BRADYCARDIAS, AND OTHER

HEART RHYTHM DISTURBANCES

BASIC

JASSIN M. JOURIA, MD

Dr. Jassin M. Jouria is a practicing Emergency Medicine physician, 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 serve 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

Electrocardiograms are valuable tests for evaluating health and to diagnose cardiac issues. But the test is only as good as the skill of the clinician performing it. Medical clinicians must commit to learning and updating their electrocardiogram procedure and interpretation skills to arrive at a correct diagnosis, and these skills start with an understanding of the basic function of the electrocardiogram. Being able to identify normal readings on an electrocardiogram rhythm strip is the first step to recognizing cardiac issues, and possibly saving lives.

1 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 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 3.5 hours. Nurses may only claim credit commensurate with the credit awarded for completion of this course activity.

Pharmacology content is 0.5 hours (30 minutes).

Statement of Learning Need

Health clinicians in general practice and cardiology need to be able to understand the function and information generated by an electrocardiogram. The correct diagnosis and proper treatment of a cardiac condition is dependent on competent and accurate interpretation of diagnostic tests, which includes the electrocardiogram in both inpatient and outpatient settings.

2 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Course Purpose

To provide health clinicians with basic knowledge about the purpose, function and diagnostic data of an electrocardiogram.

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.

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.

3 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 1. The P wave is a summation wave that is generated by the depolarization front as it transits the

a. . b. ventricles. c. bundle of His. d. atria.

2. True or False: Normally, the right depolarizes earlier than the left atrium since the depolarization wave originates in the sinoatrial node.

a. True b. False

3. An ECG reading showing a P wave with increased amplitude can be an indication of

a. hyperkalemia. b. hypokalemia. c. Wolff–Parkinson–White (WPW) syndrome. d. hypotrophy.

4. ______are known as P mitrale and indicate left-atrial abnormality, such as left-atrial dilation or hypertrophy.

a. Bifid P waves b. P waves with increased amplitude c. P wave with a flat baseline d. P waves that are not clearly delineated

5. ______is an ECG recording that was not made by the electrical activity of the heart.

a. An ECG artifact b. An ectopic c. A bifid P wave d. An ECG variant

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

An electrocardiogram indicates heart activity by recording atrial and ventricular activity. It generates waveforms that become recorded on an electrocardiogram report. Variations in the normal progression of an electrocardiogram, waveform intervals or amplitude, can be a sign that a patient may have a certain medical condition. It is important for a clinician to understand what medical condition is associated with a specific change in the electrical activity of the heart. Examination of the electrocardiogram is key to appropriate diagnosis in addition to a physical examination and accurate history taking. The goal is to determine whether heart rhythm abnormalities exist in the electrocardiogram report and to correlate those with any reported symptoms.

Atrial Depolarization And Repolarization

The electrocardiogram measures electrical impulses while they travel through the heart, using ECG patches with wires attached to the skin to measure the impulses, the impulses display on a monitor or print on paper as waves of electrical activity. The electrocardiogram measures the electrical impulses as five distinct waves. These waves are called P, Q, R, S, and T. The Q through T waves show electrical activity in the lower chambers (ventricles) of the heart. When considering the P waves and their presence, frequency, relationship to the QRS complex, appearance, and conformity, the P wave in an electrocardiogram (ECG) represents atrial depolarization that results in atrial contraction. The P wave is a summation wave that is generated by the depolarization front as it transits the atria. Normally, the right atrium depolarizes earlier than the left atrium since the depolarization wave originates in the sinoatrial node, in the high right atrium and then through the left atrium.

5 nursece4less.com nursece4less.com nursece4less.com nursece4less.com The depolarization front is carried through the atria along semi-specialized conduction pathways including Bachmann's bundle. This results in uniform shaped waves. Depolarization that originates elsewhere in the atria as with atrial ectopy results in a P wave with a different morphology compared to normal. A P wave with increased amplitude can be an indication of hypokalemia. It can also be an indication of . A P wave with decreased amplitude can be an indication of hyperkalemia. Bifid P waves are known as P mitrale and indicate left-atrial abnormality, such as left-atrial dilation or hypertrophy.19

In a situation where at least three different shaped P wave are on a given ECG lead tracing, this can imply that even if one arises from the SA node, at least two can arise elsewhere. This could be evidence of multiple ectopic foci called multifocal or multiform atrial rhythm if the rate is equal to or less than 100. It is multifocal atrial if the rate is over 100. This can be common in exacerbations of chronic obstructive lung disease.

If the baseline has a totally irregular form this could suggest fibrillatory waves of atrial . It could also suggest possible ECG artifact, which is an ECG recording that was not made by the electrical activity of the heart. A baseline with a saw tooth shape suggests the flutter waves of . With these two rhythms and a fast ventricular rate, it is easy to misinterpret the fibrillatory or flutter waves as P waves. The absence of a P wave with a flat baseline could indicate fine or sinoatrial arrest with a secondary escape rhythm. If P waves are not clearly delineated in the surface ECG, another lead can be used to better visualize the P waves.

Atrial repolarization occurs at a mean of 320 milliseconds (ms) after the end of a P wave. It has a duration of 2-3 times that of the P wave. The polarity is

6 nursece4less.com nursece4less.com nursece4less.com nursece4less.com always opposite to that of the P wave. It is represented on a surface ECG as what is called a Ta wave.

In a normal ECG, atrial and ventricular depolarization and repolarization appear on an ECG as a series of waves. The P wave is followed by the QRS complex and the . The first deflection is the P wave associated with right and left atrial depolarization. The first positive deflection in the complex is called an R wave. The normal ECG patterns are explained more specifically below.

PR Interval

In electrocardiography, the PR interval is the period that extends from the beginning of the P wave (the onset of atrial depolarization) until the beginning of the QRS complex (the onset of ventricular depolarization). It is measured in milliseconds. This interval is sometimes termed the PQ interval. Variations in the PR interval can mean an association with certain medical conditions.

A long PR interval is considered to be over 200 ms. This can indicate a first degree . Prolongation can be associated with the condition of hypokalemia, acute , or associated with Lyme disease. A short PR interval is considered to be less than 120 ms. It can be associated with Wolff–Parkinson–White (WPW) syndrome, Lown–Ganong– Levine syndrome, or junctional rhythms. A variable PR interval could mean another type of heart block. Atrial injury or could be indicated by a PR segment depression.30,31

The normal PR interval is from 0.12 - 0.2 seconds (s) and is measured on the ECG from the beginning of the P wave to the beginning of the QRS

7 nursece4less.com nursece4less.com nursece4less.com nursece4less.com complex. This interval represents the onset of atrial depolarization to the onset of ventricular depolarization. It consists of atrial depolarization, electrical conduction from the atria to the ventricles via the AV node (end of the P to the beginning of the R wave), and conduction through the His- Purkinje System.32

Anomalies in the PR interval may be physiologic or may represent abnormal progression of electrical conduction from the atria to the ventricles through the AV node. These are evident in either prolongation (PR ≥ 0.2 s) or shortening (PR ≤ 0.12 s).

The differential for an abnormal PR interval begins with exclusion of abnormality. This would be due to normal PR variability. The diagnostic algorithm to use next is based on the length of the PR interval; shortened PR or prolonged PR.

In normal physiologic states, the PR interval may vary with heart rate. This is due to variations in sympathetic tone. Increased tone mediates increased conduction through the AV node at faster heart rates and shortened PR. Withdrawal of sympathetic tone or increased vagal inputs will slow conduction through the AV node at slower heart rates with a lengthened PR. Typically, and in the majority of cases even with physiologic variability, the PR interval should be between 0.14 and 0.2 s. Individuals without known cardiac disease, such as with young adults and well-conditioned athletes, will rarely present with a PR > 0.2 s that is physiologic. In this clinical case, administration of atropine invariably shortens the PR interval. This is not the case for a patient with underlying cardiac pathophysiologic disease.

8 nursece4less.com nursece4less.com nursece4less.com nursece4less.com With a PR interval < 0.12 s, Wolff-Parkinson-White (WPW) syndrome should be considered. The differential for a PR interval less than 0.12 s is short. It is largely limited to the diagnosis of an accessory bypass tract between the atria and ventricles. In this clinical presentation, the PR interval is shortened as electrical conduction has bypassed the normal route of conduction through the AV node. The cardiac current travels directly between the atria and ventricles. The accessory conducting tissues could be between the atria and ventricles, between the atria and the AV node (atriofasicular pathways), or between the AV node and the (nodoventricular).

For a PR interval > 0.2 s, a heart block should be considered. With isolated prolonged PR intervals, patients are rarely symptomatic. For a prolonged PR interval associated with a higher grade AV block, a patient can present with symptoms. These can be fatigue, decreased exercise tolerance, and fainting. Patients, in general, with prolonged PR intervals that have symptoms tend to be older and have a history of . Young adults or well- conditioned athletes will on occasion present with asymptomatic PR prolongation. The differential of a prolonged PR interval is based on the ECG. It can be divided into first degree heart block with prolonged PR interval. It can also be divided into second degree heart block as a higher grade AV block, Mobitz Type I or Mobitz Type II.

A diagnostic approach for PR < 0.12 s is to start with accurate history taking. This can help differentiate a shortened PR due to a physiologic variant with no associated bypass tract, or accelerated conduction through the AV node, versus a shortened PR due to accelerated conduction associated via a bypass tract. A patient with a physiologic variant is asymptomatic. They come to clinical attention generally due to an ECG analysis. A patient with a shortened PR and a history of sudden palpitation

9 nursece4less.com nursece4less.com nursece4less.com nursece4less.com should be considered as a physiologic variant, as a diagnosis of exclusion only. Not all patients with bypass tracts are symptomatic. The lack of symptoms cannot be used to exclude a diagnosis of a bypass tract as associated with a shortened PR interval.

Examination of the ECG is key to appropriate diagnosis in addition to accurate history taking. The goal is to determine if the short PR is associated with other ECG abnormalities. It is appropriate to look for Wolf Parkinson White Syndrome, as it manifests with a short PR, slurring of the QRS complex (delta wave), and a widened QRS. It is also appropriate to look for Atriofasciular or Nodofasicular Pathways, which manifests with a short PR interval and normal width QRS.

A diagnostic approach for a PR interval > 0.2 s is an appropriate diagnosis of a prolonged PR based on ECG analysis. The goal is to determine the severity of the AV nodal dysfunction from simple delay in conduction to complete lack of conduction through the AV node or complete heart block. The ECG should also be examined for other abnormalities that could be associated with the prolonged PR, and evaluated for the following:

• PR interval uniformly prolonged before each QRS (first degree heart block) • PR interval progressively prolonged until there is no P wave before a QRS (Mobitz Type I, site of block usually in the AV node and proximal to the bundle of His) • PR interval following the dropped beat shorter than the PR interval prior to the dropped beat (Mobitz Type I) • QRS complexes tending to cluster together (Mobitz Type I) • Normal PR interval followed by a nonconducted P wave (Mobitz II, site of block usually infranodal)

10 nursece4less.com nursece4less.com nursece4less.com nursece4less.com • Pathologic Q waves • Changes on ECG suggestive of active (inferior MI associated with Mobitz I, anterior wall MI associated with Mobitz II)

The diagnostic differential can also be approached based on the cause of the prolonged PR. Some of the possible causes include:

• Underlying cardiac disease (previous MI, , myocarditits, electrical degeneration with age) • Ongoing active ischemia (acute inferior wall MI, acute anterior wall MI) • Medication effect (amiodarone, , beta blockers, calcium channel blockers) • Electrolyte abnormalities (hyperkalemia) • High vagal tone (young adults, well-conditioned athletes) • Hypothyroidism • Idiopathic

Historical information for treating PR < 0.12 s includes several examples of what is important in the diagnosis. Note that patients with shortened PR intervals due to bypass tracts may present with paroxysmal supraventricular tachycardia. History taking should cover a history of light headedness, palpitations, near loss of consciousness, fainting, or unexpected death in patients and family members. Some historical questions to ask the patient include:

• Have you ever experienced palpitations or the sensation of your heart racing? • Have you ever suddenly lost consciousness? • Does anyone in your family have a history of sudden cardiac death, palpitations, or sudden loss of consciousness?

11 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Historical information for PR > 0.2 s includes taking a history that determines if the prolonged PR is associated with higher grade AV block (Mobitz I or II). The clinician should investigate the following: Is the delay in nodal conduction significant enough to impair cardiac output? Does it cause syncope or lightheadedness? In addition, the patient’s history should cover reasons for conduction disease. Other questions to cover include: 1. Have you ever had an episode where you lost consciousness or felt as if you were going to pass out? If so, when? 2. Have you ever had an episode of sudden onset of dizziness? 3. What medications are you currently taking? Have you recently started or stopped any medications? 4. Have you ever been told that you have cardiac disease? To your knowledge, have you had an MI in the past?

Physical examination for PR < 0.12 seconds should include several items that will be useful in diagnosing the cause of the problem. A full cardiac exam should be part of the exam in patients with a suspected bypass tract. Patients who have bypass tracts generally have no other associated cardiac abnormalities. A physical exam should include auscultation as in some cases, though rare, a bypass tract can be associated with congenital heart disease (Ebsein’s Anomaly), heritable (glycogen storage disease), or prolapse.

Physical examination for PR > 0.2 s with a prolonged PR should include a full cardiac exam. Emphasis should be on the pulse, looking for an irregular pulse with dropped beats (Mobitz I) or an irregular pulse with some dropped beats (Mobitz II). Evaluation should also include evidence of co-existing heart disease. This should cover cardiomyopathy or .

12 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Laboratory, radiographic, and other testing for PR < 0.12 s include several considerations to be useful in diagnosing the cause of the problem. Genetic testing in specialized scenarios could be appropriate to diagnose a heritable form of Wolff-Parkinson-White syndrome. Laboratory testing is generally not helpful in diagnosis of an accessory tract.

Laboratory testing for PR > 0.2 s should consider that this type of PR abnormality can be diagnosed through ECG analysis and causes are usually determined by history. A cause can sometimes be determined through laboratory testing. This is generally in the setting of a medication-induced abnormality or severe hypothyroidism. With these cases, measuring a drug level as, such as digitalis, or thyroid stimulating hormone (TSH) is useful in determining the diagnosis.

Electrocardiogram criteria alone are not sufficient for diagnosis of a bypass tract associated with a shortened PR. This is because the findings could be intermittent. The shortened PR could also represent a physiologic variant consistent with enhanced AV conduction. Wolff-Parkinson-White could be associated with the presence of a delta wave or widened QRS. Generally, a patient with a suspected bypass tract should be referred for further evaluation to a cardiac electrophysiologist.

Any PR interval ≥ 0.2 s is considered prolonged. Criteria to differentiate between first degree heart block - simple PR prolongation - and second degree heart block - Mobitz I and II – are listed below.

• First degree heart block: PR ≥ 0.2 s, PR interval uniformly prolonged before each QRS. • Second degree heart block, Mobitz I: PR ≥ 0.2 s, gradual prolongation of the PR interval until there is failed conduction (P with no subsequent

13 nursece4less.com nursece4less.com nursece4less.com nursece4less.com QRS), shortened PR following the dropped QRS, presence of group beating. • Third degree heart block Mobitz II: PR ≥ 0.2 s, fixed duration of PR interval with abrupt appearance of the P without a subsequent QRS.

Management of PR < 0.12 s (considering WPW) while the diagnostic process is proceeding should include several considerations for this clinical problem of PR interval abnormality.

In an acute condition, a patient with an accessory bypass tract may present with supraventricular tachycardia. The ventricles could become pre-excited. This is during atrial fibrillation in patients with atrioventricular reentrant tachycardia due to conduction through the bypass tract. This poses a risk of degeneration into . Patients with a known history of pre-excitation or evidence of pre-excitation as seen on an ECG should not be given nodal agents to control their heart rate when presenting with atrial fibrillation. This could exacerbate their .

In a chronic condition, a patient can present with a shortened PR interval. This is diagnosed solely by ECG. In this situation, emphasis should be placed on determining if a patient has associated symptomatic tachycardia suggestive of a bypass tract. A patient with a symptomatic tachycardia should be referred to a cardiologist for evaluation. Possible treatment could be with radiofrequency ablation of the bypass tract if appropriate. The risk is low overall for sudden cardiac death in asymptomatic patients with a known bypass tract. However, asymptomatic patients should be referred to a cardiologist for evaluation and determination of risk.

14 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Management for PR > 0.2 s and a prolonged PR is determined by the degree of AV nodal blockade. Here are factors to consider.33-35

• First degree AV block requires no intervention.

• Second degree heart bock, Mobitz I, is generally due to reversible causes (active ischemia, medication effect) and emergency management is aimed at increasing the heart rate while the underlying cause is managed. If the heart rate is greater than 40 beats per minute and the patient is asymptomatic, there is no need for intervention to increase the heart rate. If the heart rate is less than 40 beats per minute and the patient is symptomatic, atropine 0.5 mg may be given as needed up to 3 doses every 3-5 minutes to increase conduction through the AV node.

To increase heart rate, alternative medications could be appropriate. Symptomatic patients with reversible causes could require the insertion of a temporary pacemaker while the reversible cause is addressed. Symptomatic patients with an irreversible cause require insertion of a permanent pacemaker.

• Second degree heart block Mobitz II generally represents severe infra AV nodal conduction disease and is less likely to be due to reversible cause. Emergency management is the same as that for symptomatic Mobitz I. Mobitz II is more likely to progress to complete heart block. These patients usually require insertion of a permanent pacemaker.

The following sections will include a discussion of the varied heart conditions detected through the ECG. A helpful University of Utah web-based ECG Learning Center to view related cardiac rhythm images is available at https://ecg.utah.edu.

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Bradycardia is less than 60 beats per minute in adults and involves a heart rate less than normal. Advanced cardiac life support (ACLS) refers to a set of clinical interventions for the urgent treatment of , stroke, and other life-threatening medical emergencies, as well as the knowledge and skills to deploy those interventions. A look at the ACLS Bradycardia Algorithm for management of bradycardia would be of value.35,36

The ACLS Bradycardia Algorithm outlines the steps for assessing and managing a patient who has symptomatic bradycardia. It begins with the decision that the patient's heart rate is < 60 beats per minute (bpm). This is the reason for the patient’s symptoms. Once the decision is that the heart rate is < 60 bpm and the patient is symptomatic, a clinician can assess and manage the affected patient using the primary and secondary ACLS surveys. At this point, the clinician needs to maintain the patient airway and assist with breathing as needed. The clinician should administer oxygen if oxygen saturation is less than 94% or the patient is short of breath.

The blood pressure and heart rate should be monitored. A 12-lead ECG should be obtained and reviewed. Additionally, intravenous (IV) access should be established. A problem-focused history and physical examination should be completed in search of possible contributing factors and the right treatment.

Two questions will help a clinician decide if the patient's physical signs and symptoms of poor perfusion are caused by the bradycardia.

1. Are the signs or symptoms serious, such as hypotension, pulmonary congestion, dizziness, shock, ongoing chest pain, shortness of breath,

16 nursece4less.com nursece4less.com nursece4less.com nursece4less.com congestive , weakness or fatigue, or acute altered mental status? 2. Are the signs and symptoms related to the slow heart rate?

There may be another reason for the patient’s symptoms other than the slow heart rate. The clinician should determine if the patient has adequate perfusion. Determination of a treatment sequence depends on the severity of the patient's clinical presentation. If perfusion is adequate, the clinician should monitor and observe the patient. If perfusion is poor, the clinician should move quickly through the following steps:

• Prepare for transcutaneous pacing, which is the application of electrical energy to a patient’s heart to stimulate contraction. Do not delay pacing. If no intravenous (IV) line is present, pacing can be pursued first.

• Consider administering atropine 0.5 mg IV if IV access is available. This may be repeated every 3 to 5 minutes up to 3mg or 6 doses.

• If the atropine is ineffective, begin pacing if it has not been initiated already.

Epinephrine or dopamine should be considered while waiting for the heart pacing procedure, or if pacing is ineffective. Epinephrine should be given at 2 to 10 µg/min. Dopamine should be given at 2 to 10 µg/kg per minute. The clinician should progress quickly through these actions as the patient could be in pre-cardiac arrest and need multiple interventions done in rapid succession - pacing, IV atropine, dopamine and epinephrine.

17 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Mobitz Type I, Mobitz Type II and

Mobitz Type I and Mobitz Type II is related to an atrioventricular (AV) block and is understood as a delay or interruption in the transmission of an impulse from the atria to the ventricles due to an anatomic or functional impairment in the conduction system. This conduction disturbance can be permanent or transient. Conduction can be delayed, intermittent, or absent.37,38

With a first degree AV block there is delayed conduction from the atrium to the ventricle defined as a prolonged PR interval of > 200 ms without interruption in atrial to ventricular conduction. With a second degree AV block there is intermittent atrial conduction to the ventricle, often in a regular pattern (for example, 2:1, 3:2), or higher degrees of block, which are further classified into Mobitz type I (Wenckebach) and Mobitz type II second degree AV block. With a third degree (complete AV) block there is no atrial impulse conduction to the ventricle. With a high-grade AV block, there are two or more consecutive blocked P waves.

To be more precise, a Type 1 second-degree AV block, Mobitz I or Wenckebach, is almost always a disease of the AV node. A Mobitz I heart block is characterized by progressive prolongation of the PR interval on the electrocardiogram on consecutive beats followed by a blocked P wave. This is a dropped QRS complex. After the dropped QRS complex, the PR interval resets and the cycle repeats.

A baseline assumption when determining if an individual has Mobitz I heart block is that the atrial rhythm has to be regular. With atrial rhythm that is not regular, an alternative explanation of why certain P waves does not conduct to the ventricles may exist. There could be a benign condition and

18 nursece4less.com nursece4less.com nursece4less.com nursece4less.com no specific treatment is needed. In symptomatic cases, conduction can be transiently improved with intravenous atropine or isoproterenol.

A Type 2 Second-degree AV block is also known as Mobitz II and is almost always a disease of the distal conduction system (His-Purkinje System). On a surface ECG, Mobitz II heart block is characterized by intermittently non- conducted P waves not preceded by PR prolongation and not followed by PR shortening. Typically, there is a fixed number of non-conducted P waves for every successfully conducted QRS complex. This ratio is often specified in describing Mobitz II blocks. As an example, Mobitz II block could be two P waves for every one QRS complex and could be referred to as a 2:1 Mobitz II block. Of medical significance, this type of AV block could progress rapidly to complete heart block. No escape rhythm may emerge. For such a case, the individual could experience a Stokes-Adams attack, cardiac arrest, or sudden cardiac death. The treatment for complete AV Block is an implanted pacemaker. The impairment is typically below the AV node. The term infranodal block or infrahisian block can be applied to this disorder. They refer to the anatomical location of the block.

Second-degree atrioventricular (AV) blocks are a disease of the electrical conduction system of the heart. There is a conduction block between the atria and ventricles. Diagnosis of the presence of a second degree AV block comes when one or more but not all of the atrial impulses do not conduct to the ventricles. This is due to impaired conduction. Regarding people with Wenckebach (Type I Mobitz), these people do not show symptoms. However, for those people who do show symptoms these can include lightheadedness, dizziness, and fainting.

19 nursece4less.com nursece4less.com nursece4less.com nursece4less.com With the two non-distinct types of second degree AV blocks, these are called Type 1 and Type 2. For both types, a P wave is blocked from initiating a QRS complex. In Type 1, there are increasing delays in each cycle before the omission. With Type 2, there is no such pattern. The Type 1 second degree heart block is considered to be more benign than the Type 2 second degree heart block.

Concerning the P:QRS ratios, the Type 1 Mobitz block occurs in regular cycles, and there is always a ratio that is fixed between the number of P wave and the number of QRS complexes per cycle. This ratio can be specified when describing the block. As an example, a Mobitz Type I block with 4 P waves and 3 QRS complexes per cycle could be called 4:3 Mobitz Type I block. With a Type II Mobitz block, this usually occurs with a fixed P:QRS ratio. There is a set number of P waves for every successful QRS. Frequently, this ratio is specified; for example, it could be 3:1, 4:1, 5:1, or a higher Mobitz Type II block.

Higher numbers of P waves for every QRS means a more severe block. The Type II Mobitz block is unstable by nature. It is possible for the P:QRS ratio in a Mobitz Type II block to change with time. It is also possible to not differentiate the type of a Mobitz block. For example, reference could be made to to 3:1 Mobitz block or 4:2 Mobitz block. There is no ambiguity except in the case of a 2:1 block. With a 2:1 block, there are two P waves for every QRS complex.

It is not possible to differentiate Type I from Type II Mobitz blocks based solely on the P:QRS ratio. It is not possible to differentiate either on a pattern of lengthening PR intervals. In this case, a lengthened PR interval

20 nursece4less.com nursece4less.com nursece4less.com nursece4less.com with a normal QRS width could likely indicate a type I pathology. A normal PR interval with a widened QRS is likely indicating a type II pathology.

QRS Complex

When considering the QRS complex, its interval length, and consistency of appearance, the QRS complex is typically the most visually obvious and central part of an ECG tracing. It corresponds to the right and left ventricles of the heart. It typically lasts 0.06 to 0.10 seconds. During physical activity and in children it could be shorter.

The Q wave, R wave, and S wave occur in rapid succession. They do not all appear in all leads and reflect a single event. They are usually considered together. A Q wave is any downward deflection that comes after a P wave. An R wave follows and is an upward deflection. The S wave is any downward deflection after the R wave. A T wave follows the S wave. In some cases, an additional wave follows the T wave and is called the U wave.

Concerning formation, depolarization of the heart ventricles occurs almost simultaneously via the Bundle of His and Purkinje fibers. When they work efficiently, the QRS complex duration is 80 to 120 ms. This appears as three small squares or fewer at the standard paper speed of 25 mm/second. Any abnormality of conduction takes longer and causes a widened QRS complex. In the , there is an abnormal second upward deflection. This would be within the QRS complex. In such a case, a second upward deflection is referred to as R’ or R Prime. This would be called an RSR pattern.

As ventricles contain more muscle mass than do atria, the QRS complex is considerably larger than the P wave. The QRS complex can often be used to

21 nursece4less.com nursece4less.com nursece4less.com nursece4less.com determine the axis of the electrocardiogram. It is possible, however, to determine a separate P wave axis.

Duration, amplitude, and morphology or the QRS complex can be useful in diagnosing various disease states and cardiac , conduction abnormalities, , , and electrolyte derangements. Q wave duration is up to 0.04 seconds in leads other than III and aVR. Amplitude for the Q wave is less than 1/3 QRS amplitude (R+S). The amplitude of the Q wave is less than one-fourth of the R wave. Abnormality can indicate the presence of infarction.

The QRS complex is included in estimating the QT interval. For normal Q waves, when present, they represent depolarization of the interventricular septum. They are thus called septal Q waves. They can be appreciated in the lateral leads I, aVL, V5 and V6. A pathological Q wave occurs when the electrical signal passes through stunned or scarred heart muscle. They are usually markers of previous myocardial infarctions with subsequent fibrosis.

A pathologic Q wave is defined as having a deflection amplitude of 25 percent of more of the subsequent R wave; or, it is greater than 0.04 seconds (40 ms) in width and greater than 2 mm in amplitude. Diagnosis requires the presence of this pattern in more than one corresponding lead. ST elevation is how myocardial infarctions with pathological Q waves are identified.

The normal value for QRS duration is 0.06 to 0.10 seconds. It is shorter in children. Prolonged duration indicates, for example, hyperkalemia or bundle branch block. Increased amplitude shows cardiac hypertrophy. Concerning the Q wave, an abnormality indicates the presence of infarction. The R wave

22 nursece4less.com nursece4less.com nursece4less.com nursece4less.com progression, seen in the precordial lead, usually progresses from showing an rS type complex in V1 with an increasing R and decreasing S wave when moving towards the left side. Usually there is a qR-type of complex in V5 and V6. The R wave amplitude usually is taller in V5 than in V6.

What is normal is to have a narrow QS and rSr’ pattern in V1. This is so also for qRs and R patterns in V5 and V6. A transition zone is when the QRS complex changes from predominately negative to predominately positive. The R/S ration becomes greater than 1. This usually occurs at V3 and V4. It is normal to have the transition zone at V2 called early transition, and at V5 called delayed transition. Consider that in biomedical engineering, the maximum amplitude in the R wave is typically called R Peak Amplitude or just R Peak. It is essential to have accurate R peak detection in signal processing equipment for heart rate measurement. It is the main feature used in arrhythmia detection.

Poor R wave progression (PRWP) varies in definition in the literature. A typical definition is when the R wave is less than 2 to 4 mm in leads V3 and V4 and/or there is presence of a reversed R wave progression. This is defined as 1) R in V4 < R in V3, 2) R in V3 < R in V2, 3) R in V2 < R in V1, or 4) any combination of these. It is typical for poor R wave progression to be attributed to anterior myocardial infarction. It may also be , Wolff–Parkinson–White syndrome, right and left ventricular hypertrophy and attributed to faulty ECG recording technique.

The J-point is the point where the QRS complex meets the ST segment. This J-point is easy to identify. It is when the ST segment is horizontal and forms a sharp angle with the last part of the QRS complex. When the ST segment is sloped or the QRS complex is wide, the two features do not form a sharp

23 nursece4less.com nursece4less.com nursece4less.com nursece4less.com angle. The location of the J-point is less clear. There is not a consensus on the exact location of the J-point with these circumstance. One definition could be the first point of inflection of the upstroke of the S wave. Another definition is the point where the ECG tracing becomes more horizontal than vertical.

Not every QRS complex includes a Q wave, R wave, and S wave. Any combination of these waves can be called a QRS complex. Correct interpretation of a challenging ECG requires exact labeling of various waves. Some individuals use lowercase and uppercase letters. This depends on the relative size of each wave. As an example, an Rs complex is positively deflected and rS complex is negatively deflected. If labeled RS for each of these complexes, it is not possible to see this distinction without viewing the actual electrocardiogram.

Long QT Syndrome

Long QT syndrome (LQTS) is a heart rhythm condition. It can potentially cause fast and chaotic heart beats. These rapid heartbeats can trigger a sudden fainting spell or seizure. The heart can in some cases beat erratically for so long that it causes sudden death. Some people have a genetic mutation that puts them at risk of being born with congenital long QT syndrome. Other causes of acquired long QT syndrome can be due to the use of certain medications, imbalances of the body’s salts and minerals – causing electrolyte abnormalities, and medical conditions.46

Treatment for long QT syndrome can include taking medications to prevent an erratic heart rhythm. Surgery or an implantable device is another treatment option. A patient should also avoid certain medications that can trigger long QT syndrome. A patent can do very well with the condition and

24 nursece4less.com nursece4less.com nursece4less.com nursece4less.com effective treatment. Some with long QT syndrome are even able to be active in recreational and competitive sports.

Some people have long QT syndrome and do not have signs or symptoms. Others are aware of the condition if they have a family history of long QT syndrome, get genetic test results, or discover the condition as a result of an electrocardiogram done for another reason. Those who do have symptoms can experience fainting spells. This is the most common sign of the condition. A fainting spell or syncope can be triggered by long QT syndrome or by a heart temporarily beating in an erratic manner. Fainting could happen when a person is angry, excited, or exercising.

Another symptom is losing consciousness with no warning. This can be from being startled by a ringing telephone. Some people get a warning sign before a fainting spell. This warning sign could be lightheadedness, heart palpitations, irregular heartbeat, blurred vision, or weakness. In some cases, there is little or no warning before a fainting spell from long QT syndrome.

Seizures are another symptom or sign. If a heart continues to beat erratically, the brain will not get enough oxygen. This can cause a seizure.

Sudden death is another symptom or sign. Generally, a heart will return to its normal rhythm. If this does not happen by itself, sudden death will occur unless an external defibrillator is used in time to convert the rhythm back to normal.

With congenital or inherited long QT syndrome, signs and symptoms could start for a fetus during the first weeks to months after birth. It could start also at an older age or never. Most who have signs and symptoms of long

25 nursece4less.com nursece4less.com nursece4less.com nursece4less.com QT syndrome have an episode before the age of 40. Signs and symptoms of the condition can occur during sleep or at arousal from sleep. Care from a health clinician should happen if a person suddenly faints during physical exertion, emotional excitement, or after using a new medication. This is especially if the medication is known to prolong a QT interval. As long QT syndrome can be familial, a person should ask their health clinician if they want to be tested for the condition. This would be if a first degree relation such as a parent, sibling, or child is diagnosed with long QT syndrome.84-87

Causes of LQTS

The heart rhythm disorder known as long QT syndrome can cause serious irregular heart rhythms known as arrhythmias. Normally the heart circulates blood throughout the body with each heartbeat. The chambers of a heart contract and relax as they pump blood. Electrical impulses control these actions. The electrical impulses travel through the heart and cause it to beat. After a heartbeat, the electrical system of a heart recharges itself. This is in preparation for the next heartbeat.88

With LQTS the muscle of the heart takes longer than normal to recharge between beats. This is an electrical disturbance often seen on an electrocardiogram, and is called prolonged QT interval. In the space between the start of the Q wave and end of the T wave is the QT interval. This corresponds to the time for the heart to contract and refill with blood. This comes before the beginning of the next contraction. Measurement can show if this QT interval happens in a normal amount of time. If it takes longer than normal to happen, this is called a prolonged QT interval. Age, sex, and regularity and speed of the heart rate are taken into account for the upper limit of a normal QT interval.

26 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Long QT syndrome results from abnormalities in the heart's electrical recharging system. However, the heart's structure is normal. Abnormalities in the heart's electrical system might be inherited. Or, they may be acquired due to an underlying medical condition or a medication.

Inherited LQTS

At least 17 genes associated with long QT syndrome have been found so far, and hundreds of mutations within these genes have been identified. Mutations in three of these genes account for about 75 percent of LQTS cases, while mutations in the other minor genes contribute a small percent of long QT syndrome cases.

About 20 percent of people who definitely have congenital LQTS have a negative genetic test result. On the other hand, among families with genetically established LQTS, between 10 percent and 37 percent of the relatives with a positive LQTS genetic test have a normal QT interval.

Inherited long QT syndrome is described as either Romano-Ward or Jervell and Lange-Nielsen syndromes. Romano-Ward syndrome is the more common form. It occurs in people who inherit only a single genetic variant from one parent. Jervell and Lange-Nielsen syndrome is a rare form. It usually occurs earlier and is more severe. In this syndrome, children inherit genetic variants from each parent. They are born deaf and also have long QT syndrome.

In addition, scientists are investigating a link between sudden infant death syndrome and LQTS. They discovered that about five to ten percent of babies affected by sudden infant death syndrome have a genetic defect or mutation for long QT syndrome.46,89

27 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Acquired LQTS

Acquired long QT syndrome can be caused by certain medications, electrolyte abnormalities such as hypokalemia or other medical conditions. More than 100 medications — many of them common — can lengthen the QT interval in otherwise healthy people and cause a form of LQTS known as drug-induced long QT syndrome.

Medications can lengthen the QT interval and upset the heart rhythm. These medications include certain antibiotics, certain antidepressant and antipsychotic medications, some antihistamines, diuretics, some anti-nausea medication, and medications used to maintain normal heart rhythms - antiarrhythmic medications. People who develop drug-induced long QT syndrome may have some subtle genetic defects in their . This kind of defect make them more likely to have disruptions in their heart rhythm due to certain medications.

Risk Factors for LQTS

People who may have a higher risk of inherited or acquired long QT syndrome could include children, teenagers, and young adults with unexplained fainting, unexplained near drownings or other accidents, unexplained seizures, or a history of cardiac arrest. These can also include family members of children, teenagers and young adults with similar symptoms, such as first-degree relatives of people with known LQTS, people taking medications known to cause prolonged QT intervals, and people with low potassium, magnesium or calcium blood levels, for example those with anorexia nervosa.

Inherited long QT syndrome can go undiagnosed. It can also often go misdiagnosed as a seizure disorder such as epilepsy. Long QT syndrome

28 nursece4less.com nursece4less.com nursece4less.com nursece4less.com could be responsible for other unexplained deaths in children and young adults. An example is an unexplained drowning of a young person. This could be the first clue of inherited LQTS in a family.

Complications from LQTS

In general, prolonged QT intervals in people who have LQTS do not cause problems. Stress that is physical or emotional could impact a heart that is sensitive to prolonged QT intervals. This could cause a heart’s rhythm to go out of control. This could trigger a life threatening and irregular heart rhythm. Such an arrhythmia could include Torsade de pointes and ventricular fibrillation.

Torsade de pointes also known simply as torsade is a twisting of the points and an arrhythmia where the two lower chambers of the heart – ventricles – beat fast and chaotically. This makes the waves on an electrocardiogram output look twisted. Less blood pumps out from the heart and reaches the brain. This can cause someone to suddenly faint and often with no warning. If an episode of torsade is short and under one minute the heart can correct itself. A person can regain consciousness on their own. If an episode of torsade lasts longer, this can result in a sudden fainting spell. This can be followed by a full body seizure. If a dangerous rhythm does not correct itself, what follows could be a life threatening arrhythmia called ventricular fibrillation.

Ventricular fibrillation causes the ventricles to beat so fast that the heart quivers. It also ceases to pump blood. Unless the heart is shocked back into a normal rhythm by a defibrillator, ventricular fibrillation can lead to brain damage. It can also lead to sudden death.

29 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Finally, it is also now known that a long QT syndrome can explain cases of sudden death in a young person who appears to be healthy.46,90

Prevention of LQTS

With a case of inherited long QT syndrome, a person must be careful with what medications they take. This could include appetite suppressants, decongestants, and common antibiotics that could trigger a dangerous heart rhythm. Illegal drugs such as amphetamines and cocaine can also pose a serious risk for someone with long QT syndrome.

In addition, a person should seek immediate medical treatment for an illness that could result in low blood potassium levels. This is especially if a person has vomiting and diarrhea. This kind of illness could trigger an episode of LQTS. A medical clinician could advise not to take certain drugs such as diuretics as they lower blood potassium levels. For some, as with those who are older adults with LQTS and no signs or symptoms of the condition in decades, no treatment is needed other than preventive measures.46

Wolff-Parkinson-White Syndrome

With Wolff-Parkinson-White (WPW) syndrome, a person experiences episodes of tachycardia due to an abnormal extra, electrical pathway in the heart. Some people with WPW have no symptoms. Treatment is available to those who have symptoms. The long-term outcome for someone who has WPW is excellent. This is especially true when using treatments to eliminate the abnormal conduction pathway.49

An understanding of WPW begins with an understanding of the structure of the heart and its normal electrical conduction system. To briefly review, the

30 nursece4less.com nursece4less.com nursece4less.com nursece4less.com four chambers of the heart are the right and left atria and right and left ventricles. Blood goes from the body and returns to the heart into the right atrium. The blood then goes into the right ventricle. Blood is then pumped out of the right ventricle into the lungs where red blood cells fill with oxygen and then the blood returns to the heart through the left atrium. Blood in the left atrium then goes to the left ventricle which pumps the blood to the rest of the body through the aorta.79

Electrical impulses stimulate heart muscle cells and cause them to contract. They contract in a uniform way and at a regular rate. The contraction produces a heartbeat that moves the pumping of blood out of the heart and into arteries and all parts of the body. Normally, a heartbeat is produced when the heart’s natural pacemaker, the sinoatrial or sinus node (an area of specialized cells in the upper portion of the right atrium), sends out a series of regular electrical impulses. These electrical impulses travel in an organized way along conduction tissue in the heart. First, they pass across both atria then go to an area between the atria and ventricles known as the atrioventricular (AV) node. They finally spread across the ventricles, the heart’s main pumping chambers at a normal heart rate of about 60 to 100 beats per minute.79

Causes of WPW Syndrome

A patient with WPW syndrome has an extra, electrical pathway between the atria and ventricles. This is known as an accessory pathway. In a normal heart, the atria are almost completely isolated from the ventricles electrically. This is because they are separated by fibrous atrioventricular rings. The rings are at the level of the heart valves that separate the ventricles from the atria. The AV node is normally the only electrical connection between the ventricles and atria.70

31 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Conduction in the AV node is slower than other parts of the conduction system. This is to allow time for ventricles to fill with blood before contracting. In a person with WPW syndrome the accessory pathway directly connects the atria and ventricles at a site other than the AV node. This can be considered to be a small gap in the insulation between the ventricles and atria. The connection size can be as small as a hair. An accessory pathway allows the electrical signal to from the atria to the ventricles more quickly than is normal. The signal travels in a way that bypasses the AV node where the electrical signal travels more slowly. What results is that the normal sinus impulse can travel down the normal path through the AV node or the more rapidly conducting accessory pathway. This means the impulse traveling through the accessory pathway reaches the ventricle earlier. This causes what is termed as pre-excitation and poses a risk of developing a short circuit of the normal electrical pathway, resulting in tachycardia.

Wolff-Parkinson-White syndrome occurs with a patient who has a recurring tachycardia because of this abnormal pathway. Also, a patient can have a WPW pathway but no tachycardia. This patient does not have WPW syndrome but may at some point develop it. The WPW pattern can be detected on a routine electrocardiogram.

Concerning causes of tachycardia, the existence of an accessory pathway alone does not explain tachycardia. This is because the sinus node rate generally ranges from 60 to 100 beats per minute. There are two mechanisms of tachycardia in the WPW syndrome. One is atrioventricular reentrant tachycardia. The other is atrial fibrillation.

Atrioventricular reentrant tachycardia (AVRT) is the most common mechanism of tachycardia in a patient with WPW. With this tachycardia, an

32 nursece4less.com nursece4less.com nursece4less.com nursece4less.com electrical impulse travels down one pathway either through the AV node or the accessory pathway. It then travels back up the other, creating a repeating loop. This circular or reentrant electrical activity sends impulses to the ventricles at an abnormally high rate. This causes the heart to beat from 140 to 250 times per minute. This tachycardia of WPW syndrome begins suddenly and can stop just as suddenly on its own. It can last seconds or hours. Treatment can sometimes be needed to end the tachycardia and return to a normal rhythm. A patient with WPW syndrome typically has recurrent episodes of tachycardia. The mechanism of tachycardia is rarely life threatening. However, it can degenerate into another mechanism called atrial fibrillation.80,81

Atrial fibrillation is an abnormal rhythm that a patient with WPW can less commonly develop. With atrial fibrillation the atria beat in an uncoordinated way at a rate of 350 to 600 beats per minute. Normally the AV node blocks most of these impulses and the ventricular rate is felt in the pulse and usually less than 170 beats per minute. With WPW, as conduction from the atria to the ventricles can be rapid, the result is more impulses getting to the ventricles by crossing the accessory pathway. Ventricles can beat at 200 beats per minute or more. There is a risk the heart can beat up to 300 times per minute. This kind of rapid heart rhythm can lead to cardiac arrest and sudden death. Because of the risk of this rhythm being life threatening, most patients with WPW are recommended to undergo catheter ablation.

WPW Symptoms and Diagnosis

A person with WPW syndrome can have no symptoms and no tachycardia. If a symptom does occur with WPW syndrome, this is related to development of an abnormal heart rhythm and rapid heart rate. With tachycardia can come palpitations, dizziness, fainting, lightheadedness, and rarely sudden

33 nursece4less.com nursece4less.com nursece4less.com nursece4less.com death. Sudden death can come as a result of a very rapid ventricular response seen in WPW syndrome. With a very rapid heart rate, ventricles cannot pump blood effectively to vital organs. The incidence of sudden death for people with WPW is low at 0 to 0.39 percent a year. The lowest risk is for those who have WPW with no symptoms.

No other underlying structural heart disease such as or congestive heart failure is the situation for many patients with WPW syndrome. If other heart disease is present with WPW, the heart could be less able to tolerate a rapid heart rate. In this case, there is an increase in the likelihood of serious symptoms. These symptoms include chest pain and difficulty breathing.

An electrocardiogram is what is usually used to diagnose WPW and can detect a WPW pattern even while a patient is in a normal rhythm. Specialized testing could also be required for some patients.

A characteristic ECG pattern in WPW involves conduction through the accessory pathway. A short PR and delta are classic findings. These reflect early conduction or pre-excitation to the ventricles through the accessory pathway. The PR interval is the time for conduction between atria and ventricles. If most of the impulses going from the atria to the ventricles go through the AV node, a short PR interval, delta wave, and other findings associated with a WPW pattern will not be seen.

For some people with WPW, an ECG can vary from day to day. It can even vary from hour to hour. This can depend on factors such as adrenaline released during periods of stress or caffeine intake. In addition, these factors can alter the relative proportion of impulses conducted through the

34 nursece4less.com nursece4less.com nursece4less.com nursece4less.com accessory pathway. These are the only impulses that produce the WPW pattern.

While the diagnosis of WPW syndrome is based on ECG evidence of the accessory pathway and presence of related tachycardia, for some patients a special invasive procedure called an electrophysiology study could be helpful. The results of this testing can determine the reason for the tachycardia. It can also identify the location of the accessory pathway. In addition, it can determine if the accessory pathway has dangerous properties. The location in a hospital where the test is performed is called an electrophysiology lab. The patient gets sedative medication before the procedure. Throughout testing the blood pressure, heart rate and rhythm, and oxygen levels are monitored for the patient.

To complete the electrophysiology study, a heart rhythm specialist who is specially trained threads small wires called electrode catheters typically through a vein in the inner thigh. In some situations, a vein in another area of the body could be preferred. The catheters are advanced into the heart. At this point they are positioned at various locations. The catheters provide for precise monitoring or mapping of the electrical pathways in the heart.49,70

Treatment for WPW

If a person has a WPW pattern on an ECG and has no tachycardia, the person typically needs no treatment. The person might never develop symptoms. In some young patients, conduction via the accessory pathway disappears spontaneously as they grow older. Some asymptomatic people with a WPW ECG pattern could be advised to get additional testing. These could be people in a high risk occupation or professional athletes. The

35 nursece4less.com nursece4less.com nursece4less.com nursece4less.com testing could include electrophysiology testing. This will determine if the accessory pathway is associated with high risk for sudden cardiac arrest.69

Treatment is required for a patient with WPW syndrome if the patient has an episode of tachycardia as there are serious potential risks from tachycardia. The treatment should have a focus on stopping the tachycardia and prevention of it recurring. If the tachycardia is an AVRT, interfering with the circular loop can often stop the tachycardia. To achieve this goal, the Valsalva maneuver or carotid sinus pressure maneuver could help. With the Valsalva maneuver the patient coughs or bears down as if having a bowel movement. The carotid sinus pressure maneuver involves firmly massaging the main artery in the neck of the patient. If use of these maneuvers is not effective, medications could stop the tachycardia. The choice of medication should depend on the mechanism responsible. A cardiologist with experience in the treatment of rhythm disturbances is typically the specialist who assists with treatment.

Electric cardioversion can help to stop the arrhythmia if a patient is unstable due to low blood pressure from a rapid heart rate or if medication is not immediately effective. During cardioversion, electricity is discharged into the patient’s heart using pads or paddles placed on the chest. The current has an effect on the electrical charge of the heart muscle cells to restart a normal rhythm.

Radiofrequency ablation, medication, and surgery are the three major options for preventing recurrent of tachycardia. A heart rhythm specialist or cardiac electrophysiologist with experience in treating WPW syndrome is typically the best choice for deciding on which option is best for treatment.

36 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Radiofrequency ablation of the accessory pathway for a patient with WPW syndrome is the treatment of choice. This procedure is performed in a hospital’s electrophysiology lab. The patient gets sedative medication to reduce discomfort. A wire electrode catheter is advanced into the heart from large blood vessels. Then the catheter is positioned in the chambers of the heart using fluoroscopy low energy X-rays. After localizing the accessory pathway, radiofrequency energy that is high frequency electricity is delivered to the area to destroy the accessory pathway and prevent it from conducting impulses. With an experienced specialist performing this procedure, ablation cures the WPW syndrome in over 95 percent of cases. Some patients have multiple accessory pathways. For these patients, if there is no detection of one of the pathways and it is not ablated during the initial procedure, the arrhythmia could recur. In this case, if the ablation procedure is repeated the result is generally good.82,83

The risk of major complications is low at about three percent. The primary risks are damage to the blood vessels or nerves of the thigh, bleeding, perforation of the heart, infection, and heart block that requires a pacemaker. The risk of a specific complication depends in part on the location of the accessory pathway and what critical structures are near.

Surgery is another way to disconnect the WPW pathway. The success rate for surgical ablation is close to 100 percent. The complication rate is low. Radiofrequency ablation is less invasive. Surgery now is rarely performed for this reason. If a patient is undergoing cardiac surgery for another reason, surgical ablation could be a good option. Cardiac surgery could be for a coronary artery bypass or valve surgery. Surgery is recommended when radiofrequency ablation and medication is not effective.

37 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Medications can help to prevent recurrence of tachycardia in a patient with WPW. This is typically for a patient who is not a candidate for ablation or surgery. The patient could get medication to use during an episode or to take daily to prevent the arrhythmia. The patient could also learn to perform maneuvers that can stop the tachycardia. Valsalva is a maneuver where a patient coughs or bears down as if having a bowel movement.49

Torsade de Pointes

Torsade de Pointes is an uncommon and distinctive form of polymorphic (VT). It is characterized by a gradual change in the amplitude and twisting of the QRS complexes around the isoelectric line. As mentioned, Torsade de Pointes is also called torsade. It is associated with a prolonged QT interval. It can be congenital or acquired. Torsade usually terminates spontaneously but it can frequently recur. It can also degenerate into ventricular fibrillation.

Torsade is generally described as having regular variation of the morphology of the QRS vector from positive to net negative and back again. The “twisting of the point" about the isoelectric axis has been described as with a ballet movement. Most of the cases exhibit polymorphism; axis changes may not have regularity. The form of the QRS complex varies from beat to beat. The ventricular rate can range from 150 beats per minute to 250 beats per minute (bpm). The definition can require that the QT interval is increased markedly. It can be greater than or equal to 600 msec. Torsade can occur in bursts that are not sustained.21

The management of torsade is generally different from the management of other ventricular tachycardia that is the fast heart rhythm that starts in the heart ventricles. If left untreated, a form of ventricular tachycardia could get

38 nursece4less.com nursece4less.com nursece4less.com nursece4less.com worse and lead to ventricular fibrillation. This can be life threatening. Treatment of ventricular tachycardia can include the use of group IA anti- dysrhythmic drugs, which tend to prolong the QT interval. This kind of drug should not be used in torsade and the consequences can be disastrous. It is critically important to differentiate the difference of torsade from other forms of ventricular tachycardia.

Risk factors for torsade include a congenital long QT syndrome. Additional risk factors include the female gender or an acquired long QT syndrome with causes of this including medication and electrolyte disorders such as hypokalemia and hypomagnesemia. Other risk factors include bradycardia or baseline electrocardiographic abnormalities. Renal or liver failure is another risk factor.

Torsade can also be a side effect of certain anti-arrhythmic medications, such as sotalol, procainamide, and quinidine. Also, propulsid is a gastrokinetic drug that was withdrawn from the U.S., market in 2000. It was linked to deaths caused by long QT syndrome induced torsade.22

Clinicians should be aware of the condition of torsade and that it is a distinctive form of polymorphic ventricular tachycardia characterized by a gradual change in the amplitude and twisting of the QRS complexes around the isoelectric line.40 As a heart condition associated with a prolonged QT interval, it may be congenital or acquired. It can terminate spontaneously but frequently recurs and may degenerate into ventricular fibrillation.

A case example of a patient with torsade would be one where the patient was asymptomatic and reportedly on erythromycin, and found on ECG to have marked QT prolongation in conjunction with profound hypomagnesemia

39 nursece4less.com nursece4less.com nursece4less.com nursece4less.com and hypokalemia. This would be an example of a recurrent and non- sustained Torsade de Pointes. Once erythromycin was discontinued and there was aggressive repletion of the magnesium and potassium, no further torsade de pointes occurred. The patient's QT interval returned to normal.

The management of torsade is generally different than treatment of a typical ventricular tachycardia. This includes the use of group IA antidysrhythmic drugs. These drugs tend to prolong the QT interval. The drugs can have disastrous consequences in torsade. Differentiating between ventricular tachycardia and torsade is absolutely critical.

Pathophysiology of Torsade

What is known is an association between torsade and a prolonged QT interval. The mechanisms involved at the cellular and ionic levels are now becoming clearer. The abnormality that underlies acquired and congenital long QT syndromes is in the ionic current flow during repolarization. This affects the QT interval.

Changes in ionic current may result in the effect of decreased repolarizing current. This is reflected in a long QT. These changes can secondarily lead to depolarizing currents and possible action potentials. These are called afterdepolarizations. These lead to further delay in repolarization. It also causes early afterdepolarization (the triggering event for torsade). This repolarization has three phases. With the initial upstroke of potential in a normal cardiac cell, there is a rapid influx of positive ions. This is Na+ and Ca++. The influx results in the depolarization of the cell membrane. After this there is a rapid and transient outward potassium current (Ito). This is while the influx rate of positive ions (Na+, Ca++) declines. This is the initial part of phase 1 that is the repolarization.

40 nursece4less.com nursece4less.com nursece4less.com nursece4less.com With phase 2 comes a plateau. Positive currents flowing inward and outward are almost equal during phase 2. With phase 3 of repolarization there is mediation by activation of the delayed rectifier potassium current (IK) moving outward while the inward positive current decays.

If there is slow inactivation of the Ca++ and Na+ currents, the inward window current can cause single or repetitive depolarization during phases 2 and 3. These are early afterdepolarizations that appear as pathologic U waves on a surface ECG. When they reach a threshold, they may trigger ventricular tachyarrhythmias.

Changes in repolarization do not occur in all myocardial cells. More prone to prolongation of repolarization are the deep endocardial region and mid myocardial layer – composed of M cells – in the ventricle. They are also more prone to early afterdepolarization as they have a less rapid delayed rectifier potassium current (IKr). Other regions may have shorter or normal cycles. This quality of repolarization in the myocardial cells promotes the spread of triggered activity. This is initiated by early afterdepolarizations through a reentrant mechanism. This is now thought to be responsible for the maintenance of torsade.

Currently recognized are six genetic variations that are underlying torsade. Genotypes LQT1 and LQT2 have slow potassium channels. LQT3 shows defects in the sodium channels. Treatment modalities soon could be based on the genotype of the individual.40

Causes of Torsade

Prolongation of the QT interval could be congenital. This is seen in the Jervell and Lange-Nielsen syndrome mentioned earlier that is a congenitally long QT

41 nursece4less.com nursece4less.com nursece4less.com nursece4less.com associated with congenital deafness. It is also seen in the Romano Ward syndrome where there is an isolated prolongation of the QT interval. These syndromes are associated with sudden death. This is due either to primary ventricular fibrillation or torsade that degenerates into ventricular fibrillation.

Brugada syndrome shows a coved ST segment in the right precordial leads. This syndrome can cause sudden death. This is due to polymorphic ventricle tachycardia that resembles torsade. Takotsubo cardiomyopathy is stress induced cardiomyopathy. It causes a predisposition to torsade.

An acquired condition that predisposes someone to torsade can decrease the outward potassium current. Or it can interfere with the inward sodium and calcium currents or fluxes. Reports show electrolyte disturbances that precipitate torsade include hypokalemia and hypomagnesemia. With these disturbances there is a delay in phase III that is reprolongation. The disturbances form the substrate for the emergence of the dysrhythmia. Close observation is in order for a predisposed patient, which includes individuals with cirrhosis or hypothyroidism.

Antiarrhythmic drugs reported to cause to torsade include class IA agents such as quinidine, procainamide, disopyramide. They also include class IC agents such as encainide, flecainide and class III agents such as sotalol, amiodarone. Also, what can precipitate torsade are drug interactions with the antihistamines astemizole and terfenadine that were recalled from the U.S., market. These drugs should not be used with class IA, IC, or III agents. Reports show precipitation of torsade and sudden death with the use of astemizole and terfenadine in high dosages or when used in combination with the azole antifungal drugs or the macrolide antibiotics. What has been shown to slow the hepatic metabolism of this antihistamines is grapefruit

42 nursece4less.com nursece4less.com nursece4less.com nursece4less.com juice, which also has this effect on other drugs and has been shown to prolong the QT interval for patients taking astemizole or terfenadine. The clinical implications of this interaction remain unclear.

Other drugs prolong the QT interval and are implicated in cases of torsade. They include phenothiazines, tricyclic antidepressants, lithium carbonate, ziprasidone, cisapride, highly active antiretroviral drugs, and high-dose methadone. They also include anthracycline chemotherapeutic agents such as doxorubicin, daunomycin, some fluoroquinolones, and any other medication using the CYP3A metabolic pathway.39

Ranolazine is an anti- agent. It also prolongs the QTc. Torsade is a rare complication of this therapy.40

Multiple agents can act synergistically. QT prolongation is variable among and in a single individual. The causative agent can be speculative. Lists of suspected agents increasing the QT interval could include drugs that do not have the effect.

Torsade Risk Factors

The risk factors for torsade have been raised earlier; and include being female, a congenital long QT syndrome, bradycardia. Also included is acquired long QT syndrome caused by medications and electrolyte disorders such as hypokalemia and hypomagnesemia. Baseline electrocardiographic abnormalities, renal or liver failure, and congenital long QT syndromes that are adrenergic-dependent are also implicated. Congenital syndromes associated with torsade include Jervell and Lange-Nielsen syndrome, Romano-Ward syndrome, and acquired long QT syndromes.

43 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Drugs in a number of drug classes have been associated with torsade. A more thorough summary of those drugs include: 1) antiarrhythmic drugs associated with torsade include Class IA - Quinidine, disopyramide, procainamide. It also includes Class III - Sotalol, amiodarone (rare), ibutilide, dofetilide, almokalant, 2) antibiotics, such as erythromycin, clarithromycin, azithromycin, levofloxacin, moxifloxacin, gatifloxacin, trimethoprim-sulfamethoxazole, clindamycin, pentamidine, chloroquine, 3) antifungals, such as ketoconazole, itraconazole, 4) antivirals, such as amantadine, 5) antipsychotics, such as haloperidol, phenothiazines, thioridazine, trifluoperazine, sertindole, zimeldine, ziprasidone, 5) tricyclic and tetracyclic antidepressants, 6) antihistamines, such as terfenadine, astemizole, diphenhydramine, hydroxyzine, 7) cholinergic antagonists, such as cisapride, and 8) diuretics, such as indapamide, hydrochlorothiazide, and furosemide. It should be noted that lithium, some antihypertensives, anticonvulsants (phenytoin, carbamazepine), oral hypoglycemic, citrate with massive blood transfusions, cocaine, vasopressin, fluoxetine, anesthetics (dexmedetomidine, propofol) and loperamide antidiarrheal agent have been associated with torsade. Notably, loperamide has been associated in torsade even in patients without a predisposing genetic or cardiac abnormality, typically as a result of misuse.

Some drugs such as amiodarone routinely prolong QT. These are less commonly associated with clinical consequences of long QT.

Certain conditions are associated with torsade. These include electrolyte abnormalities such as hypokalemia, hypomagnesemia, hypocalcemia. They also include endocrine disorders such as hypothyroidism, hyperparathyroidism, pheochromocytoma, hyperaldosteronism, hypoglycemia. Also included are:

44 nursece4less.com nursece4less.com nursece4less.com nursece4less.com • Cardiac conditions - Myocardial ischemia, myocardial infarction, , bradyarrhythmia, complete atrioventricular (AV) block, takotsubo cardiomyopathy • Intracranial disorders - Subarachnoid hemorrhage, thalamic hematoma, cerebrovascular accident, encephalitis, head injury • Nutritional disorders - Anorexia nervosa, starvation, liquid protein diets, gastroplasty and ileojejunal bypass, celiac disease

Epidemiology of Torsade

The prevalence of torsade is not currently known. What is known is that it is a life threatening arrhythmia. It can present as sudden cardiac death. This can be in a patient with a structurally normal heart. There are 300,000 sudden cardiac deaths occurring a year in the U.S., and estimates are that torsade accounts for less than five percent of these. The corrected QT interval is longer in a white person than a black person. This is for both genders. This could explain the lower susceptibility to acquired torsade in a black person. Southeast Asians experience Brugada syndrome more frequently.

When comparing torsade in men and women, it is 2-3 times more common in women. Women have a longer QT interval. Women have more QT prolongation secondary to drug therapy. Congenital long QT syndrome is autosomal with an autosome any of the numbered chromosomes (as opposed to the sex chromosomes). It shows a greater frequency of expression and greater lengthening of the QT interval in women than men.

The highest frequency of torsade is for patients ages 35 to 50. It occurs in a wide range of ages and include newborns to the very elderly. If torsade occurs at an early age, it is typically due to a congenital long QT syndrome.

45 nursece4less.com nursece4less.com nursece4less.com nursece4less.com For an older person it typically is due to an acquired long QT syndrome. Reports show that just over half of elderly patients aged at or over 80 with a drug induced torsade experience it as a result of “reckless administration” of a QT interval prolonging agent.40,41

Patient History

Someone with torsade typically presents with recurrent episodes of dizziness, palpitations, and fainting that correspond to arrhythmia episodes. Sudden cardiac death can happen with the first episode. These can also occur but they are non-specific and could be produced by any form of tachyarrhythmia, nausea, shortness of breath, cold sweats, and chest pain.40

For a young person with torsade, what should be considered is a diagnosis of congenital long QT. This is especially with a family history of sudden cardiac death or sudden infant death syndrome. For these patients an episode of torsade is triggered by adrenergic stimulation. This can include fear, stress, or physical exertion. Clinicians should also consider other predisposing factors.42

Clinicians should remember that family history of congenital deafness is suggestive. A prolonged QT is found is only 0.25 to 0.3 percent of deaf mute children. Deafness is usually autosomal recessive. A patient with Jervell and Lange-Nielsen syndrome typically has a congenital sensorineural deafness. This represents an autosomal dominant pattern of inheritance for cardiac abnormalities. Romano-Ward syndrome is another form for familial or congenital long QT syndrome. With this condition hearing is normal. We observe an autosomal dominant pattern.

46 nursece4less.com nursece4less.com nursece4less.com nursece4less.com It is important to ask a patient about all currently taken medications. Drug associated torsade is rare but increasingly becoming more common. The incidence is as high as 2-3 percent with certain drugs. A patient who has acquired long QT syndrome usually develops torsade during a period of bradycardia. The most common causes of acquired long QT syndrome include medication and electrolyte disorder such as hypokalemia and hypomagnesemia.

Some of the physical signs of torsade include a rapid pulse, low or normal blood pressure, or transient or prolongs loss of consciousness. Preceding this could be bradycardia or premature ventricular contractions that lead to palpitations. Diaphoresis and pallor can be noted especially if there is a sustained episode. Physical findings for torsade depend on the duration and rate of tachycardia plus the degree of cerebral hypoperfusion. The cause of the torsade determines other physical signs.

There are other conditions that share similar signs or symptoms as torsade and should be considered as a differential diagnosis. These other conditions include: • Ventricular Tachycardia • Pediatrics, Tachycardia • Syncope • Renal Failure, Chronic and Dialysis Complication • Toxicity, Anti dysrhythmic • Toxicity, Antihistamine • Ventricular Fibrillation • Sudden Cardiac Death

47 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Another consideration is differentiation of acquired long QT syndrome from congenital long QT syndrome. Torsade should also be differentiated from polymorphic ventricular tachycardia or monomorphic ventricular tachycardia. It is possible to confuse torsade with supraventricular tachycardia with aberrant conduction when the degree of aberration is variable. A clue is that atrial fibrillation could be intermixed with typical and narrower QRS complexes.40

Electrocardiography and Torsade

It is important to understand that torsade is a diagnosis made with the help of an electrocardiogram. A case example where an ECG strip shows the condition would be an older person who develops QT prolongation secondary to quinidine therapy. An ECG strip may show resolution with overdrive ventricular pacing. Another case example would be a patient with prolonged QT and atrial ectopy. An ECG strip may show a premature beat and then a run of torsade.

Patients who are at risk due to chronic conditions or drug therapy should have frequent ECG monitoring. Typically, present are a prolonged QT interval and pathological U waves. These reflect abnormal ventricular repolarization. One consistent indicator of QT prolongation is a QT of 0.60 seconds or longer. Another is a QTc corrected for heart rate of 0.45 seconds or longer.

Other electrocardiographic features are helpful in diagnosing torsade. These include its typical mode of onset and development as follows: • Patients have paroxysms of 5-20 beats at a rate faster than 200 bpm and sustained episodes are seen occasionally • Progressive change in polarity of QRS occurs about the isoelectric line

48 nursece4less.com nursece4less.com nursece4less.com nursece4less.com • Complete 180° twist of QRS complexes within 10-12 beats is present • A short-long-short sequence between the R-R intervals occurs before the trigger response

It should be noted that patients can revert spontaneously. Or they can convert to a non-polymorphic ventricular tachycardia or ventricular fibrillation. If torsade occurs in a setting of acquired long QT syndrome this is preceded by pauses in most cases. For most adult cases in congenital long QT syndrome that is adrenergic dependent, pause dependence is found in most cases. In children the onset of torsade is not pause dependent.

There can be a failure to identify this rhythm for several reasons. For a very short run of torsade, the typical twisting of the QRS complex around the isoelectric line could not be apparent. Early events are usually short lived. For a single lead ECG recording, torsade may not be obvious.

Torsade should be considered as a diagnosis for any patient with pause dependent ventricular tachycardia. Ventricular in a patient with a long QT interval could be a sign of an impending torsade.

Checking for electrolytes is important. This includes checking for hypoglycemia, hypokalemia, hypomagnesemia, and hypocalcemia. Checking for cardiac enzymes is important too. Clinicians should rule out myocardial ischemia, especially in patients without QT prolongation. Chest radiographs and echocardiography can rule out structural heart disease if a clinical suggestion is present.40

49 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Treatment of Torsade

Treatment of torsade can be short-term or long-term. Short-term management is the same in both congenital and acquired long QT syndrome. The exception is that beta1-adrenergic stimulation may be appropriate in the acquired form but is contraindicated in the congenital form.

In a patient who is otherwise, stable direct current cardioversion is to be a last resort. This is because torsade is paroxysmal in nature. In addition, it is characterized by its frequent recurrences following cardioversion. Torsade can frequently be self-terminating. But it can degenerate into ventricular fibrillation.

Offending agents should be withdrawn. Clinicians should identify and correct any predisposing conditions such as hypokalemia, hypomagnesemia, and bradycardia.

Concerning pharmacologic therapy, magnesium is the drug of choice for suppressing early afterdepolarizations and terminating an arrhythmia. Magnesium decreases the influx of calcium. This lowers the amplitude of early afterdepolarization (EAD).43

Administration of magnesium can be at 1-2 g IV initially in 30 to 60 seconds. This can be repeated in 5 to 15 minutes. As an alternative, a continuous infusion can be started at a rate of 3-10 mg/min. Even for a patient with normal magnesium levels, magnesium is effective for treatment. A patient requires close monitoring due to the danger of hypermagnesemia and depression of neuromuscular function. The recommendation can also be supplemental potassium to increase the potassium concentration to high normal. This increases the efflux of potassium from myocardial cells leading

50 nursece4less.com nursece4less.com nursece4less.com nursece4less.com to rapid repolarization. Lidocaine typically has no effect in the treatment of torsade. It can sometimes have an initial beneficial effect but in all cases torsade recurs.43

Mexiletine can be helpful in suppressing torsade. One study showed how it was used in patients with human immunodeficiency virus (HIV) who has acquired long QT interval and torsade. It suppressed the torsade effectively on a long term basis.40

Patients are treated with beta blockers if they have congenital QT syndromes as they are thought to have abnormality of sympathetic balance or tone. If a patient experiences breakthrough torsade, what can help is a short-acting such as esmolol.44

In bradycardia dependent torsade usually associated with acquired long QT syndrome that is pause dependent the use of isoproterenol can help. Administration should be as a continuous IV infusion to keep the heart rate above 90 beats per minute. Isoproterenol accelerates atrioventricular conduction and decreases the QT interval by increasing the heart rate. It also reduces temporal dispersion of repolarization. For a congenital form of long QT syndrome that is adrenergic dependent beta-adrenergic agonists such as isoproterenol are contraindicated. Due to precautions, adverse effects, and contraindications, such drugs are used as an interim agent until overdrive pacing can be started.

Pacing can be effective in terminating torsade. This is based on the QT interval shortening with a faster heart rate. Pacing is effective because it facilitates the repolarizing potassium currents and prevents long pauses. It also suppresses early afterdepolarization and decreases the QT interval.45

51 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Atrial pacing is preferred as it preserves the atrial contribution to ventricular filling. It also results in a narrower QRS complex and shorter QT. In a patient with atrioventricular block, ventricular pacing can suppress torsade. This depends on intact atrial to ventricular conduction at the necessary pacing rate.

Pacing should be at a rate of 90 to 110 beats per minute. This is until the QT interval is normalized. Overdrive pacing may be needed at a rate of up to 140 beats per minute. This is to control the rhythm. In an extremely difficult case, torsade should be treated with electrical cardioversion or defibrillation. Some reports cite successful conversion with phenytoin and lidocaine. There are cases reported of successful conversion using phenytoin and overdrive pacing. If a patient is unresponsive to conversion with phenytoin and overdrive pacing, electrical cardioversion should be attempted.

For congenital long QT syndrome, beta adrenergic antagonists at a maximum tolerated dose is used as a first line long term therapy. Propranolol is used most extensively. Other agents such as esmolol or nadolol also can be used. In congenital cases where bradycardia is a prominent feature, beta blockers should be avoided. Beta-blockers are contraindicated in acquired long QT syndrome. This is because bradycardia produced by these agents can precipitate torsade. An approach to assessing the adequacy of beta blockade is through exercise testing. An investigator recommends an aim of at least 20 percent reduction in maximum heart rate. This is compared to that of the baseline and pre beta blocker therapy. Another approach is checking blood levels of beta blockers such as propranolol as much as possible.

52 nursece4less.com nursece4less.com nursece4less.com nursece4less.com If a patient has no fainting, ventricular tachyarrhythmia, or a family history of sudden cardiac death, the patient could be observed without treatment.

Permanent pacing benefits a patient who remains symptomatic. This is despite getting a maximally tolerated dose of beta blockers. It can be used adjunctively with beta blockers. It decreases the QT interval. This is by enhancing the repolarizing potassium currents and suppressing EADs. For a patient who remains refractory to beta blockade and pacing, high left thoracic sympathectomy, another antiadrenergic therapy, is effective.

In an instance where torsade recurs despite treatment with beta blocker, pacing, and possible left thoracic sympathectomy, an implantable cardioverter defibrillator (ICD) is useful. Beta blockers should be used with ICDs. This is because shock can further precipitate torsade by adrenergic stimulation. An ICD for refractory cases may often precede sympathectomy.

Long term treatment in acquired long QT syndrome often is not needed. This is because the QT interval returns to normal when the inciting factor or predisposing condition is corrected.

In cases associated with heart block or bradycardia, pacemaker implantation is effective. Implantable cardioverter defibrillators are appropriate in cases that cannot be managed by avoidance of the offending agent. It may not always be clear where the boundary is in acquired and congenital cases. Additional factors can be present. Individuals can show increased susceptibility to QT effects. Immediate cardiology evaluation and follow-up are necessary and additional consultation could include a cardiologist, electrophysiologist and geneticist in cases of familiar or congenital long QT syndrome.

53 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Activity, Prognosis, and Education for Torsade Patients

Competitive sports are not allowed for a patient with congenital long QT syndrome. Complications can include ventricular fibrillation, monomorphic ventricular tachycardia, and sudden cardiac death.

Prognosis for congenital long QT syndrome includes that the mortality rate for an untreated patient is 50 percent for 10 years. This can be reduced 3 to 4 percent with therapy. For acquired long QT syndrome, the prognosis is excellent. This is once the inciting factor is identified and withheld reliably.

Concerning patient education, a patient should use medication with the approval of a medical clinician only. Patients should avoid competitive sports in the case of congenital long QT syndrome. Close follow up is necessary. This is because of the risk of sudden cardiac death. Cardiac support groups can help. A patient should learn how to monitor their pulse and recognize adverse drug effects. Family members should undergo training for basic life support.40

Summary

Health clinicians should be aware that electrocardiograms are valuable tools for evaluating heart health and diagnosing cardiac issues. Clinicians should also understand that the ECG report is only as good as the person reading the output and commit to developing ECG interpretation skills in order to ensure safe and appropriate diagnosis and treatment of cardiac conditions.

Being able to identify normal readings on an ECG rhythm strip is the first building block to recognizing cardiac issues and to possibly saving lives. A

54 nursece4less.com nursece4less.com nursece4less.com nursece4less.com helpful University of Utah web-based ECG Learning Center to view related cardiac rhythm images is available at https://ecg.utah.edu.

Examination of the ECG is key to appropriate diagnosis in addition to accurate history taking. The goal is to know whether ECG abnormalities exist. It is appropriate to consider certain hereditary or acquired cardiac conditions that manifest as rhythm abnormalities in the electrocardiogram.

Medications have been associated with both the prevention and cause of cardiac rhythm disturbances. It is important for clinicians to differentiate Torsade de Pointes from other cardiac arrhythmias when considering a type of drug intervention, as certain drugs have been associated with fatal events in torsade.

The ECG and other diagnostic tests have been presented, as well as varied types of treatment including cardiac defibrillation, pacing, ablation and surgery. Education of the patient and family members has been recommended for early recognition and intervention of a cardiac rhythm condition to prevent a potentially serious outcome.

Please take time to help NurseCe4Less.com course planners evaluate the nursing knowledge needs met by completing the self-assessment of Knowledge Questions after reading the article, and providing feedback in the online course evaluation.

Completing the study questions is optional and is NOT a course requirement.

55 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 1. The P wave is a summation wave that is generated by the depolarization front as it transits the

a. sinoatrial node. b. ventricles. c. bundle of His. d. atria.

2. True or False: Normally, the right atrium depolarizes earlier than the left atrium since the depolarization wave originates in the sinoatrial node.

a. True b. False

3. An ECG reading showing a P wave with increased amplitude can be an indication of

a. hyperkalemia. b. hypokalemia. c. Wolff–Parkinson–White (WPW) syndrome. d. hypotrophy.

4. ______are known as P mitrale and indicate left-atrial abnormality, such as left-atrial dilation or hypertrophy.

a. Bifid P waves b. P waves with increased amplitude c. P wave with a flat baseline d. P waves that are not clearly delineated

5. ______is an ECG recording that was not made by the electrical activity of the heart.

a. An ECG artifact b. An ectopic c. A bifid P wave d. An ECG variant

56 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 6. Atrial repolarization is represented on a surface ECG as what is called

a. a Pa wave. b. a P wave. c. a Ta wave. d. an R wave.

7. True or False: Atrial and ventricular depolarization and repolarization appear on an ECG as a series of waves and the P wave is followed by the QRS complex and the T wave.

a. True b. False

8. In electrocardiography, the PR interval is the period that extends from the beginning of the P wave until

a. the beginning of the Ta wave. b. the beginning of the QRS complex. c. the end of the R wave. d. the end of the T wave.

9. True or False: In electrocardiography, the PR interval is measured in microseconds.

a. True b. False

10. A short PR interval (less than 120 ms) can be associated with

a. acute rheumatic fever. b. carditis associated with Lyme disease. c. hypokalemia. d. junctional rhythms.

11. With a PR interval < 0.12 seconds ______should be considered.

a. acute rheumatic fever. b. carditis associated with Lyme disease. c. Wolff-Parkinson-White syndrome d. hypokalemia.

57 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 12. A patient with a shortened PR interval and a history of sudden palpitation should be considered as a physiologic variant,

a. in cases where the patient is asymptomatic. b. if a short PR interval and normal width QRS are present. c. only if there is a delay in conduction. d. as a diagnosis of exclusion only.

13. True or False: A patient with a shortened PR interval due to a physiologic variant will present asymptomatic.

a. True b. False

14. A diagnostic approach for a PR interval ______is an appropriate diagnosis of a prolonged PR based on ECG analysis.

a. > 0.02 s b. ≥ 0.12 s c. ≥ 0.2 s d. < 0.2 s

15. The criteria for third degree heart block Mobitz II are a PR interval ≥ 0.2 s, and a fixed duration of the PR interval with an abrupt appearance of the P wave

a. followed by the QRS complex. b. without a subsequent QRS complex. c. with a lengthen PR following the dropped QRS complex. d. with the presence of group beating.

16. An asymptomatic patient with a known bypass tract

a. is at low risk of sudden cardiac death. b. is at high risk of sudden cardiac death. c. does not need to be referred to a cardiologist. d. None of the above

17. True or False: First degree atrioventricular block requires no intervention.

a. True b. False

58 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 18. Which of the following refers to a heart rate that is less than 60 beats per minute in adults?

a. Hypertrophy b. Tachycardia c. Torsade de Pointes d. Bradycardia

19. If perfusion is poor for a patient, the clinician should

a. continue to monitor the patient for change on an ECG. b. administer atropine, then pacing only if atropine is ineffective. c. not delay transcutaneous pacing. d. the clinician should monitor and observe the patient.

20. A baseline assumption when determining if an individual has Mobitz I heart block is that the atrial rhythm has to be

a. regular. b. irregular. c. accompanied by poor perfusion. d. asymptomatic.

21. True or False: A Type 2 Second-degree AV block is also known as Mobitz II could progress rapidly to complete heart block.

a. True b. False

22. A higher number of P waves for every QRS indicates

a. a fine atrial fibrillation. b. sinoatrial arrest with a secondary escape rhythm. c. a more severe block. d. a physiologic variant.

23. The ______is typically the most visually obvious and central part of an ECG tracing.

a. P wave b. U wave c. R wave d. QRS complex

59 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 24. When the ventricles work efficiently, QRS complex duration is

a. 40 ms. b. 80 to 120 ms. c. 40 to 80 ms. d. 60 ms.

25. Concerning the Q wave, an abnormality indicates the presence of

a. a physiologic variant. b. a fine atrial fibrillation. c. depolarization. d. infarction.

26. If a clinician uses lowercase and uppercase letters when labeling an RS complex, an uppercase “R” and lower case “s,” written as “Rs” means the Rs complex is

a. positively deflected. b. simultaneously depolarizing via the Purkinje fibers. c. negatively deflected. d. clustering together.

27. The most common sign of long QT syndrome is

a. shortness of breath. b. nausea. c. fainting. d. chest pain.

28. True or False: A patient has Wolff-Parkinson-White syndrome if the patient has an extra, electrical pathway, with or without tachycardia.

a. True b. False

29. Torsade de Pointes is

a. an abnormality of the P wave. b. always acute and does not recur if it terminates. c. congenital, never acquired. d. associated with a prolonged QT interval.

60 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 30. Which of the following treatments is contraindicated for congenital long QT syndrome?

a. Beta1-adrenergic stimulation b. Mexiletine c. Magnesium d. Beta blockers

CORRECT ANSWERS:

1. The P wave is a summation wave that is generated by the depolarization front as it transits the

d. atria.

“The P wave is a summation wave that is generated by the depolarization front as it transits the atria.”

2. True or False: Normally, the right atrium depolarizes earlier than the left atrium since the depolarization wave originates in the sinoatrial node.

a. True

"Normally, the right atrium depolarizes earlier than the left atrium since the depolarization wave originates in the sinoatrial node, in the high right atrium and then through the left atrium.”

3. An ECG reading showing a P wave with increased amplitude can be an indication of

b. hypokalemia.

“A P wave with increased amplitude can be an indication of hypokalemia. It can also be an indication of atrial enlargement. A P wave with decreased amplitude can be an indication of hyperkalemia.”

61 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 4. ______are known as P mitrale and indicate left-atrial abnormality, such as left-atrial dilation or hypertrophy.

a. Bifid P waves

“Bifid P waves are known as P mitrale and indicate left-atrial abnormality, such as left-atrial dilation or hypertrophy.”

5. ______is an ECG recording that was not made by the electrical activity of the heart.

a. An ECG artifact

“It could also suggest possible ECG artifact, which is an ECG recording that was not made by the electrical activity of the heart.”

6. Atrial repolarization is represented on a surface ECG as what is called

c. a Ta wave.

“Atrial repolarization occurs at a mean of 320 milliseconds (ms) after the end of a P wave. It has a duration of 2-3 times that of the P wave. The polarity is always opposite to that of the P wave. It is represented on a surface ECG as what is called a Ta wave.”

7. True or False: Atrial and ventricular depolarization and repolarization appear on an ECG as a series of waves and the P wave is followed by the QRS complex and the T wave.

a. True

“Atrial and ventricular depolarization and repolarization appear on an ECG as a series of waves. The P wave is followed by the QRS complex and the T wave. The first deflection is the P wave associated with right and left atrial depolarization.”

62 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 8. In electrocardiography, the PR interval is the period that extends from the beginning of the P wave until

b. the beginning of the QRS complex.

“In electrocardiography, the PR interval is the period that extends from the beginning of the P wave (the onset of atrial depolarization) until the beginning of the QRS complex (the onset of ventricular depolarization).”

9. True or False: In electrocardiography, the PR interval is measured in microseconds.

b. False

“In electrocardiography, the PR interval is the period that extends from the beginning of the P wave (the onset of atrial depolarization) until the beginning of the QRS complex (the onset of ventricular depolarization). It is measured in milliseconds.”

10. A short PR interval (less than 120 ms) can be associated with

d. junctional rhythms.

“A long PR interval is considered to be over 200 ms. This can indicate a first degree heart block. Prolongation can be associated with the condition of hypokalemia, acute rheumatic fever, or carditis associated with Lyme disease. A short PR interval is considered to be less than 120 ms. It can be associated with Wolff– Parkinson–White (WPW) syndrome, Lown–Ganong–Levine syndrome, or junctional rhythms.”

11. With a PR interval < 0.12 seconds ______should be considered.

c. Wolff-Parkinson-White syndrome

“With a PR interval < 0.12 s Wolff-Parkinson-White syndrome should be considered.”

63 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 12. A patient with a shortened PR interval and a history of sudden palpitation should be considered as a physiologic variant,

d. as a diagnosis of exclusion only.

“A patient with a shortened PR and a history of sudden palpitation should be considered as a physiologic variant, as a diagnosis of exclusion only. Not all patients with bypass tracts are symptomatic. The lack of symptoms cannot be used to exclude a diagnosis of bypass tract as associated with a shortened PR interval.”

13. True or False: A patient with a shortened PR interval due to a physiologic variant will present asymptomatic.

a. True

“A diagnostic approach for PR < 0.12 s is to start with accurate history taking. This can help differentiate a shortened PR due to a physiologic variant with no associated bypass tract, or accelerated conduction through the AV node, versus a shortened PR due to accelerated conduction associated via a bypass tract. A patient with a physiologic variant is asymptomatic. They come to clinical attention generally due to an ECG analysis.”

14. A diagnostic approach for a PR interval ______is an appropriate diagnosis of a prolonged PR based on ECG analysis.

c. ≥ 0.2 s

“A diagnostic approach for a PR interval > 0.2 s is an appropriate diagnosis of a prolonged PR based on ECG analysis.... Any PR ≥ 0.2 s is considered prolonged.”

15. The criteria for third degree heart block Mobitz II are a PR interval ≥ 0.2 s, and a fixed duration of the PR interval with an abrupt appearance of the P wave

b. without a subsequent QRS complex.

“Criteria to differentiate between first degree heart block - simple PR prolongation - and second degree heart block - Mobitz I and II - include the following: … Third degree heart block Mobitz II: PR ≥ 0.2 s, fixed duration of PR interval with abrupt appearance of the P without a subsequent QRS.”

64 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 16. An asymptomatic patient with a known bypass tract

a. is at low risk of sudden cardiac death.

“A patient with a symptomatic tachycardia should be referred to a cardiologist for evaluation. Possible treatment could be with radiofrequency ablation of the bypass tract if appropriate. The risk is low overall for sudden cardiac death in asymptomatic patients with a known bypass tract. However, asymptomatic patients should be referred to a cardiologist for evaluation and determination of risk.”

17. True or False: First degree atrioventricular block requires no intervention.

a. True

“Management for PR > 0.2 s and a prolonged PR is determined by the degree of AV nodal blockade. Here are factors to consider. First degree AV block requires no intervention.”

18. Which of the following refers to a heart rate that is less than 60 beats per minute in adults?

d. Bradycardia

“Bradycardia is less than 60 beats per minute in adults and involves a heart rate less than normal.”

19. If perfusion is poor for a patient, the clinician should

c. not delay transcutaneous pacing.

“Determination of a treatment sequence depends on the severity of the patient's clinical presentation. If perfusion is adequate, the clinician should monitor and observe the patient. If perfusion is poor, the clinician should move quickly through the following steps: Prepare for transcutaneous pacing, which is the application of electrical energy to a patient’s heart to stimulate contraction. Do not delay pacing. If no IV is present pacing can be first. Consider administering atropine 0.5 mg IV if IV access is available. This may be repeated every 3 to 5 minutes up to 3mg or 6 doses. If the atropine is ineffective, begin pacing if it has not been initiated already.”

65 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 20. A baseline assumption when determining if an individual has Mobitz I heart block is that the atrial rhythm has to be

a. regular.

“A baseline assumption when determining if an individual has Mobitz I heart block is that the atrial rhythm has to be regular. With atrial rhythm that is not regular, an alternative explanation of why certain P waves do not conduct to the ventricles may exist.”

21. True or False: A Type 2 Second-degree AV block is also known as Mobitz II could progress rapidly to complete heart block.

a. True

“A Type 2 Second-degree AV block is also known as Mobitz II and is almost always a disease of the distal conduction system (His- Purkinje System)... Of medical significance, this type of AV block could progress rapidly to complete heart block.”

22. A higher number of P waves for every QRS indicates

c. a more severe block.

“The absence of a P wave with a flat baseline could indicate fine atrial fibrillation or sinoatrial arrest with a secondary escape rhythm.... Higher numbers of P waves for every QRS means a more severe block.”

23. The ______is typically the most visually obvious and central part of an ECG tracing.

d. QRS complex

“When considering the QRS complex, its interval length, and consistency of appearance, the QRS complex is typically the most visually obvious and central part of an ECG tracing.”

66 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 24. When the ventricles work efficiently, QRS complex duration is

b. 80 to 120 ms.

“Concerning formation, depolarization of the heart ventricles occurs almost simultaneously via the Bundle of His and Purkinje fibers. When they work efficiently, the QRS complex duration is 80 to 120 ms.”

25. Concerning the Q wave, an abnormality indicates the presence of

d. infarction.

“Concerning the Q wave, an abnormality indicates the presence of infarction.”

26. If a clinician uses lowercase and uppercase letters when labeling an RS complex, an uppercase “R” and lower case “s,” written as “Rs” means the Rs complex is

a. positively deflected.

“Some individuals use lowercase and uppercase letters. This depends on the relative size of each wave. As an example, an Rs complex is positively deflected and rS complex is negatively deflected. If labeled RS for each of these complexes, it is not possible to see this distinction without viewing the actual ECG.”

27. The most common sign of long QT syndrome is

c. fainting.

“Some people have long QT syndrome and do not have signs or symptoms. Others are aware of the condition if they have a family history of long QT syndrome, get genetic test results, or discover the condition as a result of an electrocardiogram done for another reason. Those who do have symptoms can experience fainting spells. This is the most common sign of the condition.”

67 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 28. True or False: A patient has Wolff-Parkinson-White syndrome if the patient has an extra, electrical pathway, with or without tachycardia.

b. False

“A patient with WPW syndrome has an extra, electrical pathway between the atria and ventricles. This is known as an accessory pathway.... Wolff-Parkinson-White syndrome occurs with a patient who has a recurring tachycardia because of this abnormal pathway. A patient can have a WPW pathway but no tachycardia. This patient does not have WPW syndrome but may at some point develop it. This patient has a WPW pattern which can be detected on a routine electrocardiogram.”

29. Torsade de Pointes is

d. associated with a prolonged QT interval.

“Torsade de Pointes is also called torsade. It is associated with a prolonged QT interval. It can be congenital or acquired. Torsade usually terminates spontaneously but it can frequently recur. It can also degenerate into ventricular fibrillation.”

30. Which of the following treatments is contraindicated for congenital long QT syndrome?

a. Beta1-adrenergic stimulation

“Treatment can be short-term or long-term. Short-term management is the same in both congenital and acquired long QT syndrome. The exception is that beta1-adrenergic stimulation may be appropriate in the acquired form but is contraindicated in the congenital form.... Patients are treated with beta blockers if they have congenital QT syndromes as they are thought to have abnormality of sympathetic balance or tone.”

68 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Reference Section

The References below include published works and in-text citations of published works that are intended as helpful material for your further reading. [These References are for a multi-part series on Basic Electrocardiography].

1. Prutkin, J.M. (2017). ECG tutorial: Basic principles of ECG analysis. UpToDate. Retrieved online at https://www.uptodate.com/contents/ecg-tutorial-basic-principles-of- ecg- analysis?source=search_result&search=electrocardiogram&selectedTitl e=1~150. 2. O’Brien, T. (2016). Introduction to cardiac rhythm strip analysis. EKG.Academy. Retrieved online at https://ekg.academy/learn- ekg?courseid=318&seq=1 3. Tso, Colin, et al (2015). Electrocardiography: A Technologist’s Guide to Interpretation. Journal of Nuclear Medicine Technology. Vol. 43 no. 4 247-252. 4. Prutkin, J. (2017). ECG tutorial: Electrical components of the ECG. UpToDate. Retrieved online at https://www.uptodate.com/contents/ecg-tutorial-electrical- components-of-the- ecg?soure=search_result&search=6+second+method+ECG+rhythm+s trip&selectedTitle=4~150 5. Goldberger, A. (2016). Basic principles of electrocardiographic interpretation. UpToDate. Retrieved online at https://www.uptodate.com/contents/basic-principles-of- electrocardiographic-interpretation?source=see_link 6. Goldberger, A., et al (2017). Goldberger's Clinical Electrocardiography: A Simplified Approach, 9th ed; Retrieved from Elsevier, Philadelphia. 7. Mirvis, D.M. and Goldberger, A. (2014). Electrocardiography. In: Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 10th ed, Bonow, RO, Mann, DL, Zipes, DP, Libby, P (Eds), W.B. Saunders Company, Philadelphia 8. Sauer, W.H. (2017). Left bundle branch block. UpToDate. Retrieved online at https://www.uptodate.com/contents/left-bundle-branch- block?source=see_link 9. Jones & Barlett Learning. (n.d.). Rhythms. Retrieved online at http://samples.jbpub.com/9780763712846/12841_CH08_Garcia.pdf 10. Hampton, John R (2013). The ECG Made Easy (8th ed.). Retrieved from Edinburgh: Churchill Livingstone. p. 4. ISBN 9780702046421.

69 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 11. Mayo Clinic (2014). Premature ventricular contractions. Retrieved online at http://www.mayoclinic.org/diseases-conditions/premature- ventricular-contractions/basics/causes/con-20030205 12. Manolis, A. (2017). Supraventricular premature beats. Retrieved online at https://www.uptodate.com/contents/supraventricular-premature- beats?source=search_result&search=premature+ventral+contraction& selectedTitle=2~150 13. Conen, D., et al. (2012). Premature atrial contractions in the general population: frequency and risk factors. Circulation 126:2302. 14. Prutkin, J. (2015). ECG tutorial: Ventricular arrhythmias. UpToDate. Retrieved online at https://www.uptodate.com/contents/ecg-tutorial- ventricular- arrhythmias?source=search_result&search=torsades+de+pointes&sele ctedTitle=5~150 15. Seslar, S.P., et. al. (2014). Clinical features of congenital long QT syndrome. UpToDate. Retrieved online at https://www.uptodate.com/contents/clinical-features-of-congenital- long-qt- syndrome?source=search_result&search=torsades+de+pointes&select edTitle=3~145 16. Baldzizhar, A., et al. (2016). Ventricular Tachycardias: Characteristics and Management. Critical care nursing clinics of North America; 28 (3): 317-29. 17. EKG.Academy. (2017). Introduction to pacemaker rhythms. Clinical Skills Education. Retrieved online at www.ekg.academy/pacemaker- rhythms. 18. Prutkin, J. (2017). EKG Tutorial: Pacemakers. UpToDate. Retrieved from https://www.uptodate.com/contents/ecg-tutorial- pacemakers?source=search_result&search=pacemaker+rhythm&select edTitle=2~150 19. Mount, D. (2017). Clinical manifestations and treatment of hypokalemia in adults. UpToDate. Retrieved online at https://www.uptodate.com/contents/clinical-manifestations-and- treatment-of-hypokalemia-in- adults?source=search_result&search=hypokalemia&selectedTitle=1~1 50. 20. He, J., Tse, et. al. (2017). P-Wave indices and risk of ischemic stroke. American Heart Association. Retrieved online at http://stroke.ahajournals.org/content/early/2017/07/05/STROKEAHA. 117.017293?download=true 21. Zimetbaum, P. et al. (2017). Clinical features of congenital long QT syndrome. UpToDate. Retrieved online at https://www.uptodate.com/contents/clinical-features-of-congenital- long-qt-

70 nursece4less.com nursece4less.com nursece4less.com nursece4less.com syndrome?source=search_result&search=torsades%20de%20pointes& selectedTitle=3~150. 22. Yap, Y.G. and Camm, A.J. (2017). "Drug induced QT prolongation and ". Heart. 89 (11): 1363–1372. ISSN 1355-6037. PMC 1767957 23. Park, D.S. and Fishman, G. (2017). Development and Function of the Cardiac Conduction System in Health and Disease. J Cardiovasc Dev Dis; 4(2). pii: 7. doi: 10.3390/jcdd4020007. 24. Mayo Clinic. (n.d.). Supraventricular tachycardia. Mayo. Retrieved online at http://www.mayoclinic.org/diseases- conditions/supraventricular-tachycardia/symptoms-causes/syc- 20355243 25. Mayo Clinic. (n.d.). Ventricular tachycardia. Mayo. Retrieved online at http://www.mayoclinic.org/diseases-conditions/ventricular- tachycardia/symptoms-causes/syc-20355138 26. Shah, S.N. (2015). . Retrieved from http://emedicine.medscape.com/article/757257-overview 27. van der Lende, M., et al. (2016). Cardiac arrhythmias during or after epileptic seizures. J Neurol Neurosurg Psychiatry. 87 (1):69-74 28. Shah, S.N. (2016). Pulseless electrical activity. Retrieved online at http://emedicine.medscape.com/article/161080-overview 29. Mayo Clinic. (n.d.). Pacemakers. Mayo. Retrieved online at http://www.mayoclinic.org/tests-procedures/pacemaker/home/ovc- 20198445 30. The Journal of Family Medicine. (n.d.). EKG PR interval abnormalities. Retrieved online at http://www.mdedge.com/jfponline/dsm/4899/hospital-medicine/ekg- pr-interval-abnormalities 31. MedicineNet.com. (2016). Syncope. Retrieved online at https://www.medicinenet.com/script/main/art.asp?articlekey=5612 32. Iyasere, C.A. (n.d.). EKG: PR interval abnormalities. Journal of family practice. Retrieved online at http://www.mdedge.com/jfponline/dsm/4899/hospital-medicine/ekg- pr-interval-abnormalities 33. Goldberger’s Clinical Electrocardiography: A Simplified Approach, 7th ed. ISBN-13: 978-0323087865 34. Ferri, F. (2014). Ferri's Clinical Advisor. 1st Ed. eBook ISBN: 9780323084307 35. Homoud, M.K. (2017). . UpToDate. Retrieved online at https://www.uptodate.com/contents/sinus- bradycardia?source=search_result&search=bradycardia&selectedTitle= 1%7E150 36. ACLS Training Center. (2017). ACLS bradycardia algorithm. Retrieved online at https://www.acls.net/acls-bradycardia-algorithm.htm

71 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 37. Sauer, W. (2017). Second degree atrioventricular block: Mobitz type I (Wenckebach type). UpToDate. Retrieved online at https://www.uptodate.com/contents/second-degree-atrioventricular- block-mobitz-type-i-wenckebach- block?source=search_result&search=mobitz&selectedTitle=1~40 38. Sauer, W. (2017). Second degree atrioventricular block: Mobitz type II. UpToDate. Retrieved online at https://www.uptodate.com/contents/second-degree-atrioventricular- block-mobitz-type- ii?source=search_result&search=mobitz&selectedTitle=2~40 39. Colucci, W.S. (2017). Drugs that should be avoided or used with caution in patients with heart failure. UpToDate. Retrieved online at https://www.uptodate.com/contents/drugs-that-should-be-avoided-or- used-with-caution-in-patients-with-heart- failure?source=search_result&search=torsade&selectedTitle=50~145 40. Dave, J. (2017). Torsade de Pointes. Medscape. Retrieved online at http://emedicine.medscape.com/article/1950863-overview 41. Jackobson, G., et al. (2016). Reckless administration of QT interval- prolonging agents in elderly patients with drug-induced torsade de pointes. Z Gerontol Geriatr. 42. Cho Y. (2016). Management of patients with long QT syndrome. Korean Circ J. 46 (6):747-52. 43. Baker, W.L. (2016). Treating arrhythmias with adjunctive magnesium: identifying future research directions. Eur Heart J Cardiovasc Pharmacother. 44. Kaye, A.D., et al. (2013). QT interval abnormalities: risk factors and perioperative management in long QT syndromes and Torsades de Pointes. J Anesth. 2013. 44 45. Overbey, A.N., et. al. (2013). Overdrive pacing in a patient with incessant torsades de pointes. BMJ Case Rep. doi: 10.1136/bcr-2013- 200146. PMCID: PMC3822076. Retrieved online at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3822076/ 46. Mayo Clinic. (n.d.). Long QT Syndrome. Mayo. Retrieved online at http://www.mayoclinic.org/diseases-conditions/long-qt- syndrome/symptoms-causes/syc-20352518 47. Knight, B.P. (2017). Patient education: Implantable cardioverter- fibrillators. UpToDate. Retrieved online at https://www.uptodate.com/contents/implantable-cardioverter- defibrillators-beyond-the- basics?source=search_result&search=cardiac+rhythms&selectedTitle= 1~29 48. Ganz, L.I. (2017). General principles of the implantable cardioverter- defibrillator. UpToDate. Retrieved online at https://www.uptodate.com/contents/general-principles-of-the-

72 nursece4less.com nursece4less.com nursece4less.com nursece4less.com implantable-cardioverter- defibrillator?source=search_result&search=ICD&selectedTitle=1%7E15 0 49. Knight, B.P. (2017). Patient education: Wolff-Parkinson-White syndrome. UpToDate. Retrieved online at https://www.uptodate.com/contents/wolff-parkinson-white-syndrome- beyond-the- basics?source=search_result&search=cardiac+resynchronization&selec tedTitle=10~35 50. Knight, B.P. (2017). Patient education: Cardioversion. UpToDate. Retrieved online at https://www.uptodate.com/contents/cardioversion- beyond-the- basics?source=search_result&search=tachycardia&selectedTitle=4~27 51. Mayo Clinic. (n.d.). Cardioversion. Mayo. Retrieved online at http://www.mayoclinic.org/home/ovc-20336882 52. Chen, M.A. (2016). Cardioversion. National Institutes for Health. Retrieved online at www.nlm.nih.gov/medlineplus/ency/article/007110.htm 53. National Heart, Lung, and Blood Institute. (2016). Cardioversion. Retrieved online at https://www.nhlbi.nih.gov/health/health- topics/topics/crv/ 54. American Heart Association. (2016). Non-surgical procedures for atrial fibrillation (AFib or AF). AHA. Retrieved online at http://www.heart.org/HEARTORG/Conditions/Arrhythmia/AboutArrhyth mia/Non-surgical-Procedures-for- AF_UCM_423782_Article.jsp#.Wd7AsRNSyT8 55. Heart Rhythm Society. (n.d.). Cardioversion. Retrieved online at http://www.hrsonline.org/Patient- Resources/Treatment/Cardioversion#axzz2QAR9BBOa 56. Prutkin, J.M. (2017). ECG tutorial: Pacemakers. UpToDate. Retrieved online at https://www.uptodate.com/contents/ecg-tutorial- pacemakers?source=search_result&search=pacemaker+rhythm&select edTitle=2~150 57. Prutkin, J.M. (2016). ECG tutorial: Physiology of the conduction system. UpToDate. Retrieved online at http://www.uptodate.com/contents/ecg-tutorial-physiology-of-the- conduction-system 58. Prutkin, J.M. (2016). ECG tutorial: Electrical components of the ECG. UpToDate. Retrieved online at https://www.uptodate.com/contents/ecg-tutorial-electrical- components-of-the-ecg. source=search_result&search=ECG+leads&selected 59. Aruda-Olson, A.M. (2017). Overview of stress echocardiography. UpToDate. Retrieved online at

73 nursece4less.com nursece4less.com nursece4less.com nursece4less.com https://www.uptodate.com/contents/overview-of-stress- echocardiography?source=search_result&search=echo+cardiogram&se lectedTitle=1~150 60. Patel, A. (2015). Principles of Doppler echocardiography. UpToDate. Retrieved online at https://www.uptodate.com/contents/principles-of- doppler- echocardiography?source=search_result&search=doppler+echocardiog ram&selectedTitle=1~150 61. Ahmed, H. (2017). Contrast echocardiography: Clinical applications. UpToDate. Retrieved online at https://www.uptodate.com/contents/contrast-echocardiography- clinical- applications?source=search_result&search=echo+cardiogram&selected Title=6~150 62. Mor-Avi, V. and Lang, R.M. (2015). Three dimensional echocardiography. UpToDate. Retrieved online at https://www.uptodate.com/contents/three-dimensional- echocardiography?source=search_result&search=echocardiography&se lectedTitle=2~150 63. Callans, D.J. (2017). Bundle branch reentrant ventricular tachycardia. UpToDate. Retrieved online at http://www.uptodate.com/contents/bundle-branch-reentrant- ventricular- tachycardia?source=search_result&search=bundle+branch&selectedTit le=3~150 64. Bauer, W. (2016). Normal sinus rhythm and sinus arrhythmia. UpToDate. Retrieved online at http://www.uptodate.com/contents/normal-sinus-rhythm-and-sinus- arrhythmia?source=search_result&search=sinus+rhythm&selectedTitle =1~150 65. Zimetbaum, P.J. and Wylie, J.V. (2016). Nonsustained ventricular tachycardia clinical manifestations, evaluation, and management. UpToDate. Retrieved from http://www.uptodate.com/contents/nonsustained-ventricular- tachycardia-clinical-manifestations-evaluation-and- management?source=search_result&search=ventricular+tachycardia& selectedTitle=1~150 66. Giardina, E. (2016). Therapeutic use of ibutilde. UpToDate. Retrieved online at http://www.uptodate.com/contents/therapeutic-use-of- ibutilide?source=search_result&search=ibutilide&selectedTitle=1~28 67. Knight, P.B. (2017). Cardioversion for specific arrhythmias. UpToDate. Retrieved online at http://www.uptodate.com/contents/cardioversion- for-specific-

74 nursece4less.com nursece4less.com nursece4less.com nursece4less.com arrhythmias?source=search_result&search=cardioversion&selectedTitl e=1~150 68. Knight, P.B. (2017). Basic principles and technique of electrical cardioversion and defibrillation. UpToDate. Retrieved online at http://www.uptodate.com/contents/basic-principles-and-technique-of- electrical-cardioversion-and- defibrillation?source=search_result&search=cardioversion&selectedTitl e=3~150 69. Biase, L.D., Walsh, E.P. (2016). Treatment of arrhythmias associated with the Wolff-Parkinson-White syndrome. UpToDate. Retrieved online at http://www.uptodate.com/contents/treatment-of-symptomatic- arrhythmias-associated-with-the-wolff-parkinson-white- syndrome?source=search_result&search=Wolff&selectedTitle=1~86 70. Biase, L.D. and Walsh, E.P. (2016). Epidemiology, clinical manifestations, and diagnosis of the Wolff-Parkinson-White syndrome. UpToDate. Retrieved online at http://www.uptodate.com/contents/epidemiology-clinical- manifestations-and-diagnosis-of-the-wolff-parkinson-white- syndrome?source=search_result&search=Wolff&selectedTitle=2~86 71. Ganz, L.I. (2017). Cardiac implantable electronic devices: Long term complications. UpToDate. Retrieved online at http://www.uptodate.com/contents/cardiac-implantable-electronic- devices-long-term- complications?source=search_result&search=implantable+cariac+defi brillator&selectedTitle=3~150 72. Ganz, L.I. and Hayes, D.L. (2016). Cardiac implantable electronic devices: Patient follow-up. UpToDate. Retrieved online at http://www.uptodate.com/contents/cardiac-implantable-electronic- devices-patient-follow- up?source=search_result&search=implantable+cariac+defibrillator&sel ectedTitle=4~150 73. Ganz, L.I. (2016). General principles of the implantable cardioverter- defibrillator. UpToDate. Retrieved online at http://www.uptodate.com/contents/general-principles-of-the- implantable-cardioverter- defibrillator?source=search_result&search=implantable+cariac+defibril lator&selectedTitle=2~150 74. Kirkfeldt, R.E., et. al. (2013). Complications after cardiac implantable electronic device implantations: an analysis of a complete, nationwide cohort in Denmark. European Heart Journal, Volume 35, Issue 18, 7 May 2014, Pages 1186–1194, https://doi.org/10.1093/eurheartj/eht511. Retrieved from https://academic.oup.com/eurheartj/article/35/18/1186/461882/Com plications-after-cardiac-implantable-electronic

75 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 75. Weinstock, J., et al. (2016). Subcutaneous implantable cardioverter defibrillators. UpToDate. Retrieved online at https://www.uptodate.com/contents/subcutaneous-implantable- cardioverter- defibrillators?source=search_result&search=implantable+defibrillator& selectedTitle=8~150 76. Garlitski, A.C. (2017). Cardiac implantable electronic device lead removal. UpToDate. Retrieved online at http://www.uptodate.com/contents/cardiac-implantable-electronic- device-lead- removal?source=search_result&search=implantable+cariac+defibrillat or&selectedTitle=8~150 77. Schulman, P.M. (2017). Perioperative management of patients with a pacemaker or implantable cardioverter-defibrillator. UpToDate. Retrieved online at http://www.uptodate.com/contents/perioperative- management-of-patients-with-a-pacemaker-or-implantable- cardioverter- defibrillator?source=search_result&search=implantable+cariac+defibril lator&selectedTitle=6~150 78. American Heart Association. (2016). Living with your implantable cardioverter defibrillator. AHA. Retrieved online at http://www.heart.org/HEARTORG/Conditions/Arrhythmia/PreventionTr eatmentofArrhythmia/Living-With-Your-Implantable-Cardioverter- Defibrillator-ICD_UCM_448462_Article.jsp#.WeE6ihNSyT8 79. Mayo Clinic. (n.d.). Wolff-Parkindson-White Syndrome. Mayo. Retrieved online at https://www.mayoclinic.org/diseases- conditions/wolff-parkinson-white-syndrome/symptoms-causes/syc- 20354626 80. Biase, L.D., Walsh, E.P. (2016). Atrioventricular reentrant tachycardia (AVRT) associated with an accessory pathway. UpToDate. Retrieved online at https://www.uptodate.com/contents/atrioventricular- reentrant-tachycardia-avrt-associated-with-an-accessory- pathway?source=search_result&search=Atrioventricular+reentrant+ta chycardia&selectedTitle=1~60 81. Knight, B.P. (2017). Atrioventricular nodal reentrant tachycardia. UpToDate. Retrieved online at https://www.uptodate.com/contents/atrioventricular-nodal-reentrant- tachycardia?source=search_result&search=Atrioventricular+reentrant +tachycardia&selectedTitle=2~60 82. Ganz, L.I. (2017). Overview of catheter ablation of cardiac arrhythmias. UpToDate. Retrieved online at https://www.uptodate.com/contents/overview-of-catheter-ablation-of- cardiac-

76 nursece4less.com nursece4less.com nursece4less.com nursece4less.com arrhythmias?source=search_result&search=radiofrequency+ablation+ cardiac&selectedTitle=1~150 83. Passman, R. (2016). Catheter ablation to prevent recurrent atrial fibrillation: Clinical applications. UpToDate. Retrieved online at https://www.uptodate.com/contents/catheter-ablation-to-prevent- recurrent-atrial-fibrillation-clinical- applications?source=search_result&search=radiofrequency+ablation+c ardiac&selectedTitle=2~150 84. Seslar, S.P., et al. (2014). Clinical features of congenital long QT syndrome. UpToDate. Retrieved online at https://www.uptodate.com/contents/clinical-features-of-congenital- long-qt- syndrome?source=search_result&search=long+qt+syndrome&selected Title=6~150 85. Zimetbaum, P.J. (2017). Pathophysiology of the long QT syndrome. UpToDate. Retrieved online at https://www.uptodate.com/contents/pathophysiology-of-the-long-qt- syndrome?source=search_result&search=long+qt+syndrome&selected Title=5~150 86. Berul, C.I., et al. (2017) Acquired long QT syndrome. UpToDate. Retrieved online at https://www.uptodate.com/contents/acquired- long-qt- syndrome?source=search_result&search=long+qt+syndrome&selected Title=1~150 87. Schwartz, P.J., Ackerman, M.J. (2017). Congenital long QT syndrome. UpToDate. Retrieved online at https://www.uptodate.com/contents/congenital-long-qt-syndrome- diagnosis?source=search_result&search=long+qt+syndrome&selected Title=2~150 88. Zimetbaum, P.J., et al. (2017). Prognosis and management of congenital Long QT Syndrome. UpToDate. Retrieved online at https://www.uptodate.com/contents/prognosis-and-management-of- congenital-long-qt- syndrome?source=search_result&search=long+qt+syndrome&selected Title=3~150 89. Zimetbaum, P.J. (2016). Genetics of congenital and acquired long QT syndrome. UpToDate. Retrieved online at https://www.uptodate.com/contents/genetics-of-congenital-and- acquired-long-qt- syndrome?source=search_result&search=long+qt+syndrome&selected Title=4~150 90. National Institutes of Health. (2011). What is Long QT Syndrome? NIH. Retrieved online at https://www.nhlbi.nih.gov/health/health- topics/topics/qt

77 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 91. Patel, A. (2017). Transthoracic echocardiography: Normal cardiac anatomy and tomographic views. UpToDate. Retrieved online at https://www.uptodate.com/contents/transthoracic-echocardiography- normal-cardiac-anatomy-and-tomographic- views?source=search_result&search=echocardiograms&selectedTitle= 1~150 92. Patel, A. and Kannam, J.P. (2017). Transesophageal echocardiography: Indications, complications, and normal views. UpToDate. Retrieved online at https://www.uptodate.com/contents/transesophageal- echocardiography-indications-complications-and-normal- views?source=search_result&search=echocardiograms&selectedTitle= 4~150 93. Gorcsan, J. (2015). Tissue Doppler echocardiography. UpToDate. Retrieved online at https://www.uptodate.com/contents/tissue- doppler- echocardiography?source=search_result&search=echocardiograms&sel ectedTitle=5~150 94. Goldberger, A.L. (2017). Basic Principles of Electrocardiographic Interpretation. UpToDate. Retrieved online at https://www.uptodate.com/contents/basic-principles-of- electrocardiographic-interpretation?source=see_link 95. The Standard 12 Lead EKG (2016). University of Utah. Retrieved online at https://ecg.utah.edu/lesson/1

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