior symptoms of HF with reduced ejection fraction

(HFrEF), unless contraindicated, to reduce morbidity and mortality.

Chronic kidney disease (CKD) and hypertension: Regardless of race or

diabetes status, the use of an ACE inhibitor (ACEI) or angiotensin receptor

blocker (ARB) as initial therapy is recommended to improve kidney outcomes.

In the general nonblack population (without CKD) including those with

diabetes, initial antihypertensive treatment should consist of a thiazide-type

diuretic, calcium channel blocker, ACEI, or ARB. In the general black

population (without CKD) including those with diabetes, initial

antihypertensive treatment should consist of a thiazide-type diuretic or a

calcium channel blocker instead of an ACEI or ARB.

Coronary artery disease (CAD) and hypertension: The American Heart

Association, American College of Cardiology and American Society of

Hypertension (AHA/ACC/ASH) 2015 scientific statement for the treatment of

hypertension in patients with coronary artery disease (CAD) recommends the

use of a beta blocker as part of a regimen in patients with hypertension and

chronic stable angina with a history of prior MI.

A BP target of <140/90 mm Hg is reasonable for the secondary prevention of

cardiovascular events.

A lower target BP (<130/80 mm Hg) may be appropriate in some individuals

with CAD, previous MI, stroke or transient ischemic attack, or CAD risk

equivalents.


Acebutolol

Brand Names:

Sectral



Antihypertensive

Beta-Blocker With Intrinsic Sympathomimetic Activity


Dosing:

Angina, ventricular arrhythmia: Oral: 400 mg/day in 2 divided doses;

maintenance: 600 to 1200 mg/day in divided doses; maximum: 1200 mg/day

Hypertension: Oral: Initial: 400 mg in 1 to 2 divided doses; optimal response

usually seen at 400 to 800 mg daily (larger doses may be divided) although

some patients may respond to as little as 200 mg daily; usual dose range:

200 to 400 mg daily; maximum dose: 1200 mg in 2 divided doses

Chronic stable angina (off-label use): Oral: Usual dose: 400 to 1200

mg/day in 2 divided doses; low doses (i.e., 400 mg/day) may also be given

as once daily.


Treatment of hypertension; management of ventricular arrhythmias

The 2014 guideline for the management of high blood pressure in adults

(Eighth Joint National Committee, JNC 8; James, 2013) recommends initiation

of pharmacologic treatment to lower blood pressure for the following patients:

• Patients ≥60 years of age with systolic blood pressure (SBP) ≥150 mm Hg

or diastolic blood pressure (DBP) ≥90 mm Hg. Goal of therapy is SBP <150

mm Hg and DBP <90 mm Hg.

• Patients <60 years of age with SBP ≥140 mm Hg or DBP ≥90 mm Hg. Goal

of therapy is SBP <140 mm Hg and DBP <90 mm Hg.

• Patients ≥18 years of age with diabetes and SBP ≥140 mm Hg or DBP ≥90

mm Hg. Goal of therapy is SBP <140 mm Hg and DBP <90 mm Hg.


• Patients ≥18 years of age with chronic kidney disease (CKD) and SBP ≥140

mm Hg or DBP ≥90 mm Hg. Goal of therapy is SBP <140 mm Hg and DBP

<90 mm Hg.

In patients with CKD, regardless of race or diabetes status, the use of an ACE

inhibitor (ACEI) or angiotensin receptor blocker (ARB) as initial therapy is

recommended to improve kidney outcomes. In the general nonblack

population (without CKD), including those with diabetes, initial

antihypertensive treatment should consist of a thiazide-type diuretic, calcium

channel blocker, ACEI, or ARB. In the general black population (without CKD),

including those with diabetes, initial antihypertensive treatment should

consist of a thiazide-type diuretic or a calcium channel blocker instead of an

ACEI or ARB.

Bisoprolol

Brand Names:

Zebeta


Antihypertensive


Dosing: Adult

Hypertension: Oral: Initial: 2.5 to 5 mg once daily; may be increased to 10

mg and then up to 20 mg once daily, if necessary; usual dose range: 5 to 10

mg once daily.

Atrial fibrillation (rate control) (off-label use): Usual maintenance dose:

2.5 to 10 mg once daily.

Heart failure (off-label use): Oral: Initial: 1.25 mg once daily; maximum

dose: 10 mg once daily. (Note: Initiate only in stable patients or hospitalized

patients after volume status has been optimized and IV diuretics,

vasodilators, and inotropic agents have all been successfully discontinued).


Caution should be used when initiating in patients who required inotropes

during their hospital course. Increase dose gradually and monitor for

congestive signs and symptoms of HF making every effort to achieve target

dose shown to be effective


Hypertension: Treatment of hypertension, alone or in combination with

other agents

Hypertension: The 2014 guideline for the management of high blood pressure

in adults (Eighth Joint National Committee [JNC 8]) recommends initiation of

pharmacologic treatment to lower blood pressure for the following patients:

• Patients ≥60 years of age, with systolic blood pressure (SBP) ≥150 mm Hg



• Patients <60 years of age, with SBP ≥140 mm Hg or DBP ≥90 mm Hg. Goal


• Patients ≥18 years of age with diabetes, with SBP ≥140 mm Hg or DBP ≥90


• Patients ≥18 years of age with chronic kidney disease (CKD), with SBP

≥140 mm Hg or DBP ≥90 mm Hg. Goal of therapy is SBP <140 mm Hg and

DBP <90 mm Hg.













Hypertension 2015 scientific statement for the treatment of hypertension in

patients with coronary artery disease (CAD) recommends the use of a beta

blocker as part of a regimen in patients with hypertension and chronic stable

angina with a history of prior MI.


cardiovascular events. A lower target BP (<130/80 mm Hg) may be

appropriate in some individuals with CAD, previous MI, stroke or transient

ischemic attack, or CAD risk equivalents.

Carvedilol

Brand Names:

Coreg

Coreg CR


Antihypertensive

Beta-Blocker With Alpha-Blocking Activity

Dosing: Adult

Reduce dosage if heart rate drops to <55 beats/minute.

Hypertension: Oral:

Immediate release: 6.25 mg twice daily; if tolerated, dose should be

maintained for 1 to 2 weeks, then increased to 12.5 mg twice daily. If

necessary, dosage may be increased to a maximum of 25 mg twice daily after

1 to 2 weeks. Usual dosage range: 6.25 to 25 mg twice daily.

Extended release: Initial: 20 mg once daily, if tolerated, dose should be

maintained for 1 to 2 weeks then increased to 40 mg once daily if necessary;

if this dose is tolerated, maintain for 1 to 2 weeks then, if necessary, increase

to 80 mg once daily; maximum dose: 80 mg once daily.


Heart failure: Oral:

(Note: Initiate only in stable patients or hospitalized patients after volume

status has been optimized and IV diuretics, vasodilators, and inotropic agents

have all been successfully discontinued. Caution should be used when

initiating in patients who required inotropes during their hospital course.

Increase dose gradually and monitor for congestive signs and symptoms of

HF making every effort to achieve target dose shown to be effective).

Immediate release: 3.125 mg twice daily for 2 weeks; if this dose is

tolerated, may increase to 6.25 mg twice daily. Double the dose every 2

weeks to the highest dose tolerated by patient. (Prior to initiating therapy,

other heart failure medications should be stabilized and fluid retention

minimized).

Maximum recommended dose:

Mild-to-moderate heart failure -

<85 kg: 25 mg twice daily

>85 kg: 50 mg twice daily

Severe heart failure: 25 mg twice daily.

Extended release: Initial: 10 mg once daily for 2 weeks; if the dose is

tolerated, increase dose to 20 mg, 40 mg, and 80 mg over successive

intervals of at least 2 weeks. Maintain on lower dose if higher dose is not

tolerated. (Note: The 2013 ACCF/AHA heart failure guidelines recommend a

maximum dose of 80 mg once daily).

Left ventricular dysfunction following MI: Oral: (Note: Should be

initiated only after patient is hemodynamically stable and fluid retention has

been minimized).

Immediate release: Initial 3.125 to 6.25 mg twice daily; increase dosage

incrementally (i.e., from 6.25 to 12.5 mg twice daily) at intervals of 3 to 10

days, based on tolerance, to a target dose of 25 mg twice daily. (Note: The

2013 ACCF/AHA heart failure guidelines recommend a maximum dose of 50

mg twice daily).


Extended release: Initial: Extended release: Initial: 10 to 20 mg once daily;

increase dosage incrementally at intervals of 3 to 10 days, based on

tolerance, to a target dose of 80 mg once daily.

Angina pectoris (off-label use): Oral: Immediate release: 25 to 50 mg

twice daily.

Atrial fibrillation (rate control) (off-label use): Usual maintenance dose:

3.125 to 25 mg twice daily. In patients with heart failure, the initial dose of

3.125 mg twice daily may be increased at 2-week intervals to a target dose of

25 mg twice daily (50 mg twice daily for patients weighing >85 kg).

Conversion from immediate release to extended release (Coreg CR):

Current dose immediate release tablets 3.125 mg twice daily: Convert to

extended release capsules 10 mg once daily.





Current dose immediate release tablets 25 mg twice daily: Convert to



Hypertension: Management of hypertension.

The 2014 guideline for the management of high blood pressure in adults

recommends initiation of pharmacologic treatment to lower blood pressure for

the following patients:











DBP <90 mm Hg.

In patients with CKD, regardless of race or diabetes status, the use of an ACE

inhibitor (ACEI) or angiotensin receptor blocker (ARB) as initial therapy is

recommended to improve kidney outcomes. In the general non-black


antihypertensive treatment should consist of a thiazide-type diuretic, calcium

channel blocker, ACEI, or ARB. In the general black population (without CKD)

including those with diabetes, initial antihypertensive treatment should

consist of a thiazide-type diuretic or a calcium channel blocker instead of an

ACEI or ARB.

Heart failure: Mild to severe chronic heart failure of ischemic or

cardiomyopathic origin (usually in addition to standard therapy, i.e., diuretics,

ACE inhibitors). The ACCF/AHA 2013 heart failure guidelines recommend the

use of 1 of the 3 beta blockers (i.e., bisoprolol, carvedilol, or extended-

release metoprolol succinate) for all patients with recent or remote history of

MI or ACS and reduced ejection fraction (rEF) to reduce mortality, for all

patients with rEF to prevent symptomatic HF (even if no history of MI), and

for all patients with current or prior symptoms of HF with reduced ejection

fraction (HFrEF), unless contraindicated, to reduce morbidity and mortality.

Left ventricular dysfunction following myocardial infarction (MI): Left

ventricular dysfunction following MI (clinically stable with LVEF ≤40%).

Propafenone


Mortality:

In the National Heart, Lung, and Blood Institute's Cardiac Arrhythmia

Suppression Trial (CAST), a long-term, multicenter, randomized, double-blind

study in patients with asymptomatic non–life-threatening ventricular

arrhythmias who had a myocardial infarction (MI) more than 6 days but less


than 2 years previously, an increased rate of death or reversed cardiac arrest

rate (7.7%) was seen in patients treated with encainide or flecainide (class IC

antiarrhythmics) compared with that seen in patients assigned to placebo

(3%). The average duration of treatment with encainide or flecainide in this

study was 10 months.

The applicability of the CAST results to other populations (i.e., those without

recent MI) or other antiarrhythmic drugs is uncertain, but at present, it is

prudent to consider any IC antiarrhythmic to have a significant risk in patients

with structural heart disease. Given the lack of any evidence that these drugs

improve survival, generally avoid antiarrhythmic agents in patients with non–

life-threatening ventricular arrhythmias, even if the patients are experiencing

unpleasant, but not life-threatening, symptoms or signs.

Brand Names:

Rythmol

Rythmol SR


Antiarrhythmic Agent, Class Ic

Dosing:

Patients who exhibit significant widening of QRS complex or second- or third-

degree AV block may need dose reduction.

Atrial fibrillation (to prevent recurrence): Oral:

Extended release capsule: Initial: 225 mg every 12 hours; dosage increase

may be made at a minimum of 5-day intervals; may increase to 325 mg

every 12 hours; if further increase is necessary, may increase to 425 mg

every 12 hours

Immediate release tablet: Initial: 150 mg every 8 hours; dosage increase

may be made at minimum of 3- to 4-day intervals, may increase to 225 mg

every 8 hours; if further increase is necessary, may increase to 300 mg every

8 hours.


Paroxysmal supraventricular tachycardia (to prevent recurrence),

ventricular arrhythmias: Oral: Immediate release tablet: Initial: 150 mg

every 8 hours (US labeling) or 300 mg every 12 hours (Canadian labeling);

dosage increase may be made at minimum of 3- to 4-day intervals, may

increase to 225 mg every 8 hours; if further increase is necessary, may

increase to 300 mg every 8 hours.

Paroxysmal atrial fibrillation, pharmacologic cardioversion (off-label

use): Oral: Immediate release tablet: Outpatient: "Pill-in-the-pocket" dose:

450 mg (weight <70 kg), 600 mg (weight ≥70 kg). May not repeat in ≤24

hours. (Note: An initial inpatient cardioversion trial should have been

successful before sending patient home on this approach. Patient must be

taking an AV nodal-blocking agent (e.g., beta-blocker, nondihydropyridine

calcium channel blocker) prior to initiation of antiarrhythmic).


Treatment of life-threatening ventricular arrhythmias; to prolong the time to

recurrence of paroxysmal atrial fibrillation/flutter (PAF) or paroxysmal

supraventricular tachycardia (PSVT) in patients with disabling symptoms

without structural heart disease.

Extended release capsule: Prolong the time to recurrence of symptomatic

atrial fibrillation in patients without structural heart disease

Disopyramide


Mortality:



study in patients with asymptomatic non-life-threatening ventricular

arrhythmias who had an MI more than 6 days but less than 2 years

previously, an excessive mortality or nonfatal cardiac arrest rate (7.7%) was

seen in patients treated with encainide or flecainide compared with that seen

in patients assigned to carefully matched placebo-treated groups (3%).


The average duration of treatment with encainide or flecainide in this study

was 10 months.


recent MI) is uncertain. Considering the known proarrhythmic properties of

disopyramide and the lack of evidence of improved survival for any

antiarrhythmic drug in patients without life-threatening arrhythmias, the use

of disopyramide as well as other antiarrhythmic agents should be reserved for

patients with life-threatening ventricular arrhythmias.

Brand Names:

Norpace

Norpace CR


Antiarrhythmic Agent, Class Ia

Dosing:

Arrhythmias: Oral: Immediate release:

<1 year: 10 to 30 mg/kg/24 hours in 4 divided doses

1 to 4 years: 10 to 20 mg/kg/24 hours in 4 divided doses




Life-threatening ventricular arrhythmias (i.e., sustained ventricular

tachycardia)

Mexiletine


Mortality:



study in patients with asymptomatic non–life-threatening ventricular


arrhythmias who had an myocardial infarction (MI) more than 6 days but less

than 2 years previously, an excessive mortality or nonfatal cardiac arrest rate

(7.7%) was seen in patients treated with encainide or flecainide compared

with that seen in patients assigned to carefully matched placebo-treated

groups (3%). The average duration of treatment with encainide or flecainide

in this study was 10 months.


recent MI) is uncertain. Considering the known proarrhythmic properties of

mexiletine and the lack of evidence of improved survival for any

antiarrhythmic drug in patients without life-threatening arrhythmias, the use

of mexiletine as well as other antiarrhythmic agents should be reserved for

patients with life-threatening ventricular arrhythmias.

Acute liver injury:

In postmarketing experience, abnormal liver function tests have been

reported, some in the first few weeks of therapy with mexiletine. Most of

these have been observed in the setting of congestive heart failure or

ischemia and their relationship to mexiletine has not been established.

Brand Names:

Novo-Mexiletine


Antiarrhythmic Agent, Class Ib

Dosing:

Ventricular arrhythmias (life-threatening): Oral: Initial: 200 mg every 8

hours (may load with 400 mg if necessary); adjust dose in 50 or 100 mg

increments no more frequently than every 2 to 3 days; usual dose: 200 to

300 mg every 8 hours; maximum dose: 1.2 g/day. (Note: Once controlled,

patients may be transferred to an every 12-hour dosing schedule; do not

exceed 450 mg every 12 hours with this regimen).


Conversion:

Switching from other oral antiarrhythmics (i.e., disopyramide, quinidine

sulfate): Initiate 200 mg dose of mexiletine 6 to 12 hours after the last dose

of the former agent.

Switching from IV lidocaine: Initiate 200 mg dose of mexiletine when

lidocaine infusion is stopped.

Switching from oral procainamide: Initiate a 200 mg dose of mexiletine 3 to 6

hours after the last dose of procainamide.

Premature ventricular complex (symptomatic) suppression (off-label

use): Oral: 100 or 150 mg 3 times daily; if not controlled, may increase to

200 mg 3 times daily (Saikawa 1992; Tanabe 1991) or 100 or 200 mg 2 to 3

times daily; may progressively increase to a maximum dose of 500 mg 3

times daily.


Ventricular arrhythmias: Management of life-threatening ventricular

arrhythmias. (Note: The American College of Cardiology/American Heart

Association/European Society of Cardiology (ACC/AHA/ESC) states that

mexiletine may be considered for those with long QT syndrome who present

with torsades de pointes).

Propranolol


Cardiac ischemia after abrupt discontinuation (Inderal LA, Inderal XL,

Innopran XL): Following abrupt discontinuation of therapy with beta-blockers,

exacerbations of angina pectoris and myocardial infarction (MI) have

occurred. When discontinuing long-term administration of propranolol,

particularly in patients with ischemic heart disease, gradually reduce the dose

over a period of 1 to 2 weeks and monitor the patient. If angina markedly

worsens or acute coronary insufficiency develops, promptly resume therapy,

at least temporarily, and take other measures appropriate for the

management of unstable angina.


Warn patients against interruption or discontinuation of therapy without

health care provider's advice. Because coronary artery disease is common

and may be unrecognized, avoid abrupt discontinuation of propranolol

therapy, even in patients treated only for hypertension.

Brand Names:

Hemangeol

Inderal LA

Inderal XL

InnoPran XL


Antianginal Agent


Antihypertensive


Dosing: Pediatric

Proliferating infantile hemangioma (Hemangeol): Infants ≥2 kg:

(Note: Initiate treatment at age 5 weeks to 5 months; doses should be

administered at least 9 hours apart. Refer to product labeling for detailed

weight-based dosing tabulation).

Week 1: 0.15 mL/kg (~0.6 mg/kg) twice daily

Week 2: 0.3 mL/kg (~1.1 mg/kg) twice daily

Week 3 (maintenance): 0.4 mL/kg (~1.7 mg/kg) twice daily; maintain this

dose for 6 months.

Readjust dose periodically as the child's weight increases. Treatment may be

reinitiated if hemangiomas recur.

Hypertension (off-label use): Children and Adolescents: Oral: Immediate-

release formulations: Initial: 1 to 2 mg/kg/day divided in 2 to 3 doses/day;

titrate dose to effect; maximum dose: 4 mg/kg/day up to 640 mg/day;

sustained-release formulation may be dosed once daily.


Thyrotoxicosis (off-label use): Adolescents: Oral: Immediate-release

formulations: 10 to 40 mg/dose every 6 to 8 hours; may also consider

administering extended or sustained release formulations.


Management of hypertension; angina pectoris; pheochromocytoma; essential

tremor; supraventricular arrhythmias (such as atrial fibrillation and flutter, AV

nodal re-entrant tachycardias), ventricular tachycardias (catecholamine-

induced arrhythmias, digoxin toxicity); prevention of myocardial infarction;

migraine headache prophylaxis; symptomatic treatment of obstructive

hypertrophic cardiomyopathy (formerly known as hypertrophic subaortic

stenosis); treatment of proliferating infantile hemangioma requiring systemic

therapy (Hemangeol only).


in adults recommends initiation of pharmacologic treatment to lower blood

pressure for the following patients:










DBP <90 mm Hg.






diuretic, calcium channel blocker, ACEI, or ARB.


In the general black population (without CKD) including those with diabetes,

initial antihypertensive treatment should consist of a thiazide-type diuretic or

a calcium channel blocker instead of an ACEI or ARB. Beta-blockers are no

longer recommended as first-line therapy in the general patient population.


Association, American College of Cardiology, and American Society of


hypertension in patients with CAD recommends the use of a beta blocker as

part of a regimen in patients with hypertension and chronic stable angina with

a history of prior MI. A BP target of <140/90 mm Hg is reasonable for the

secondary prevention of cardiovascular events. A lower target BP (<130/80

mm Hg) may be appropriate in some individuals with CAD, previous MI,

stroke or transient ischemic attack, or CAD risk equivalents (AHA/ACC/ASH)

Ibutilide


Life-threatening arrhythmias:

Ibutilide fumarate can cause potentially fatal arrhythmias, particularly

sustained polymorphic ventricular tachycardia usually in association with QT

prolongation (torsades de pointes), but sometimes without documented QT

prolongation. In registration studies, these arrhythmias, which require

cardioversion, occurred in 1.7% of treated patients during or within a number

of hours of using ibutilide fumarate. These arrhythmias can be reversed if

treated promptly. It is essential that ibutilide be administered in a setting of

continuous ECG monitoring and by personnel trained in identification and

treatment of acute ventricular arrhythmias, particularly polymorphic

ventricular tachycardia. Patients with atrial fibrillation of more than 2 to 3

days' duration must be adequately anticoagulated, generally at least 2 weeks.

Appropriate treatment environment:

Choice of patients: Patients with chronic atrial fibrillation have a strong

tendency to revert after conversion to sinus rhythm and treatments to

maintain sinus rhythm carry risks.


Patients to be treated with ibutilide fumarate, therefore, should be carefully

selected such that the expected benefits of maintaining sinus rhythm

outweigh the immediate risks of ibutilide, and the risks of maintenance

therapy, and are likely to offer an advantage compared with alternative

management.

Brand Names:

Corvert



Dosing:

Atrial fibrillation/flutter: IV:

<60 kg: 0.01 mg/kg over 10 minutes

≥60 kg: 1 mg over 10 minutes

(Note: Discontinue infusion if arrhythmia terminates, if sustained or

nonsustained ventricular tachycardia occurs, or if marked prolongation of

QT/QTc occurs. If the arrhythmia does not terminate within 10 minutes after

the end of the initial infusion, a second infusion of equal strength may be

infused over a 10-minute period).

Dofetilide


Arrhythmias:

To minimize the risk of induced arrhythmia, patients initiated or re-initiated

on dofetilide should be placed for a minimum of 3 days in a facility that can

provide calculations of creatinine clearance, continuous electrocardiographic

monitoring, and cardiac resuscitation.

Brand Names:

Tikosyn




Dosing:

(Note: CrCl and QTc (or QT interval if heart rate is <60 beats/minute) must

be determined prior to first dose. If QTc >440 msec (>500 msec in patients

with ventricular conduction abnormalities), dofetilide is contraindicated).

Atrial fibrillation/atrial flutter:

Initial: 500 mcg twice daily orally (maximum dose: 500 mcg twice daily).

Initial dosage must be adjusted in patients with estimated CrCl <60

mL/minute (see dosage adjustment in renal impairment). Dofetilide may be

initiated at lower doses than recommended based on health care provider

discretion.

Modification of dosage in response to initial dose: QTc interval should be

measured 2 to 3 hours after the initial dose. If the QTc increases to more

than 15% above baseline QTc or if the QTc is >500 msec (>550 msec in

patients with ventricular conduction abnormalities), dofetilide dose should be

reduced.

If the starting dose was 500 mcg twice daily, then reduce to 250 mcg twice

daily. If the starting dose was 250 mcg twice daily, then reduce to 125 mcg

twice daily. If the starting dose was 125 mcg twice daily, then reduce to 125

mcg once daily. If at any time after the second dose is given the QTc is >500

msec (>550 msec in patients with ventricular conduction abnormalities),

dofetilide should be discontinued.

Maintenance therapy: No further down titration of dose based on QTc is

recommended following modification of initial dose. Renal function and QTc

should be re-evaluated every 3 months or as medically warranted. If QTc

>500 msec (>550 msec in patients with ventricular conduction

abnormalities), discontinue therapy. If renal function deteriorates, adjust dose

as described in dosage adjustment in renal impairment.



Atrial fibrillation/atrial flutter: Maintenance of normal sinus rhythm in

patients with chronic atrial fibrillation/atrial flutter of longer than 1-week

duration who have been converted to normal sinus rhythm; conversion of

atrial fibrillation and atrial flutter to normal sinus rhythm.

Dronedarone


Increased risk of death, stroke, and heart failure:

Dronedarone is contraindicated in patients with symptomatic heart failure

with recent decompensation requiring hospitalization or New York Heart

Association (NYHA) class IV heart failure. Dronedarone doubles the risk of

death in these patients. Dronedarone is contraindicated in patients in atrial

fibrillation (AF) who will not or cannot be cardioverted into normal sinus

rhythm. In patients with permanent AF, dronedarone doubles the risk of

death, stroke, and hospitalization for heart failure.

Brand Names:

Multaq



Dosing:

(Note: Prior to initiation of dronedarone, class I or III antiarrhythmics (i.e.,

amiodarone, flecainide, propafenone, quinidine, disopyramide, dofetilide,

sotalol) or drugs that are strong inhibitors of CYP3A (i.e., ketoconazole) must

be stopped).

Paroxysmal or persistent atrial fibrillation: Oral: 400 mg twice daily.


Paroxysmal or persistent atrial fibrillation: To reduce the risk of

hospitalization for atrial fibrillation (AF) in patients in sinus rhythm with a

history of paroxysmal or persistent AF.


Verapamil

Brand Names:

Calan

Calan SR

Covera-HS [DSC]

Isoptin SR

Verelan

Verelan PM


Antianginal Agent

Antiarrhythmic Agent, Class IV

Antihypertensive

Calcium Channel Blocker

Calcium Channel Blocker, Nondihydropyridine

Dosing:

SVT: (Note: Verapamil is no longer included in the Pediatric Advanced Life

Support (PALS) tachyarrhythmia algorithm).

Children: 1-15 years: IV: 0.1 to 0.3 mg/kg/dose over 2 minutes; maximum:

5 mg/dose, may repeat dose in 30 minutes if inadequate response; maximum

for second dose: 10 mg


IV: Supraventricular tachyarrhythmia (PSVT, atrial fibrillation/flutter [rate

control])

Oral: Treatment of hypertension; angina pectoris (vasospastic, chronic stable,

unstable) (Calan, Covera-HS); supraventricular tachyarrhythmia (PSVT, atrial

fibrillation/flutter [rate control])

Acute coronary syndrome (ACS): The ACCF/AHA guidelines for the

management of unstable angina/non-ST-elevation myocardial infarction

recommend verapamil to treat hypertension or ongoing ischemia if beta-

blocker therapy is ineffective or contraindicated and in the absence of left

ventricular dysfunction, pulmonary congestion, or AV block.



in adults recommends initiation of pharmacologic treatment to lower blood

pressure for the following patients:

• Patients ≥60 years of age with systolic blood pressure (SBP) ≥150 mm Hg



• Patients <60 years of age with SBP ≥140 mm Hg or DBP ≥90 mm Hg. Goal


• Patients ≥18 years of age with diabetes with SBP ≥140 mm Hg or DBP ≥90


• Patients ≥18 years of age with chronic kidney disease (CKD) with SBP ≥140

mm Hg or DBP ≥90 mm Hg. Goal of therapy is SBP <140 mm Hg and DBP

<90 mm Hg.













hypertension in patients with coronary artery disease (CAD) recommends that

a non-dihydropyridine CCB (verapamil, diltiazem) may be used as a substitute

for a beta blocker in patients who have an intolerance or contraindication to

beta blockers with ongoing ischemia, hypertension and chronic stable angina,

or if angina or hypertension continues to be uncontrolled while receiving

standard therapies (i.e., beta blocker). However, a non-dihydropyridine CCB

(i.e., verapamil, diltiazem) should be avoided in patients with LV dysfunction

or heart failure (with reduced ejection fraction).



cardiovascular events. A lower target BP (<130/80 mm Hg) may be

appropriate in some individuals with CAD, previous MI, stroke or transient

ischemic attack, or CAD risk equivalents.

Dipyridamole

Brand Names:

Persantine


Antiplatelet Agent

Vasodilator

Dosing:

Adjunctive therapy for prophylaxis of thromboembolism with cardiac valve

replacement: Oral: 75 to 100 mg 4 times/day

Evaluation of coronary artery disease: IV: 0.56 mg/kg over 4 minutes;

maximum dose: 70 mg.

Following completion of dipyridamole infusion, inject radiotracer (i.e.,

thallium-201) in 3 to 5 minutes. (Note: To reverse complications and side

effects of dipyridamole, aminophylline (50 to 250 mg IV push over 30 to 60

seconds given at least 1 minute after the radiotracer injection) should be

available for urgent/emergent use).

Obesity: Dosing for patients who are obese or morbidly obese is not

established; in these patients, it is customary to use doses up to the weight

of 125 kg.


Oral: Used with warfarin to decrease thrombosis in patients after artificial

heart valve replacement.

IV: Diagnostic agent in CAD.


Cardiac Pacemakers And Defibrillators

Pacemakers sense electrical events and respond when necessary by

delivering electrical stimuli to the heart. Permanent pacemaker leads

are placed via thoracotomy or transvenously, but some temporary

emergency pacemaker leads can be placed on the chest wall.

Indications for Pacemaker Placement

Indications are numerous but generally involve symptomatic

bradycardia or high-grade atrioventricular (AV) block. Some

tachyarrhythmias may be terminated by overdrive pacing with a brief

period of pacing at a faster rate; the pacemaker is then slowed to the

desired rate. Nevertheless, ventricular tachyarrhythmias are better

treated with devices that can cardiovert and defibrillate as well as

pace (implantable cardioverter defibrillators).

Types of Pacemakers

Types of pacemakers are designated by 3 to 5 letters, representing

which cardiac chambers are paced, which chambers are sensed, how

the pacemaker responds to a sensed event (inhibits or triggers

pacing), whether it can increase heart rate during exercise (rate-

modulating), and whether pacing is multisite (in both atria, both

ventricles, or more than one pacing lead in a single chamber). For

example, a VVIR pacemaker paces (V) and senses (V) events in the

ventricle, inhibits pacing in response to sensed event (I), and can

increase its rate during exercise (R).

VVI and DDD pacemakers are the devices most commonly used. They

offer equivalent survival benefits. Compared with VVI pacemakers,


physiologic pacemakers (AAI, DDD, VDD) appear to reduce risk of

atrial fibrillation (AF) and heart failure and slightly improve quality of

life.32,183

Advances in pacemaker design include lower-energy circuitry, new

battery designs, and corticosteroid-eluting leads (which reduce pacing

threshold), all of which increase pacemaker longevity. Mode switching

refers to an automatic change in the mode of pacing in response to

sensed events (i.e., from DDDR to VVIR during AF).83,84

Complications of Pacemaker Use

Pacemakers may malfunction by oversensing or undersensing events,

failing to pace or capture, or pacing at an abnormal rate.

Tachycardias are an especially common complication. Rate-

modulating pacemakers may increase stimuli in response to vibration,

muscle activity, or voltage induced by magnetic fields during MRI. In

pacemaker-mediated tachycardia, a normally functioning dual-

chamber pacemaker senses a ventricular premature or paced beat

transmitted to the atrium through the AV node or a retrograde-

conducting accessory pathway, which triggers ventricular stimulation

in a rapid, repeating cycle.25

Additional complications associated with normally functioning devices

include cross-talk inhibition, in which sensing of the atrial pacing

impulse by the ventricular channel of a dual-chamber pacemaker

leads to inhibition of ventricular pacing, and pacemaker syndrome, in

which AV asynchrony induced by ventricular pacing causes

fluctuating, vague cerebral (i.e., light-headedness), cervical (i.e.,

neck pulsations), or respiratory (i.e., dyspnea) symptoms. Pacemaker


syndrome is managed by restoring AV synchrony by atrial pacing

(AAI), single-lead atrial sensing ventricular pacing (VDD), or dual-

chamber pacing (DDD), most commonly the latter.

Environmental interference comes from electromagnetic sources such

as surgical electrocautery and MRI, although MRI may be safe when

the pacemaker generator and leads are not inside the magnet.

Cellular telephones and electronic security devices are a potential

source of interference; telephones should not be placed close to the

device but are not a problem when used normally for talking. Walking

through metal detectors does not cause pacemaker malfunction as

long as patients do not linger.

Defibrillators

Direct-Current (DC) Cardioversion-Defibrillation

A transthoracic DC shock of sufficient magnitude depolarizes the

entire myocardium, rendering the entire heart momentarily refractory

to repeat depolarization. Thereafter, the most rapid intrinsic

pacemaker, usually the sinoatrial node, reassumes control of heart

rhythm. Thus, DC cardioversion-defibrillation very effectively

terminates tachyarrhythmias that result from reentry. However, it is

less effective for terminating tachyarrhythmias that result from

automaticity because the return rhythm is likely to be the automatic

tachyarrhythmia. For tachyarrhythmias other than ventricular

fibrillation (VF), the DC shock must be synchronized to the QRS

complex (called DC cardioversion) because a shock that falls during

the vulnerable period (near the peak of the T wave) can induce VF. In

VF, synchronization of a shock to the QRS complex is neither


necessary nor possible. A DC shock applied without synchronization

to a QRS complex is DC defibrillation.

Procedure for DC cardioversion

When DC cardioversion is elective, patients should fast for 6 to 8 h to

avoid the possibility of aspiration. Because the procedure is

frightening and painful, brief general anesthesia or IV analgesia and

sedation (i.e., fentanyl 1 mcg/kg, then midazolam 1 to 2 mg q 2 min

to a maximum of 5 mg) is necessary. Equipment and personnel to

maintain the airways must be present.

The electrodes (pads or paddles) used for cardioversion may be

placed anteroposteriorly (along the left sternal border over the 3rd

and 4th intercostal spaces and in the left infrascapular region) or

anterolaterally (between the clavicle and the 2nd intercostal space

along the right sternal border and over the 5th and 6th intercostal

spaces at the apex of the heart). After synchronization to the QRS

complex is confirmed on the monitor, a shock is given. The most

appropriate energy level varies with the tachyarrhythmia being

treated. Cardioversion efficacy increases with use of biphasic shocks,

in which the current polarity is reversed part way through the shock

waveform.85 DC cardioversion-defibrillation can also be applied

directly to the heart during a thoracotomy or through use of an

intracardiac electrode catheter; then, much lower energy levels are

required.

Complications of DC cardioversion

Complications are usually minor and include atrial and ventricular

premature beats and muscle soreness. Less commonly, but more


likely if patients have marginal left ventricular function or multiple

shocks are used, cardioversion precipitates myocyte damage and

electromechanical dissociation.

Implantable Cardioverter-Defibrillators

Implantable cardioverter-defibrillators cardiovert or defibrillate the

heart in response to ventricular tachycardia (VT) or ventricular

fibrillation (VF). Contemporary tiered-therapy ICDs also provide

antibradycardia pacing and antitachycardia pacing (to terminate

responsive atrial or ventricular tachycardias) and store intracardiac

electrograms.

The ICDs are implanted subcutaneously or subpectorally, with

electrodes inserted transvenously into the right ventricle and

sometimes also the right atrium. A biventricular ICD also has a left

ventricular epicardial lead placed via the coronary sinus venous

system or via thoracotomy. ICDs are the preferred treatment for

patients who have had an episode of VF or hemodynamically

significant VT not due to reversible or transient conditions (i.e.,

electrolyte disturbance, antiarrhythmic drug proarrhythmia, acute

MI). ICDs may also be indicated for patients with VT or VF inducible

during an electrophysiologic study and for patients with idiopathic or

ischemic cardiomyopathy, a left ventricular ejection fraction

of < 35%, and a high risk of VT or VF. Other indications are less

clear.86

Because ICDs treat rather than prevent VT or VF, patients prone to

these arrhythmias may require both an ICD and antiarrhythmic drugs


to reduce the number of episodes and need for uncomfortable

shocks; this approach also prolongs the life of the ICD.

Impulse generators for ICDs typically last about 5 years. ICDs may

malfunction by delivering inappropriate pacing or shocks in response

to sinus rhythm, SVTs, or nonphysiologically generated impulses (i.e.,

due to lead fracture). They also may malfunction by not delivering

appropriate pacing or shocks when needed because of factors such as

lead or impulse generator migration, undersensing, an increase in

pacing threshold due to fibrosis at the site of prior shocks, and

battery depletion.

In patients who report that the ICD has discharged but that no

associated symptoms of syncope, dyspnea, chest pain or persistent

palpitations occurred, follow up with the ICD clinic and/or the

electrophysiologist within the week is appropriate. The ICD can then

be electronically interrogated to determine the reason for discharge.

If such associated symptoms were present, or the patient received

multiple shocks, emergency department referral is indicated to look

for a treatable cause (i.e., coronary ischemia, electrolyte

abnormality) or device malfunction.87

Cardiac Resynchronization Therapy

In some patients, the normal, orderly, sequential relationship

between contraction of the cardiac chambers is disrupted (becomes

dyssynchronous). Dyssynchrony may be: 1) Atrioventricular, between

atrial and ventricular contraction, 2) Interventricular, between left

and right ventricular contraction, and 3) Intraventricular, between

different segments of left ventricular contraction.


Patients at risk for dyssynchrony include those with: ischemic or

nonischemic dilated cardiomyopathy, prolonged QRS interval (≥ 130

msec), left ventricular end-diastolic dimension ≥ 55 mm, and left

ventricular ejection fraction ≤ 35% in sinus rhythm.

Cardiac resynchronization therapy (CRT) involves use of a pacing

system to resynchronize cardiac contraction. Such systems usually

include a right atrial lead, right ventricular lead, and left ventricular

lead. Leads may be placed transvenously or surgically via

thoracotomy. In heart failure patients with New York Heart

Association (NYHA) class II, III, and IV symptoms, CRT can reduce

hospitalization for heart failure and reduce all-cause mortality.

However, there is little to no benefit in patients with permanent atrial

fibrillation, right bundle branch block, nonspecific intraventricular

conduction delay, or only mild prolongation of QRS duration (< 150

msec).

Cardiac Ablation

If a tachyarrhythmia depends on a specific pathway or ectopic site of

automaticity, the site can be ablated by low-voltage, high-frequency

(300 to 750 MHz) electrical energy, applied through an electrode

catheter. This energy heats and necroses an area < 1 cm in diameter

and up to 1 cm deep. Before energy can be applied, the target site or

sites must be mapped during an electrophysiologic study.

Success rate is > 90% for reentrant supraventricular tachycardias

(via the atrioventricular [AV] node or an accessory pathway), focal

atrial tachycardia and flutter, and focal idiopathic ventricular

tachycardia (VT—right ventricular outflow tract, left septal, or bundle


branch reentrant VT). Because atrial fibrillation (AF) often originates

or is maintained by an arrhythmogenic site in the pulmonary veins,

this source can be electrically isolated by ablations at the pulmonary

vein – left atrial junction or in the left atrium. Alternatively, in

patients with refractory AF and rapid ventricular rates, the AV node

may be ablated after permanent pacemaker implantation. RF ablation

is sometimes successful in patients with VT refractory to drugs

particularly when ischemic heart disease is present.58

The mortality rate of RF ablation is < 1/2000 and the procedure is

considered to be safe. Complications include valvular damage,

pulmonary vein stenosis or occlusion (if used to treat atrial

fibrillation), stroke or other embolism, cardiac perforation,

tamponade (1%), and unintended AV node ablation.40

Summary

An arrhythmia is any abnormality in the rate, regularity, or site of

origin or a disturbance in conduction that disrupts the normal

sequence of activation in the atria or ventricles. Arrhythmias can be

due to a variety of reasons, such as electrolyte abnormalities,

structural abnormalities, metabolic derangements, genetic mutations,

and drug toxicity. Arrhythmias have varying degrees of severity and

significance based on site of origin, symptoms, frequency, and

duration.

Abnormal heart rates in children are often not a cause of concern, but

it is absolutely vital that a healthcare professional be able to

recognize when an arrhythmia has the potential to become serious or

life threatening, and to identify appropriate treatment options.


Arrhythmias may or may not present with secondary symptoms and

it often requires some investigation to determine if a cause for the

arrhythmia is present. Understanding the mechanics of arrhythmias

as well as the treatment options will ensure that you are able to

communicate with your patient and his or her parents to determine

the right course of action.

Please take time to help NurseCe4Less.com course planners evaluate

the nursing knowledge needs met by completing the self-assessment

of Knowledge Questions after reading the article, and providing

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considered

a. a depolarization event.

b. an atrioventricular (AV) impulse. c. an arrhythmia.

d. a repolarization event.


a. a slow outward leak of sodium.

b. depolarization. c. a slow outward leak of potassium.

d. All of the above

3. True or False: Some arrhythmias are so common as to be

considered as almost normal variants.

a. True b. False

4. The conduction system in the ventricles is more elaborate than that in the atria because

a. the muscle mass is larger. b. of the location of the bundle of His. c. the superior vena cava enters through the ventricles.

d. of fiber stretch.



a. atria via

b. atrioventricular (AV) node

c. coronary sinus



6. In general, arrhythmia mechanisms are described as

abnormalities in

a. electrical development.

b. electrical conduction. c. a combination of electrical development and conduction.

d. All of the above

7. _________________ ions cause the actual muscular contraction by coupling with the muscle fibers.

a. Potassium b. Calcium

c. Sodium

d. None of the above

8. The atrial muscle and ventricular muscle are separated by insulation of the fibrous mitral and tricuspid valve rings,

and normally the only connection between them is via

a. the superior vena cava.

b. the Bachmann bundle. c. the His bundle.

d. the Purkinje fibers.

9. The ventricle is activated through the dense network of

_____________ originating from the bundle branches.

a. the Bachmann bundle

b. Purkinje fibers c. the His bundle

d. the superior vena cava

10. True or False: The mechanism of abnormal automaticity is

NOT similar to the normal automaticity of sinus node

cells.

a. True

b. False


11. Conduction block or conduction delay is a frequent cause

of ____________________, especially if the conduction

block is located in the cardiac conduction system.

a. bradyarrhythmias b. tachyarrhythmias

c. depolarization

d. muscular contraction

12. Ion channels are passages for ions that facilitate

a. muscular contraction. b. movement through the cell membrane.

c. and AV reentry.

d. and fiber stretch.

13. True or False: By far the most common tachycardia presenting in early infancy is orthodromic AV reentry.

a. True b. False

14. Depolarization is initiated by

a. the sodium channel closing b. a slow inward leak of sodium. c. an outward movement of potassium ions.

d. a complex exchange of sodium, calcium, and potassium.

15. The final conducting components of the ventricles are the ____________, which emanate from the bundle branches

to stimulate the ventricular cardiac muscle to contract.

a. bundle of His

b. catecholamines

c. Purkinje fibers

d. tricuspid valve rings

16. The QRS complex from an electrocardiogram measures

a. both ventricular depolarization and repolarization.

b. depolarization of the ventricles.

c. repolarization.

d. atrial activity.


17. The conduction pathways through the atrium to the AV-

node show preferential conduction due to

a. their connection to the Bachmann bundle.

b. their specialized conduction properties. c. phase 4 diastolic depolarization.

d. their anatomical structure.

18. True or False: Conduction between the AV node and the

bundle of His is measured by the P-R interval (the time

between atrial activity and ventricular activity).

a. True

b. False

19. The anterior internodal pathway (through the atrium to the AV-node) connects to the anterior interatrial band,

also known as

a. the anterior internodal pathway. b. the Purkinje fibers.

c. the Bachmann bundle. d. the His bundle.

20. The connection between atria and ventricles is facilitated

through

a. the AV node. b. the sinus node. c. the interventricular septum.

d. the junction with the septum.

21. The normal average heart rate of children

a. is higher than that of adults.

b. varies from 60 bpm (at rest). c. varies up to 220 bpm during strenuous activities.

d. All of the above


22. True or False: Many children with palpitations do not have

an arrhythmia and a detailed first-hand history is

essential before assessing the likelihood of an arrhythmia and the necessity of further investigation.

a. True

b. False

23. When diagnosing a child with an arrhythmia, diagnosis is based mainly on

a. the child’s age and the age of onset of arrhythmia. b. the history (palpitations, heart failure, syncope, etc.).

c. the ECG findings.

d. All of the above

24. Infants generally have heart rates

a. greater than 60 bpm and less than 120 bpm. b. greater than 60 bpm and less than 140 bpm. c. greater than 80 bpm and less than 170 bpm.

d. greater than 80 bpm and less than 220 bpm.

25. Common arrhythmias in neonates with structurally

normal hearts include a. sinus tachycardia.

b. sinus bradycardia. c. atrioventricular reentry tachycardia (AVRT).

d. complete AV block.

26. A head-up tilt test is sometimes used for investigation of ______________ with recurrent syncope or presyncope.

a. infants

b. children older than 6 years

c. children between 3 and 6 years d. neonates


27. During the head-up tilt test,

a. blood pressure is recorded continuously. b. the ECG is recorded continuously. c. The patient is passively tilted to an angle of 60–80.

d. All of the above

28. True or False: The first scheme (Vaughan-Williams) is still

the one that most physicians use when speaking of

antiarrhythmic drugs.

a. True

b. False

29. In the Vaughan-Williams antiarrhythmic drugs classifications, _____________ are a class I drug.

a. sodium channel blockers

b. beta-blockers c. nondihydropyridine calcium channel blockers

d. digoxin and adenosine

30. Class Ic antiarrhythmic drugs have slow kinetics so they

express their electrophysiologic effects at _____ heart

rates.

a. fast b. slow

c. intermediate d. all

31. __________________________ are not included in the

Vaughan Williams classification.

a. Sodium channel blockers

b. Digoxin and adenosine

c. Beta-blockers d. Nondihydropyridine calcium channel blockers


32. True or False: Dronedarone is contraindicated in patients in

atrial fibrillation (AF) who will not or cannot be

cardioverted into normal sinus rhythm.

a. True b. False

33. Class I drugs are subdivided based on the kinetics of the

sodium channel effects: Class Ia drugs have ___________ kinetics.

a. fast b. slow

c. intermediate

d. intermittent

34. In the Vaughan-Williams antiarrhythmic drugs classifications, _____________ are a class II drug.

a. sodium channel blockers b. beta-blockers

c. nondihydropyridine calcium channel blockers d. digoxin and adenosine

35. True or False: Proarrhythmia is a drug-related arrhythmia that is worse than the arrhythmia being treated, and it is an adverse effect of class I drugs.

a. True

b. False

36. Class Ib drugs have fast kinetics so they

a. have major effects on atrial tissue.

b. are very potent antiarrhythmics.

c. express their electrophysiologic effects only at fast heart

rates. d. All of the above


37. Class II drugs are contraindicated in

a. glaucoma patients. b. older patients.

c. asthma patients. d. patients with sinus tachycardia.

38. ______________ is intended for use only in patients with

indicated life-threatening arrhythmias because its use is accompanied by substantial toxicity.

a. Nadolol b. Amiodarone

c. Sotalol

d. Diltiazem

39. When discontinuing nadolol administered long-term, particularly in patients with ischemic heart disease,

a. gradually reduce dose over a period of 1 to 2 days. b. nadolol may not be reintroduced.

c. the drug should be stopped abruptly. d. gradually reduce dose over a period of 1 to 2 weeks.

40. The use of an ACE inhibitor (ACEI) or angiotensin receptor blocker (ARB) as initial therapy is recommended to improve kidney outcomes

a. in non-white populations.

b. in non-black populations. c. depending on diabetes status.

d. regardless of race or diabetes status.

41. True or False: It may be prudent not to discontinue nadolol

therapy abruptly in patients with possible coronary artery

disease but it is prudent in patients being treated ONLY for hypertension.

a. True

b. False


42. Abnormal liver function tests have been reported, some in

the first few weeks of therapy with

a. an ACE inhibitor (ACEI).

b. angiotensin receptor blocker (ARB). c. mexiletine.

d. bisoprolol.

43. Permanent pacemaker leads are placed

a. via thoracotomy or transvenously.

b. on the chest wall. c. in the diaphragm.

d. on the front of the breastbone.

44. Pacemakers may malfunction by

a. oversensing events.

b. undersensing events. c. failing to pace or capture, or pacing at an abnormal rate. d. All of the above

45. In patients with permanent atrial fibrillation (AF),

__________ doubles the risk of death, stroke, and

hospitalization for heart failure. a. dofetilide

b. dronedarone c. bisoprolol

d. digoxin

46. True or False: To minimize the risk of induced arrhythmia, patients initiated or re-initiated on dofetilide should be

placed in a facility for at least 3 days for calculations of

creatinine clearance, continuous ECG monitoring, and

cardiac resuscitation.

a. True

b. False


47. Severe exacerbation of angina and the occurrence of

myocardial infarction (MI) and ventricular arrhythmias

have been reported in patients with angina following the abrupt discontinuation of therapy with

a. dofetilide

b. beta-blockers.

c. bisoprolol

d. digoxin

48. Class III drugs are membrane stabilizing drugs, primarily

a. fast-channel blockers.

b. beta-blockers.

c. calcium channel blockers. d. potassium channel blockers.

49. True or False: Because class Ia drugs have intermediate

kinetics, their fast-channel tissue conduction slowing effects WILL be evident on an ECG obtained during normal rhythm at normal rates.

a. True

b. False

50. Class IV drugs are the nondihydropyridine

a. fast-channel blockers. b. beta-blockers.

c. calcium channel blockers. d. potassium channel blockers.


CORRECT ANSWERS:


considered

c. an arrhythmia.


b. depolarization.

3. True or False: Some arrhythmias are so common as to be considered as almost normal variants.

a. True

4. The conduction system in the ventricles is more elaborate

than that in the atria because

a. the muscle mass is larger.




6. In general, arrhythmia mechanisms are described as abnormalities in

d. All of the above

7. _________________ ions cause the actual muscular

contraction by coupling with the muscle fibers.

b. Calcium

8. The atrial muscle and ventricular muscle are separated by

insulation of the fibrous mitral and tricuspid valve rings,

and normally the only connection between them is via

c. the His bundle.


9. The ventricle is activated through the dense network of

_____________ originating from the bundle branches.

b. Purkinje fibers

10. True or False: The mechanism of abnormal automaticity is

NOT similar to the normal automaticity of sinus node

cells.

b. False

11. Conduction block or conduction delay is a frequent cause of ____________________, especially if the conduction

block is located in the cardiac conduction system.

a. bradyarrhythmias

12. Ion channels are passages for ions that facilitate

b. movement through the cell membrane.

13. True or False: By far the most common tachycardia presenting in early infancy is orthodromic AV reentry.

a. True

14. Depolarization is initiated by

b. a slow inward leak of sodium.

15. The final conducting components of the ventricles are the

____________, which emanate from the bundle branches to stimulate the ventricular cardiac muscle to contract.

c. Purkinje fibers

16. The QRS complex from an electrocardiogram measures

b. depolarization of the ventricles.

17. The conduction pathways through the atrium to the AV-

node show preferential conduction due to

d. their anatomical structure.


18. True or False: Conduction between the AV node and the

bundle of His is measured by the P-R interval (the time

between atrial activity and ventricular activity).

a. True

19. The anterior internodal pathway (through the atrium to

the AV-node) connects to the anterior interatrial band,

also known as

c. the Bachmann bundle.

20. The connection between atria and ventricles is facilitated

through

a. the AV node.

21. The normal average heart rate of children

d. All of the above

22. True or False: Many children with palpitations do not have an arrhythmia and a detailed first-hand history is

essential before assessing the likelihood of an arrhythmia

and the necessity of further investigation.

a. True

23. When diagnosing a child with an arrhythmia, diagnosis is

based mainly on

d. All of the above

24. Infants generally have heart rates

c. greater than 80 bpm and less than 170 bpm.

25. Common arrhythmias in neonates with structurally

normal hearts include

c. atrioventricular reentry tachycardia (AVRT).


26. A head-up tilt test is sometimes used for investigation of

______________ with recurrent syncope or presyncope.

b. children older than 6 years

27. During the head-up tilt test,

d. All of the above

28. True or False: The first scheme (Vaughan-Williams) is still

the one that most physicians use when speaking of

antiarrhythmic drugs.

a. True

29. In the Vaughan-Williams antiarrhythmic drugs

classifications, _____________ are a class I drug.

a. sodium channel blockers

30. Class Ic antiarrhythmic drugs have slow kinetics so they

express their electrophysiologic effects at _____ heart rates.

d. all

31. Vaughan Williams classification.

b. Digoxin and adenosine

32. True or False: Dronedarone is contraindicated in patients

in atrial fibrillation (AF) who will not or cannot be cardioverted into normal sinus rhythm.

a. True

33. Class I drugs are subdivided based on the kinetics of the

sodium channel effects: Class Ia drugs have ___________ kinetics.

c. intermediate


34. In the Vaughan-Williams antiarrhythmic drugs

classifications, _____________ are a class II drug.

b. beta-blockers

35. True or False: Proarrhythmia is a drug-related arrhythmia

that is worse than the arrhythmia being treated, and it is

an adverse effect of class I drugs.

a. True

36. Class Ib drugs have fast kinetics so they

c. express their electrophysiologic effects only at fast heart

rates.

37. Class II drugs are contraindicated in

c. asthma patients.

38. ______________ is intended for use only in patients with

indicated life-threatening arrhythmias because its use is accompanied by substantial toxicity.

b. Amiodarone 39. When discontinuing nadolol administered long-term,

particularly in patients with ischemic heart disease,

d. gradually reduce dose over a period of 1 to 2 weeks.

40. The use of an ACE inhibitor (ACEI) or angiotensin receptor blocker (ARB) as initial therapy is recommended to

improve kidney outcomes

d. regardless of race or diabetes status.

41. True or False: It may be prudent not to discontinue

nadolol therapy abruptly in patients with possible

coronary artery disease but it is prudent in patients being treated ONLY for hypertension.

b. False


42. Abnormal liver function tests have been reported, some in

the first few weeks of therapy with

c. mexiletine.

43. Permanent pacemaker leads are placed

a. via thoracotomy or transvenously.

44. Pacemakers may malfunction by

d. All of the above

45. In patients with permanent atrial fibrillation (AF),

__________ doubles the risk of death, stroke, and hospitalization for heart failure.

b. dronedarone

46. True or False: To minimize the risk of induced arrhythmia,

patients initiated or re-initiated on dofetilide should be

placed in a facility for at least 3 days for calculations of creatinine clearance, continuous ECG monitoring, and

cardiac resuscitation.

a. True

47. Severe exacerbation of angina and the occurrence of myocardial infarction (MI) and ventricular arrhythmias

have been reported in patients with angina following the abrupt discontinuation of therapy with

b. beta-blockers.

48. Class III drugs are membrane stabilizing drugs, primarily

d. potassium channel blockers

49. True or False: Because class Ia drugs have intermediate

kinetics, their fast-channel tissue conduction slowing effects WILL be evident on an ECG obtained during normal

rhythm at normal rates.

b. False


50. Class IV drugs are the nondihydropyridine

c. calcium channel blockers

References Section

The reference section of in-text citations include published works

intended as helpful material for further reading. Unpublished works

and personal communications are not included in this section, although

may appear within the study text.

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