Download atrial fibrillation

ATRIAL
FIBRILLATION
Dana Bartlett, BSN, MSN, MA,
CSPI
Dana Bartlett is a professional nurse and
author. His clinical experience includes 16
years of ICU and ER experience and over 20
years of as a poison control center information
specialist. Dana has published numerous CE
and journal articles, written NCLEX material
and textbook chapters, and done editing and
reviewing for publishers such as Elsevier, Lippincott, and Thieme. He has written widely on
the subject of toxicology and was recently named a contributing editor, toxicology section,
for Critical Care Nurse journal. He is currently employed at the Connecticut Poison Control
Center and is actively involved in lecturing and mentoring nurses, emergency medical
residents and pharmacy students.
ABSTRACT
The primary treatment of atrial fibrillation involves rate control, prevention
of thromboembolic events and restoring the heart to sinus rhythm. Control
of atrial fibrillation is achieved through pharmacological treatment and
cardioversion. Refractory atrial fibrillation may benefit from surgical
approaches to treatment. Diagnosis of atrial fibrillation requires investigation
into possible reversible causes as a first approach to therapy. New guidelines
influencing how atrial fibrillation is understood and treated, including newer
pharmacological agents, are discussed.
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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.
Pharmacology content is .5 hours (30 minutes).
Statement of Learning Need
Ongoing education is needed on the public health burden of atrial fibrillation.
Current medical, surgical and pharmacological guidelines for the treatment
of atrial fibrillation support clinicians caring for patients with an acute or
chronic atrial fibrillation condition.
Course Purpose
To provide clinicians with current knowledge of the symptoms, diagnosis and
treatment of patients with atrial fibrillation.
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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
Dana Bartlett, BSN, MSN, MA, CSPI, William S. Cook, PhD,
Douglas Lawrence, MA, Susan DePasquale, MSN, FPMHNP-BC –
all have no disclosures
Acknowledgement of Commercial Support
There is no commercial support for this course.
Please take time to complete a self-assessment of knowledge, on
page 4, sample questions before reading the article.
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Opportunity to complete a self-assessment of knowledge learned
will be provided at the end of the course.
1.
The incidence of atrial fibrillation:
a.
b.
c.
d.
2.
Which of the following are established risk factors for atrial
fibrillation?
a.
b.
c.
d.
3.
signs and symptoms
identification of risk factors
blood tests
a 12-lead ECG
Cardioversion is used if the patient with atrial fibrillation:
a.
b.
c.
d.
5.
African American ethnicity, chronic kidney disease
Hypertension, heart failure
Coronary artery disease, COPD
Cirrhosis of the liver, stroke
The diagnosis of atrial fibrillation can only be made by:
a.
b.
c.
d.
4.
increases with age
decrease with age
is not affected by age
increases with age but only for women
is > age 80
has a history of COPD
is hemodynamically unstable
is < age 40
Rhythm control in patients who have atrial fibrillation can be
attained by using:
a.
b.
c.
d.
beta blockers, diltiazem, or digoxin
electrical or pharmacological cardioversion
supportive care and life style changes
the Cox maze procedure
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Introduction
Atrial fibrillation is the most common arrhythmia. It is characterized by
ectopic atrial activity and an irregular, often rapid ventricular response.
Atrial fibrillation is typically seen in patients who have common
cardiovascular diseases such as hypertension and heart failure or who have
lifestyle risk factors such as alcohol and or obesity. It is a significant cause of
morbidity and mortality, the presence of atrial fibrillation increases the risk
of developing heart failure and thromboembolism, and it is a common cause
of stroke. Treatment of atrial fibrillation is rate and/or rhythm control,
anticoagulant medication to reduce the risk of thromboembolism and stroke,
and lifestyle modifications. These interventions can reduce morbidity and
mortality and improve quality of life but despite the therapeutic options in
use, atrial fibrillation is still widespread and it is a significant public health
problem. Current information on the public health burden of atrial fibrillation,
pathogenesis of the arrhythmia, risk factors that cause atrial fibrillation or
are thought to be associated with its development, the complications of
atrial fibrillation (especially stroke), the classification of atrial fibrillation and
how atrial fibrillation is diagnosed, (i.e., electrocardiographic changes, signs
and symptoms), and current medical, pharmacological, and surgical
treatments for atrial fibrillation are reviewed in this course.
Atrial Fibrillation: Statistics
Atrial fibrillation is the most common sustained arrhythmia.1,2 The true
prevalence of atrial fibrillation is not known as 10%-40% of patients who
have this arrhythmia are asymptomatic and not diagnosed,1 but prevalence
estimates of 2%-3.4% are typical3,4 and the life time risk of developing atrial
fibrillation has been estimated to be 1 in 4.4,5 The prevalence of atrial
fibrillation increases with age;5 more men than women have atrial
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fibrillation,6,7 it is more common in Caucasians than in African Americans,5
and it is a rare arrhythmia in children and teenagers.8,9 The prevalence of
atrial fibrillation has been slowly increasing1,2 (caused in part by the aging of
the population), and people who have atrial fibrillation are approximately
twice as likely to be hospitalized as those who do not.10
Clearly, atrial fibrillation is a significant public health problem. It is
associated with a greatly increased risk of the comorbidities of heart failure
and stroke. Given how common this arrhythmia is and the projected
increase in prevalence, atrial fibrillation is a serious health concern.
Pathogenesis Of Atrial Fibrillation
The pathogenesis of atrial fibrillation is complex and not completely
understood, but there is substantial evidence for two pathogenic
mechanisms by which this arrhythmia is initiated and sustained: a triggering
focus and atrial remodeling, respectively.5,11 Atrial fibrillation may also be
caused in part by changes in the autonomic nervous system, abnormal
myocardial metabolic processes, atrial dilation, fibrosis caused by cardiac
disease, re-entry mechanisms (rotors), or a pro-thrombotic state.2,11,12 It is
also possible that in any single patient there are multiple ways that atrial
fibrillation begins and is sustained and these pathologic processes probably
interact and influence each other.
Triggering Focus
The pulmonary veins have been confirmed as a common site of the
triggering focus - or foci - that initiates atrial fibrillation11,13 but other areas
of the myocardium have been identified that can initiate atrial fibrillation and
there may be multiple sites that act as triggering foci.11
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Atrial Remodeling
Electrophysiologic studies and
examination of the myocardium have
shown that there are electrical and
structural changes in the heart, aka
remodeling, that sustain atrial
fibrillation once a triggering focus has
begun to initiate the arrhythmia.11,14
These changes in the electrical and
structural part of the heart can include a decreased refractory period, altered
functioning of ion channels, autonomic dysfunction, development of re-entry
circuits, sinus node dysfunction, fibrosis of the myocardium, and other
damage that allows abnormal atrial impulses to be both conducted and
sustained.11,14-18 How these changes occur is not entirely clear, but it may be
that the triggering focus/foci induce them in a vulnerable heart.
The triggering focus or foci in atrial fibrillation depolarize the atria between
300-600 times per minute. This extremely rapid rate of atrial depolarization
has two important effects: 1) the rate of atrial fibrillation is much faster than
the rhythmic depolarization rate of the sinoatrial (SA) node so ventricular
depolarization and contraction is determined by the ectopic foci in the atria,
and 2) transmission of every impulse through the atrioventricular (AV) node
and the other parts of the cardiac conduction system is not possible because
of the refractory period of these structures, and the number of atrial
impulses that reaches the ventricles is variable and always changing.
The rapid atrial depolarization of atrial fibrillation that supersedes the SA
node as the cardiac pacemaker and the inability of the AV to transmit to the
ventricles the hundreds of atrial impulses that are firing each minute cause
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the characteristic electrocardiographic changes of atrial fibrillation. Atrial
fibrillation involves an absence of P waves and an irregularly, irregular
ventricular rate. These cardiac abnormalities also cause loss of atrial systole
and several other changes in cardiac performance that will be discussed later
in this study.
Risk Factors Of Atrial Fibrillation
There are many factors that can or may increase the risk of developing atrial
fibrillation. Some are proven risk factors while others are considered risks by
association. A complete discussion of the established, emerging, and
potential risk factors would be quite lengthy; readers are referred to
Andrade, et al. (2014) for detailed information.15 Established risk factors will
be covered here, and the emerging and potential risk factors will simply be
listed.
There are also several medical conditions that are direct causes of atrial
fibrillation. These are listed in Table 3 shown later in the course. It’s
important to understand that many patients who have atrial fibrillation have
specific cardiovascular diseases, chronic diseases, and/or life style issues
that are risk factors for atrial fibrillation or are thought to contribute to its
development. However, Huxley, et al. (2011) studied almost 15,000 adults
and found that 43% of the cases of atrial fibrillation were not explained by
common risk factors for the disease.19
Established Risk Factors
Age and Gender
The risk of developing atrial fibrillation increases with age, and the
prevalence of atrial fibrillation doubles with each decade starting at age 50.15
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Although age is undoubtedly a risk factor for
atrial fibrillation the reasons for this (aside
from age increasing the incidence of other
risk factors) are not completely
understood.20-23
Men have a higher risk of symptomatic and
asymptomatic fibrillation than do
women.15,21,24,25 Women who have atrial
fibrillation: 1) have a higher mortality rate
and are more likely to have a stroke than
men; 2) they are equally as likely as men to progress from paroxysmal atrial
fibrillation to sustained atrial fibrillation; 3) the clinical picture of
symptomatic atrial fibrillation is slightly different for women; and, 4) women
have been reported to have longer and more symptomatic episodes of atrial
fibrillation and more episodes of paroxysmal atrial fibrillation.24-27
Hypertension
A consistent association between hypertension and atrial fibrillation has been
clearly established.15,21,28 The relative risk for someone who has
hypertension of developing atrial fibrillation has been estimated to be 1.2%
to 1.5%.15 Most cases of atrial fibrillation occur in people who have
hypertension,29 and hypertension increases the risk of paroxysmal atrial
fibrillation progressing to permanent atrial fibrillation.30 The mechanisms by
which hypertension may cause or contribute to atrial fibrillation include atrial
stretching, fibrosis, myocardial inflammation, renal dysfunction, changes in
the renin-angiotensin system, and structural and electrical remodeling.31-33
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Valvular Heart Disease
Any valvular abnormality that causes regurgitation or stenosis can cause
atrial fibrillation.21 Left heart valvular lesions, especially lesions caused by
rheumatic heart disease and resulting in stenosis, are associated with the
highest prevalence of atrial fibrillation15 and the worse the lesion, the higher
the risk. In addition, atrial fibrillation associated with rheumatic heart
disease may increase the risk of mortality and stroke.34
Aortic stenosis increases the risk for
developing atrial fibrillation.35,36 Patients
who have mild to moderate aortic stenosis
can have a 9.1% prevalence of atrial
fibrillation. The prevalence increases to
almost 27% with a severe stenosis,36 and
aortic stenosis and atrial fibrillation together
increase mortality risks and the risk for
stroke.36
Heart Failure and Cardiac Myopathy
Atrial fibrillation and heart failure often coexist. Studies have shown that
one-third to almost two-thirds of patients with heart failure have atrial
fibrillation,37,38 and Chugh, et al. (2014) reported that patients who had
heart failure had a six-fold increase in risk for atrial fibrillation.39 The close
association between these two diseases is further underscored by cardiac
and myocardial pathologies that are common to both, and many researchers
have noted that heart failure may cause atrial fibrillation and, alternatively,
atrial fibrillation may cause heart failure.37,40
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The prognosis for people who have atrial fibrillation and heart failure is very
poor, with a significant increase in the risk of mortality.37,38,41 Depending on
the time of diagnosis of atrial fibrillation, the prevalence of atrial fibrillation
in patients who have hypertrophic cardiomyopathy has been reported to be
5%-28%.42,43
Alcohol Consumption
Heavy alcohol use is a well-known and welldocumented cause of atrial fibrillation;44,45
the risk of atrial fibrillation increases by up to
30% if more than two drinks a day are
consumed;46-48 and, the risk is progressive, the
A drink is defined as an
alcoholic beverage that
contains 14 grams/0.6
ounces of pure alcohol.
This amount of alcohol is
more alcohol that is consumed the greater the
in 12 ounces of beer, 5
risk.49 Acute alcohol intoxication or sporadic
ounces of wine, and 1.5
binge drinking can also cause atrial fibrillation,
ounces of hard liquor.
a phenomenon called holiday heart
syndrome.50
It is unclear how alcohol increases the risk for atrial fibrillation. Studies in
animals and humans have identified issues such as conduction
abnormalities, electrolyte abnormalities, and increased vagal tone as
possible pathologic mechanisms.49 Current (2016) research suggests that
the primary way by which alcohol causes atrial fibrillation is physical damage
to the left atrium.45
Obesity
The relationship between body weight and atrial fibrillation is complex and
still being worked out. Obesity is a risk factor for atrial fibrillation15,51,52 but
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being underweight has been identified as a risk factor, as well.53 There is
also research that has shown that in specific situations body weight can have
a negative or positive effect vis-a-vis atrial fibrillation. Examples of this
include: Phan, et al. (2016) found that obese patients had a higher risk of
developing atrial fibrillation in the post-operative period;53 and, Sandhu, et
al. (2016) found that obese patients who had atrial fibrillation and were
treated with anticoagulants had a better prognosis than normal weight
patients who received the same treatment.55
Table 1: Emerging Risk Factors15
Prehypertension
Increased pulse pressure
Obstructive sleep apnea
Physical activity: Cumulative lifetime practice >1500 h
Diastolic dysfunction
Familial and genetic
Hypertrophic cardiomyopathy
Congenital heart disease
Table 2: Potential Risk Factors15
Coronary artery disease
Chronic kidney disease
Inflammation
Pericardial fat
Tobacco use
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Table 3: Medical Conditions As A Cause Of Atrial Fibrillation
Hyperthyroidism
Myocardial infarction
Pheochromcytoma
Pulmonary embolism
Thyrotoxicosis
Classification Of Atrial Fibrillation
Atrial fibrillation is classified into five categories.56 These are described below
as: 1) Paroxysmal atrial fibrillation, 2) Persistent atrial fibrillation,
3) Long-standing persistent atrial fibrillation, 4) Permanent atrial fibrillation,
and; 5) Non-valvular atrial fibrillation.
Paroxysmal Atrial Fibrillation
Paroxysmal atrial fibrillation terminates spontaneously or with intervention
within seven days of onset. Paroxysmal atrial fibrillation may recur and it
frequently progresses to persistent and/or permanent atrial fibrillation.
Persistent Atrial Fibrillation
Persistent atrial fibrillation persists for longer than seven days.
Longstanding, Persistent Atrial Fibrillation
Longstanding, persistent atrial fibrillation persists for more than 12 months.
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Permanent Atrial Fibrillation
The term permanent atrial fibrillation is used when the patient and the
medical clinician have decided not to make further attempts to restore sinus
rhythm.
Non-valvular Atrial Fibrillation
Non-valvular atrial fibrillation occurs in the absence of rheumatic mitral
stenosis, a mechanical or bio-prosthetic heart valve, or mitral valve repair.
Valvular atrial fibrillation occurs in patients found to have the arrhythmia
and mitral stenosis or an artificial heart valve.
The term lone atrial fibrillation is still used in the literature to describe atrial
fibrillation that occurs in young adults who do not have cardiac disease,
diabetes mellitus, or hypertension. There is no standard, accepted definition
of lone atrial fibrillation and use of the term is discouraged by the current
(2014) guidelines from the American Heart Association (AHA) and the
American College of Cardiology (ACC) and other authorities.56,57
Diagnosis Of Atrial Fibrillation
Risk factors can help clinicians consider a diagnosis of atrial fibrillation in
certain patients, and there are signs and symptoms that can indicate its
presence. But atrial fibrillation can only be diagnosed by examining a 12lead electrocardiogram (ECG).
Electrocardiogram
The two identifying characteristics of atrial fibrillation as seen on a 12-lead
ECG are: 1) Absence of P waves; and, 2) An irregularly, irregular ventricular
rate. The QRS complex is usually narrow. Small fibrillatory waves called F
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waves may be seen but their absence or presence is not needed for a
diagnosis of atrial fibrillation. The ventricular rate can be quite variable and
it is usually rapid, between 110-140 beats per minute but it may be much
faster or abnormally slow. Because atrial fibrillation may not be present
when the patient is examined or when a 12-lead ECG is done, continuous,
telemetric ECG monitoring may be needed to detect the arrhythmia.
Patient Physical Examination and History
The clinical presentation of atrial fibrillation can be completely benign or the
patient may have mild and nonspecific symptoms such as dizziness, fatigue,
or palpitations. Patients may also have significant signs and symptoms such
as chest pain, dyspnea, heart failure, hypotension, or syncope. Some cases
of atrial fibrillation may be detected only after a life-threatening event like
cardiogenic shock or a stroke.
Less serious presentations may be seen only during times of stress. This
phenomenon is due to loss of atrial systole, decreased coronary blood flow,
impaired ventricular filling, and irregular ventricular response.
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Loss of Atrial Systole
In atrial fibrillation, the atria do not contract in response to an SA node
impulse. Instead, the very rapid atrial ectopic impulses cause the atria to
“quiver” and effectively eliminate atrial systole. Approximately 20% - 30% of
stroke volume comes from the volume of blood delivered by atrial systole,
and patients may tolerate this loss of stroke volume until the heart rate
increases or there is a demand for a higher than normal cardiac output.
When these situations occur so can the signs and symptoms of loss of
cardiac output such as dyspnea and dizziness.
Decreased Coronary Blood Flow
Atrial fibrillation is also associated with decreased coronary blood flow.57 If
the heart rate increases or there is a demand for a higher than normal
myocardial perfusion, the myocardium may be deprived of blood flow and
oxygen.
Impaired Ventricular Filling
Atrial fibrillation is associated with cardiomyopathy, hypertension, and mitral
stenosis and these can all impair ventricular filling. This effect combined with
loss of atrial systole can further decrease stroke volume.
Irregular Ventricular Response
The ventricular response to the atrial impulses is irregular and the filling
time and stroke volume vary, as well. When interviewing someone who may
have atrial fibrillation the clinician should ask about symptoms of chest pain,
dizziness, dyspnea, dyspnea on exertion, fatigue, palpitations, or syncope. If
any of these symptoms have occurred the clinician should also find out when
they occurred and what the patient was doing when they occurred. During
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the physical examination, attention should be paid to the patient’s breath
sounds, heart sounds, and peripheral circulation.
Detecting atrial fibrillation can be difficult as episodes of atrial fibrillation can
be brief. They may last for only a few seconds and the patient may be
asymptomatic, especially if the patient has paroxysmal atrial fibrillation.40
The detection and diagnosis of atrial fibrillation, however, is very important
to prevent stroke and as atrial fibrillation can easily go unrecognized this is a
significant challenge.
Atrial Fibrillation And Stroke
Stroke is the most common and most serious complication of atrial
fibrillation. A stroke caused by atrial fibrillation is almost always an ischemic
stroke caused by a thromboembolism. The embolism is typically part of a
mural thrombus that has formed in the atria, caused by inefficient and/or
absence of atrial systole.
Atrial fibrillation is also responsible for approximately 20% of all cryptogenic
(obscure or of unknown origin) strokes.58 A 2014 study by Kishore, et al.
found that 11% of all the patients they studied who suffered a stroke had
atrial fibrillation that had not been detected prior to the stroke.59
The risk for stroke is increased five-fold by atrial fibrillation. Atrial fibrillation
accounts for ≥15% of all strokes in the United States and for 36% of all
strokes in people >age 8058, and these numbers are probably
underestimates.60 The risk for stroke from atrial fibrillation increases from
1.5% in patients aged 50-59 to 23.5% in patients aged 80-89,61 and atrial
fibrillation is a significant cause of silent cerebral infarction and transient
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ischemic attack (TIA).62-64 Additionally,
there is a high rate of recurrence of stroke
caused by atrial fibrillation.60
Even brief episodes of atrial fibrillation are
considered to increase the risk for
stroke;65 and, patients who have a stroke
caused by atrial fibrillation are more likely
to have significant physical impairment
when compared to stroke from other causes.58,66,67
A stroke caused by atrial fibrillation is associated with increased
hospitalization costs, increased subsequent risk of hospitalization, and a
higher risk for hospital readmission,68,69 and ischemic stroke caused by atrial
fibrillation has been estimated to triple the mortality rate.66 Furthermore,
this risk appears to persist well beyond the immediate post-stroke period.66
Treatment Of New Onset Atrial Fibrillation
Treatment of new onset atrial fibrillation should focus on the issues
highlighted here.

Note the signs and symptoms of atrial fibrillation. Is the patient
asymptomatic, symptomatic but clinically stable, or having evidence of
cardiac, neurological, or pulmonary distress?

Is there an identifiable and potentially correctable cause of the atrial
fibrillation such as electrolyte imbalance, hyperthyroidism, intoxication,
myocardial ischemia, or pulmonary embolism?
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
Does the patient need emergency cardioversion and if so, how should
this be done?

Should rate control, rhythm control, or both be initiated?

Prevention of systemic embolization.
Signs and Symptoms
Many patients who have undiagnosed atrial fibrillation will have signs and
symptoms that are caused by decreased cardiac output and/or a rapid
ventricular rate, i.e., chest pain, dyspnea on exertion, fatigue, or
palpitations. These often occur intermittently, the patient may be
asymptomatic at the time of the examination, and not all patients who have
atrial fibrillation have symptoms.70
Serious cardiac, neurological, and/or pulmonary signs or symptoms caused
by new onset atrial fibrillation are unusual.
Identifiable and Correctable Causes
Identifiable and correctable causes of atrial fibrillation represent a small
percentage of all cases of new onset atrial fibrillation. The appropriate
referrals should be made and treatments done in these cases.
Emergency or Immediate Cardioversion
Emergency or immediate cardioversion to restore sinus rhythm in a patient
who has new onset atrial fibrillation and a rapid ventricular rate should be
performed, or at least considered, if the patient has any of the following.56,71

Active myocardial ischemia

Evidence of organ hypo-perfusion
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
Hypotension

Severe heart failure

First episode of atrial fibrillation with duration of < 48 hours

Wolf-Parkinson-White syndrome, atrial fibrillation, and hemodynamic
compromise
Cardioversion to restore sinus rhythm
can be done electrically or
pharmacologically and it can be done
as an outpatient procedure or when
the patient is hospitalized. Both
electrical cardioversion and
pharmacological cardioversion have
been proven to be effective; each has
its own risk-benefit ratio, but there
are no controlled trials that have
directly compared the two.72 If the
patient is young, has persistent
symptoms that interfere with health or quality of life, or attempts at rate
control have failed, rhythm control would be the best approach.71,73
Direct current cardioversion involves placing electrodes on the patient’s
chest and delivering a synchronized electrical shock at a specific time in the
cardiac cycle. The risks of direct current cardioversion include bradyarrhythmias, burns, complications of sedation used during the procedure,
thromboembolism, reprogramming/altering the functions of an implanted
cardiac device, sinus arrest, and ventricular fibrillation or tachycardia.71,73
Sinus arrest may happen if the patient has sinus node dysfunction, and
ventricular fibrillation or tachycardia are rare complications.73 Elective
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cardioversion should not be done if the patient has digoxin toxicity,
hypokalemia, or hypomagnesemia.71-74 The basics of the procedure are
highlighted below:

Serum electrolytes and oxygen saturation should be measured before
the procedure is done.

During the procedure, the patient should be sedated and blood
pressure, heart rate, CO2 capnography, oxygen saturation, and cardiac
rhythm should be continuously monitored.

Depending on the circumstances some patients may be pretreated
with an antiarrhythmic drug, i.e., amiodarone, propafenone, flecainide
ibutilide, or sotalol.

An electrical current of 100-200 joules is delivered.

It is reasonable to make several attempts at electrical cardioversion if
the initial attempt is unsuccessful.
Given the high risk for embolic stroke associated with atrial fibrillation and
also with cardioversion for atrial fibrillation,75 anticoagulant therapy is an
important consideration when performing direct current cardioversion. The
risk of a stroke is the highest in the first 72 hours after cardioversion and
most strokes will happen within 10 days of the procedure.71,73 The American
College of Cardiology/American Heart Association 2014 guidelines for the
management of patients who have atrial fibrillation have the following
recommendations for anticoagulation and cardioversion.71

Appropriate anticoagulation management around the time of a
cardioversion is essential for reducing thromboembolic risk.

In patients with atrial fibrillation clearly of <48 hours duration, it is
common practice to perform a cardioversion without transesophageal
echocardiogram (TEE) or antecedent anticoagulation.
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
For patients with atrial fibrillation requiring emergency cardioversion
because of hemodynamic instability, the initiation of anticoagulation
should not delay interventions to stabilize the patient. In these cases,
it is reasonable to administer heparin (an intravenous bolus of
unfractionated heparin [UFH] followed by infusion, or low molecular
weight heparin [LMWH]), or a newer anticoagulant and to continue
coagulation therapy after cardioversion, unless contraindicated.

For patients with atrial fibrillation of less than 48-hours duration and
with high risk of stroke, intravenous heparin, LMWH, or administration
of a factor Xa or direct thrombin inhibitor is recommended as soon as
possible before or immediately after cardioversion, followed by longterm anticoagulation therapy.

Decisions regarding whether to initiate long-term systemic
anticoagulation at the time of cardioversion in a patient with atrial
fibrillation of <48 hours duration should be based on the patient's
long-term risk of stroke using the CHA2DS2-VASc risk score.

For patients with atrial fibrillation of 48-hours duration or longer or of
unknown duration who have not been anticoagulated for the preceding
3 weeks, it is reasonable to perform a transesophageal
echocardiogram (TEE) prior to cardioversion and proceed with
cardioversion if no left atrial thrombus is identified, including in the left
atrial appendage, if anticoagulation is achieved before TEE and
maintained after cardioversion for at least 4 weeks.

For patients with atrial fibrillation of ≥48 hours or uncertain duration,
oral anticoagulation is recommended for ≥4 weeks after emergency
cardioversion (as with patients undergoing elective cardioversion). If
warfarin is used, bridging with UFH or LMWH is indicated until the INR
is therapeutic.
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Pharmacological cardioversion can also be tried on an immediate basis using
intravenous amiodarone, flecainide, or ibutilide,74 but this approach is less
effective than electrical cardioversion.74
Treatment Of Persistent Or Permanent Atrial Fibrillation
The treatment issues for patients with persistent or permanent atrial
fibrillation are control or management of comorbidities and risk factors, rate
and rhythm control, and prevention of embolization with anticoagulant
drugs. General treatment of persistent or permanent atrial fibrillation is
covered here; a discussion of control and management of comorbidities and
risk factors is beyond the scope of this study.
Rate Control or Rhythm Control
Rate control or rhythm control (or the two together) can be used to treat
atrial fibrillation. Comparisons between the two have shown that rhythm
control is only moderately effective for abolishing atrial fibrillation, it does
not have as strong an effect on mortality, and it is associated with a greater
number of adverse effects.76-79 Neither rate control or rhythm control
reverse the structural remodeling that helps to sustain atrial fibrillation.80,81
Pharmacologic Rhythm Control
Amiodarone, disopyramide, dofetilide, dronedarone, ibutilide, flecainide,
propafenone, and quinidine can be used for rhythm control and, hopefully,
cardioversion of atrial fibrillation.71,74 Drug choice is guided by the patient’s
clinical conditions and comorbidities and by safety concerns and
contraindications. The administration, doses, and the risks and benefits of
each drug used for rhythm control are not included here; however, the
online 2014 Guideline for the Management of Patients with Atrial Fibrillation
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provides this information at
(http://circ.ahajournals.org/content/early/2014/03/27/CIR.0000000000000041.full.pdf).
Rate Control
Rate control improves quality of life, decreases the potential for developing
tachycardia-induced cardiomyopathy, and reduces morbidity.71 There are
four clinical situations that indicate the need for rate control.76

As a well-controlled heart rate is important for patient health, rate
control should be the first treatment for patients who have new onset
atrial fibrillation.

Rate control is a sensible first-choice treatment for patients who do not
need sinus rhythm, i.e., patients >80 years of age and who have no
symptoms or only minor symptoms.

Rate control is the only option when rhythm control by cardioversion,
medications, or ablation has failed.

Rate control is the treatment of choice for patients for whom the risk
of restoring sinus rhythm is greater than the benefits, i.e., patients
who have sick sinus syndrome or paroxysmal atrial fibrillation with a
high ventricular response rate.
Pharmacological rate control can be done by using beta-blockers,
nondihydropyridine calcium channel blockers (diltiazem or verapamil),
digoxin, or amiodarone.71,76 Beta-blockers have been considered the first-line
drug of choice for rate control in atrial fibrillation, followed by a
nondihydropyridine calcium channel blockers (diltiazem or verapamil)
digoxin, and amiodarone. Evidence comparing the effectiveness of the rate
control drugs is lacking so the clinical situation and the patient’s
comorbidities will determine which drug should be used.71,76,82
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A complete discussion of the administration, doses, and the risks and
benefits of each drug used for rate control is beyond the scope of this study
module. Readers are referred to the 2014 Guideline for the Management of
Patients with Atrial Fibrillation for more information. This article is available
online at the following web link:
http://circ.ahajournals.org/content/early/2014/03/27/CIR.0000000000000041.full.pdf.
The American College of Cardiology/American Heart Association Task Force
has outlined some general principles of pharmacologic rate control.71

Heart rate control (resting heart rate <80 bpm) is reasonable for
symptomatic management of atrial fibrillation.

Control of the ventricular rate using a beta-blocker or
nondihydropyridine calcium channel antagonist is recommended for
patients with paroxysmal, persistent, or permanent atrial fibrillation.

Intravenous administration of a beta-blocker or nondihydropyridine
calcium channel blocker is recommended to slow the ventricular heart
rate in the acute setting in patients without pre-excitation.
Hemodynamically unstable patients should be electrically cardioverted.

If the patient has atrial fibrillation-related symptoms during activity,
rate control should be assessed during exertion and necessary
adjustments made.

Intravenous amiodarone can be useful for rate control in critically ill
patients who do not have pre-excitation. Oral amiodarone may be
useful for ventricular rate control when other measures are
unsuccessful or contraindicated.

AV nodal ablation with permanent ventricular pacing is reasonable to
control the heart rate when pharmacological therapy is inadequate and
rhythm control cannot be achieved.
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
A lenient rate-control strategy (resting heart rate <110 bpm) may be
reasonable if the patient remains asymptomatic and left ventricular
systolic function is preserved.

AV nodal ablation with permanent ventricular pacing should not be
performed to improve rate control without prior attempts to achieve
rate control with medications.

Nondihydropyridine calcium channel antagonists should not be used in
patients with decompensated heart failure; this may cause further
hemodynamic compromise.

In patients with pre-excitation and atrial fibrillation, digoxin,
nondihydropyridine calcium channel antagonists, or intravenous
amiodarone should not be administered as they may increase the
ventricular response and may result in ventricular fibrillation.

Dronedarone should not be used to control the ventricular rate in
patients who have permanent atrial fibrillation; it increases the risk of
the combined endpoints of stroke, MI, systemic embolism, or
cardiovascular death.
The goals of rate control are to: 1) prevent bradycardia; 2) reduce the risk
of tachycardia-induced cardiomyopathy and heart failure; and, 3) attain a
heart rate that produces a cardiac output that meets the physiological
demands of the patient. The last point has been somewhat controversial and
requires consideration of the patient’s needs; should a heart rate of <80
bpm (the so-called strict approach) or a heart rate of <110 bpm (the socalled lenient approach) be the goal?82,83 The only large randomized trial
that addressed this question found that lenient rate control was safe and
effective and should be considered if the patient has few symptoms.83 But
the ACC/AHA 2014 guidelines71 and recent (2016) expert commentary82,83
(which included the lead author of the aforementioned study) have both
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suggested that the optimal heart rate for atrial fibrillation is not known and
further study is needed. Using the strict approach or the lenient approach
must be decided on a case-by-case basis.
Catheter ablation or pacemaker implantation can be used for rate control
and will be discussed in the following section.
Catheter Ablation
The goal of catheter ablation is to destroy the focus or foci that initiate atrial
fibrillation. Catheter ablation is typically done using cyroablation or
radiofrequency ablation, and the ablation procedure can target the
pulmonary veins, the AV node, or other structures.79,84,85 Indications for
catheter ablation as a treatment for atrial fibrillation include, but are not
limited to: 1) patients who have symptomatic paroxysmal atrial fibrillation
that is refractory to at least one class I or III antiarrhythmic drug, or who
are intolerant of these drugs; and, 2) patients who have symptomatic
persistent atrial fibrillation that is refractory to at least one class I or class
III antiarrhythmic drug, or who are intolerant of these drugs.
Key points to know about catheter ablation for atrial fibrillation are:

The success for catheter ablation of paroxysmal atrial fibrillation is
higher than for persistent atrial fibrillation.85,86

Catheter ablation is considered superior to antiarrhythymic drugs for
treating atrial fibrillation and preventing recurrences.85,87

No single catheter ablation approach is effective for all patients. This
point is underscored by differing opinions about the effectiveness of
pulmonary vein ablation alone versus pulmonary vein ablation plus
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ablation of other sites; some authors have concluded pulmonary vein
ablation by itself is sufficient while others have not.84-87

The success rate for catheter ablation has been reported to be 75%93% for paroxysmal atrial fibrillation and 63%-74% for nonparoxysmal atrial fibrillation.85 Many patients will require a repeat
ablation, but early recurrences can be treated with medications or
cardioversion.74 It is not clear if catheter ablation reduces the risk of
stroke. There is some evidence that it reduces the risk of mortality.88

Cryoablation has some procedural advantages that radiofrequency
ablation does not. The outcomes of each approach for paroxysmal
atrial fibrillation and persistent atrial fibrillation are comparable.89-91

Anticoagulation should be started one month before the procedure and
continued for three months after.85 If the patient has persistent atrial
fibrillation, TEE should be done prior to ablation to rule out presence of
a left atrial or left atrial appendage clot.85

Complications/side effects include (but are not limited to) adverse
effects from sedation used during the procedure, arterio-venous fistula
or pseudo-aneurysm at the access site, cardiac tamponade, fluid
overload, hematoma at the access site, phrenic nerve palsy
(cryoablation), stroke, and transient ischemic attack.85,86,88
AV Node Ablation
AV node ablation and pacemaker insertion is used if: 1) rate and rhythm
control medications strategies have failed or medications cannot be
tolerated; 2) ablation did not work; 3) the patient has become
symptomatic, i.e., have heart failure; and, 4) the patient develops a longterm rapid ventricular rate, a risk for cardiomyopathy.71,76,79,92 AV node
ablation is also used for patients who have atrial fibrillation and require
biventricular pacing for management of systolic heart failure.92
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The success rate of AV node ablation
in abolishing atrial fibrillation has
been reported to be up to 95%,79,92
the complication rate is low, and it
can improve quality of life and longterm survival.79 However, the
procedure is not reversible so AV
node ablation with pacemaker
implantation “... should be restricted
until, and only if, absolutely
necessary.76
Cox Maze Procedure
The Cox maze is a surgical procedure that can be used to abolish atrial
fibrillation. The Cox maze procedure was first performed in the 1980s and it
has gone through several iterations since it was developed. The original
procedure involved cutting and sewing to create lesions (the maze) in the
atria that would block ectopic electrical impulses from reaching the
ventricles. The Cox maze procedure had a high rate of success at achieving
rate control but it is a very complex and technically demanding operation to
perform. The iteration that is currently used, the Cox maze IV, has replaced
the cut and sew technique with radiofrequency ablation and cryoablation,93,94
and the success rate (absence of atrial fibrillation) at 12-24 months postprocedure has been reported to be 90%.94
The Cox maze IV can also be combined with radiofrequency ablation that is
done six to eight weeks after the surgery.93 Indications for surgical ablation
(including Cox maze IV) are: 1) patients who have symptomatic atrial
fibrillation and who have not responded to medical therapy and/or have had
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one more unsuccessful catheter ablation, or patients who prefer surgery;
and, 2) patients who are having cardiac surgery and have symptomatic atrial
fibrillation, regardless of whether or not antiarrhythmic medications have
been started.95
Cardioversion
Patients who have persistent or permanent
atrial fibrillation can be cardioverted, but if
the cardioversion is elective they should be
A transesophageal
echocardiogram (TEE) is an
ultrasound done using a
treated with warfarin for at least three weeks
flexible tube with a
before and four weeks after the procedure to
ultrasound transducer at its
avoid left atrial thrombus.71 The 2014
guidelines notes that “ ... it is reasonable to
perform a TEE prior to cardioversion and
proceed with cardioversion if no LA (left
atrial) thrombus is identified, including in the
tip. A TEE is capable of
producing an ultrasound
image of the heart that is
typically clearer than the
image produced by transthoracic echocardiography.
LAA (left atrial appendage), provided that
anticoagulation is achieved before TEE and maintained after cardioversion
for at least 4 weeks.”71 If the cardioversion must be done immediately,
anticoagulation should be started as soon as possible and continued for at
least four weeks after the procedure.71 Continuing anticoagulation past four
weeks post-cardioversion may be needed, depending on the patient’s risk for
thromboembolism. (Risk assessment will be discussed later in the study).
Prevention Of Embolization
Prevention of embolization in patients who have atrial fibrillation is critically
important. The primary preventive technique is anticoagulation using oral
medications,96 and oral anticoagulation has been shown to be very effective
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at preventing thromboembolic events in patients who have atrial
fibrillation.96 There are three decisions that must be made before initiating
oral anticoagulation therapy: 1) assessment of stroke risk; 2) assessment of
bleeding risk; and, 3) choosing an anticoagulant.
Assessment of Stroke Risk
Assessment of stroke risk was traditionally done using the CHADS2
algorithm, but the currently accepted tool is the CHA2DS2-VASc
algorithm.71,96 In most cases of atrial fibrillation, a CHA2DS2-Vasc score of
≥2 indicates the need for anticoagulation.96
CHADS2
Congestive heart failure (1 point)
Hypertension (1 point)
Age ≥75 years (1 point)
Diabetes (1 point)
Prior stroke, TIA or thromboembolism (2 points)
CHA2DS2-VASc
Congestive heart failure (1 point)
Hypertension (1 point)
Age ≥75 (2 points)
Diabetes (1 point)
Stroke or transient ischemic attack (2 points)
Vascular disease (1 point)
Age 65-74 (1 point)
Sex category (1 point for female)
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Assessment of Bleeding Risk
Oral anticoagulants increase the risk of bleeding, so assessment of a
patient’s risk for bleeding must be done before starting anticoagulation
therapy. Assessment of bleeding risk is not as straightforward as assessment
of risk for stroke. Multiple assessments tools have been developed such as
ATRIA, HAS-BLED, HEMORRHAGES, ORBIT, and REITE, and each of these
has its advocates and critics.
Table 6: Assessment Tools For Assessing Bleeding Risk
Atria
(Anticoagulation and Risk factors in Atrial Fibrillation)
HAS-BLED
(Hypertension, Abnormal renal/liver function, Stroke, Bleeding history or
predisposition, Labile INR, Elderly, Drugs/alcohol concomitantly)
HEMORRHAGES
(Hepatic or renal disease, Ethanol abuse, Malignancy, Older age, Reduced
Platelet Count Reduced platelet count or function, Re-bleeding, Hypertension,
Anemia, Genetic Factors, Excessive Fall Risk and Stroke)
ORBIT
(Older than 74, Reduced hemoglobin, abnormal hemoglobin, or anemia, Bleeding
history, Insufficient kidney function, Treatment with any antiplatelet drug
RIETE
Computerized Registry of Patients with Venous Thromboembolism
The question of course, is which one is the best and should be used. The
ACC/AHA 2014 guidelines note that “... these scores may be helpful in
defining patients at elevated bleeding risk, their clinical utility is insufficient
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for use as evidence for the recommendations in this guideline.”71 Steinberg
(2016) writes that: 1) There have been no randomized clinical trials that
have shown that withholding anticoagulation because of a high risk for
bleeding is beneficial; and, 2) Large observational studies suggest that there
is a preventative benefit to oral anticoagulation, even if there is a high risk
for bleeding as per one of these assessment tools. Steinberg also points out
that these assessment tools “... help remind clinicians of bleed risk factors,
and particularly to highlight management of reversible risk factors for
bleeding.”96
Choosing an Anticoagulant
Anticoagulants have been proven to lower the risk for thromboembolic
stroke in patients who have atrial fibrillation. The anticoagulants that are
used for this purpose are warfarin, and the new oral anticoagulants
apixaban, dabigatran, edoxaban, and rivaroxaban. Warfarin inhibits vitamin
K-dependent synthesis of the clotting factors II, VII, IX, and X. Apixaban,
deoxidant, and rivaroxaban inhibit the clotting factor Xa; dabigatran is a
direct thrombin inhibitor.
Choosing between warfarin and a new anticoagulant - and if the latter is
chosen, which of the four to use - is challenging. The decision should be
made on a case-by-case basis but unless a newer anticoagulant is
contraindicated, these drugs are the preferred choice.96 However, if a patient
is well managed on warfarin there is no reason to stop using it.71
Points to consider when choosing an anticoagulant for a patient who has
atrial fibrillation are highlighted below.
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
The new anticoagulants are as effective as warfarin (and in some
cases, more so), and they have a smaller risk of intracranial bleeding
than warfarin.96,97 Patients who have valvular atrial fibrillation should
be treated with warfarin.71

The new anticoagulants have fewer drug-drug interactions than
warfarin and fewer dietary effects, as well, but a higher risk for
gastrointestinal bleeding than warfarin.71 The onset of effect is faster
and more predictable than it is for warfarin.71

There is no laboratory test that can be used to evaluate the
effectiveness of the new oral anticoagulants; there is no reversal agent
for bleeding caused by apixaban, edoxaban, or rivaroxaban, and these
drugs are more expensive than warfarin.71,96 In addition, these drugs
have short half-lives so missing even one dose can put the patient at
risk.96

There are no head-to-head clinical trials that compared any new
anticoagulant to another. Choosing which one to use must be done on
a case-by-case basis by considering the patient’s clinical
characteristics and the risks and benefits of each drug.

The new anticoagulants should not be used for patients who have
valvular atrial fibrillation or significant liver disease.96 These drugs are
excreted by the kidneys so they must be used cautiously in patients
who have renal impairment, or not all.96
General concerns that are common to all the new anticoagulants include:98

There are no laboratory tests that are used to monitor the
effectiveness of these drugs and routine measurements of
coagulation parameters are not recommended. If the patient is
having a stroke, or needs surgery on an urgent basis it might be
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useful to measure specific coagulation tests such as direct thrombin
inhibitor or anti-factor Xa levels.

Idarucizumab is an FDA approved reversal agent for bleeding
caused by dabigatran. There are no reversal agents for the other
new anticoagulants.

One month after drug therapy has been initiated the patient should
be assessed for adherence to the medication regimen and for
adverse effects. Periodic assessments should be made to check for
adverse effects and compliance.

Apixaban can be taken with or without food. Dabigatran and
rivaroxaban should be taken with food.

Non-steroidal anti-inflammatories should be avoided. Aspirin can be
used in some patients.
Antiplatelet Therapy
Antiplatelet therapy with aspirin or aspirin and clopidogrel has limited use as
a preventive therapy in patients with atrial fibrillation.71,96 Aspirin alone or
aspirin and clopidogrel have been shown to be inferior to warfarin for
preventing thromboembolic events and stroke and the risk for bleeding is
higher.71,96,99,100
Prevention of Atrial Fibrillation
Atrial fibrillation is considered in part a heritable disease101,102 and having a
family member who has atrial fibrillation has been associated with an
increased risk for developing atrial fibrillation and some of its
complications.71,102 Genetic variation mutations that increase the risk for
developing atrial fibrillation and that may influence individual response to
treatment have been identified.101,102,104 Widespread practical use of this
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information is not yet possible and genetic screening of the population is not
recommended at this time.71,105
The angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor
blockers (ARBs), aldosterone inhibitors (i.e., spironolactone), beta-blockers,
corticosteroids, and the statin drugs have all been investigated - and some
have been used - as therapies for the prevention of atrial fibrillation.106-108
These medications hopefully provide upstream protection against pathologic
mechanisms such as atrial remodeling, inflammation, and oxidative stress
that contribute to the development of atrial fibrillation. The evidence for the
effectiveness of this approach is mixed and conflicting and more research is
needed.
The ACC/AHA guidelines comments on upstream therapies are shown
below.71

An ACE inhibitor or an ARB is reasonable for primary prevention of
new-onset atrial fibrillation in patients with heart failure and reduced
left ventricular ejection fraction.

Therapy with an ACE inhibitor or an ARB may be considered for
primary prevention of new-onset atrial fibrillation in the setting of
hypertension.

Statin therapy may be reasonable for primary prevention of new-onset
atrial fibrillation after coronary artery surgery.

Therapy with an ACE inhibitor, ARB, or statin is not beneficial for
primary prevention of atrial fibrillation in patients without
cardiovascular disease.
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Summary
Atrial fibrillation is the most common arrhythmia. It affects millions of
people, the incidence increases with each decade after age 50, and it is a
major cause of morbidity and mortality, especially embolic stroke. The
pathogenesis of atrial fibrillation is thought to involve an initial triggering
focus and atrial remodeling that sustains the arrhythmia. The triggering
focus or foci in atrial fibrillation depolarize the atria between 300-600 times
a minute, and this extremely rapid rate of atrial depolarization has several
important effects.
Firstly, ventricular depolarization and contraction is determined by the
ectopic foci in the atria resulting in rapid and irregular ventricular
contraction. Secondly, transmission of these impulses through the AV node
and the other parts of the cardiac conduction system is not possible because
of the refractory period of these structures, and the number of atrial impulse
that reaches the ventricles is variable and always changing. Finally, loss of
atrial systole decreases stroke volume. The result of these three changes in
impulse formation and conduction is a rapid, irregular heart rate and
decreased cardiac output.
The five categories of atrial fibrillation were reviewed as paroxysmal atrial
fibrillation, persistent atrial fibrillation, longstanding, persistent atrial
fibrillation, permanent atrial fibrillation, and non-valvular atrial fibrillation.
Hypertension, alcohol consumption, obesity, valvular heart disease, heart
failure, increasing age and male gender significantly increase the risk for
developing atrial fibrillation. Many other risk factors have been associated
with atrial fibrillation such as coronary artery disease and smoking, and
atrial fibrillation is a heritable disease, as well.
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Most patients who have atrial fibrillation will have nonspecific signs and
symptoms such as dyspnea on exertion, fatigue, or palpitations and these
usually occur during exercise or times of stress. However, some patients will
be asymptomatic and a small number will present with hemodynamic
instability, myocardial ischemia, or a stroke. Often a stroke will be the first
sign of atrial fibrillation. A clinical examination and checking for precipitating
causes are important, but a 12-lead ECG is needed to make the diagnosis of
atrial fibrillation; characterized by the absence of P waves and an irregularly,
irregular R-to-R interval. The hart rate is usually rapid, up to 140 beats a
minute or faster, but it may be abnormally slow, as well.
The treatment of atrial fibrillation will depend on patient characteristics, the
type of atrial fibrillation, the duration of the arrhythmia, and the presenting
signs and symptoms. For every patient with atrial fibrillation, consideration
should be given to the need for immediate cardioversion, rate control,
rhythm control, and prevention of embolization. Cardioversion can be done
emergently or electively, and it can be done using direct current electrical
cardioversion, cardioversion using rhythm control drugs, or a combination of
the two. Rate control can be accomplished using beta-blockers, digoxin,
diltiazem or verapamil, or amiodarone. Rhythm control can be accomplished
by using amiodarone, disopyramide, dofetilide, dronedarone, flecainide,
ibutilide, propafenone, or quinidine.
Surgical procedures for treatment of atrial fibrillation include AV node
ablation, catheter ablation, and the Cox maze procedure. Pacemakers have a
limited role for the treatment of atrial fibrillation. Anticoagulation to prevent
embolization is accomplished by using warfarin, apixaban, edoxaban,
dabigatran, or rivaroxaban. Anticoagulation can significantly reduce the risk
of stroke, but the anticoagulants can cause bleeding. The newer
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anticoagulants, apixaban, dabigatran, edoxaban or rivaroxaban are at least
as effective at preventing stroke as warfarin, they are easier to use, and for
most patients they are the preferred anticoagulant. Upstream therapies such
as ACE inhibitors, ARBs, aldosterone inhibitors, and the statin drugs may be
effective for the prevention of new onset atrial fibrillation in certain patient
populations.
Health clinicians must continuously educate themselves on evolving
professional guidelines that address the diagnosis and treatment of atrial
fibrillation. Importantly, medical and nursing clinicians have a key role in
guiding patients to understand risk factors associated with atrial fibrillation
and corresponding complications, such as stroke. Prevention strategies have
been specifically highlighted here to guide clinicians to help patients learn
lifestyle choices that increase their risk for atrial fibrillation, such as use of
alcohol and drugs, and obesity.
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1.
The incidence of atrial fibrillation:
a.
b.
c.
d.
2.
Which of the following are considered pathogenic mechanisms
of atrial fibrillation?
a.
b.
c.
d.
3.
African American ethnicity, chronic kidney disease
Hypertension, heart failure
Coronary artery disease, COPD
Cirrhosis of the liver, stroke
The diagnosis of atrial fibrillation can only be made by:
a.
b.
c.
d.
5.
Infarcts in the atria and scarring of the SA node
Abnormal conduction pathways and ventricular hypertrophy
An initiating focus and atrial remodeling
Decreased myocardial oxygen delivery and abnormal AV
pathways
Which of the following are established risk factors for atrial
fibrillation?
a.
b.
c.
d.
4.
increases with age
decrease with age
is not affected by age
increases with age but only for women
signs and symptoms
identification of risk factors
blood tests
a 12-lead ECG
The heart rate of someone who has atrial fibrillation is typically:
a.
b.
c.
d.
very
very
very
very
rapid and irregularly irregular
slow and irregular
rapid and regular
rapid and regular
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6.
Cardioversion is used if the patient with atrial fibrillation:
a.
b.
c.
d.
7.
Rhythm control in patients who have atrial fibrillation can be
attained by using:
a.
b.
c.
d.
8.
beta blockers, diltiazem, or digoxin
electrical or pharmacological cardioversion
supportive care and life style changes
the Cox maze procedure
Rate control in patients who have atrial fibrillation is typically
attained by using:
a.
b.
c.
d.
9.
is > age 80
has a history of COPD
is hemodynamically compromised
is < age 40
AV node ablation
sotalol or amiodarone
a pacemaker
beta blockers or certain calcium channel blockers
The most common and most serious complication of atrial
fibrillation is:
a.
b.
c.
d.
hypertension
chronic kidney disease
stroke
myocardial infarction
10. Prevention of thromboembolism in atrial fibrillation is achieved
by:
a.
b.
c.
d.
aspirin and warfarin
warfarin, apixaban, dabigatran, edoxoban, or rivaroxaban
ACE inhibitors and statins
emergency or elective cardioversion
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11. The risk for stroke is increased _______ by atrial fibrillation.
a.
b.
c.
d.
two-fold
three-fold
five-fold
ten-fold
12. True or False. The new anticoagulants have fewer drug-drug
interactions than warfarin and fewer dietary effects, as well, as
well as lower risk for gastrointestinal bleeding than warfarin.
a. True.
b. False.
13. Aspirin alone or aspirin and clopidogrel have been shown to be
_______________ to warfarin for preventing thromboembolic
events and stroke and the risk for bleeding is higher.
a.
b.
c.
d.
inferior
superior
equal
None of the above.
14. The Cox maze IV can also be combined with ______________
that is done six to eight weeks after the surgery.
a.
b.
c.
d.
Cardioversion
Inderal
Radiofrequency ablation
Plavix
15. In patients with pre-excitation and atrial fibrillation should not
be administered as they may increase the ventricular response
and may result in ventricular fibrillation.
a. inderal, alpha blocking agents, or IV digoxin
b. digoxin, nondihydropyridine calcium channel antagonists, or
intravenous amiodarone
c. procainamide, clonidine, or dopamine
d. amiodarone, dopamine, or lidocaine
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16. True or False. Nondihydropyridine calcium channel antagonists
should not be used in patients with decompensated heart
failure; this may cause further hemodynamic compromise.
a. True.
b. False.
17. The risk of atrial fibrillation increases by up to ______% if more
than two drinks a day are consumed.
a.
b.
c.
d.
10%
20%
30%
40%
18. Warfarin inhibits vitamin K-dependent synthesis of the clotting
factors II, VII, IX, and X.
a.
b.
c.
d.
Vitamin
Vitamin
Vitamin
Vitamin
A
K
D
B
19. Rhythm control can be accomplished by all of the following
medication, EXCEPT:
a.
b.
c.
d.
Lasix.
Amiodarone.
Dofetilide.
Quinidine.
20. Surgical procedures for treatment of atrial fibrillation include
a.
b.
c.
d.
AV node ablation.
catheter ablation.
Cox maze procedure.
All of the above.
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21. Cardioversion to restore sinus rhythm can be done electrically or
pharmacologically and it can be done as an outpatient procedure
or when the patient is hospitalized.
a. True.
b. False.
22. In most cases of atrial fibrillation, a CHA2DS2-Vasc score of
______ indicates the need for anticoagulation.
a.
b.
c.
d.
<
≥2
≥5
≤5
23. Comparisons between rate control and rhythm control have
shown that _________________________ are/is only
moderately effective for abolishing atrial fibrillation, it does not
have as strong an effect on mortality, and it is associated with a
greater number of adverse effects.
a.
b.
c.
d.
Rhythm control
Rate control
Both rate and rhythm control
None of the above.
24. The risks of direct current cardioversion include all EXCEPT
a.
b.
c.
d.
burns.
thromboembolism.
hemorrhage.
sinus arrest.
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25. Indications for catheter ablation as a treatment for atrial
fibrillation include, but are not limited to:
a. patients who have symptomatic paroxysmal atrial fibrillation that is
refractory to at least one class I or III antiarrhythmic drug, or who are
intolerant of these drugs
b. patients who have symptomatic persistent atrial fibrillation that is
refractory to at least one class I or class III antiarrhythmic drug, or
who are intolerant of these drugs.
c. patients who have symptomatic persistent atrial fibrillation that is
refractory to at least one class I or class III antiarrhythmic drug, or
who have developed tolerance of these drugs.
d. Both a. and b. above.
CORRECT ANSWERS:
1.
The incidence of atrial fibrillation:
a. increases with age
p. 8: “The risk of developing atrial fibrillation increases with age, and
the prevalence of atrial fibrillation doubles with each decade starting at
age 50.”
2.
Which of the following are considered pathogenic mechanisms
of atrial fibrillation?
c. An initiating focus and atrial remodeling
p. 6: “The pathogenesis of atrial fibrillation is complex and not
completely understood, but there is substantial evidence for two
pathogenic mechanisms by which this arrhythmia is initiated and
sustained: a triggering focus and atrial remodeling, respectively.”
3.
Which of the following are established risk factors for atrial
fibrillation?
b. Hypertension, heart failure
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pp. 9-10: “Most cases of atrial fibrillation occur in people who have
hypertension, and hypertension increases the risk of paroxysmal
atrial fibrillation progressing to permanent atrial fibrillation… Atrial
fibrillation and heart failure often coexist. Studies have shown that
one-third to almost two-thirds of patients with heart failure have
atrial fibrillation.”
4.
The diagnosis of atrial fibrillation can only be made by:
d. a 12-lead ECG
p. 14: “Risk factors can help clinicians consider a diagnosis of atrial
fibrillation in certain patients, and there are signs and symptoms that
can indicate its presence. But atrial fibrillation can only be diagnosed
by examining a 12-lead electrocardiogram (ECG).”
5.
The heart rate of someone who has atrial fibrillation is typically:
a. very rapid and irregularly irregular
pp. 7-8: “The rapid atrial depolarization of atrial fibrillation that
supersedes the SA node as the cardiac pacemaker and the inability of
the AV to transmit to the ventricles the hundreds of atrial impulses
that are firing each minute cause the characteristic
electrocardiographic changes of atrial fibrillation. Atrial fibrillation
involves an absence of P waves and an irregularly, irregular ventricular
rate.”
6.
Cardioversion is used if the patient with atrial fibrillation:
c. is hemodynamically compromised
pp. 19-20: “Emergency or immediate cardioversion to restore sinus
rhythm in a patient who has new onset atrial fibrillation and a rapid
ventricular rate should be performed, or at least considered, if the
patient has any of the following.
• Active myocardial ischemia
• Evidence of organ hypo-perfusion
• Hypotension
• Severe heart failure
• First episode of atrial fibrillation with duration of < 48 hours
• Wolf-Parkinson-White syndrome, atrial fibrillation, and
hemodynamic compromise”
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7.
Rhythm control in patients who have atrial fibrillation can be
attained by using:
b. electrical or pharmacological cardioversion
p. 20: “Cardioversion to restore sinus rhythm can be done electrically
or pharmacologically …”
8.
Rate control in patients who have atrial fibrillation is typically
attained by using:
d. beta blockers or certain calcium channel blockers
p. 24: “Pharmacological rate control can be done by using betablockers, nondihydropyridine calcium channel blockers (diltiazem or
verapamil) ...”
9.
The most common and most serious complication of atrial
fibrillation is:
c. stroke
p. 17: “Stroke is the most common and most serious complication of
atrial fibrillation.”
10. Prevention of thromboembolism in atrial fibrillation is achieved
by:
b. warfarin, apixaban, dabigatran, edoxaban, and rivaroxaban
p. 33: “Anticoagulants have been proven to lower the risk for
thromboembolic stroke in patients who have atrial fibrillation. The
anticoagulants that are used for this purpose are warfarin, and the new
oral anticoagulants apixaban, dabigatran, edoxaban, and rivaroxaban.”
11. The risk for stroke is increased _______ by atrial fibrillation.
c. five-fold
p. 17: “The risk for stroke is increased five-fold by atrial fibrillation.”
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12. True or False. The new anticoagulants have fewer drug-drug
interactions than warfarin and fewer dietary effects, as well, as
well as lower risk for gastrointestinal bleeding than warfarin.
b. False.
p. 34: “The new anticoagulants have fewer drug-drug interactions than
warfarin and fewer dietary effects, as well, but a higher risk for
gastrointestinal bleeding than warfarin.”
13. Aspirin alone or aspirin and clopidogrel have been shown to be
_______________ to warfarin for preventing thromboembolic
events and stroke and the risk for bleeding is higher.
a. inferior
p. 35: “Aspirin alone or aspirin and clopidogrel have been shown to be
inferior to warfarin for preventing thromboembolic events and stroke
and the risk for bleeding is higher.”
14. The Cox maze IV can also be combined with ______________
that is done six to eight weeks after the surgery.
c. Radiofrequency ablation
p. 29: “The Cox maze IV can also be combined with radiofrequency
ablation that is done six to eight weeks after the surgery.”
15. Patients with pre-excitation and atrial fibrillation should not be
administered the following medication as they may increase the
ventricular response and may result in ventricular fibrillation.
b. digoxin, nondihydropyridine calcium channel antagonists, or
intravenous amiodarone
p. 26: “In patients with pre-excitation and atrial fibrillation, digoxin,
nondihydropyridine calcium channel antagonists, or intravenous
amiodarone should not be administered as they may increase the
ventricular response and may result in ventricular fibrillation.”
16. True or False. Nondihydropyridine calcium channel antagonists
should not be used in patients with decompensated heart
failure; this may cause further hemodynamic compromise.
a. True.
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p. 26: “Nondihydropyridine calcium channel antagonists should not be
used in patients with decompensated heart failure; this may cause
further hemodynamic compromise.”
17. The risk of atrial fibrillation increases by up to ______% if more
than two drinks a day are consumed.
c. 30%
p. 11: “the risk of atrial fibrillation increases by up to 30% if more than
two drinks a day are consumed…”
18. Warfarin inhibits vitamin K-dependent synthesis of the clotting
factors II, VII, IX, and X.
b. Vitamin K
p. 33: “Warfarin inhibits vitamin K-dependent synthesis of the clotting
factors II, VII, IX, and X.”
19. Rhythm control can be accomplished by all of the following
medication, EXCEPT:
a. Lasix.
p. 38: “Rhythm control can be accomplished by using amiodarone,
disopyramide, dofetilide, dronedarone, flecainide, ibutilide,
propafenone, or quinidine.”
20. Surgical procedures for treatment of atrial fibrillation include
a.
b.
c.
d.
AV node ablation.
catheter ablation.
Cox maze procedure.
All of the above.
p. 38: “Surgical procedures for treatment of atrial fibrillation include AV
node ablation, catheter ablation, and the Cox maze procedure.”
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21. Cardioversion to restore sinus rhythm can be done electrically
or pharmacologically and it can be done as an outpatient
procedure or when the patient is hospitalized.
a. True.
p. 20: “Cardioversion to restore sinus rhythm can be done electrically
or pharmacologically and it can be done as an outpatient procedure or
when the patient is hospitalized.”
22. In most cases of atrial fibrillation, a CHA2DS2-Vasc score of
______ indicates the need for anticoagulation.
b. ≥2
p. 31: “In most cases of atrial fibrillation, a CHA2DS2-Vasc score of ≥2
indicates the need for anticoagulation.”
23. Comparisons between rate control and rhythm control have
shown that _________________________ are/is only
moderately effective for abolishing atrial fibrillation, it does not
have as strong an effect on mortality, and it is associated with a
greater number of adverse effects.
a. Rhythm control
p.23: “Rate control or rhythm control (or the two together) can be
used to treat atrial fibrillation. Comparisons between the two have
shown that rhythm control is only moderately effective for abolishing
atrial fibrillation, it does not have as strong an effect on mortality, and
it is associated with a greater number of adverse effects.”
24. The risks of direct current cardioversion include all EXCEPT
c. hemorrhage.
p. 20: “The risks of direct current cardioversion include bradyarrhythmias, burns, complications of sedation used during the
procedure, thromboembolism, reprogramming/altering the functions of
an implanted cardiac device, sinus arrest, and ventricular fibrillation or
tachycardia.”
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25. Indications for catheter ablation as a treatment for atrial
fibrillation include, but are not limited to:
a. patients who have symptomatic paroxysmal atrial fibrillation that is
refractory to at least one class I or III antiarrhythmic drug, or who
are intolerant of these drugs
b. patients who have symptomatic persistent atrial fibrillation that is
refractory to at least one class I or class III antiarrhythmic drug, or
who are intolerant of these drugs.
c. patients who have symptomatic persistent atrial fibrillation that is
refractory to at least one class I or class III antiarrhythmic drug, or
who have developed tolerance of these drugs.
d. Both a. and b. above.
p. 27: “Indications for catheter ablation as a treatment for atrial
fibrillation include, but are not limited to: 1) patients who have
symptomatic paroxysmal atrial fibrillation that is refractory to at least
one class I or III antiarrhythmic drug, or who are intolerant of these
drugs; and, 2) patients who have symptomatic persistent atrial
fibrillation that is refractory to at least one class I or class III
antiarrhythmic drug, or who are intolerant of these drugs.”
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