INTERVENTIONAL TREATMENTS FOR ATRIAL

CARDIOVERSION AND ABLATION

JASSIN M. JOURIA

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

Atrial arrhythmias are serious disorders that can cause an irregular and/or rapid heartbeat, which can lead to serious clinical sequelae. Atrial is an example of an atrial that can lead to blood clots, stroke, or failure. Electrical cardioversion and ablation are two procedures that can minimize these risks and treat atrial arrhythmia. Each of these treatments have risks and neither offers a complete success rate, but they

1 nursece4less.com nursece4less.com nursece4less.com nursece4less.com can be very effective in providing greater quality of life, and extending the life expectancy of patients. 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 hours. Nurses may only claim credit commensurate with the credit awarded for completion of this course activity.

Statement of Learning Need

Cardioversion and cardiac ablation for the treatment of resistant atrial arrhythmia has been analyzed in the medical literature, including benefits and risks. Clinicians need to understand the indications and efficacy of both procedures to treat atrial arrhythmia and to reduce cardiac system burden. Clinical research is growing with evolving recommendations for clinicians managing refractory atrial arrhythmia and to plan cardioversion or .

Course Purpose

2 nursece4less.com nursece4less.com nursece4less.com nursece4less.com To provide clinicians with knowledge of cardiac atrial arrhythmias and of the treatments of cardioversion and cardiac catheter ablation to reverse symptoms of atrial arrhythmia and potentially adverse outcomes.

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.

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Please take time to complete a self-assessment of knowledge, on page 4, sample questions before reading the article. Opportunity to complete a self-assessment of knowledge learned will be provided at the end of the course.

1. It is the ______that generates the electrical impulses in the heart.

a. nervous system b. Bachmann’s bundle c. heart d. hypothalamus

2. In a healthy person, the ______initiates the electrical activity to cause an electrical signal to move from the atria toward the lower chambers of the heart.

a. sinoatrial (SA) node b. bundle of His c. pinus d. atrioventricular (AV) node

3. When examining an ECG of a patient with , the sequences are typically manifested as a fast and often irregular rhythm, with

a. a dramatically irregular QRS complex. b. exaggerated P waves. c. well-defined PR intervals. d. no P waves.

4. When comparing the atrial cells to the ventricular cells, the cells in the atria

a. have a longer refractory period. b. have a continuous action. c. initiate another action potential faster than the ventricular cells. d. initiate action potential at the same rate as the ventricular cells.

5. A patient with atrial fibrillation (AF) is considered to have recurrent AF when the patient

4 nursece4less.com nursece4less.com nursece4less.com nursece4less.com a. requires treatment for the condition. b. suffers from two or more episodes of fibrillation. c. has episodes that are not self-limiting. d. has episodes that are persistent, not sporadic.

Introduction

Atrial arrhythmias are serious conditions that can cause multiple complications if they are not well-managed. Atrial arrhythmias include atrial fibrillation, supraventricular , bradycardia, premature atrial contractions, sick sinus syndrome, atrioventricular heart blocks, amongst other heart rhythm and rate abnormalities originating within the atria. Atrial fibrillation is the most prevalent type of atrial arrhythmia, which can cause potentially life-threatening consequences, including thrombosis and stroke. Understanding atrial arrhythmias is crucial to treating patients with these conditions to restore a normal heart rhythm and to improve health and a greater sense of wellbeing. Interventional cardiac procedures may be done to treat these arrhythmias when more conservative medical interventions fail, and can include cardiac ablation and cardioversion.

Electrical Activity Of The Heart

Before discussion of the different definitions of arrhythmias, it is necessary to define some of the particular mechanisms that are involved with the electrical activity of the heart. Although some of the rate of cardiac conduction is controlled by the nervous system, it is the heart itself that actually generates the electrical impulses. The heart’s ability to generate its rhythm through its specialized conduction system is known as auto- rhythmicity, which is a function that is unique to the heart muscle in comparison to other types of muscles in the body.

5 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Sinoatrial Node

The electrical current begins in the sinoatrial (SA) node at the top of the right , which is located near the connection between the atrium and the superior vena cava.2 The SA node initiates the electrical activity to cause an electrical signal to move from the atria through specified pathways, known as internodal pathways, through the atrioventricular (AV) node and toward the base of the ventricles to cause the heart to contract; that is, the impulse starts in the right atrium, then it moves to the left atrium via the Bachmann’s bundle, which is an internodal tract that passes between the two atria and allows the impulse to pass through, before moving along further toward the ventricles.

Interestingly, this impulse generated from the SA node moves through the heart cell-by-cell; the cells next to each other are stimulated and the impulse spreads through them when they are near cells with a faster pace. In other words, a cell that has a faster pace from the SA node sets the pace for which surrounding cells imitate and follow, thus setting off the process that leads to a contraction. For this reason, the SA node is also referred to as the pacemaker of the heart.

The electrical impulses generated from the cells of the SA node are referred to as action potential, which occurs when ions cross through channels to move in and out of the heart’s cells. The action potential refers to the

6 nursece4less.com nursece4less.com nursece4less.com nursece4less.com changes in voltage within each cardiac cell. The transmembrane potential is a term used to describe the difference between the voltage within the cell compared to the outside of the cell. As the impulse travels through the atria, the action potential essentially triggers the action potential in the next cell through a series of connections between the cells known as gap junctions. In this manner, the action potential is able to travel from cell to cell. The cells in the atria have a faster conduction velocity than those within the actual SA node but ventricular tissue has a faster conduction velocity than the cells of the atria.2,10,11

Atrial cells have a shorter refractory period and ventricular cells have a longer refractory period, meaning that cells in the atria will be ready to initiate another action potential at a faster rate than those of the ventricles.10,11 The action potential is different from the cardiac resting potential, which is the opposite polarization and voltage from inside the cell. In the resting state, there are more negative ions inside the cell when compared to the outside. However, the action potential can develop as various ions move across the cell membrane.

Blood Flow

When the electrical signal is at the level of the SA node, the atria contract and blood is shunted through the valves to the ventricles. From the SA node, the signal travels to the AV node, which is found at the junction between the right atrium and the right . When the impulse reaches the AV node, it is briefly suspended before moving on, which allows the atria to fully contract and send enough blood on to the ventricles. The blood passes through the valves, filling the ventricles, and the signal moves on to the atrioventricular bundle, or bundle of His, which is found along the walls of

7 nursece4less.com nursece4less.com nursece4less.com nursece4less.com the ventricles. At this time, the valves between the atria and ventricles have closed, allowing the atria to refill with blood for the next contraction.2,10,11

Beyond the bundle of His, the impulse travels through the right and left bundle branches that span the ventricles and the septum between the right and left sides. The system further splits off into the Purkinje fibers, continuing to extend across the ventricles and causing them to contract. The impulse is also received by the papillary muscles, which are attached to the ventricular wall and the mitral and tricuspid valves. When the papillary muscles receive the impulse, they also contract so that with the contraction of the ventricles, blood is prevented from flowing back into the atria.

The left ventricle contracts just slightly before the right, and blood is moved through the valves, where it either travels toward the lungs or into general circulation. As the ventricles relax after their contractions, the system resets to begin again in the SA node.

Depolarization and Repolarization

As the electrical impulse travels through the channels of the heart, it undergoes several phases, representing the cardiac conduction cycle that allows the heart to contract.

Phase 0: Depolarization

Sodium ions enter the cardiac cells during depolarization. When this occurs in one cell, it triggers other cells nearby to also allow sodium ions to enter through their membranes and the transmembrane potential becomes positive. Consequently, the process of depolarization moves cell by cell through the heart. The pace at which one cell triggers the next into depolarization is known as conduction velocity. The cells repeatedly undergo

8 nursece4less.com nursece4less.com nursece4less.com nursece4less.com the process of depolarization but cannot replicate the process again until they have repolarized. As soon as depolarization has occurred within a cell, it begins the process of repolarization.10,11

Phases 1 and 2: Early Repolarization

Phase 1 is considered the initial phase of repolarization. During Phase 2, calcium ions enter the cell and it initiates what is known as the plateau phase, where the actual process of repolarization is slowed somewhat. Phases 1 and 2 are known as the refractory period and the cell will not react to any new stimuli during these phases.

Phase 3: Repolarization

At phase 3, the repolarization process is completed and the refractory period ends. The amount of calcium entering the cells is restricted and the cell again nears the stage where it was just before depolarization.

Phase 4: Resting or Quiet Phase

During the resting or quiet phase there is no exchange of ions across the cell membranes, repolarization is complete, and the cell is preparing for depolarization once again.10,11

Atrial Arrhythmias

A cardiac arrhythmia is an abnormality in the natural rhythm of the heart. The cell-to-cell process described above may also explain how arrhythmias can develop. When a myocardial cell sets a faster or irregular pace, the cells

9 nursece4less.com nursece4less.com nursece4less.com nursece4less.com nearby respond in the same way, setting off an abnormal rhythm or rate that leads to irregularities with the timing of contractions.25

Atrial arrhythmias are those that originate at some point within the atria of the heart. These types of arrhythmias can extend to and impact the ventricles as well but they start in the upper chambers. Depending on the particular type, an atrial arrhythmia could originate within the SA node or somewhere along the continuum between this node and the AV node. The abnormality could impact one or both atria at the same time or it could start in one and cross over to the other. When this occurs, conduction of the heart’s electrical impulse takes place through the Bachmann’s bundle, which acts as a bridge between the left and right atria during the conduction sequence. Therefore, an arrhythmia could develop in one of the atria but could then pass over through the Bachmann’s bundle to impact the other side.10,11,25

When an arrhythmia develops, the heart beats at an aberrant pace, which may or may not be irregular. For instance, tachycardia, which occurs when the heart beats at an abnormally fast rate, is considered a type of tachyarrhythmia. When tachycardia develops, though, the heart often beats too quickly but not necessarily irregularly.12 Alternatively, when an arrhythmia develops, the heart may beat irregularly, but the rate is not necessarily too fast or too slow.

People who develop arrhythmias may or may not experience symptoms related to the condition. Depending on the severity of the arrhythmia and the extent to which it impacts blood flow, symptoms may be slow to develop.

10 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Understanding the differences between the types of arrhythmias is important in determining the appropriate intervention. At times, an arrhythmia occurs that is noted but simply monitored without intervention. There are many arrhythmias that do not self-resolve and that require rapid treatment. Some of the more significant arrhythmias, including atrial arrhythmias and the supraventricular arrhythmias require prompt intervention to prevent these conditions from deteriorating into potentially life-threatening events. Overall, arrhythmias can be classified into four different categories; those that cause extra beats, supraventricular arrhythmias, ventricular arrhythmias, and bradyarrhythmias.12 One of the more common atrial arrhythmias is atrial fibrillation.

Atrial Fibrillation

Atrial fibrillation occurs when the atria beat in a manner that is uncoordinated and irregular. Normally, as the heart contracts, the atria and the ventricles keep pace with each other according to the conduction system of the heart. When atrial fibrillation (AF) occurs, the different chambers of the heart – the atria and the ventricles – beat rapidly and out of sync. The atria contract at a faster pace than the ventricles and their efforts are uncoordinated. As each electrical impulse is released from within the atrium, it may follow an abnormal pattern through the heart, causing irregularities in the rate and rhythm of contractions. Because of the abnormally fast that occurs with atrial fibrillation, blood flow through each of the heart’s chambers is incomplete and less blood is pumped into circulation.

If the SA node becomes damaged in some way, the pacemaker role of generating electrical impulses could be taken over by another node located elsewhere in the heart.

11 nursece4less.com nursece4less.com nursece4less.com nursece4less.com With atrial fibrillation, the entire process of the electrical impulse passing through the different areas of the heart is disordered. Instead of one impulse at a time being fired from the SA node, there may be multiple signals sent from different parts of the atria.22,25 When all of these impulses are generated at the same time, the atria then beat chaotically and rapidly and blood does not flow normally into the ventricles.

When examining an electrocardiogram (ECG) of a patient with atrial fibrillation, the sequences are typically manifested as a fast and often irregular rhythm, with no P waves. The area of the P wave is typically flat and it is not well-defined. The PR interval is absent but the QRS complex often appears relatively normal or it may be slightly widened, because the ventricles are still contracting, although these contractions may be at a fairly reasonable but irregular rate. Clinically, the patient may complain of discomfort or the feeling of palpitations in the chest, shortness of breath, or dizziness. The assessed pulse rate is rapid and irregular, and blood pressure may be low. When atrial fibrillation is identified on an ECG, the clinician must then determine whether it is an isolated episode or if the patient is consistently experiencing repeated rounds of atrial fibrillation. A patient’s medical history may help answer this question.

Isolated occurrences of atrial fibrillation are often benign and may resolve spontaneously without further problems. Atrial fibrillation may develop into a persistent or even permanent condition. With persistent and ongoing atrial fibrillation, the patient is at risk of potentially life-threatening complications associated with decreased cardiac output, including sudden or heart failure.5,22 The affected individual is also at risk of thrombosis and stroke. These secondary conditions are discussed more fully below.

12 nursece4less.com nursece4less.com nursece4less.com nursece4less.com The increase in cases of atrial fibrillation is on the rise, with more people detecting the condition and being diagnosed at earlier stages. Throughout the world, approximately 2 percent of the general population has some form of AF. The prevalence of the condition is only expected to increase with time; estimated projections are that by the year 2050, the overall frequency of AF will increase by three-fold.6

Risk Factors

The risk of AF is thought to increase with advancing age. This particular arrhythmia may occur more often in older adults. When diagnosed, it is thought that up to 85 percent of patients with AF are older than age 65 years.13 This statistic can be particularly problematic, as this specific population may already have an increased risk of stroke due to heart disease, as well as increased risk of other adverse events, such as falls or accidents due to dizziness and syncope, both of which may also be more likely to occur as a result of AF.

Causes

Atrial fibrillation has been shown to have a number of potential causes. Many of the related conditions contribute to AF because they can have a significant impact on the heart’s conduction system, thereby affecting normal contractions. While arrhythmias can be caused by a number of cardiac conditions, including heart disease or heart failure, they may also occur transiently as a result of social, emotional, or environmental factors. For example, some people may be more likely to suffer from cardiac arrhythmias when outside factors are present, such as increased stress and fatigue, sleep difficulties (obstructive sleep apnea), drug and alcohol use, or even dietary alterations. Some causes that have been noted as contributing to AF include

13 nursece4less.com nursece4less.com nursece4less.com nursece4less.com hypertension, , heart failure, valve disease, and diabetes.5,22

Hypertension

Hypertension is one of the more common conditions associated with the development of atrial fibrillation. While high blood pressure often causes few symptoms initially, some patients may develop complications of untreated hypertension combined with problems associated with AF. In addition to its frequent link with AF, hypertension is also often associated with a number of other health conditions that could also contribute negative symptoms to a person’s state of health.

Over time, elevated blood pressure can increase the size of the atria, affecting pacing abilities and contributing to an arrhythmia. A review published in the Methodist DeBakey Cardiovascular Journal also noted that various other factors, including the effects of angiotensin II, are associated with blood pressure regulation. Angiotensin II may promote AF development because it can affect ion channels in the cells. Further, increased levels of aldosterone, a hormone that is also connected to blood pressure, has been shown to contribute to arrhythmia by promoting fibrosis, which can impact the source of the abnormal impulse that produces AF.54

Heart Disease

Cardiac arrhythmia, such as bradycardia, can be caused by damage to the cardiovascular system. This damage may be caused by coronary artery disease or a previous myocardial infarction.

Valve Disease

14 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Cardiac issues such as valve disease can contribute to AF by impacting blood flow through the heart. When the valves between the chambers do not work properly, blood flow is slowed and blood can build up or regurgitate, potentially increasing the size of the atria. The heart has to work harder to pump blood, which increases the risk of AF development.

Scarring of the tissue of the atria due to arteriosclerosis can also affect how electrical impulses are generated and the pathways through which they are sent. The scarring can affect not only the rate and degree of impulses generated, but also the location of where the impulse originates from. For example, excessive scarring could prevent the SA node from acting as a pacemaker and the impulse could be generated from another area, such as the AV node, thereby contributing to an abnormal heart rhythm.

Type 2 Diabetes

While many of the causes of AF are related to the cardiovascular system overall, there are some conditions that can still perpetuate AF development but that seem to be associated with other body systems entirely. A metabolic condition such as diabetes would seem less likely to cause an arrhythmia such as AF, but studies have shown that there is a connection.

One study published in the Archives of Cardiovascular Diseases examined the relationship between type 2 diabetes and development of atrial fibrillation. Of the kinds of diabetes diagnosed, type 2 is much more common and may be more likely to be related to modifiable factors such as obesity or activity levels. Type 2 diabetes is also more likely to be related to insulin resistance, in which the body’s cells no longer respond to the effects of insulin. The study examined the different mechanisms noted in the

15 nursece4less.com nursece4less.com nursece4less.com nursece4less.com relationship between AF and type 2 diabetes to look for connections that would indicate a causative relationship.

One notable connection that was identified in the study was that diabetes is associated with endothelial dysfunction, in which the disease can cause damage to the endothelial layer of the blood vessels when blood glucose levels are not adequately controlled. This endothelial dysfunction also increases the risk of clot formation and thrombosis that could further diminish blood flow. Recurrent Arterial Fibrillation

A patient with atrial fibrillation is considered to have recurrent atrial fibrillation when the patient suffers from two or more episodes of fibrillation.52 These episodes can be very sporadic and self-limiting, producing few symptoms and rarely requiring treatment. Alternatively, AF episodes may become unrelenting in their frequency, with a patient experiencing episodes of fibrillation more often than a normal heart rhythm. Recurrent AF is further classified as being paroxysmal AF or persistent AF. It is important to determine whether a patient is having intermittent or continuous periods of AF. Some of this information can be established based on the patient’s history of symptoms.

Paroxysmal Atrial Fibrillation

One particular type of atrial fibrillation that is commonly seen among patients is known as paroxysmal AF, which is considered to be more serious than occasional, self-limiting episodes of the arrhythmia. Alternatively, paroxysmal AF is not considered to be as serious as other types, including persistent AF. Paroxysmal AF is considered when an individual has two or more episodes of atrial fibrillation, lasting more than 30 seconds each, within seven days of each other. Each of the episodes are fairly benign and they

16 nursece4less.com nursece4less.com nursece4less.com nursece4less.com self-resolve. This particular type of AF is thought to account for up to 60 percent of diagnosed cases.6

Although paroxysmal AF is a relatively common form of atrial fibrillation, it can be dangerous for the affected patient. First, an individual who experiences occasional bouts of AF may never seek treatment. If the episodes are self-limiting and symptoms are tolerable, the affected person may reason that it will resolve on its own without further need for care or actual diagnosis. The lack of symptoms, in some cases, may mean that the person is unaware that he/she even has the condition.

When paroxysmal AF is eventually diagnosed, it can be difficult to determine when the condition actually began, as the individual has ignored or adjusted to the symptoms somewhat over time. Secondly, repeated episodes of paroxysmal AF can cause structural changes in the tissue within the heart that will eventually lead to more persistent atrial fibrillation as well as decreased cardiac output overall. Without treatment of paroxysmal AF, the individual may develop further heart damage, more frequent episodes of AF, and eventual development of persistent atrial fibrillation.

Paroxysmal AF is thought to contribute to a process of structural remodeling within the heart, sometimes known as atrial arrhythmogenic remodeling. The process involves enough damage to the heart’s tissue that over time, it eventually promotes further atrial arrhythmias. In essence, longer periods of untreated AF cause structural remodeling within the heart that eventually stimulate further AF and more frequent episodes.6,7 Paroxysmal atrial fibrillation, in itself, is a progressive disease that can continually worsen over time if the patient does not receive proper care and treatment.

17 nursece4less.com nursece4less.com nursece4less.com nursece4less.com One article published in the Journal of the American College of stated that AF typically contributes to further AF through one of four different mechanisms. It may cause electrical remodeling in which the ion channels within the heart muscle cells are altered, an increase in intracellular calcium occurs, and irregularities in the gap junctions develops. Structural remodeling describes a condition of when the atria are enlarged over time and there is fibrosis development that interrupts the normal conduction cycle. There may be autonomic nervous system changes that contribute to AF development. Though the heart itself is responsible for generating electrical impulses to promote contraction, the autonomic nervous system plays a role in regulating electrical activity from within the atria and when there is increased activity from adrenergic receptors, there may be greater ectopic activity, thereby contributing to abnormalities with generation of cardiac impulses.

Finally, calcium handling abnormalities are thought to contribute to perpetuating AF. Recall that since the heart is a muscle, it needs a certain amount of calcium to contract normally. Abnormalities in calcium levels within the human heart contribute to a pro-fibrillatory state in which there is an increase in ectopic beats, in addition to prolonging AF when it develops.7 All of these mechanisms increase the complexity of atrial fibrillation, and when one or more mechanisms are present, a person affected with AF can have a much greater risk of developing a more persistent arrhythmia because of their stimulating effects.

Persistent Atrial Fibrillation

Persistent atrial fibrillation is a condition that lasts longer than paroxysmal AF. This means that it is technically longer than seven days’ duration and it

18 nursece4less.com nursece4less.com nursece4less.com nursece4less.com requires some form of intervention for correction. This may involve prescription medication to stimulate the heart to contract at a normal rate and rhythm, or further procedures, including cardioversion or ablation, to correct the arrhythmia.

Persistent AF may be further classified as longstanding persistent AF, described as episodes that last longer than one year. Longstanding persistent AF is more likely to develop after an individual has had paroxysmal AF. As discussed, the paroxysmal form of the arrhythmia can perpetuate further episodes that increase in frequency, often because of the structural or electrical remodeling that can occur within the heart, as well as the effects of the autonomic nervous system. Over time, when changes within the heart muscle occur due to paroxysmal AF, the individual may eventually develop persistent AF that is longstanding.

Longstanding persistent AF is a subcategory of persistent AF, which occurs when the arrhythmia episodes last longer than a year. At this point, the condition is generally considered to be ongoing, despite attempts to eliminate it. Treatment is more focused on managing the condition and preventing the AF from worsening.7

Permanent Atrial Fibrillation

In contrast to recurrent AF, a patient who has suffered from atrial fibrillation for over a year may be diagnosed with permanent AF. This condition is somewhat similar to longstanding persistent AF, in that the patient has experienced episodes and symptoms of AF for a long time. With permanent AF, there is a certain amount of acceptance of the situation and there are no longer attempts at procedures such as cardioversion or catheter ablation to correct the AF.

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Patients with permanent AF may remain on prescription antiarrhythmic medications, with the understanding that long-term AF increases the risk of thrombosis. However, there are few other attempts to try to eradicate the arrhythmia or restore the heart to normal .5

Although a patient with permanent AF may not pursue more invasive forms of treatment for arrhythmia resolution, the condition can still be managed to prevent complications. The risk of stroke among patients in this population is elevated, so stroke prevention measures are essential. A study by Senoo, et al.,57 in the journal Stroke compared the prognosis of two different groups of patients: those with permanent AF and those with non-permanent AF. Both groups were using anticoagulant medications. Overall, there were more patients with permanent AF who also had heart failure (29%) compared to those with non-permanent AF (16%). Further, there was a greater risk of mortality from cardiovascular causes and stroke in the permanent AF group compared to those with non-permanent AF, even though patients in both groups were taking anticoagulants.57

The study by Senoo, et al., suggests that anticoagulation is important in all patients with AF, regardless of whether it is classified as permanent or not.57 However, among those with permanent AF, further measures of prevention against development of other complications, including cardiovascular disease and heart failure, are necessary.

Electrocardiogram Testing

When a patient with atrial fibrillation presents for care, the clinician will have to determine whether the patient is having intermittent or continuous periods of AF. This may be evaluated using an electrocardiogram (ECG).

20 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Paroxysmal AF may or may not be manifested during a routine ECG; the chance of identifying the rhythm during an ECG is typically contingent on whether the rhythm actually appears during the test.

Persistent or permanent AF will most likely show up on an ECG because the arrhythmia is often ongoing for longer periods. Technically, an episode of AF is confirmed when it is documented through ECG analysis and when it has a duration of at least 30 seconds; however, it can sometimes be difficult to capture an arrhythmia on an ECG when paroxysmal AF is present.55 If there is a question of the persistence of AF, the patient may need further evaluation through use of a , in which the patient can wear the device for a period of 24 hours or more to record ECG and determine how long the AF episodes are lasting.

Symptoms

Some patients who develop atrial fibrillation have few to no symptoms. Consequently, the condition could go unnoticed for long periods until an affected individual develops complications or the condition worsens to the point that the patient eventually does start to notice symptoms. At times, a patient may find out that he or she has AF during a routine screening for another health condition or following an ECG that shows the abnormalities. Approximately 20 percent of people with AF are not aware they have the condition.6 Even if symptoms seem insignificant or if the patient is asymptomatic entirely, the risks of AF remain the same.

When symptoms are present, they are typically related to the heart’s contractions and the effects on blood flow. Because AF leads to a decrease in cardiac output due to the irregularity, the patient may have symptoms that are related to the effects of decreased circulation. The very rapid pace of the

21 nursece4less.com nursece4less.com nursece4less.com nursece4less.com atria does not allow the ventricles to properly keep up. Consequently, when the ventricles do contract, they are not sufficiently filled with blood from the atria, and less blood is pumped toward the lungs and into circulation overall. This is more notable with a faster pulse rate. An affected person may have the feeling of heart palpitations or fluttering in the chest, sometimes described as a racing or pounding heartbeat, or a feeling of fluttering or thumping in the chest with each heartbeat. Some people feel dizzy or lightheaded or they may faint.3,5 A patient feels dizziness or lightheadedness with AF because of diminished blood flow to the brain. Over time, the consistently diminished levels of blood flow may eventually cause confusion or memory loss. Decreased circulation to the skeletal muscles may contribute to overall feelings of weakness or fatigue. Some people experience difficulty breathing, a feeling of not being able to stop for a breath, or overall activity intolerance when decreased cardiac output affects blood flow to the lungs.1

For some people, symptoms of AF may also mimic that of angina, and they experience chest pain and pressure when the irregularity arises. The chest discomfort is actually quite similar to angina, which occurs as a result of decreased blood flow to the heart. When AF develops and the heart beats irregularly, there may also be a reduction in overall blood flow to the heart muscle tissue. While traditional angina is thought to be caused by decreased blood flow due to an obstruction in the coronary vessels, such as atherosclerosis, a reduction in blood flow because of decreased cardiac output due to AF could also reduce circulation to the heart that is significant enough to cause angina.

Increased severity of symptoms is not necessarily associated with more severe or persistent AF; however, even mild symptoms of the condition can

22 nursece4less.com nursece4less.com nursece4less.com nursece4less.com contribute to increased risk of stroke or damage to the heart. Additionally, when an arrhythmia is ongoing and when it affects an individual because of symptoms (frequent syncope, for example), intervention is needed for the safety and comfort of the patient. There are also some arrhythmias that are quite noticeable and that can quickly become life-threatening without appropriate intervention.1,71

Complications and Anticoagulation

Atrial fibrillation can increase the risk of thrombosis because circulation through the heart and into the blood vessels is impaired. Blood is more likely to pool and coagulate when it is poorly pumped from the atria to the ventricles. Consequently, blood clots could develop within the atria and could then be passed on to the ventricles or into the . Because of this risk of blood clots, anticoagulant medications are often needed for patients with AF.

The risk of blood clots can also differ depending on the type of AF present. With persistent AF, the increased possibility places the affected patient at risk of serious and potentially life-threatening complications of stroke or myocardial infarction. Patients who already have underlying heart disease, such as atherosclerosis or hypertension are at even greater risk of stroke when AF is present, although even those who are otherwise healthy (without concomitant heart disease) are still at higher risk when AF emerges.13 Often, anticoagulant drugs are prescribed in these cases when risk of blood clots is high. In fact, one study has shown that atrial fibrillation is associated with a five-fold greater risk of stroke, which could potentially lead to lethal consequences.4

23 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Evaluation of the need for anticoagulants may be on a case-by-case basis that considers the patient’s age, sex, and health history, and how long he or she has been experiencing AF. Unfortunately, when an individual has developed AF, that person is also at greater risk of developing some other types of atrial arrhythmias, including , which occurs when the atria beat at a rapid pace and are out of sync with the ventricles. Atrial flutter may cause the atria to beat at a pace of upwards of 300 beats per minute, while the ventricles may beat at approximately half the same pace, or around 150 beats per minute.7,9

Atrial fibrillation can also lead to irreversible cardiac complications such as heart failure, when the atria are stretched and become larger over time. The decrease in blood flow into circulation combined with the pooling and backing up of blood within the heart can lead to symptoms of heart failure and further health problems.

24 nursece4less.com nursece4less.com nursece4less.com nursece4less.com As stated, if a patient is evaluated to have AF, it can technically be classified as one of several actual types of the arrhythmia. In order to understand atrial fibrillation better, it is essential to first revisit what occurs with the electrical conduction of impulses and define the different types of AF based on their symptoms, patterns of illness, and presentation.3,5

Normally, the heart rate is defined as the number of electrical impulses generated by the SA node per minute. Because the SA node starts the electrical impulse that causes the heart to contract, each impulse is equal to one heartbeat. When AF occurs, the electrical signals sent from the SA node are disorganized; the signals may actually originate in other locations besides the SA node. As a result, the atria do not contract in a synchronized manner. Instead of normal contractions, they may only contract partially, which is ineffective for blood flow. Blood can back up within the atria when only some of it passes into the ventricles. This not only causes a decrease in overall blood flow pumped into circulation with each cardiac contraction, but the patient is at greater risk from blood clots that can develop when blood pools and then coagulates within the atria.3

An episode of atrial fibrillation is technically defined as this quivering or vibration of the atria that lasts for more than 30 seconds at a time, according to guidelines from several professional medical organizations, including the American College of Cardiology and the American Heart Association.5 The rate and length of time that a person experiences episodes of AF can vary. Some patients experience random episodes on an intermittent basis that self-resolve and cause no long-term effects; alternatively, some people develop constant AF that causes continuous symptoms and is permanent.

25 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Supraventricular Tachycardia

Supraventricular tachycardia, commonly referred to as SVT, is sometimes described as an individual condition but is actually a collection of types of heart rhythms in which the heart rate is abnormally fast. The condition describes a rapid heart rate over 100 beats per minute that originates above the ventricles. Because the heart rate is so fast, blood flow from the heart with each contraction is insufficient. The lungs and the tissues of the rest of the body do not receive adequate blood flow and may become hypoxic if the SVT continues over a period of time. The heart works much harder than normal because there is too little time for the heart muscle to rest between contractions. An affected patient may experience dizziness, syncope, weakness, shortness of breath, sweating, or a feeling of pounding in the chest or neck.58

Supraventricular tachycardia does not describe a situation in which a patient is exercising or engaging in intense activity that would normally elevate the heart rate. Instead, because of a trigger, the ventricles begin to contract rapidly when the electrical impulse returns to the atria in a loop, such as that formed with the combination of Wolff-Parkinson-White syndrome, discussed in the next section, and atrial fibrillation. This re-entry of the impulse from the ventricles back into the atria is what causes the heart to beat so quickly as the impulse continues repeatedly through the loop in a cyclical manner.

For many patients, SVT can develop based on an event or stimulus that causes the heart to rapidly increase the rate at which electrical impulses are generated. Some of these triggers include environmental or emotional stimuli, including excessive caffeine or alcohol intake, smoking, or use of stimulant drugs. Supraventricular tachycardia can also develop without warning in a person who already has underlying heart disease or who has

26 nursece4less.com nursece4less.com nursece4less.com nursece4less.com already been diagnosed with another arrhythmia, such as Wolff-Parkinson- White (WPW) syndrome. People with a history of heart failure or chronic lung disease may also be more likely to experience episodes of SVT.58

There are several arrhythmias that are technically classified as types of SVT. One example is , which is relatively common and often conditional. Sinus tachycardia occurs when the heart beats at a rate faster than 100 beats per minute with normal activity, increasing to upwards of 200 beats per minute or more with activity. The rhythm of sinus tachycardia is regular.58,60

Overall, sinus tachycardia is usually considered a benign condition and can be caused by a number of factors that are situational and can be corrected easily. Common causes of sinus tachycardia include use of some medications, such as epinephrine or pseudoephedrine, dietary factors, including caffeine consumption, nicotine or alcohol intake, and anxiety or stress. Often, sinus tachycardia is resolved when the cause has been eliminated. Resolution is typically gradual, with the heart rate progressively slowing down until it has reached normal limits.

Atrial tachycardia is another type of SVT that exhibits many of the opposite effects of heart block, described later as well. Instead of the heart rate being too slow, resulting in bradycardia, atrial tachycardia involves an abnormally fast rate that originates in the atria. The arrhythmia is generated in a manner similar to that seen with atrial flutter.

Paroxysmal Atrial Tachycardia

Paroxysmal atrial tachycardia (PAT) begins and ends suddenly, and there may be little impetus that triggers an event. Episodes can be infrequent and

27 nursece4less.com nursece4less.com nursece4less.com nursece4less.com self-limiting, and the heart rate can be up to 240 beats per minute. As with other types of cardiac arrhythmias, PAT develops when there is an abnormality in how the cardiac impulses are released from the SA node or when the impulses are generated from locations other than the SA node. Typically, the P wave will appear abnormal when PAT is present, as the impulse is not traveling normally from the SA to the AV node.6

The individual who experiences PAT often feels the sensation of fluttering in the chest as the heart beats. The condition is episodic and typically resolves on its own without further intervention. However, the situation could also change from paroxysmal atrial tachycardia to a sustained rhythm; when this occurs, the affected person often suffers from symptoms related to poor blood flow throughout circulation. Common symptoms include dizziness or lightheadedness, particularly if normal cardiac output is not restored with resolution of the tachycardia.6

Because PAT is episodic and tends to self-resolve, treatment is often unnecessary. A patient who is in a sustained rhythm may convert back to a normal rhythm after stimulating the vagal reflex, which often acts to reset the arrhythmia back into a normal pattern and rate. Sustained atrial tachycardia often needs further treatment through cardioversion when the vagal response cannot be stimulated.

Vagal maneuvers may be used to stop an episode of SVT. Performing a vagal maneuver involves stimulating the vagus nerve through the face and neck. In adults, this can be done by holding the breath and bearing down in a manner of having a bowel movement, known as the Valsalva maneuver.59 A cold washcloth placed over the face or touching the back of the throat to stimulate the gag reflex can also act as vagal maneuvers. When an infant is

28 nursece4less.com nursece4less.com nursece4less.com nursece4less.com having episodes of SVT, a small ice bag or cold cloth placed over the face for several seconds can often convert the tachycardia back into a normal rate.

The vagus nerve is one of the cranial nerves and is actually very long, extending from the head and neck down into the abdomen. The vagus nerve has a connection with the heart in that it provides parasympathetic innervation to the SA node. When a vagal maneuver is performed, the vagus nerve is stimulated, causing a release of acetylcholine that affects the SA node and slows the heart rate.59 There are various forms of vagal maneuvers that can be attempted before trying other treatments for SVT. A patient who can tolerate vagal maneuvers and who recognizes when he or she is having an episode of SVT may be taught how to perform one or more specific maneuvers to try to correct the situation before attempting other measures of treatment, including medication or more invasive procedures.

Atrioventricular Node Re-entrant Tachycardia

Atrioventricular node re-entrant tachycardia (AVNRT) is the most common type of SVT. When this occurs, the cardiac impulse may travel from the SA node through the atrium but as it reaches the AV node, it does not progress to the bundle of His. Instead, the impulse circles the AV node because there is more than one nodal pathway present. The impulse then remains near the AV node, continuing to circle it without progressing further in the conduction cycle. The ventricles are repeatedly stimulated to contract, so the ventricular rate increases rapidly and the overall heart rate is much faster than normal.

Patients with AVNRT typically exhibit symptoms related to a very rapid ventricular rate combined with disorganized atrial and ventricular contractions. Common symptoms include dizziness and lightheadedness, syncope, weakness and fatigue, shortness of breath, chest palpitations,

29 nursece4less.com nursece4less.com nursece4less.com nursece4less.com sweating, and mild chest discomfort.52 Because the condition could be stimulated by environmental conditions, such as stress or caffeine intake, lifestyle modifications are the first course of treatment for managing AVNRT.

Some patients are taught how to perform vagal maneuvers so that if they feel that the arrhythmia has started and begin to develop symptoms, they can convert the heart back to normal sinus on their own. When vagal maneuvers are not successful and the AVNRT has started to affect the patient’s quality of life, medication is the next step of treatment. Typically, drugs such as beta blockers or calcium channel blockers are prescribed, although some patients respond best to digoxin as well. Ultimately, catheter ablation is sometimes needed to prevent the arrhythmia from continuing to recur, even after treatment.

Atrioventricular Re-entrant Tachycardia

Atrioventricular re-entrant tachycardia (AVRT) occurs when the electrical impulse follows a loop in an abnormal manner that stimulates the ventricles to contract at a faster rate. With AVRT, there is an extra pathway that develops somewhere between the atria and the ventricles. The impulse can jump from the atrium to the ventricle through this pathway and stimulate the ventricle to contract. The signal can also travel in reverse through the pathway and can loop back from the ventricles back to the atria.60 Wolff- Parkinson-White syndrome is an example of AVRT.

The symptoms of AVRT are similar to those seen with other forms of SVT, including dizziness, lightheadedness, weakness, and near-syncope. Some people may also feel chest discomfort or have poor activity tolerance. Although the accessory pathway cannot be eliminated, many patients can

30 nursece4less.com nursece4less.com nursece4less.com nursece4less.com reduce the number of episodes of AVRT they experience by making lifestyle modifications and healthy choices.

If symptoms are more severe, other treatment may be considered, including antiarrhythmic drugs, beta blockers, and calcium channel blockers. When medication use is not feasible for a patient or the arrhythmia still has not resolved, catheter ablation is the final option for treatment.61 Catheter ablation is the only means of resolving the accessory pathway and preventing further episodes of AVRT.

Other Atrial Arrhythmias

While atrial fibrillation is the more common form of atrial arrhythmia, there are other types of heart rhythm irregularities. These are described in this section.

Wolff-Parkinson-White Syndrome

Yet another syndrome that affects the heart’s conduction system is Wolff- Parkinson-White syndrome (WPW). As with various other types of atrial arrhythmias, WPW syndrome develops due to abnormalities in the conduction system and in the location of where the electrical impulse is generated. Wolff-Parkinson-White syndrome is a congenital anomaly in which an affected individual has an accessory pathway in the heart. The development of this extra pathway is related to a specific type of genetic mutation, although this explains only a percentage of cases.

For a significant number of people, the actual cause of WPW syndrome is unknown. When the accessory pathway is present, the electrical impulse can potentially bypass the AV node when it travels from the atria to the

31 nursece4less.com nursece4less.com nursece4less.com nursece4less.com ventricles. This pathway is known as the bundle of Kent. When impulses pass through the bundle of Kent instead of the normal pathway through the AV node, the heart contracts at a much faster rate. Additionally, the bundle of Kent may generate its own impulses and send them backward toward the atria, forming a loop.20

A person with the syndrome will often experience symptoms associated with tachycardia, including a bounding heart rate, a feeling of thumping or fluttering in the chest, dizziness and lightheadedness, and syncope. Wolff- Parkinson-White syndrome is known to be one of the more common causes of supraventricular tachycardia.20 If the individual with WPW also develops atrial fibrillation, the effects can be life-threatening and he will need immediate treatment. Because the syndrome can not only cause abnormal movement of impulses from the atria to the ventricles but also a reversal of impulses backward from the ventricles to the atria, if atrial fibrillation develops, the heart cannot regulate the rate of contractions by using the AV node. The ventricular rate then increases rapidly and the affected person is at risk of developing , a life-threatening arrhythmia.21

Wolff-Parkinson-White syndrome is typically episodic in nature and the affected individual may have few symptoms. Although it is a congenital condition, an affected person could live with the syndrome for years without it being diagnosed. It may be discovered when an adolescent or young adult exhibits signs or symptoms of a cardiac arrhythmia.

The usual treatment for WPW is cardioversion to shock the heart out of the abnormal rhythm and resume normal conduction patterns. If AF is also present, the patient should only be treated through cardioversion, rather than more conservative approaches of medication. In fact, some medications

32 nursece4less.com nursece4less.com nursece4less.com nursece4less.com normally used for rhythm control, such as digoxin or , are contraindicated in cases where WPW syndrome is present with concurrent AF, as they could increase the risk of ventricular fibrillation.21 The condition requires immediate response through rapid cardioversion to prevent the arrhythmia from becoming life-threatening and causing sudden death.

The atrial arrhythmias listed here can impact the heart’s rate and rhythm in many ways, sometimes causing bradyarrhythmias where the heart beats too slowly; tachyarrhythmias, where the rate is too fast; or even a combination of the two, such as that seen with sick sinus syndrome. Supraventricular arrhythmias also originate in the atria and can affect the ventricles and the rates at which they contract.

Sinus Bradycardia

Sinus bradycardia describes a condition in which the heart beats at a slower- than-normal pace. With a normal heart rate for adults being 60 to 100 beats per minute, sinus bradycardia occurs when the heart rate is slower than 60 beats per minute. The rhythm is regular with this situation, although it is slow. Sinus bradycardia can be transient and can be caused by various circumstances, including use of some medications such as digoxin or beta- blockers. The condition is considered an atrial arrhythmia because it is an abnormality in the rate of the heart’s contractions and it typically originates in the SA node.

Due to circumstances that affect the heart’s ability to generate impulses at a normal rate, the SA node instead creates impulses at a slower rate than average, and the number of the heart’s contractions slows because of fewer impulses overall. Some patients with sinus bradycardia can be asymptomatic

33 nursece4less.com nursece4less.com nursece4less.com nursece4less.com and the condition goes unnoticed; alternatively, decreased blood flow can cause organ hypoperfusion that can lead to significant symptoms.

Some people normally live with heart rates that are technically considered to be sinus bradycardia because they are less than 60 beats per minute. For example, some athletes have normal resting heart rates that are much slower than average because extensive exercise builds up the heart muscle and causes larger stroke volumes. Consequently, when an athlete engages in routine activities, the heart rate does not necessarily increase as much when compared to an average adult because more oxygen is already being delivered to the tissues with each heartbeat. This explains why conditioned athletes tend to have slower heart rates overall that could be considered sinus bradycardia, but they are otherwise asymptomatic.

Bradyarrhythmia

A bradyarrhythmia describes a heart rate or pace in which the heart beats abnormally slow. Often, a person with consistent bradycardia can benefit from a pacemaker that can recognize the arrhythmia and stimulate the heart to contract if the heart rate is too slow. Recall that a pacemaker is a device that regulates the heart rate; when the heart beats too slowly, a pacemaker will stimulate the heart’s contractions by sending electrical signals to the heart. A pacemaker may be implanted under the skin as a permanent placement, or a temporary pacemaker may be put into place to stimulate the heart when the SA node is not generating enough impulses to stimulate contractions.12,13

Often, bradycardia can be caused from persistent damage to the cardiovascular system because of heart disease, such as coronary artery disease or a previous myocardial infarction. The condition is technically

34 nursece4less.com nursece4less.com nursece4less.com nursece4less.com observed when the heart rate falls below 60 beats per minute, although some people can tolerate a very low rate without any adverse effects.

A consistently low heart rate decreases the amount of blood flow through circulation, since the heart is not contracting as often each minute. Consequently, the individual with bradycardia may suffer from the effects of poor circulation and diminished blood flow, including decreased oxygen to the brain, causing dizziness, lightheadedness, and syncope.12,13

Premature Atrial Contractions

Another type of atrial arrhythmia, premature atrial contractions (PACs) are extra beats that occur within the atria. They originate at a location other than the SA node and cause random and erratic atrial contractions. With PACs, instead of the electrical impulse starting in the normal location of the SA node, it is typically generated just after another normal signal has been sent that results in a regular contraction. The atria then contract again quickly, even though a normal contraction has just occurred. This results in an extra atrial beat and the patient may complain of the feeling of a skipped heartbeat.

The affected individual may feel a flopping sensation in the chest with each irregular beat. The ventricles may or may not contract with atrial contractions. Premature atrial contractions are typically harmless and do not cause long-term complications, especially when they are random and infrequent. When they occur on occasion, they may be more likely to develop in cases where a person consumes certain substances such as caffeine or alcohol, which tend to stimulate the irregularity.14

35 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Although most PACs self-resolve and are episodic, there has been some evidence that unremitting PACs can contribute to adverse cardiovascular outcomes, including stroke and atrial fibrillation. Increased frequency of PACs can also be associated with advancing age, and older adults are more likely to suffer from these kinds of arrhythmias when compared to young adults. One study published in Circulation assessed the frequency of PACs in adults over age 50 years by having subjects wear continuous Holter monitors for a specified period. The study showed that with increasing age, the subjects were more likely to experience more PACs per hour (0.8 per hour among 50 to 55 year olds compared to 2.6 PACs per hour among those over age 70 years). Additionally, the study also found that several factors, including history of cardiovascular disease, physical activity, natriuretic peptide levels, and HDL cholesterol had significant associations with development of PACs. Overall, 99 percent of the subjects in the study had at least one PAC during the Holter monitoring period.14

Basically, clinicians should understand that PACs are mostly benign and will resolve on their own without long-term problems. Even with advancing age and increasing numbers of the arrhythmia, PACs do not usually cause long- term problems in otherwise healthy individuals. Among those with history of heart disease or other chronic health conditions, PACs could lead to more significant arrhythmias, including atrial flutter.

Treatment of the condition typically first involves eliminating substances from the diet that can contribute to the arrhythmia, including caffeine and alcohol. When an individual develops regular PACs to the point that it is disrupting his health and quality of life, he may need medication or other intervention to prevent the condition from progressing and worsening. Some

36 nursece4less.com nursece4less.com nursece4less.com nursece4less.com interventional medications prescribed may include digitalis, or beta blocker medications, such as propranolol.14

Premature Junctional Contractions

Similarly, premature junctional contractions (PJCs) are also types of ectopic beats that occur within the atria. PJCs may occur as extra beats in otherwise normal sinus rhythm. The impulse is not generated from the SA node but instead, it originates just before the AV node near the junction of the atria and the ventricles.18 Premature junctional contractions are so named because the contraction occurs before the anticipated, normal beat. The early contraction then disrupts the normal heartbeat.

The frequency of PJCs can vary between occasional and infrequent beats to recurrent contractions that cause discomfort. The causes of PJCs can also vary, as several etiologies have been identified. They are typically related to increased stress, heart disease, fatigue, and even diet; in some cases, though, there is no identifiable cause. On an ECG, premature junctional contractions may appear as an irregular rhythm and the P wave may not be apparent. With these types of contractions, the P wave may occur before or after the QRS complex, or sometimes within the QRS complex itself.18 The P wave may also appear larger or smaller in size when compared to normal.

Atrial Flutter

Another type of atrial arrhythmia is atrial flutter, a relatively common condition in which there is a very rapid atrial rate of contractions. Atrial flutter is not diagnosed as often as atrial fibrillation, but both conditions can lead to problems with poor circulation and an increased risk of thrombosis. With atrial flutter, the electrical signal is generated from a location other than the SA node and the impulse may originate closer to the AV node.

37 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Consequently, the atria depolarize at a much faster rate than normal. The actual rate of atrial contractions can be up to 300 to 350 beats per minute. Alternatively, the ventricles do not contract as quickly and there is usually a large discrepancy in rate between the two sections of the heart.15,17

With atrial flutter, the atria beat at a rate that is typically much faster than the ventricles, and the rate of the atria is too fast for the ventricles to keep up. Consequently, on the ECG, the patient may exhibit several extra P waves for every QRS complex, meaning that the atrial contractions are occurring but there are not necessarily as many corresponding ventricular contractions occurring at the same time. Atrial flutter is more commonly seen among older adults and in those with diagnosed heart disease.

Atrial flutter may or may not include episodes of atrial fibrillation; and the affected patient does not necessarily experience symptoms of the event. Atrial flutter has about half as much risk of causing thrombosis as atrial fibrillation, but the risk is still present and should be accounted for.15 The affected patient may need anticoagulant therapy to prevent blood clots and the possibility of stroke.

Medications that help to regulate the rate of atrial contractions, such as digitalis, beta blockers, or calcium channel blockers, may be implemented. Some of these drugs have been shown to be successful, but they are often not as effective in controlling atrial contractions as when they are used as treatment of atrial fibrillation.15 Further treatments by cardiac ablation or cardioversion is often necessary when the atrial flutter is recurrent and cannot be controlled through medication alone.

Sick Sinus Syndrome

38 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Sick sinus syndrome, also known as sinus node dysfunction, describes a condition in which there is an abnormality in the SA node that leads to cardiac arrhythmias. Because the SA is the normal pacemaker for the heart, SSS causes some form of arrhythmia because the heart is not pacing in a normal manner. Consequently, the atria are not able to contract at a rate and rhythm that meets physiological requirements of the body. The term actually covers several types of abnormalities, including brady- and tachyarrhythmias.23,24 The cause of the abnormality in the sinus node can vary; age-related fibrotic conditions can cause scarring and tissue degeneration within the atria, ultimately impacting the SA node; heart disease, including ischemia, can affect blood flow to the SA node and cause functional abnormalities; there are some genetic conditions that affect the SA node, and sometimes, tissue degeneration over time and with aging can cause irregularities to develop. Outside factors such as drug use, endocrine disorders, or toxicity can also cause SSS.23

Many cases of SSS are asymptomatic or produce few symptoms. Some people are unaware of the condition until it either progresses to the point that it causes more significant symptoms or it is diagnosed through testing to rule out another condition. Patients with SSS may exhibit symptoms associated with the type of arrhythmia it causes. When bradycardia develops, an affected person may experience the effects of decreased perfusion, including lightheadedness, dizziness, and activity intolerance. Near-fainting and syncope are thought to affect almost 50 percent of patients with SSS.24

Alternatively, SSS that causes some form of tachyarrhythmia may be manifested as the feeling of heart palpitations and syncope. Some people

39 nursece4less.com nursece4less.com nursece4less.com nursece4less.com also experience gastrointestinal issues, decrease urine output, and fatigue, typically as a result of decreased blood flow to particular organs.

On an ECG, sick sinus syndrome may be manifested in a number of ways. When it causes intermittent bradycardia, the patient may exhibit pauses in between the R wave of the QRS complex and the next P wave, sometimes referred to as sinus arrest. It is a temporary condition that has the appearance of an extremely long beat between one contraction and the next. Tachy-brady syndrome, characterized by irregular periods of tachycardia followed by sporadic bradycardia may also be seen on an ECG, as a patient will alternate between a very rapid heart rate followed by a very slow heart rate. Tachy-brady syndrome appears in approximately 50 percent of cases of SSS.24

Patients with SSS are at risk of developing consistent arrhythmias that can cause further complications of decreased end-organ perfusion and stroke. When atrial fibrillation develops due to SSS, the patient not only can experience decreased cardiac output overall, but he is also at much greater risk of thrombosis. A review published in American Family Physician explained that at least 50 percent of patients with SSS who develop tachy- brady syndrome manifest atrial fibrillation or atrial flutter as tachyarrhythmias and are at greater risk of developing some form of heart block that produces consistent bradycardia, with up to one-half of patients with SSS developing AV block.24

Since SSS causes a malfunction in the SA node, the main treatment is pacing through implantation of a cardiac pacemaker to regulate the rate and rhythm of atrial contractions. Pacing is done only in patients that have bradycardia and that are symptomatic. Correction of extrinsic causes, such

40 nursece4less.com nursece4less.com nursece4less.com nursece4less.com as by changing some prescription medications can also alleviate some of the dysfunction. Placement of a pacemaker can reduce symptoms and improve a patient’s activity tolerance; studies have shown, though, that a pacemaker as treatment for SSS does not impact overall survival rates.24

Atrioventricular Heart Block

Atrioventricular heart block, is another condition that may be classified as an atrial arrhythmia. Heart block occurs when there is some type of blockage in the conduction of the electrical signal as it passes from the SA to the AV nodes, usually because of some abnormality within the AV node. This typically results in bradycardia, which can be significant enough to cause symptoms for the patient.

Heart block is often classified into one of several different sub-categories, depending on the degree of the defect. With first-degree heart block, the electrical signal is still able to pass through to the ventricles, but this may occur at a pace that is slower than usual. An ECG typically shows a slower heart rate with a prolonged P-R interval (longer than 0.2 seconds), but the rest of the ECG appears normal. In general, treatment is not usually necessary and first-degree heart block may self-resolve.19,36

Second-degree heart block is divided into two further sub-categories: type 1 (Mobitz I/Wenckebach) and type 2 (Mobitz II). Although second-degree heart block is more serious than first-degree, type 1 is still usually considered to be a benign condition that is almost comparable to first-degree block. The two types of second-degree heart block are named after Woldemar Mobitz, a German physician who studied cardiac arrhythmias during the early part of the 20th century. Type 1 of second-degree heart block is referred to as Mobitz I; it may also be called Wenckebach, which is

41 nursece4less.com nursece4less.com nursece4less.com nursece4less.com named after Karel Wenckebach, a cardiologist from the Netherlands who actually discovered the phenomenon of second-degree heart block before Mobitz.

Type 1, while mostly asymptomatic, still involves the slowing of electrical impulses between the SA and AV nodes in the heart. The impulses travel at a slower pace than those that occur during first-degree heart block. The rhythm, as noted on the ECG, will appear to be a deterioration of first- degree AV block, with prolonged P-R intervals that may reach the point where a QRS complex does not follow a P wave because of the length of the interval, and there is a dropped beat.

A patient may develop type 1 second-degree AV block with undue cause, although it has been associated with acute myocardial infarction.19 Alternatively, an individual may have type 1 second-degree block for a period of time that eventually self-resolves. In comparison to type 2, Mobitz I usually does not require a pacemaker for the slow heart rate unless the patient becomes symptomatic. There is also the possibility that if left unchecked, a patient with this type of heart block may progress to type 2 or another serious cardiac arrhythmia.

Type 2 of second-degree heart block is sometimes referred to as Mobitz II. This particular type is more serious than type 1 and may require more intervention. With this type of heart block, the irregularity extends to the ventricles, and they may also beat at an irregular pace. There may be prolonged P-R intervals noted on the ECG. For each P wave, there is not always an associated QRS complex. The QRS complexes still appear normal, but they may be widened.

42 nursece4less.com nursece4less.com nursece4less.com nursece4less.com The atrial contractions sometimes fail to set off ventricular contractions, so they may simply be absent in the presence of P waves. The dropped beats may happen regularly or infrequently. The more often a dropped beat occurs in comparison with normal beats, a patient is more likely to experience symptoms. For example, if there is a skipped beat after every 3 contractions, the individual may be more likely to experience symptoms when compared to a dropped beat after every 10 to 12 contractions. Often, the affected patient requires a pacemaker to regulate cardiac impulses and to prevent the condition from worsening.

Type 2 second-degree AV block is notable in that it typically commences in the bundle of His, which originates near the AV node. Therefore, it may begin as an atrial arrhythmia, but it more commonly impacts the ventricles. The condition is more likely to develop as a result of some type of disease process that affects the heart, including autoimmune conditions such as myocarditis, myocardial infarction that has affected the bundle branches of the anterior wall, or infection, as well as an imbalance in potassium levels that can affect the electrical conduction system. This particular type of second-degree block often requires treatment to prevent it from progressing to third-degree AV block.

Third-degree heart block is also called complete heart block. In this situation, the impulses are completely blocked from reaching the ventricles. The ventricles respond by attempting to generate their own impulses by using the AV node or the bundle of His, and they contract at a different rate and rhythm than the atria. If the impulse is generated from within the ventricles, beyond the bundle of His, the ventricular rate is likely to be slower when compared to impulses generated within the AV node.19 The ventricles may or may not be able to keep pace with the atria; depending on

43 nursece4less.com nursece4less.com nursece4less.com nursece4less.com the location of where their impulses are generated, the ventricular rate can be extremely slow and the patient will exhibit significant symptoms.

The heart rate overall may be 60 beats per minute or less. On the ECG, there are often normal P waves and QRS complexes that are either normal or widened, but these items are independent of each other and have no relationship.19 Third-degree AV block may occur as a progression of another type of heart block that worsened in severity. Development of this type of block often indicates damage to the heart, including cardiac ischemia or a myocardial infarction; consequently, the situation typically requires rapid treatment to prevent the obstruction in the atria and to restore normal cardiac conduction. Intervention and treatment involve promptly implanting a pacemaker to regulate the rhythm and to prevent further ischemia and consequences of severe bradycardia that can occur with this particular rhythm.

Persons with complete heart block may exhibit several kinds of symptoms; most symptoms are related to decreased blood flow and poor tissue oxygenation when the heart is not functioning at full capacity. The most common symptoms of heart block, particularly in second- and third-degree block, include dizziness and lightheadedness, syncope, poor exercise tolerance, and shortness of breath. Untreated, heart block can progress from one stage to the next and the condition can worsen. For example, a patient with Mobitz I could eventually progress to Mobitz II over time and can develop more serious symptoms if there is no intervention.36 Untreated heart block can also lead to other cardiac complications and increased risk of poor outcomes, including hypoxia, severe hypotension, and cardiac arrest.

44 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Summary

Atrial arrhythmias are those that originate at some point within the atria of the heart. Atrial arrhythmias are serious conditions that can cause multiple complications if they are not well-managed. Atrial fibrillation can cause potentially life-threatening consequences, including thrombosis or stroke.

Understanding the differences between the types of atrial arrhythmias is important to determine the appropriate medical intervention. At times, an arrhythmia occurs that is noted but simply monitored without intervention. There are many arrhythmias that do not self-resolve and that require rapid treatment. Some of the more significant atrial arrhythmias require prompt intervention to prevent these conditions from deteriorating into potentially life-threatening events.

45 nursece4less.com nursece4less.com nursece4less.com nursece4less.com

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.

1. It is the ______that generates the electrical impulses in the heart.

a. nervous system b. Bachmann’s bundle c. heart d. hypothalamus

2. In a healthy person, the ______initiates the electrical activity to cause an electrical signal to move from the atria toward the lower chambers of the heart.

a. sinoatrial (SA) node b. bundle of His c. pinus d. atrioventricular (AV) node

3. When examining an ECG of a patient with atrial fibrillation, the sequences are typically manifested as a fast and often irregular rhythm, with

a. a dramatically irregular QRS complex. b. exaggerated P waves. c. well-defined PR intervals. d. no P waves.

4. When comparing the atrial cells to the ventricular cells, the cells in the atria

a. have a longer refractory period. b. have a continuous action. c. initiate another action potential faster than the ventricular cells. d. initiate action potential at the same rate as the ventricular cells.

46 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 5. A patient with atrial fibrillation (AF) is considered to have recurrent AF when the patient

a. requires treatment for the condition. b. suffers from two or more episodes of fibrillation. c. has episodes that are not self-limiting. d. has episodes that are persistent, not sporadic.

6. Atrial arrhythmias are those that originate

a. in the Purkinje fibers. b. at some point within the atria of the heart. c. at or after the atrioventricular (AV) node. d. anywhere within the heart.

7. True or False: Atrial arrhythmias can extend to and impact the ventricles as well.

a. True b. False

8. A patient with tachycardia is someone who has a heart rhythm that beats

a. too slowly. b. regularly but slowly. c. irregularly. d. too quickly.

9. Because of the abnormally fast heart rate that occurs with atrial fibrillation,

a. less blood is pumped into circulation. b. blood flow through the heart’s chambers is increased. c. increased cardiac output occurs. d. high blood pressure always results.

10. Which of the following conditions is known to contribute to arterial fibrillation?

a. Hypertension b. disease

47 nursece4less.com nursece4less.com nursece4less.com nursece4less.com c. Diabetes d. All of the above

11. Hypertension may directly affect the pacing abilities of the heart and contribute to arrhythmia because hypertension

a. causes the heart muscle to thin. b. promotes fibrosis. c. can increase the size of the atria. d. affects ion channels in the cells. 12. A patient with arterial fibrillation (AF) is considered to have recurrent atrial fibrillation when the patient experiences

a. two or more episodes of AF. b. AF for more than 7 days. c. symptoms related to AF. d. more AF episodes than normal heart rhythms.

13. Paroxysmal AF may be present when an individual has two or more episodes of atrial fibrillation, lasting more than 30 seconds each

a. for more than seven days. b. that do not self-resolve. c. that require intervention to control the symptoms. d. within seven days of each other.

14. With permanent AF, the patient may have to

a. begin cardioversion procedures. b. receive catheter ablation since the condition is not self-resolving. c. accept the permanence of the condition and treat with antiarrhythmic medications. d. stop taking antiarrhythmic medications and replace them with cardioversion.

15. Which of the following conditions is least likely to show up on an electrocardiogram?

a. Persistent AF b. Paroxysmal AF c. Permanent AF d. Atrial flutter

48 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 16. True or False: An episode of arterial fibrillation (AF) is confirmed when it is documented through ECG analysis and when it has a duration of at least 30 seconds.

a. True b. False

17. Sinus tachycardia is a type of supraventricular tachycardia (SVT) that

a. is characterized by an irregular rhythm. b. is usually considered a benign condition. c. originates in the ventricles or below the lower heart chambers. d. is not self-resolving.

18. Sinus tachycardia is resolved

a. when the irregular rhythm returns to normal. b. using medications such as epinephrine or pseudoephedrine. c. gradually and when the cause has been eliminated. d. when the heart rate drops below 200 beats per minute.

19. When an infant is having episodes of supraventricular tachycardia (SVT), the tachycardia can often be converted back to a normal rate using a vagal maneuver by

a. placing the infant on his or her stomach. b. administering a low dose of pseudoephedrine. c. holding the infant’s breath for 10 seconds. d. placing a cold cloth over the face for several seconds.

20. True or False: When a vagal maneuver is performed, the vagus nerve is stimulated, causing a release of acetylcholine that affects the SA node and slows the heart rate.

a. True b. False

21. ______, a type of SVT, occurs when the cardiac impulse travels from the SA node through the atrium but as it reaches the AV node, it does not progress to the bundle of His.

49 nursece4less.com nursece4less.com nursece4less.com nursece4less.com

a. Atrioventricular node re-entrant tachycardia (AVNRT) b. Sinus tachycardia c. Wolff-Parkinson-White syndrome d. Atrial tachycardia

22. A person who engages in routine exercises may have a slower heartbeat that appears to be sinus bradycardia because

a. hypoperfusion occurs as a result of exercise. b. exercise causes the heart to have smaller stroke volume. c. more oxygen is delivered to the tissues with each heartbeat. d. exercise creates more pathways for conduction.

23. A patient with bradycardia may suffer from

a. hyperperfusion. b. heart muscle quivers. c. oxygen toxicity. d. dizziness, lightheadedness, and syncope.

24. ______heart block, also called complete heart block, is a condition where the heart impulses are completely blocked from reaching the ventricles.

a. Type 1 (Mobitz I/Wenckebach) b. Third-degree c. Second-degree d. Type 2 (Mobitz II)

25. Wolff-Parkinson-White syndrome is a congenital anomaly in which an affected individual has

a. Type 1 (Mobitz I/Wenckebach) heart block. b. an accessory pathway in the heart. c. an irregular, slow heart rhythm. d. sinus node dysfunction.

50 nursece4less.com nursece4less.com nursece4less.com nursece4less.com

CORRECT ANSWERS:

1. It is the ______that generates the electrical impulses in the heart.

c. heart

“Although some of the rate of cardiac conduction is controlled by the nervous system, it is the heart itself that actually generates the electrical impulses.”

2. In a healthy person, the ______initiates the electrical activity to cause an electrical signal to move from the atria toward the lower chambers of the heart.

a. sinoatrial (SA) node

“The SA node initiates the electrical activity to cause an electrical signal to move from the atria through specified pathways, known as internodal pathways, toward the lower chambers of the heart.”

3. When examining an ECG of a patient with atrial fibrillation, the sequences are typically manifested as a fast and often irregular rhythm, with

d. no P waves.

“When examining an ECG of a patient with atrial fibrillation, the sequences are typically manifested as a fast and often irregular rhythm, with no P waves. The area of the P wave is typically flat and it is not well-defined. The PR interval is absent but the QRS complex often appears relatively normal or it may be slightly widened, because the ventricles are still contracting, although these contractions may be at a fairly reasonable but irregular rate.”

51 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 4. When comparing the atrial cells to the ventricular cells, the cells in the atria

c. initiate another action potential faster than the ventricular cells.

“Atrial cells have a shorter refractory period and ventricular cells have a longer refractory period, meaning that cells in the atria will be ready to initiate another action potential at a faster rate than those of the ventricles.” 5. A patient with atrial fibrillation (AF) is considered to have recurrent AF when the patient

b. suffers from two or more episodes of fibrillation.

“A patient with AF is considered to have recurrent atrial fibrillation when the patient suffers from two or more episodes of fibrillation. These episodes can be very sporadic and self-limiting, producing few symptoms and rarely requiring treatment.”

6. Atrial arrhythmias are those that originate

b. at some point within the atria of the heart.

“Atrial arrhythmias are those that originate at some point within the atria of the heart.”

7. True or False: Atrial arrhythmias can extend to and impact the ventricles as well.

a. True

“Atrial arrhythmias are those that originate at some point within the atria of the heart. These types of arrhythmias can extend to and impact the ventricles as well but they start in the upper chambers.”

8. A patient with tachycardia is someone who has a heart rhythm that beats

d. too quickly.

“For instance, tachycardia, which occurs when the heart beats at an abnormally fast rate, is considered a type of tachyarrhythmia.”

52 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 9. Because of the abnormally fast heart rate that occurs with atrial fibrillation,

a. less blood is pumped into circulation.

“Because of the abnormally fast heart rate that occurs with atrial fibrillation, ... less blood is pumped into circulation.... The assessed pulse rate is rapid and irregular, and blood pressure may be low.”

10. Which of the following conditions is known to contribute to arterial fibrillation?

a. Hypertension b. Heart valve disease c. Diabetes d. All of the above [correct answer]

“Some causes that have been noted as contributing to AF include hypertension, coronary artery disease, heart failure, valve disease, and diabetes.”

11. Hypertension may directly affect the pacing abilities of the heart and contribute to arrhythmia because hypertension

c. can increase the size of the atria.

“Over time, elevated blood pressure can increase the size of the atria, affecting pacing abilities and contributing to an arrhythmia.”

12. A patient with arterial fibrillation (AF) is considered to have recurrent atrial fibrillation when the patient experiences

a. two or more episodes of AF.

“A patient with AF is considered to have recurrent atrial fibrillation when the patient suffers from two or more episodes of fibrillation.”

13. Paroxysmal AF may be present when an individual has two or more episodes of atrial fibrillation, lasting more than 30 seconds each

d. within seven days of each other.

53 nursece4less.com nursece4less.com nursece4less.com nursece4less.com “Paroxysmal AF is considered when an individual has two or more episodes of atrial fibrillation, lasting more than 30 seconds each, within seven days of each other. Each of the episodes are fairly benign and they self-resolve. This particular type of AF is thought to account for up to 60 percent of diagnosed cases.”

14. With permanent AF, the patient may have to

c. accept the permanence of the condition and treat with antiarrhythmic medications.

“With permanent AF, there is a certain amount of acceptance of the situation and there are no longer attempts at procedures such as cardioversion or catheter ablation to correct the AF.”

15. Which of the following conditions is least likely to show up on an electrocardiogram?

b. Paroxysmal AF

“Paroxysmal AF may or may not be manifested during a routine ECG; the chance of identifying the rhythm during an ECG is typically contingent on whether the rhythm actually appears during the test.”

16. True or False: An episode of arterial fibrillation (AF) is confirmed when it is documented through ECG analysis and when it has a duration of at least 30 seconds.

a. True

“Technically, an episode of AF is confirmed when it is documented through ECG analysis and when it has a duration of at least 30 seconds; however, it can sometimes be difficult to capture an arrhythmia on an ECG when paroxysmal AF is present.”

17. Sinus tachycardia is a type of supraventricular tachycardia (SVT) that

b. is usually considered a benign condition.

54 nursece4less.com nursece4less.com nursece4less.com nursece4less.com

“[An SVT] condition describes a rapid heart rate over 100 beats per minute that originates above the ventricles.... Sinus tachycardia occurs when the heart beats at a rate faster than 100 beats per minute with normal activity, increasing to upwards of 200 beats per minute or more with activity. The rhythm of sinus tachycardia is regular. Overall, sinus tachycardia is usually considered as a benign condition and can be caused by a number of factors that are situational and can be corrected easily.”

18. Sinus tachycardia is resolved

c. gradually and when the cause has been eliminated.

“Common causes of sinus tachycardia include use of some medications, such as epinephrine or pseudoephedrine; dietary factors, including caffeine consumption; nicotine or alcohol intake, and anxiety or stress. Often, sinus tachycardia is resolved when the cause has been eliminated. Resolution is typically gradual, with the heart rate progressively slowing down until it has reached normal limits.”

19. When an infant is having episodes of supraventricular tachycardia (SVT), the tachycardia can often be converted back to a normal rate using a vagal maneuver by

d. placing a cold cloth over the face for several seconds.

“When an infant is having episodes of SVT, a small ice bag or cold cloth placed over the face for several seconds can often convert the tachycardia back into a normal rate.”

20. True or False: When a vagal maneuver is performed, the vagus nerve is stimulated, causing a release of acetylcholine that affects the SA node and slows the heart rate.

a. True

“When a vagal maneuver is performed, the vagus nerve is stimulated, causing a release of acetylcholine that affects the SA node and slows the heart rate.”

21. ______, a type of SVT, occurs when the cardiac impulse travels from the SA node through the atrium but

55 nursece4less.com nursece4less.com nursece4less.com nursece4less.com as it reaches the AV node, it does not progress to the bundle of His.

a. Atrioventricular node re-entrant tachycardia (AVNRT)

“Atrioventricular node re-entrant tachycardia (AVNRT) is the most common type of SVT. When this occurs, the cardiac impulse may travel from the SA node through the atrium but as it reaches the AV node, it does not progress to the bundle of His.”

22. A person who engages in routine exercises may have a slower heartbeat that appears to be sinus bradycardia because

c. more oxygen is delivered to the tissues with each heartbeat.

“… when an athlete engages in routine activities, the heart rate does not necessarily increase as much when compared to an average adult because more oxygen is already being delivered to the tissues with each heartbeat. This explains why conditioned athletes tend to have slower heart rates overall that could be considered sinus bradycardia, but they are otherwise asymptomatic.”

23. A patient with bradycardia may suffer from

d. dizziness, lightheadedness, and syncope.

“Consequently, the individual with bradycardia may suffer from the effects of poor circulation and diminished blood flow, including decreased oxygen to the brain, causing dizziness, lightheadedness, and syncope.”

24. ______heart block, also called complete heart block, is a condition where the heart impulses are completely blocked from reaching the ventricles.

b. Third-degree

“Third-degree heart block is also called complete heart block. In this situation, the impulses are completely blocked from reaching the ventricles.”

25. Wolff-Parkinson-White syndrome is a congenital anomaly in which an affected individual has

56 nursece4less.com nursece4less.com nursece4less.com nursece4less.com

b. an accessory pathway in the heart.

“Wolff-Parkinson-White syndrome is a congenital anomaly in which an affected individual has an accessory pathway in the heart.

Reference Section The reference section of in-text citations includes published works intended as helpful material for further reading. [References are for a multi-part series on CARDIOVERSION AND ABLATION].

1. Mitchell, L. (2017). Atrial fibrillation (AF). Retrieved from http://www.merckmanuals.com/professional/cardiovascular- disorders/arrhythmias-and-conduction-disorders/atrial-fibrillation-af 2. National Heart, Lung, and Blood Institute. (n.d.). How the heart works. Retrieved from https://www.nhlbi.nih.gov/health/health- topics/topics/hhw/electrical 3. Thompson, A. (2015). Atrial fibrillation. JAMA 313(10): 1070. Retrieved from https://jamanetwork.com/journals/jama/fullarticle/2190988 4. Emdin, C., et al. (2017). Usual blood pressure, atrial fibrillation and vascular risk: evidence from 4.3 million adults. International Journal of Epidemiology 46(1): 162-172. Retrieved from https://academic.oup.com/ije/article/46/1/162/2617172 5. Cantillon, D. (2014). Atrial fibrillation. Retrieved from http://www.clevelandclinicmeded.com/medicalpubs/diseasemanageme nt/cardiology/atrial-fibrillation/ 6. Howlett, P., et al. (2015). Diagnosing paroxysmal atrial fibrillation: are biomarkers the solution to this elusive arrhythmia? BioMed Research International, Article ID 910267. Retrieved from https://www.hindawi.com/journals/bmri/2015/910267/ 7. Nattel, S., Harada, M. (2014). Atrial remodeling and atrial fibrillation: recent advances and translational perspectives. Journal of the American College of Cardiology 63(22); 2335-2345. 8. Camm, J. (2015). NOACS in AF patients undergoing cardioversion. [PowerPoint]. St. George’s University of London. 9. Burns, E. (2017) Atrial flutter. LITFL ECG library. Retrieved from https://lifeinthefastlane.com/ecg-library/atrial-flutter/

57 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 10. Fogors, R. (n.d.). Cardiac anatomy and physiology – the cardiac action potential. The EP Lab.com. Retrieved from http://www.theeplab.com/B-The-Members-Center/C-Cardiac- AnatomyPhysiology/F-Action-Potential/CF00-Action-Potential.php 11. Ikonnikov, G. and Yelle, D. (2009). Cardiac conducting system. Clin Anat. 22(1): 99-113. Retrieved from http://www.pathophys.org/physiology-of-cardiac-conduction-and- contractility/ 12. National Heart, Lung, and Blood Institute. (n.d.). Arrhythmia. Retrieved from https://www.nhlbi.nih.gov/health-topics/arrhythmia 13. Atlantic Cardiology Group, LLP. (2018). Atrial arrhythmias. Retrieved from http://www.mccardio.com/handler.cfm?event=practice,template&cpid =3330 14. Conen, D., et al. (2012). Premature atrial contractions in the general population. Circulation 2012; 126: 2302-2308. Retrieved from http://circ.ahajournals.org/content/126/19/2302 15. Mitchell, B. (2017). Atrial flutter. Retrieved from http://www.merckmanuals.com/professional/cardiovascular- disorders/arrhythmias-and-conduction-disorders/atrial-flutter 16. Aksu, T., et al (2015). of typical atrial flutter via right jugular vein due to bilateral obstructed iliac veins in a patient with dilated cardiomyopathy. Case Reports in Cardiology, Article ID 401580, 3 pages. Retrieved from https://www.hindawi.com/journals/cric/2015/401580/ 17. Dewland, T., Glidden, D., Marcus, G. (2014). Healthcare utilization and clinical outcomes after catheter ablation of atrial flutter. PLOS One. Retrieved from http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0100 509 18. EKG.Academy.com. (2017). Junctional dysrhythmias – premature junctional complex (PJC) and junctional escape beats. Retrieved from https://ekg.academy/learn-ekg?courseid=314&seq=6 19. Nurses Learning Network. (2018). EKG interpretation. Retrieved from https://www.nurseslearning.com/courses/nrp/nrp1619/section%202/p 02.html 20. U.S. National Library of Medicine Genetics Home Reference. (2017). Wolff-Parkinson-White syndrome. Retrieved from https://ghr.nlm.nih.gov/condition/wolff-parkinson-white-syndrome 21. Mitchell, B. (2017). Atrial fibrillation and Wolff-Parkinson-White Syndrome (WPW). Retrieved from http://www.merckmanuals.com/professional/cardiovascular- disorders/arrhythmias-and-conduction-disorders/atrial-fibrillation-and- wolff-parkinson-white-syndrome-wpw

58 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 22. Mahida, S., et al. (2015). Science linking pulmonary veins and atrial fibrillation. Arrhythmia & Review 4(1): 40-43. 23. Tidy, C. (2014). Sick sinus syndrome. Retrieved from https://patient.info/doctor/sick-sinus-syndrome 24. Semelka, M., Gera, J., Usman, S. (2013). Sick sinus syndrome: a review. Am Fam Physician 87(10): 691-696. Retrieved from https://www.aafp.org/afp/2013/0515/p691.html 25. Lumen Learning. (n.d.). and electrical activity. Retrieved from https://courses.lumenlearning.com/ap2/chapter/cardiac-muscle-and- electrical-activity/ 26. Knight, B. (2017). Cardioversion (beyond the basics). Retrieved from https://www.uptodate.com/contents/cardioversion-beyond-the-basics 27. American College of Cardiology. (2018). Recommended doses of anticoagulant/antithrombotic therapies for patients with atrial fibrillation. Retrieved from http://www.acc.org/tools-and-practice- support/clinical-toolkits/atrial-fibrillation-afib/anticoagulant-dosing- table 28. Hansen, M., et al. (2015). Thromboembolic risk in 16274 atrial fibrillation patients undergoing direct current cardioversion with and without oral anticoagulant therapy. EP Europace 17(1): 18-23. Retrieved from https://academic.oup.com/europace/article/17/1/18/503751 29. Lippincott. (2016). Lippincott nursing procedures. (7th ed.). Philadelphia, PA: Lippincott Williams & Wilkins 30. Baumrind, D. (2013). The trouble with sinus tachycardia. Retrieved from http://www.ems12lead.com/2013/04/30/the-trouble-with-sinus- tachycardia/ 31. Custer, A., Lappin, S. (2017). Rhythm, tachycardia, multifocal atrial (MAT). Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK459152/ 32. Jung, P., et al. (2013). Contrast enhanced transesophageal in patients with atrial fibrillation referred to electrical cardioversion improves atrial thrombus detection and may reduce associated thromboembolic events. Cardiovascular Ultrasound 11(1). Retrieved from https://cardiovascularultrasound.biomedcentral.com/articles/10.1186/ 1476-7120-11-1 33. Yava, A., et al (2012). Effectiveness of local cold application on skin burns and pain after transthoracic cardioversion. Emergency Medicine Journal 29(7): 544-549. 34. Jin, Q., et al (2017). Prediction and prognosis of recurrence after catheter ablation with remote magnetic

59 nursece4less.com nursece4less.com nursece4less.com nursece4less.com navigation for electrical storm in patients with ischemic cardiomyopathy. Clinical Cardiology 40(11): 1083-1089. 35. Hellman, T., et al. (2017). Prediction of ineffective elective cardioversion of atrial fibrillation: a retrospective multi-center patient cohort study. BMC Cardiovascular Disorders 17(33). Retrieved from https://bmccardiovascdisord.biomedcentral.com/articles/10.1186/s128 72-017-0470-0 36. Mann, D., et al (Eds.). (2015). Braunwald’s heart disease: a textbook of cardiovascular medicine. (10th ed.). Philadelphia, PA: Elsevier Saunders 37. Babic, D., Benussi, S., Schwarz, U., Valli, P., Matter, C. (2016). Endocarditis, hemiparesis, and upper GI bleeding 4 weeks after radiofrequency ablation for atrial fibrillation. European Heart Journal – Cardiovascular Imaging 17(6): 703. 38. Hamaya, R., et al. (2017). Management of cardiac tamponade in catheter ablation of atrial fibrillation: single-centre 15 year experience on 5222 procedures. EP Europace. doi: 10.1093/europace/eux307. 39. Wynn, G., et al. (2016). Long-term outcomes after ablation of persistent atrial fibrillation: an observational study over 6 years. Open Heart. doi: 10.1136/openhrt-202015-000394 40. Canadian Heart Rhythm Society. (n.d.). (EPS) and catheter ablation. Retrieved from https://www.chrsonline.ca/index.php/heart-rhythm-health- resources/electrophysiology-study-eps-and-catheter-ablation 41. Peichl, P., et al (2014). Complications of catheter ablation and ventricular tachycardia: a single-center experience. Circulation: Arrhythmia and Electrophysiology, 7: 684-690. Retrieved from http://circep.ahajournals.org/content/7/4/684 42. Maruyama, M. (2014). Management of electrical storm: the mechanism matters. Journal of Arrhythmia 30(4): 242-249. 43. Medtronic. (2017). Micra transcatheter pacing system. Retrieved from http://www.medtronic.com/us-en/patients/treatments- therapies/pacemakers/our/micra.html 44. Ho, J., Prutkin, J. (2017). Simultaneous atrioventricular node ablation and leadless pacemaker implantation. Heart Rhythm Case Rep. 3(3): 186-188. 45. Lewis, S., et al (2015). Anaesthetic and sedative agents used for electrical cardioversion. Cochrane Database of Systematic Reviews. doi: 10.1002/14651858.CD010824.pub2 46. Srinivasa, V. and Kodali, B. (2017). Capnography during sedation. Capnography. Harvard Medical School. Boston, Mass. Retrieved from http://www.capnography.com/capnosedation/capnography-is-vital- during-sedation

60 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 47. Merit Medical. (2018). Safeguard® pressure assisted device. Retrieved from https://www.merit.com/cardiac- intervention/hemostasis/compression-devices/safeguard-pressure- assisted-device/ 48. Schreiber, D., et al. (2015). Five-year follow up after catheter ablation of persistent atrial fibrillation using the “stepwise approach” and prognostic factors for success. Circulation: Arrhythmia and Electrophysiology 8(2): 308-317. 49. Steinberg, J., et al. (2014). Very long-term outcome after initially successful catheter ablation of atrial fibrillation. Heart Rhythm 11(5): 771-776. 50. Mathew, D. (2018). . Heart Rhythm Consultants. Sarasota, Florida. Retrieved from https://www.heartrhythmdoc.com/arrhythmia-treatment- options/cryoablation/ 51. Desai, P., Kane, D., Sarkar, M. (2015). Cardioversion: what to choose? Etomidate or propofol. Ann Card Anaesth. 18(3): 306-311. 52. Washington Heart Rhythm Associates. (2015). AV Nodal Reentrant Tachycardia (AVNRT). Retrieved from http://www.washingtonhra.com/arrhythmias/av-nodal-reentrant- tachycardia-avnrt.php 53. Shukla, A. and Curtis, A. (2014). Avoiding permanent atrial fibrillation: treatment approaches to prevent disease progression. Vasc Health Risk Manag. 10: 1-12. 54. Ogunsua, A., et al (2015). Atrial fibrillation and hypertension: mechanistic, epidemiologic, and treatment parallels. Methodist Debakey Cardiovasc J. 11(4): 228-234. 55. Mody, B., et al. (2017). Ablation of long-standing persistent atrial fibrillation. Ann Transl Med. 5(15): 305. 56. Di Biase, L., Santangeli, P., Natale, A. (2013). How to ablate long- standing persistent atrial fibrillation? Current Opinion in Cardiology 28(1): 26-35. Retrieved from http://journals.lww.com/co- cardiology/fulltext/2013/01000/How_to_ablate_long_standing_persist ent_atrial.6.aspx 57. Senoo, G., et al (2015). Residual risk of stroke and death in anticoagulated patients according to the type of atrial fibrillation. Stroke 46(9). Retrieved from http://stroke.ahajournals.org/content/46/9/2523.full 58. Mayo Clinic. (2017). Supraventricular tachycardia. Retrieved from https://www.mayoclinic.org/diseases-conditions/supraventricular- tachycardia/symptoms-causes/syc-20355243 59. ACLS Certification Institute. (2018). Vagal maneuvers. Retrieved from https://acls.com/free-resources/knowledge-base/tachycardia/vagal- maneuvers

61 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 60. Yoo, B. (2018). Atrioventricular reentrant tachycardia (AVRT) & AV nodal reentrant tachycardia (AVNRT). Retrieved from https://www.khanacademy.org/science/health-and- medicine/circulatory-system-diseases/dysrhythmias-and- /v/avrt-avnrt 61. Washington Heart Rhythm Associates. (2015). Wolff-Parkinson White Syndrome (WPW) and atrioventricular reciprocating tachycardia (AVRT). Retrieved from http://www.washingtonhra.com/arrhythmias/wolff-parkinson-white- syndrome-wpw-and-atrioventricular-reciprocating-tachycardia- avrt.php 62. Bushoven, P., et al (2015). Optimal anticoagulation strategy for cardioversion in atrial fibrillation. Arrhythm Electrophysiol Rev. 4(1): 44-46. 63. American Heart Association. (n.d.). Anticoagulation. Retrieved from http://www.heart.org/idc/groups/heart- public/@wcm/@hcm/documents/downloadable/ucm_317635.pdf 64. Ozkan, G., et al. (2016). Sedoanalgesia for cardioversion: comparison of alfentianil, remifentanil and fentanyl combined with propofol and midazolam: a prospective, randomized, double-blind study. European Review for Medical and Pharmacological Sciences, 20: 1140-1148. 65. Rull, G. (2017). and cardioversion. Retrieved from https://patient.info/doctor/defibrillation-and-cardioversion 66. Pozner, C. (2018). Advanced cardiac life support (ACLS) in adults. Retrieved from https://www.uptodate.com/contents/advanced- cardiac-life-support-acls-in-adults 67. METsis Medikal. (2015). PLUS defibrillator. Retrieved from http://www.metsismedikal.com/en/defibrillator/ 68. Tse, H., Lip, G., Coats, A. (Eds.). (2011). Oxford desk reference cardiology. Oxford, UK: Oxford University Press 69. Stanford Health Care. (2017). How epicardial ablation works. Retrieved from https://stanfordhealthcare.org/medical-treatments/e/epicardial- ablation/procedures.html 70. Deng, Y., et al (2016). Anesthetic management in radiofrequency catheter ablation of ventricular tachycardia. Tex Heart Inst J. 43(6): 496-502. 71. Passman, R. (2017). 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?search=Pulmonary%20vein%20radiofrequency%20cathet er%20ablation%20therapy%20for%20atrial%20fibrillation.&source=se arch_result&selectedTitle=1~150&usage_type=default&display_rank= 1

62 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 72. Bunch, J. and Cutler, M. (2015). Is pulmonary vein isolation still the cornerstone in atrial fibrillation ablation? J Thoracic Dis. 7(2): 132- 141. 73. Gasparini, M., et al. (2013). Cardiac resynchronization therapy in patients with atrial fibrillation. JACC: Heart Failure. Retrieved from http://heartfailure.onlinejacc.org/content/1/6/500 74. MedMovie.com. (2018). 3D electrical mapping of the heart. Retrieved from http://medmovie.com/library_id/7556/topic/cvml_0307a/ 75. Nedios, S., et al (2016). Advanced mapping systems to guide atrial fibrillation ablation: electrical information that matters. J Atr Fibrillation 8(6): 1337. 76. Kern, M. (2013). Back to basics: femoral artery access and hemostasis. Digest 21(10). Retrieved from https://www.cathlabdigest.com/articles/Back-Basics-Femoral-Artery- Access-Hemostasis 77. Yasgur, B. (2016). Cryoablation vs. radiofrequency ablation in atrial fibrillation. Cardiology Advisor. Retrieved from http://www.thecardiologyadvisor.com/arrhythmia/atrial-fibrillation- ablation-techniques/article/503405/ 78. Angiodynamics. (n.d.). How does RFA work? Retrieved from http://www.angiodynamics.com/uploads/pdf/Understanding%20Radiof requency%20Ablation.pdf 79. Radiology Info.org. (2018). Cryotherapy. Retrieved from https://www.radiologyinfo.org/en/info.cfm?pg=cryo 80. Lee, R.L. (2018). Surgical ablation to prevent recurrent atrial fibrillation. UpToDate. Retrieved online at https://www.uptodate.com/contents/surgical-ablation-to-prevent- recurrent-atrial- fibrillation?search=surgical%20ablation%20a%20fib&source=search_r esult&selectedTitle=1~150&usage_type=default&display_rank=1. 81. Blecher, G. et al. (2012). Use of rate control medication before cardioversion of recent-onset atrial fibrillation or flutter in the emergency department is associated with reduced success rates. Canadian Journal of Emergency Medicine 14(3), 169-177.

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