Chamaeleons.com
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 and the continuing nursing education requirements of the American Nurses Credentialing Center's Commission on Accreditation for registered nurses. It is the policy of 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)/ |Sinoatrial (SA) node becomes dysfunctional and is no longer a reliable pacemaker, most commonly|
|Tachy-Brady Syndrome |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 |Originates above the bundle of His. Reentrant circuits generally have an abrupt onset and |
|(SVT) SVT is used as a |termination, i.e., are paroxysmal. |
|collective term | |
| |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 |Intermittent block of conduction of atrial beats to the ventricle resulting in dropped QRS |
|I, Wenckebach) |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 |Patterned dropping of QRS complex with a fixed ratio of atrial depolarizations (P waves) to |
|II; Classical type) |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 block of AV node resulting in AV dissociation between atrial and ventricular events. |
|Complete Heart Block |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/ |Myocardial ischemia from severe left ventricular outflow obstruction, LV |
|Aortic Valve Surgery |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 |Accessory pathways; AV Block: 2nd & 3rd degree; ventricular ectopy. Congenital AV |
|the Great Arteries (cc-TGA/ L-TGA) |block may preexist due to intrinsic structural malformation. |
|Cor–Triatriatum |Sinus bradycardia, atrial tachyarrhythmias, AV conduction disturbances |
|D-Transposition of the Great Arteries |Sinus bradycardia, sinoatrial block, junctional rhythm, JET, premature atrial |
|(D-TGA) |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|Rare rhythm disturbances observed. Ventricular arrhythmias if coronary sinusoids |
|Septum |with ischemia. |
|Pulmonary Atresia with a VSD |Sometimes AV conduction abnormalities observed. |
|Single Ventricle - Hypoplastic Left Heart|Atrial arrhythmias. |
|Syndrome (HLHS) | |
|Single Ventricle – Bidirectional |Transient sinus node dysfunction. |
|Cavopulmonary (Glenn) Connection | |
|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 |Atrial arrhythmias, JET, sinus bradycardia, AV conduction disturbances. |
|(TAPVR) | |
|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 |VT, SCD. |
| |septal hypertrophy. | |
|Dilated Cardiomyopathy (DCM) |Dilated poorly contractile ventricles. |SVT, VT, SCD. |
|Arrhythmogenic Right Ventricular (RV) |A form of dilated cardiomyopathy. |RV tachyarrhythmias with variable response|
|Cardiomyopathy (ARVC) or Dysplasia |Fibrofatty replacement of the RV wall |to beta-blockers and to catheter ablation.|
| |myocytes and patchy areas of fibrosis with | |
| |progressive RV dysfunction and enlargement.| |
Channelopathies – Electrical Myopathies:8,36
|CARDIOMYOPATHIES |PATHOPHYSIOLOGY |CARDIAC ARRHYTHMIAS |
|Long QT Syndrome (LQTS) |Identified by prolonged QT interval |High risk of bursts of VT such as runs of|
| |corrected for heart rate (QTc). QT interval|Torsades de Pointes, progressing to VF |
| |greater than 0.46 seconds, with upper |and SCD. May present with syncope, |
| |normal limit of 0.44 seconds. |seizures or SCD. |
| | | |
| |Acquired or congenital; can be secondary | |
| |due to drugs, i.e., amiodarone, | |
| |procainamide, sotolol, tricyclic | |
| |antidepressants and/or electrolyte | |
| |imbalance (hypokalemia, hypomagnesemia). | |
|Catecholaminergic Polymorphic Ventricular|Polymorphic ventricular tachycardia. CPVT |VT, ventricular fibrillation, and SCD. |
|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. | |
|Brugada Syndrome (BrS) |Autosomal dominant genetic In 20% of cases,|History of ventricular arrhythmias – |
| |mutations in the sodium channel are thought|ventricular fibrillation, syncope and |
| |to be causative. |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 |Risk SCD from VT and AV block. |
| |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. | |
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 |Ventricular rate control is important goal; |
| |digitalis |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 |PVCs are often benign and do not require treatment |
| |magnesium sulfate | |
|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 |
| |
|Pharmacologic Category |
|Antianginal Agent |
|Antihypertensive |
|Beta-Blocker, Nonselective |
|Sotalol |
| |
|Proarrhythmic effects: |
|To minimize the risk of induced arrhythmia, patients initiated or reinitiated on sotalol or sotalol AF and patients who |
|are converted from IV to oral administration should be placed for a minimum of 3 days (on their maintenance dose) in a |
|facility that can provide cardiac resuscitation, continuous electrocardiographic (ECG) monitoring, and calculations of |
|creatinine clearance (CrCl). |
| |
|Sotalol injection and oral solution (Sotylize): |
|Sotalol can cause life threatening ventricular tachycardia associated with QT interval prolongation. Do not initiate |
|sotalol therapy if the baseline QTc is longer than 450 msec. If the QT interval prolongs to 500 msec or greater, the dose |
|must be reduced, the interval between doses prolonged, the duration of the infusion prolonged (sotalol injection), or the |
|drug discontinued. |
| |
|Adjust the dosing interval based on CrCl. |
| |
|Renal impairment: |
|Calculate CrCl prior to dosing. |
| |
|Product interchange: |
|Do not substitute sotalol for sotalol AF because of significant differences in labeling (i.e., patient package insert, |
|dosing administration, safety information). |
| |
|Brand Names: |
|Betapace |
|Betapace AF |
|Sorine |
|Sotylize |
| |
|Pharmacologic Category |
|Antiarrhythmic Agent, Class II |
|Antiarrhythmic Agent, Class III |
|Beta-Blocker, Nonselective |
| |
|Dosing: |
|Baseline QTc interval and creatinine clearance must be determined prior to initiation. If CrCl ≤60 mL/minute, dosing |
|interval adjustment is necessary. Sotalol should be initiated and doses increased in a hospital for at least 3 days with |
|facilities for cardiac rhythm monitoring and assessment. Proarrhythmic events can occur after initiation of therapy and |
|with each upward dosage adjustment. (Note: Dosing per manufacturer, based on pediatric pharmacokinetic data; wait at least|
|36 hours between dosage adjustments to allow monitoring of QTc intervals). |
| |
|Atrial fibrillation/flutter (symptomatic): Oral: Betapace AF, Sotylize - |
|Infants and Children ≤2 years: Dosage should be adjusted (decreased) by plotting of the child's age on a logarithmic |
|scale; see graph or refer to manufacturer's package labeling. |
|Children >2 years and Adolescents: Initial: 90 mg/m2/day in 3 divided doses; may be incrementally increased to a maximum |
|of 180 mg/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 |
| |
|Pharmacologic Category |
|Antiarrhythmic Agent, Miscellaneous |
|Diagnostic Agent |
| |
|Dosing: |
|Rapid IV push (over 1 to 2 seconds) via peripheral line, followed by a normal saline flush. |
| |
|Paroxysmal supraventricular tachycardia (Adenocard): Infants and Children - IV: |
|Manufacturer's labeling: |
|Children 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 |
|5 mg/hour = 180 mg daily |
|7 mg/hour = 240 mg daily |
|11 mg/hour = 360 mg daily |
|Atenolol |
| |
|Advise patients with coronary artery disease who are being treated with atenolol against abrupt discontinuation of |
|therapy. Severe exacerbation of angina and the occurrence of myocardial infarction (MI) and ventricular arrhythmias have |
|been reported in patients with angina following the abrupt discontinuation of therapy with beta-blockers. The last 2 |
|complications may occur with or without preceding exacerbation of the angina pectoris. As with other beta-blockers, when |
|discontinuation of atenolol is planned, observe the patient carefully and advise the patient to limit physical activity to|
|a minimum. If the angina worsens or acute coronary insufficiency develops, it is recommended that atenolol be promptly |
|reinstituted, at least temporarily. Because coronary artery disease is common and may be unrecognized, it may be prudent |
|not to discontinue atenolol therapy abruptly, even in patients treated only for hypertension. |
|Brand Names: |
|Tenormin |
| |
|Pharmacologic Category |
|Antianginal Agent |
|Antihypertensive |
|Beta-Blocker, Beta-1 Selective |
| |
|Dosing: |
|Hypertension: Oral: Children: 0.5 to 1 mg/kg/dose given daily; range of 0.5 to 1.5 mg/kg/day; maximum dose: 2 mg/kg/day up|
|to 100 mg/day. |
|Esmolol |
| |
|Brand Names: |
|Brevibloc |
|Brevibloc in NaCl |
| |
|Pharmacologic Category |
|Antiarrhythmic Agent, Class II |
|Antihypertensive |
|Beta-Blocker, Beta-1 Selective |
| |
|Dosing: |
|Intraoperative and postoperative tachycardia and/or hypertension: |
|Immediate control: Initial IV bolus: 1 mg/kg over 30 seconds, followed by a 150 mcg/kg/minute infusion, if necessary. |
|Adjust infusion rate as needed to maintain desired heart rate and/or blood pressure (up to 300 mcg/kg/minute) |
|Gradual control: Initial bolus: 0.5 mg/kg over 1 minute, followed by a 50 mcg/kg/minute infusion for 4 minutes. Infusion |
|may be continued at 50 mcg/kg/minute or, if the response is inadequate, titrated upward in 50 mcg/kg/minute increments |
|(increased no more frequently than every 4 minutes) to a maximum of 300 mcg/kg/minute; may administer an optional loading |
|dose equal to the initial bolus (0.5 mg/kg over 1 minute) prior to each increase in infusion rate. |
|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 |
| |
|Pharmacologic Category |
|Antiarrhythmic Agent, Miscellaneous |
|Cardiac Glycoside |
| |
|Dosing: |
| |
|Preterm infant |
|• Total digitalizing dose: |
|– Oral: 20-30 mcg/kg |
|– IV or IM: 15-25 mcg/kg |
|• Daily maintenance dose: |
|– Oral: 5-7.5 mcg/kg |
|– IV or IM: 4-6 mcg/kg |
| |
|Full-term infant: |
|• Total digitalizing dose: |
|– Oral: 25-35 mcg/kg |
|– IV or IM: 20-30 mcg/kg |
|• Daily maintenance dose: |
|– Oral: 6-10 mcg/kg; and, IV or IM: 5-8 mcg/kg |
|1 month to 2 years: |
|• Total digitalizing dose: |
|– Oral: 35-60 mcg/kg |
|– IV or IM: 30-50 mcg/kg |
|• Daily maintenance dose: |
|– Oral: 10-15 mcg/kg |
|– IV or IM: 7.5-12 mcg/kg |
|2-5 years: |
|• Total digitalizing dose: |
|– Oral: 30-40 mcg/kg |
|– IV or IM: 25-35 mcg/kg |
|• Daily maintenance dose: |
|– Oral: 7.5-10 mcg/kg |
|– IV or IM: 6-9 mcg/kg |
|5-10 years: |
|• Total digitalizing dose: |
|– Oral: 20-35 mcg/kg |
|– IV or IM: 15-30 mcg/kg |
|• Daily maintenance dose: |
|– Oral: 5-10 mcg/kg |
|– IV or IM: 4-8 mcg/kg |
|>10 years: |
|• Total digitalizing dose: |
|– Oral: 10-15 mcg/kg |
|– IV or IM: 8-12 mcg/kg |
|• Daily maintenance dose: |
|– Oral: 2.5-5 mcg/kg |
|– IV or IM: 2-3 mcg/kg |
| |
|Heart failure: A lower serum digoxin concentration may be adequate to treat heart failure (compared to cardiac |
|arrhythmias); consider doses at the lower end of the recommended range for treatment of heart failure; a digitalizing dose|
|(loading dose) may not be necessary when treating heart failure. |
|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 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 |
| |
|Pharmacologic Category |
|Antianginal Agent |
|Antihypertensive |
|Beta-Blocker, Beta-1 Selective |
| |
|Dosing: |
|Hypertension: Oral: |
|Immediate release tablet (metoprolol tartrate): Children: 1 to 17 years: Initial: 1 to 2 mg/kg/day; maximum 6 mg/kg/day |
|(≤200 mg daily); administer in 2 divided doses. |
|Extended release tablet (metoprolol succinate): Children ≥6 years: Initial: 1 mg/kg once daily (maximum initial dose: 50 |
|mg daily). Adjust dose based on patient response (maximum: 2 mg/kg/day or 200 mg daily). |
| |
|Use: Labeled Indications |
|Immediate-release tablets (metoprolol tartrate): Treatment of angina pectoris, hypertension, or hemodynamically-stable |
|acute myocardial infarction. |
| |
|Extended-release tablets (metoprolol succinate): Treatment of angina pectoris or hypertension; to reduce |
|mortality/hospitalization in patients with heart failure (HF) (stable NYHA Class II or III) already receiving ACE |
|inhibitors, diuretics, and/or digoxin. |
| |
|Injectable (metoprolol tartrate): Treatment of hemodynamically-stable acute myocardial infarction when used in conjunction|
|with metoprolol oral maintenance therapy. |
| |
|Acute coronary syndromes (i.e., myocardial infarction, unstable angina): According to the ACCF/AHA 2013 guidelines for the|
|management of 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 ................
................
In order to avoid copyright disputes, this page is only a partial summary.
To fulfill the demand for quickly locating and searching documents.
It is intelligent file search solution for home and business.
Related searches
- getroman com reviews
- acurafinancialservices.com account management
- acurafinancialservices.com account ma
- getroman.com tv
- http cashier.95516.com bing
- http cashier.95516.com bingprivacy notice.pdf
- connected mcgraw hill com lausd
- education.com games play
- rushmorelm.com one time payment
- autotrader.com used cars
- b com 2nd year syllabus
- gmail.com sign in