ARRHYTHMIAS IN CHILDREN:

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1 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. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 1

2 Continuing Nursing Education Course Planners William A. Cook, PhD, Director, Douglas Lawrence, MA, Webmaster, Susan DePasquale, MSN, FPMHNP-BC, Lead Nurse Planner Policy Statement This activity has been planned and implemented in accordance with the policies of NurseCe4Less.com and the continuing nursing education requirements of the American Nurses Credentialing Center's Commission on Accreditation for registered nurses. It is the policy of NurseCe4Less.com to ensure objectivity, transparency, and best practice in clinical education for all continuing nursing education (CNE) activities. Continuing Education Credit Designation This educational activity is credited for 4.5 hours. Nurses may only claim credit commensurate with the credit awarded for completion of this course activity. Pharmacology content is 1 hour. Statement of Learning Need There are unique challenges associated with arrhythmias in children and the treatment options for childhood arrhythmia. This information is needed to guide the healthcare professional who is treating children with arrhythmia. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 2

3 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. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 3

4 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 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 4

5 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. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 5

6 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 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 6

7 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. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 7

8 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. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 8

9 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 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 9

10 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 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. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 10

11 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 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 11

12 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 (123) 1-2 days (123) 3-6 days (129) 1-3 weeks (148) 1-2 months (149) 3-5 months (141) 6-11 months (134) 1-2 years (119) 3-4 years (108) 5-7 years (100) 8-11 years (91) years (85) > 16 years nursece4less.com nursece4less.com nursece4less.com nursece4less.com 12

13 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 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 13

14 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 +, Ca 2+ 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 (Ca 2+ ) ions (both from the inside (sarcoplasmatic reticulum) and outside of the cell). These Ca 2+ ions cause the actual muscular contraction by nursece4less.com nursece4less.com nursece4less.com nursece4less.com 14

15 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) Ca 2+ 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 (I Na ) and subsequent activation of the outward K + channel (I to ) and the Na + /Ca 2+ exchanger (I Na,Ca ), which exchanges 3 Na + for 1 Ca 2+, 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. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 15

16 The inward movement of Ca 2+ through the open L-type Ca 2+ channels (I Ca-L ) and the exchange of Na + for internal Ca 2+ by the Na + /Ca 2+ exchanger (I Na,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 + (I Kur and Ks ). Phase 3: Final Rapid Repolarization Final repolarization is mainly caused by inactivation of Ca 2+ channels, reducing the influx of positive ions. Furthermore repolarizing K + currents (delayed rectifier current I Ks and I Kr and inwardly rectifying current I K1 and I K,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 I f, the funny current. Furthermore they lack I K1, a K + ion channel that maintains the resting membrane potential in atrial and ventricular tissue. The I f 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 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 16

17 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 PCO 2, 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. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 17

18 A single circuit of the fibers may induce a premature contraction, whereas continuous cycling of impulses might produce sustained tachycardia. This process may occur in both atrial and ventricular tissue. Conduction block occurs when the normal conduction pathway is blocked and the impulse either expires or conducts through an alternative inappropriate route to depolarize the myocardium. 5 Mechanisms of Arrhythmia Structural abnormalities or electric changes in the cardiomyocytes can impede impulse formation or change cardiac propagation, therefore facilitating arrhythmias. Arrhythmogenic mechanisms can arise in single cells (automaticity, triggered activity), but other mechanisms require multiple cells for arrhythmia induction (reentry). Briefly highlighted is the pathophysiological mechanisms of the main causes of arrhythmia. 2,11 Abnormal Automaticity The mechanism of abnormal automaticity is similar to the normal automaticity of sinus node cells. Abnormal automaticity can be caused by changes in the cell ion channel characteristics due to drugs (digoxin) or changes in the electrotonic environment (myocardial infarction). Abnormal automaticity can result from an increase of normal automaticity in non-sinus node cells or a truly abnormal automaticity in cells that don't exhibit a phase 4 diastolic depolarization. An important phenomenon in (both normal and abnormal) automaticity is overdrive suppression. In overdrive suppression the automaticity of cells is reduced after a period of high nursece4less.com nursece4less.com nursece4less.com nursece4less.com 18

19 frequency excitation. The cellular mechanism responsible for this effect is an increased activity of the Na +, K + pump (I Na, 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. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 19

20 Delayed afterdepolarizations occur after the cell has recovered after completion of repolarization. In delayed afterdepolarization an abnormal Ca 2+ handling of the cell is responsible for the afterdepolarizations due to release of Ca 2+ from the storage of Ca 2+ in the sarcoplasmatic reticulum. The accumulation of Ca 2+ 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 Ca 2+ 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 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 20

21 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 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 21

22 arrhythmias (in other words, a common arrhythmia is often a more likely diagnosis than a rare one). Probably fewer than half of new tachycardias present in the first year of life. By far the most common tachycardia presenting in early infancy is orthodromic AV reentry. Most of these infants have a normal ECG in sinus rhythm but some show ventricular preexcitation. Other neonatal tachycardias are much less common and include atrial flutter, permanent junctional reciprocating tachycardia, atrial tachycardia, and ventricular tachycardia. 12 The most common tachycardia in childhood is also orthodromic AV reentry tachycardia, although AV nodal re-entry tachycardia becomes progressively more common after the age of 5 years. Less common tachycardias in this age group are antidromic AV re-entry, atriofascicular re-entry, ventricular tachycardias, and atrial tachycardias. 5 Arrhythmias presenting with palpitations include most of the common types of supraventricular tachycardia and a few cases of ventricular tachycardia. Many children with palpitations do not have an arrhythmia and a detailed first-hand history is essential before assessing the likelihood of an arrhythmia and the necessity of further investigation. Similarly, very few children with chest pain have arrhythmias (or indeed any cardiac abnormality) and only a few with syncope have an arrhythmia. Again it all depends on the history. Incessant tachycardias presenting with heart failure or apparent cardiomyopathy include focal atrial tachycardia, permanent junctional nursece4less.com nursece4less.com nursece4less.com nursece4less.com 22

23 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 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 23

24 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 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 24

25 Mechanisms of tachyarrhythmias can be enhanced automaticity with triggered foci or enhanced conduction with the presence of reentrant circuits. Similarly, bradycardia can result from suppressed automaticity or suppressed conduction, where normal conduction is delayed or blocked. Understanding the mechanism informs the optimal treatment choice. Types of Arrhythmias The following tables provide a general overview of the different types of arrhythmias. 2,7,15,16 Sections of this course later on will provide more detailed information on the most common types. CARDIAC ARRHYTHMIA Sick sinus syndrome (SSS)/ Tachy-Brady Syndrome CHARACTERISTICS Sinoatrial (SA) node becomes dysfunctional and is no longer a reliable pacemaker, most commonly manifested as bradycardia, although there can also be tachycardia. When the sinus rate is slower than another potential pacemaker in the heart, it may no longer be the dominant pacemaker. SSS can also cause an alternating bradycardia and tachycardia. A number of rhythms result including sinus bradycardia, sinus arrest and junctional rhythm, and ectopic atrial and nodal rhythms. The term SSS includes SA node dysfunction plus symptoms of dizziness, syncope or sudden cardiac death. Bradycardias Often caused by hypoxia, vagal tone, hypothyroidism, cardiac surgery, endocarditis and myocarditis, hyperkalemia, sleep, hypothermia, sedation and anesthesia. Sinus bradycardia: Sinus node slower than normal for age related normal values. Slow junctional escape rhythm/nodal rhythm: Spontaneous depolarization of the AV node. The sinus node has either failed to fire or is slower than the AV node. Rates beats/min in children less than 3 yrs. and beats/min for children older than 3yrs. Can be common after atrial surgery and are usually transient. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 25

26 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 Wandering Atrial Pacemaker Supraventricular Tachycardias (SVT) SVT is used as a collective term Premature atrial, junctional and ventricular ectopic beats are common and may occur in patterns of bigeminy, trigeminy, quadrageminy or couplets. These are generally benign. 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. Originates above the bundle of His. Reentrant circuits generally have an abrupt onset and termination, i.e., are paroxysmal. Sinus tachycardia: Sinus node is faster than age-related normal values due to enhanced automaticity. Usually due to fever, pain, anxiety, anemia, medications, hypovolemia or in the presence of increased catecholamines. While not generally an indication of conduction system pathology, sinus tachycardia may be an important indicator of significant cardiovascular compromise. Reentrant tachycardias: Reentrant tachyarrhythmias require the presence of two possible conduction pathways with different conduction and refractory properties. The tachycardia uses both pathways; one as an antegrade limb and one as a retrograde limb of the reentry circuit. a) Within the atria: atrial flutter, atrial fibrillation; intraatrial reentrant tachycardia (IART) atrial flutter- or incisional tachycardia represents macroreentry within the atrial muscle and may be slower than atrial flutter. b) Atrioventricular reentrant tachycardias include: - atrioventricular reentrant tachycardia (AVRT): commonly associated with Wolff- Parkinson-White. Accessory pathway present allowing impulses that entered via the AV node to enter the atria - atrioventricular nodal reentry tachycardia (AVNRT): uses a slow-fast AV nodal pathway. Antegrade conduction limb is the slow pathway and retrograde limb fast one. Simulation of the atria by the retrograde pathway produces inverted p- waves. Concurrent stimulation of the ventricles. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 26

27 - 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 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 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. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 27

28 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) 1st Degree Heart Block 2nd Degree Heart Block (Mobitz I, Wenckebach) 2nd Degree Heart Block (Mobitz II; Classical type) 3rd Degree Heart Block/ Complete Heart Block 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. Slowed conduction through the AV node resulting in prolonged duration of PR interval. Intermittent block of conduction of atrial beats to the ventricle resulting in dropped QRS complexes. Progressive lengthening of the PR interval until a QRS is dropped and the cycle starts again with a shorter PR interval that progressively lengthens. Patterned dropping of QRS complex with a fixed ratio of atrial depolarizations (P waves) to conducted beats with a consistent PR interval throughout. It is higher risk than Mobitz I. Intermittent block of conduction of some beats to the ventricle without progressive prolongation of the PR interval. Potentially may progress to complete heart block. Related to His bundle or bundle branch dysfunction. Complete block of AV node resulting in AV dissociation between atrial and ventricular events. No relationship between the P waves and QRS complexes. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 28

29 Specific Categories of Cardiac Arrhythmias As noted earlier, there are many reasons for arrhythmias. Increased end diastolic pressures resulting in atrial or ventricular stretch, valvular dysfunction, tumors, multiple surgeries, scarring and ischemia all play a significant role in arrhythmia generation. Cardiac swelling, pro-arrhythmic drugs, acid/base and electrolyte imbalance are also frequent etiologies of rhythm issues. Neonatal Arrhythmias Common arrhythmias in neonates with structurally normal hearts are premature atrial contractions (PAC s), atrial flutter, atrioventricular reentry tachycardia (AVRT), permanent junctional reciprocating tachycardia (PJRT), ventricular tachycardia, and heart block. Neonatal heart block is associated with maternal autoimmune disease, i.e., systemic lupus. Post-operative Arrhythmias Early post-operative arrhythmias usually seen are sinus tachycardia, sinus bradycardia, SVT, JET, complete AV block, and less frequently ventricular tachycardia. Post-operative arrhythmias result from manipulation or injury of the conduction system. The site of surgical repair may increase the risk of certain types of arrhythmias observed. Late post operative arrhythmias such as atrial flutter, and/or intraatrial reentrant tachycardia are seen months to years after surgery. These arrhythmias are observed more often with Fontan, Mustard, Senning and tetralogy of Fallot repairs. These tachyarrhythmias can result in poor ventricular function and decreased quality of life. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 29

30 Common late post operative arrhythmias include atrial tachycardia, which may be seen in 50% of Fontan patients and tend to recur after a period of time. Arrhythmias associated with specific congenital cardiac malformations are highlighted in this section. 4,28,17 Aortic Arch with VSD Severe Aortic Stenosis/ Aortic Valve Surgery JET Myocardial ischemia from severe left ventricular outflow obstruction, LV hypertrophy and strain resulting in ventricular arrhythmias. Conduction abnormalities and complete heart block may be seen post surgical resection of sub-aortic obstructive tissue. Although remote to the conduction system, junctional tachycardia may occur. Prone to VT. Atrial Septal Defect (ASD) Atrioventricular Septal Defect (AVSD) Congenitally Corrected Transposition of the Great Arteries (cc-tga/ L-TGA) Cor Triatriatum D-Transposition of the Great Arteries (D-TGA) Sinus node dysfunction and transient atrial arrhythmias, atrial flutter, atrial fibrillation, ventricular tachycardias. 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. Accessory pathways; AV Block: 2nd & 3rd degree; ventricular ectopy. Congenital AV block may preexist due to intrinsic structural malformation. Sinus bradycardia, atrial tachyarrhythmias, AV conduction disturbances Sinus bradycardia, sinoatrial block, junctional rhythm, JET, premature atrial contractions, Mobitz 1, VT. Prone to VT if repaired with atrial level switch procedures, Senning or Mustard. Late complications of arrhythmias in the Jatene arterial switch procedure are rare. Late complications of atrial switch (Senning/Mustard) are that greater than 50% of patients have serious arrhythmias. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 30

31 Ebstein s Anomaly of the Tricuspid Valve Heart Transplant Pulmonary Atresia with Intact Ventricular Septum Pulmonary Atresia with a VSD Single Ventricle - Hypoplastic Left Heart Syndrome (HLHS) Single Ventricle Bidirectional Cavopulmonary (Glenn) Connection Single Ventricle Fontan Tetralogy of Fallot (TOF) Total Anomalous Pulmonary Venous Return (TAPVR) Truncus Arteriosus Tricuspid Atresia Ventricular Septal Defect (VSD) 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. 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. Rare rhythm disturbances observed. Ventricular arrhythmias if coronary sinusoids with ischemia. Sometimes AV conduction abnormalities observed. Atrial arrhythmias. Transient sinus node dysfunction. Sinus node dysfunction, atrial reentrant tachycardia: atrial flutter, atrial fibrillation, intra-atrial tachycardia, VT. Early or late SVT, junctional rhythm, accelerated junctional rhythm and VT. Sinus node dysfunction, supraventricular tachycardias atrial flutter, accelerated junctional rhythm, JET, AV blocks, VT. Right bundle branch block (RBBB). Prone to VT due to the volume loading on the RV causing RV dilation, failure, and increased right sided pressures. Predisposes patient to SCD. Atrial arrhythmias, JET, sinus bradycardia, AV conduction disturbances. AV conduction disturbances; ventricular arrhythmias due to the right ventriculotomy. Supraventricular arrhythmias; atrial ectopy, flutter, fibrillation. Junctional rhythm, accelerated junctional rhythm, JET, VT (Grosse-Wortmann, 2010), AV conduction block. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 31

32 Inherited Cardiomyopathies Genetic predisposition to cardiac arrhythmias with an increased risk of sudden cardiac death are reviewed in the section below. 1,7 CARDIOMYOPATHIES PATHOPHYSIOLOGY CARDIAC ARRHYTHMIAS Hypertrophic Cardiomyopathy (HCM) Hypertrophic myocardium with asymmetric septal hypertrophy. VT, SCD. Dilated Cardiomyopathy (DCM) Arrhythmogenic Right Ventricular (RV) Cardiomyopathy (ARVC) or Dysplasia Dilated poorly contractile ventricles. A form of dilated cardiomyopathy. Fibrofatty replacement of the RV wall myocytes and patchy areas of fibrosis with progressive RV dysfunction and enlargement. SVT, VT, SCD. RV tachyarrhythmias with variable response to beta-blockers and to catheter ablation. Channelopathies Electrical Myopathies: 8,36 CARDIOMYOPATHIES PATHOPHYSIOLOGY CARDIAC ARRHYTHMIAS Long QT Syndrome (LQTS) Identified by prolonged QT interval corrected for heart rate (QTc). QT interval greater than 0.46 seconds, with upper normal limit of 0.44 seconds. Acquired or congenital; can be secondary due to drugs, i.e., amiodarone, procainamide, sotolol, tricyclic antidepressants and/or electrolyte imbalance (hypokalemia, hypomagnesemia). High risk of bursts of VT such as runs of Torsades de Pointes, progressing to VF and SCD. May present with syncope, seizures or SCD. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 32

33 Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT) Brugada Syndrome (BrS) Polymorphic ventricular tachycardia. CPVT is initiated by stimulation of the adrenergic receptors from stress, emotion or exertion/physical activity; found in normal hearts with normal coronary arteries and normal ECG s. Autosomal dominant genetic In 20% of cases, mutations in the sodium channel are thought to be causative. VT, ventricular fibrillation, and SCD. History of ventricular arrhythmias ventricular fibrillation, syncope and SCD. Marked by RBBB and striking ST elevation in V1-V3. ECG manifestation and arrhythmias most likely during times of fever. Inflammatory Disease: 8 Myocarditis ACQUIRED PATHOPHYSIOLOGY CARDIAC Viral myocarditis is a cell mediated immunologic reaction. Myocardium may have lymphocyte infiltration, necrosis and scarring. Myocarditis may lead to cardiomegaly and congestive heart failure, hemodynamic compromise, shock and death. Cells undergo lymphocyte infiltration, necrosis and scarring. ARRHYTHMIAS Risk SCD from VT and AV block. Clinical Evaluation Of The Pediatric Patient The following components of clinical assessment are necessary when a health provider approaches the pediatric patient to evaluate for a cardiac arrhythmia. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 33

34 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 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 34

35 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. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 35

36 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. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 36

37 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 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 37