ATRIAL FIBRILLATION
INTRODUCTION
Atrial fibrillation is a supraventricular arrhythmia. It is defined as rapid,
uncoordinated atrial activity with a rapid, irregular ventricular response.
Atrial fibrillation also features deterioration of atrial function.
Atrial fibrillation is the most common arrhythmia. It is a significant cause of morbidity
such as stroke, thromboembolisms, and heart failure. There are medical conditions that
are clearly the cause of some cases of atrial fibrillation, but often times the reason why
atrial fibrillation happens is not known. Risk factors have been identified that increase the
chances of developing atrial fibrillation. However, atrial fibrillation can also occur in
healthy individuals when these risk factors are absent.
Atrial fibrillation is treated by with medications that control the heart rate and rhythm
and reduce the risk of complications. It can also be treated surgically and with procedures
that restore the heart to a normal sinus rhythm.
OBJECTIVES
When the student has finished this module, he/she will be able to:
1. Identify the correct definition of atrial fibrillation.
2. Identify the two basic pathophysiological causes of atrial fibrillation.
3. Identify the four types of atrial fibrillation.
4. Identify three signs and symptoms of atrial fibrillation.
5. Identify the characteristics of the ECG in a patient with atrial fibrillation.
6. Identify the four basic causes of atrial fibrillation
7. Identify two drugs that are known to cause atrial fibrillation.
8. Identify three medical conditions that are causes/risk factors for atrial fibrillation.
9. Identify two types of surgical procedures that are risk factors for atrial fibrillation.
10. Identify three cardiac disease that are risk factors for atrial fibrillation.
11. Identify the most important cardiac risk factor for atrial fibrillation.
12. Identify three important complications of atrial fibrillation.
13. Identify the two drugs commonly used to prevent stroke in patients with atrial
fibrillation.
14. Identify three drugs that are used for rate control of atrial fibrillation.
15. Identify the drug most commonly used for rhythm control of atrial fibrillation.
16. Identify the two methods that are used for cardioversion in patients with atrial
fibrillation.
17. Identify the scoring system used to asses the risk of stroke in patients with atrial
fibrillation.
18. Identify the most common non-pharmacological treatment for correcting atrial
fibrillation.
19. Identify a surgical technique that can be used to correct atrial fibrillation.
20. Identify the indications for immediate, emergency cardioversion of atrial fibrillation.
THE NORMAL CARDIAC CYCLE
In a normal heart beat, the cardiac contraction is initiated by an electrical impulse from
the sinoatrial (SA) node. This electrical impulse exits the SA node and travels through the
atria (producing the P wave) and stimulates atrial contraction. At the same time, the
electrical impulse moves though intranodal tracts in the atria to the atrioventricular (AV)
junction. The impulse is paused briefly at the AV, and is then conducted through the AV
junction, through the bundle of His, through the left and right bundle branches and into
the Purkinje fibers in the ventricles. At that point the impulse stimulates depolarization
and contraction of the ventricles.
Approximately 70% of the ventricular volume that is ejected with each heart beat
(stroke volume) comes from passive drainage from the vena cavae and the pulmonary
veins, and approximately 20% to 30% is contributed from atrial contraction. The heart
beat is normally initiated at the SA, but almost every part of the myocardium is capable
of spontaneous depolarization that can initiate a contraction.
EPIDEMIOLOGY
As mentioned previously, atrial fibrillation is the most common arrhythmia. It affects
approximately 2.2 million Americans and approximately 5.5% of the population over the
age of 69.1 It accounts for approximately one-third of all hospitalizations related to
cardiac arrhythmias. The incidence of atrial fibrillation increases with age.
Approximately 13.7% of individuals over the age of 80 have atrial fibrillation, and most
people with atrial fibrillation are between the ages of 65 and 85.2,3 Atrial fibrillation is
slightly more common in men than in women. It is less common in African Americans
and Latinos.4
Precisely identifying those at risk for developing atrial fibrillation has always been
challenging. A system for assessing the 10-year risk was recently developed. The system
included information about age, body mass index , blood pressure, age of diagnosis of
heart failure and/or heart murmur, presence of heart failure, the PR interval, and the use
of antihypertensive medications.5 The authors felt that their assessment tool could be
clinically useful, but it is not known if it is being widely used.
The incidence of atrial fibrillation is expected to rise by 2 to 2.5 fold by 2050.6 This
increase will most likely be caused by better and more aggressive diagnostic techniques,
the aging of the population, and people living longer with diseases such as hypertension,
congestive heart failure and coronary artery disease that are considered to be significant
risk factors for developing atrial fibrillation.
PATHOPHYSIOLOGY
The exact cause of atrial fibrillation is not known.7 However, it is generally thought
that atrial fibrillation is basically caused by a triggering event in an abnormal atrial
myocardium.8,9 In the past, these processes were considered independent, but they are
probably both necessary for atrial fibrillation to begin and to continue.
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The triggering event may be an automatic focal point – or multiple focal points –
that discharges rapidly and irregularly, or it may be something that has been
termed the multiple wavelet hypothesis. The focal points are often located in the
pulmonary veins, but may be found in other areas, as well. The multiple wavelet
hypothesis considers atrial fibrillation to be the result of many reentry circuits (the
wavelets) in the atrium.
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The atrial myocardium in patients with atrial fibrillation is often dilated and
fibrotic and these patients have also have decreased atrial muscle mass. The
fibrosis may be due to inflammation or by disorders in the renin-angiotensin
system. The atrial dilation is likely caused by cardiovascular diseases such as
hypertension, valvular heart disease, congestive heart failure, or coronary
atherosclerosis. It can also be a direct result of the arrhythmia itself. All of these
changes may give rise to ectopic foci, and the fibrotic changes, dilation, and loss
of muscle mass lead to erratic conduction.10
Regardless of the mechanism of any particular case of atrial fibrillation, the result is
atrial impulses formed at the rate of between 350 and 600 beats per minute. These
impulses are obviously formed at a more rapid rate than the rate of impulse formation
from the SA node, so the heart responds to the ectopic foci rather than the SA node.
Because of the refractory period of the cardiac conduction system, only a certain number
of these beats are transmitted to the ventricles: the ventricular rate in atrial fibrillation is
often very fast, up to 160 to 180 beats per minute.
Learning Break: Reentry is common cause of arrhythmias. Reentry occurs when an
ectopic foci fires a premature impulse. This premature impulse is blocked due to an
abnormality in the myocardium, but it finds an alternative pathway. The impulse moves
through this pathway in a circular fashion, creating a loop – the reentry loop – of
depolarization that is stimulated over and over by the same impulse.
Learning Break: The exact number of atrial beats that is transmitted through the cardiac
conduction system varies and is very irregular. Consequently, the heart rate is irregularly
irregular.
CLASSIFICATION OF ATRIAL FIBRILLATION
Atrial fibrillation is divided into four primary categories that are based on the length of
the symptoms, the onset, and the cause.11 Atrial fibrillation can also be secondary to a
specific medical condition.

Lone atrial fibrillation: Lone atrial fibrillation occurs in people under the age of
60 who have no clinical or electrocardiographic evidence of cardiopulmonary
disease. People with lone atrial fibrillation are less likely to develop
complications, and their mortality rate is similar to people who never had atrial
fibrillation.12
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Paroxysmal atrial fibrillation: This form of the arrhythmia is defined as atrial
fibrillation that terminates in seven days or less and often within 24 hours. In
approximately 25% of all patients with paroxysmal atrial fibrillation, the
arrhythmia will become permanent within five years.
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Persistent atrial fibrillation: Persistent atrial fibrillation lasts more than seven days
and requires treatment.
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Permanent atrial fibrillation: If the arrhythmia persists beyond on year and is
refractory to treatment, it is designated as permanent atrial fibrillation.
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Secondary: Secondary atrial fibrillation is caused by reversible influences such as
a myocardial infarction, pericarditis, cardiothoracic surgery, hyperthyroidism,
drugs, or other exogenous influences. In these cases, once the underlying problem
has resolved, the arrhythmia disappears.
SIGNS AND SYMPTOMS OF ATRIAL FIBRILLATION
The typical signs and symptoms of atrial fibrillation are irregular palpitations, chest
pain, fatigue, shortness of breath, irregular heart rate, and dyspnea on exertion.13 The
heart rate is often quite rapid with rates up to 150-160 or higher. However, patients may
have periods during which they are asymptomatic.14 Occasionally, the first sign of atrial
fibrillation is a complication such as a stroke.
Learning Break: Although the heart rate in atrial fibrillation is usually > 100 beats per
minute, the ventricular response can at times be < 100 beats per minute.
Learning Break: The signs and symptoms of atrial fibrillation are due to the
asynchronous atrial activity, loss of atrial contribution to cardiac output (up to 20% to
30%), rapid, irregular ventricular response, and decreased coronary artery blood flow.
THE ELECTROCARDIOGRAM AND ATRIAL FIBRILLATION
The electrocardiogram (ECG) is atrial fibrillation is characterized by:15
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Absence of regular, distinct P waves.
Replacement of the P waves with rapid oscillatory waves that vary in amplitude,
shape, and timing.
A rapid and irregularly irregular ventricular response.
A narrow QRS complex.
CAUSES OF ATRIAL FIBRILLATION
There are many causes of atrial fibrillation. These can be conveniently divided into
four basic categories: cardiac, medical/surgical, pharmacological, and genetic.
Genetic
There are rare forms of atrial fibrillation that are due to genetic single mutations.16
There is also increasing evidence that the risk of developing atrial fibrillation increases as
much as 30% to 41% – even when risk factors have been accounted for – if one’s first or
second degree relatives have atrial fibrillation. This appears to be especially so for
patients with lone atrial fibrillation.17,18
Pharmacological
There are several drugs that can cause atrial fibrillation. Ethanol – drinking alcohol –
has long been known to be a cause of atrial fibrillation. Atrial fibrillation can occur as a
result of chronic ethanol abuse and can occur acutely after binge drinking – the latter
syndrome being called “holiday heart.”19 It is not clear why ethanol causes atrial
fibrillation. In acute cases, it may be that metabolic breakdown products of ethanol, e.g.,
acetylaldeyde, stimulate the release of catecholamines from the myocardium. When it is
chronically abused, ethanol may cause structural damage and metabolic derangements to
the heart. In people who drink heavily, the risk for developing atrial fibrillation is
approximately 1.6 times greater than among people who abstain or drink less.20,21
Stimulants such as cocaine, methamphetamine, and caffeine (in excess) may cause atrial
fibrillation. It does not appear that moderate consumption of caffeine increases the risks
of developing atrial fibrillation.22 Cigarette smoking may increase the risk of developing
trial fibrillation.23
Medical/Surgical
There are many medical conditions that can cause atrial fibrillation. Atrial fibrillation
occurs in approximately 15% of all patients with hyperthyroidism, and sub-clinical
hyperthyroidism is associated with a three-fold increase in the incidence of atrial
fibrillation.24 Diabetes has long been considered to be a risk factor for the development
of atrial fibrillation. There is evidence for and against this association, but a recent study
that controlled for other risk factors associated with atrial fibrillation indicated that for
some people, diabetes can definitely increase the risk of developing atrial fibrillation.25
Atrial fibrillation is commonly seen (up to 76% incidence) after subarachnoid
hemorrhage.26 Obstructive sleep apnea has also been strongly implicated as a risk
factor for atrial fibrillation.27 Obesity increases the risk of atrial fibrillation by
approximately 49%, and the level of risk increases as body mass index increases.28
Atrial fibrillation is common as a postoperative event after cardiac surgery, and to a
lesser extent, pulmonary surgery. Approximately 40% of all patients who have coronary
artery bypass graft surgery or valvular surgery develop atrial fibrillation after the
operation; if the two surgeries are combined this rate is approximately 60%.29 Advanced
age, obesity, the metabolic syndrome, and cardiopulmonary disease are thought to
increase the risk of post-operative atrial fibrillation.30. It has been associated with an
increase in morbidity and mortality and prolonged hospital stay.31 The arrhythmia is
usually transient, and preoperative treatment with amiodarone, beta-blockers,
corticosteroids, sotalol, magnesium, ACE inhibitors, and some calcium channel blockers
has been shown to reduce the incidence of post-operative atrial fibrillation.32,33 Postoperative atrial fibrillation is also a relatively common occurrence after pulmonary
surgery.34,35
Atrial fibrillation also commonly occurs during renal dialysis. However, it generally
resolves spontaneously within several hours after the dialysis session has ended.36
Cardiac
There are strong associations between cardiac disease and atrial fibrillation.
Hypertension, congestive heart failure, valvular heart disease, and coronary artery
disease are all important risk factors for the development of atrial fibrillation.37
Hypertension, especially, is considered to be the most reliable predictor of risk for
atrial fibrillation.38 There is ongoing research that is attempting to discover the exact
incidence and the relationship between these diseases an atrial fibrillation: one of the
biggest questions seems to be whether or not some of the conditions are the cause of
atrial fibrillation or an effect of the arrhythmia.39,40,41
COMPLICATIONS OF ATRIAL FIBRILLATION
Atrial fibrillation is associated with a 1.5 to 1.9 fold increase in risk of death when
compared to people with sinus rhythm.42,43 It is also strongly associated with a
substantial increase in the risk for stroke due to embolism. The fibrillation in the atria
leads to stasis, and atrial fibrillation itself causes a hypercoaguable state. Approximately
15% to 25% of all strokes in the United States are directly related to atrial fibrillation,
and the presence of atial fibrillation increases the risk of stroke 4 to 5 fold.44,45 Patients
with atrial fibrillation who have had a prior stroke or a transient ischemic attack, who
have hypertension, diabetes, or valvular disease, or are over the age of 75 are especially
at risk for a stroke.46 Most of the embolic strokes caused by atrial fibrillation are caused
by a thrombus in the atria, but this is not always the case.47 A stroke that is caused by
atrial fibrillation is usually serious: the one-year mortality rate has been estimated to be
50%.48
Atrial fibrillation is also considered to be a cause for congestive heart failure (or at
the least a strong contributor to its development and progression) and tachycardiainduced cardiomyopathy.49 Patients with atrial fibrillation have approximately three
times the risk of developing congestive heart failure when compared to the general
population.
EMERGENCY TREATMENT OF UNSTABLE ATRIAL FIBRILLATION
Patients with atrial fibrillation who are hemodynamically unstable, or who have chest
pain or dyspnea related to the arrhythmia are candidates for emergent cardioversion.
Cardioversion applies electrical current to the heart that is synchronized to the QRS
complexes, and it converts the heart to a sinus rhythm. It is performed while the patient is
sedated.
TREATMENT OF ATRIAL FIBRILLATION
Atrial fibrillation is treated in order to increase the quality of life, decrease the
frequency and intensity of symptoms, and decrease the risk of complications and death.
Unfortunately, there is no conclusive evidence that the therapies available reduce the
mortality rate associated with atrial fibrillation.50 However, treatment is appropriate for
patients who are hemodynamically unstable, patients who have a high risk for embolic
complications, and patients whose quality of life is severely impacted. The basic goals of
the treatment atrial fibrillation are to 1) Correct the arrhythmia, 2) control the rate and/or
rhythm, and 3) prevent the embolic complications.
Learning Break: It is also important to treat atrial fibrillation because there is strong
evidence that atrial fibrillation causes changes in the myocardium that sustain and worsen
the arrhythmia. “Atrial fibrillation begets atrial fibrillation,” is the common wisdom.
Prevention of Embolic Complications
Preventing the thromboembolic complications of atrial fibrillation – especially
stroke – is one of the most important goals in treating this arrhythmia.51
Patients with atrial fibrillation have a higher risk of suffering a stroke than the general
population, but this risk varies significantly. The medications that can be used to prevent
a stroke can have serious side effects, so it is important that the right patients are treated
prophylactically with the right drugs. Physicians often use an assessment system called
CHADS2. CHADS stands for cardiac failure, history of hypertension, age of 75 years or
older, diabetes mellitus, and history of stroke or transient ischemic attack (TIA). In the
CHADS2 scoring system, cardiac failure, hypertension, age, age of 75 year or older, and
diabetes are each assigned one point; a stroke or a TIA are assigned two points. The
relative risk and the treatment decisions are based on the total number of points. Fr
example, a CHADS2 score of 3 reflects a 5.9% risk of stroke; a CHADS2 score of 5
reflects a risk for stroke of 12.5%.52
Treating patients with oral anticoagulants – most often with warfarin – has been the
primary method for preventing the embolic complications of atrial fibrillation.53
Unfortunately, warfarin therapy has significant drawbacks. There is a narrow therapeutic
index, very unpredictable dose-response relationship, the need for constant monitoring,
drug and diet interactions, and risk for bleeding and hemorrhagic stroke.54 Because of
these issues, many patients with atrial fibrillation who need anti-thrombotic therapy do
not receive it or are treated sub-optimally, and this has a significant affect on these
patient’s health.55
The common therapies used to prevent stroke in patients with atrial fibrillation are:

Antiplatelet therapy with aspirin: Aspirin prevents platelet activation, which is
one of the important steps in thrombus formation. In several large studies, it has
been shown that aspirin reduces the risk of stroke in patients with atrial
fibrillation by 21% to 22%.56,57
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Warfarin therapy: Warfarin is effective at preventing stroke in patients who have
atrial fibrillation. It has been estimated that anti-coagulation with warfarin reduces
the risk of stroke by approximately three fold, from 4.5% in a control group to
1.4% in a group treated with warfarin.58 Warfarin appeared to more effective than
aspirin.59
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Warfarin and aspirin combination therapy: There is no evidence that using a
combination of warfarin and aspirin is more effective than using warfarin alone,
and using both definitely increases the risk of bleeding.60

Combination antiplatelet therapy: There have been several studies that have
examined the use of combining antiplatelet drugs for preventing the embolic
complications of atrial fibrillation. These studies used aspirin and clopidogrel
(Plavix®), a drug that prevents platelet aggregation. This combination was more
effective than aspirin alone, but not as effective as warfarin, and compared to
aspirin alone, there was greater risk of bleeding.61,62
Learning Break: The goal for a patient receiving warfarin is to maintain an international
normalized ratio (INR) of between 2.0 to 3.0. This decreases the risk of stroke. If the INR
is below 2.0, the risk of stroke increases dramatically.
These are the only currently FDA-approved drugs for the use of stroke prevention in
patients with atrial fibrillation. Patients with atrial fibrillation who have a moderate to
high risk of stroke, e.g., several risk factors such as a history of embolic events, etc.,
might need both warfarin and aspirin, but this approach should be used very cautiously. If
the risk of stroke is less, warfarin or aspirin can be used.63
Short-Term Management of Atrial Fibrillation
For the patient who is hemodynamically unstable and symptomatic, immediate direct
current caridoversion should be performed.64 If the patient is hemodynamically stable but
symptomatic, oral or intravenous medications that block transmission through the AV
node can be used; the goal of therapy is rate control. These would include calcium
channel blockers, β-blockers, and possibly digoxin.65
Patients who are symptomatic and do not respond to rate controlling drugs should be
cardioverted to establish a sinus rhythm. This can be accomplished using direct
electrical current cardioversion or drugs. Ideally, the patient who is a candidate for
electrical cardioversion will have been in atrial fibrialltion for 48 hours or less; if so, the
patient does not need anticoagulation. If the arrhythmia has peristed longer than 48, the
patient should be anticoagulated with warfarin for four weeks before the procedure. The
presence of a thrombus in the atria can also be ruled out using transesophageal
electorcardiography. There is a risk of stroke after cardioversion – a mural thrombus can
be dislodged from the atria – but this can be greatly reduced by anticoagulation before
and after cardioversion. Electrical current cardioversion will correct the arrhythmia in
approximately 90% of all cases. However, atrial fibrillation commonly recurs.66
Class I or Class II antiarrhythmic drugs can be used for cardioversion, as well. If this
therapy is started within 24 hours, the rate of conversion has been reported to be 47% to
84%. If the therapy is initiated after atrial fibrillation has been present for longer than 48
hours, the conversion rate has been reported to be 15% to 30%.67 Pharmacologic
conversion is considered less effective than electrical cardioversion.68
Long-Term Management of Atrial Fibrillation: Rate Control and Rhythm Control
with Medications
There has long been a question as to whether or rate control or rhythm control was a
better strategy for treating atrial fibrillation. An analysis of several large clinical trials did
not show that either approach was preferable or more effective; the outcomes were
essentially the same.69
However, because atrial fibrillation frequently recurs, rate control should be attempted
first. It is safe and very often effective. Β-blockers, calcium channel blockers and digoxin
can be used.
If rate control is unsuccessful, rhythm control should be tried. Either medications or
non-pharmacological treatments can be used. Amiodarone, sotalol, flecainide,
propafenone, and dofetilide can all be used. The choice of drug will depend on the
presence of other cardiac diseases such as hypertension, coronary artery disease and
valvular heart disease; for example, flecainide should be avoided if the patient has
structural heart disease.70 Amiodarone is probably the most effective and most
popular drug used for maintaining rhythm, but it is also associated with many serious
side effects.71 The long-term success rate of pharmacological cardioversion has not been
not high. In several large studies, the recurrence rate was 67% to 94% within a year 72,73
Dronedarone is a relatively recently introduced drug that has shown an effectiveness
equivalent to amiodarone in maintaining a normal rhythm, and it appears to have fewer
and less serious side effects.74
Long-Term Management of Atrial Fibrillation: Rate Control and Rhythm Control
with Non-Pharmacologic Measures
The long-term effectiveness of medications in restoring and maintaining a normal rate
and/or rhythm is poor, and the drugs available have serious side effects. In addition, there
is evidence that suggests that there is electrical and structural remodeling of the
myocardium that occurs during atrial fibrillation, and this would limit the effectiveness of
medications for correcting the arrhythmia.75 Non-pharmacological approaches to rate and
rhythm control have gained popularity. They appear to be more effective and safer than
treatment with drugs.75,76
The most popular of these procedures is catheter-based radiofrequency ablation.
This procedure is used if the patient with atrial fibrillation continues to have symptoms
and antiarrhythmic drugs were tried and discontinued because of ineffectiveness or
intolerable side effects.
Pulmonary vein ablation is the most commonly performed technique of radiofrequency
ablation. The patient is heparinized and a catheter is placed in the pulmonary vein, the
ectopic foci are identified and radiofrequency energy, cold thermal energy, microwave
energy, laser, or ultrasound are used to eliminate them. Pulmonary vein ablation is most
effective for treating paroxysmal atrial fibrillation in patients with a normal atrial
myocardium. The success rate for this procedure is usually reported to be from 60% to
70%77, but it can vary from 31% to 88%.78 Major complications of this procedure include
pulmonary vein stenosis, thrombomembolic events, and left atrial-esophageal fistula.
Many patients with atrial fibrillation do not have a normal atrial myocardium, and
pulmonary vein foci are not the cause of the arrhythmia. In these situations, there are
ablation techniques that can be used. Another approach is surgical ablation. Surgery for
atrial fibrillation is designed to a) reduce the amount of atrial tissue that is capable of
forming reentry circuits by resection, and b) creating large, full-thickness lesions that will
prevent conduction of ectopic impulses.79 There are three surgical techniques that are
commonly used.

Cox-Maze III: This procedure has been reported to be highly effective, and has
been use to treat persistent and permanent atrial fibrillation. The success in
maintaining sinus rhythm has been reported to be between 85% and 95%80,81 and
it has also been shown to be very effective in reducing the incidence of stroke.
Full thickness lesions are created in the left atrium and pulmonary veins by
cutting and sewing, and the left atrial appendage is removed. These lesions, as
mentioned previously, block aberrant electrical impulses. Because the operation
is difficult to perform and there are complications that can be difficult to treat,
this operation is not first-line therapy and the Cox-Maze III is not often done.
Learning Break: The left atrial appendage is a muscular sac that is part of the left
atrium. It acts as a reservoir for blood, and it can often be a source of ectopic foci that
cause atrial fibrillation.

Pulmonary vein isolation: Pulmonary vein isolation surgery can be very effective
(a 9% recurrence rate) for patients who have paroxysmal atrial fibrillation, but it
is ineffective for patients who do not have this form of the arrhythmia.82,83

Other techniques: There are other surgical approaches used for treating atrial
fibrillation. These techniques use an energy source (radiofrequency, laser,
microwave, ultrasound, cryothermy) to form atrial lesions – left atrial or bi-atrial
– that will block conduction. The pulmonary vein and the left atrial appendage
are isolated, as well.84,85,86
SUMMARY
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Atrial fibrillation is the most common arrhythmia.
Atrial fibrillation is defined as rapid, uncoordinated atrial activity with a rapid,
irregular ventricular response.
The basic causes of atrial fibrillation are a triggering event in an abnormal atrial
myocardium.
In atrial fibrillation, the atria beat very rapidly and irregularly, and a varying and
irregular number of those atrial impulses are transmitted through the AV node.
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People with atrial fibrillation typically experience a rapid, irregular heart beat,
palpitations, shortness of breath, dyspnea on exertion, and chest pain.
The signs and symptoms of atrial fibrillation are basically caused by a decrease in
cardiac output; this is caused by the absence of regular, forceful atrial
contractions. Decreased coronary blood flow also is part of the cause of the signs
and symptoms.
The ECG is atrial fibrillation features a lack of P waves, rapid oscillatory waves
of varying size and shape, narrow QRS complexes, and an irregularly irregular
ventricular response.
Atrial fibrillation can be paroxysmal, persistent, permanent, or lone.
Atrial fibrillation has genetic, pharmacological, medical-surgical, and cardiac
causes.
Hypertension is one of the biggest risk factors for developing atrial fibrillation.
Complications of atrial fibrillation include embolic stroke, congestive heart
failure, and cardiomyopathy.
The CHADS2 is used to assess the risk of stroke in patients with atrial fibrillation.
Either warfarin or aspirin are given to patients who have atrial fibrillation in order
to prevent embolic stroke.
Treatment of atrial fibrillation focuses on rate control or rhythm control.
Rate control is accomplished using cardioversion or medications such as βblockers, calcium channel blockers, and digoixin.
Rhythm control is accomplished using medications such as amiodarone.
Rhythm control can also be accomplished using radiofrequency ablation or
surgical techniques.
REFERENCES
1. Rosenthal L. McManus DD. Atrial fibrillation. eMedicine. June 1, 2010.
http://emedicine.medscape.com/article/151066-overview. Accessed July 9, 2010.
2. Sanoski C. Prevalence, pathogenesis, and impact of atrial fibrillation. American
Journal of Health-System Pharmacy. 2010;67:S11-S16.
3. Nottingham F. Diagnosis and treatment of atrial fibrillation. Journal of the American
Academy of Nurse Practitioners. 2010;22:280-287.
4. Go A, Hylek E, Phillips K, Change Y, Henault L, Selby J, et al. Prevalence of
diagnosed atrial fibrillation in adults: National implications for rhythm management and
stroke prevention: the anticoagulation and risk factors in atrial fibrillation (ATRIA)
study. Journal of the American Medical Association. 2001;285:2370-2375.
5. Schnabel RB, Sullivan LM, Levy D, Pencina MJ, Massaro JM, D’Agostino RB, et al.
Development of a risk score for atrial fibrillation (Framingham Heart Study): a
community-based cohort. Lancet. 2009;373-:739-745.
6. Naccarelli GV Varker H, Lin J, Schulman KL. Increasing prevalence of atrial
fibrillation and flutter in the United States. American Journal of Cardiology.
2009;104:1534-1549.
7. Crandall MA, Bradley DJ, Packer DL, Asirvatham SJ. Contemporary management of
atrial fibrillation: Update on anticoagulation and invasive management strategies. Mayo
Clinic Proceedings. 2009;84:643-662.
8. Crandall MA, Bradley DJ, Packer DL, Asirvatham SJ. Contemporary management of
atrial fibrillation: Update on anticoagulation and invasive management strategies. Mayo
Clinic Proceedings. 2009;84:643-662.
9. Crandall MA, Bradley DJ, Packer DL, Asirvatham SJ. Contemporary management of
atrial fibrillation: Update on anticoagulation and invasive management strategies. Mayo
Clinic Proceedings. 2009;84:643-662.
10. Fuster V, Rydén LE, Cannom DS, Crjins HJ, Curtis AB, Ellenbogen KA, et al.
ACC/AHA/ESC 2006 guidelines for management of patients with atrial fibrillation.
Circulation. 2006;114:e257-e354.
11. Crandall MA, Bradley DJ, Packer DL, Asirvatham SJ. Contemporary management of
atrial fibrillation: Update on anticoagulation and invasive management strategies. Mayo
Clinic Proceedings. 2009;84:643-662.
12. Jahangir A, Lee V, Friedman PA, Trusty JM, Hodge DO, Kopecky SL, et al. Longterm progression and outcomes with aging in patients with lone atrial fibrillation.
Circulation. 2007;115:3050-3056.
13. Fuster V, Rydén LE, Cannom DS, Crjins HJ, Curtis AB, Ellenbogen KA, et al.
ACC/AHA/ESC 2006 guidelines for management of patients with atrial fibrillation.
Circulation. 2006;114:e257-e354.
14. Fuster V, Rydén LE, Cannom DS, Crjins HJ, Curtis AB, Ellenbogen KA, et al.
ACC/AHA/ESC 2006 guidelines for management of patients with atrial fibrillation.
Circulation. 2006;114:e257-e354.
15. Fuster V, Rydén LE, Cannom DS, Crjins HJ, Curtis AB, Ellenbogen KA, et al.
ACC/AHA/ESC 2006 guidelines for management of patients with atrial fibrillation.
Circulation. 2006;114:e257-e354.
16. Elinor PT, Shin JT, Moore RK, Yoerger DM, MacRae CA. Locus for atrial
fibrillation maps to chromosome 6q14-16. Circulation. 2003;107:2880-2883.
17. Marcus GM, Smith LM, Vittinghoff E, Tseng ZH, Badhwar N, Lee, BK, et al. A first
degree family history in lone atrial fibrillation patients. Heart Rhythm. 2008;5:826-830.
18. Fox CS, Parise H, B’Agostino RB, Lloyd-Jones DM, Vasan RS, Wang TJ, et al.
Parental atrial fibrillation as a risk factor for atrial fibrillation in offspring. Journal of the
American Medical Association. 2004; 291:2851-2855.
19. Ettinger PO, Wu CF, De La Cruz C, Weisse AB, Ahmed SS, Regan TJ. Arrhyhtmias
and the “holiday heart”: alcohol-associated cardiac rhythm disorders. American Heart
Journal. 1978;95:555-562.
20.Falcone AM, Schussler JM. Sudden atrial fibrillation associated with acute alcohol
ingestion and cor triatriatum. Proceedings of the Baylor University Medical Center.
2009;22:335-336.
21. Mukamal KJ, Tolstrup JS, Friberg J, Jensen G, Gronbaek M. Alcohol consumption
and the risk of atrial fibrillation in men and women: The Copenhagen City Heart Study.
Circulation. 2005;112:1736-1742.
22. Conen D, Chiuve SE, Evert BM, Zhang SM, Buring JE, Albert CM. Caffeine
consumption and incident atrial fibrillation in women. American Journal of Clinical
Nutrition. 2010, June 23, ahead of print.
23. Heeringa J, Kors JA, Hofman A, van Rooij FJ, Witteman JC. Cigarette smoking and
the risk of atrial fibrillation: the Rotterdam study. American Heart Journal.
2008;156:1163-1169.
24. Bielecka-Dabrowa A, Mikhailidis DP, Rysz J, Banach M. The mechanisms of atrial
fibrillation in hyperthyroidism. Thyroid Research. 2009;2:4.
25. Nichols GA, Kyndaron R, Chugh SS. Independent contribution of diabetes to the
increased prevalence and incidence of atrial fibrillation. Diabetes Care. 2009;32:18511856.
26. Frontera JA, Parra A, Simbo D, Fernandez A, Schimdt JM, Peter P, et al. Cardiac
arrhythmias after subarachnoid hemorrhage: risk factors and impact on outcome.
Cerebrovascular Disease. 2008;26:71-78.
27. Capampangan DJ, Wellik KE, Parish JM, Aguilar MI, Snyder CR, Wingerchuk D, et
al. Is obstructive sleep apnea an independent risk factor for stroke? A critically appraised
topic. Neurologist. 2010. 16:269-273.
28. Crandall MA, Bradley DJ, Packer DL, Asirvatham SJ. Contemporary management of
atrial fibrillation: Update on anticoagulation and invasive management strategies. Mayo
Clinic Proceedings. 2009;84:643-662.
29. Jongnarangsin K, Oral H, Postoperative atrial fibrillation. Medical Clinics of North
America. 2008;92:87-99.
30. Echahidi N, Pibart P, O’Hara G, Mathieu P. Mechanisms, treatment, and prevention
of atrial fibrillation after cardiac surgery. Journal of the American College of Cardiology.
2008;51:793-801.
31. Echahidi N, Pibart P, O’Hara G, Mathieu P. Mechanisms, treatment, and prevention
of atrial fibrillation after cardiac surgery. Journal of the American College of Cardiology.
2008;51:793-801.
32. Burgess DC, Kilborn MJ, Keech AC. Interventions for for preventions of postoperative atrial fibrillation and its complications after cardiac surgery: a meta analysis.
European Heart Journal. 2006;27:2846-2857.
33. Mayson SE, Greenspon AJ, Adams S, DeCaro MV, Sheth M, Weitz HH, et al. The
changing face of post-operative atrial fibrillation prevention: a review of current medical
therapy. Cardiology Review.2007;15:231-241.
34. Hollings DD, Higgins RS, Faber LP, Warren WH, Liptay MJ, Basu M, et al. Age is a
strong risk factor for atrial fibrillation after pulmonary lobectomy. American Journal of
Surgery. 2010;199;558-561.
35. Neragi-Miandoab S, Weiner S, Sugarbaker DJ. Incidence of atrial fibrillation after
extrapleural pneumonectomy vs pleurectomy in patients with malignant plural
mesothelioma. Interactive Cardiovascular and Thoracic Surgery. 2008;7:1039-1042.
36. Zebe H. Atrial fibrillation in dialysis patients. Nephrology, Dialysis, and
Transplantation. 2000;15:765-768.
37. Crandall MA, Bradley DJ, Packer DL, Asirvatham SJ. Contemporary management of
atrial fibrillation: Update on anticoagulation and invasive management strategies. Mayo
Clinic Proceedings. 2009;84:643-662.
38. Go O, Rosendorff C. Hypertension and atrial fibrillation. Current Cardiology
Reports. 2009;11:430-435.
39. Bouzas-Mosquera A, Petiero J, Broullón JF, Alvarez-García N, Mosquera VX, Casas
S, et al. Effect of atrial fibrillation outcome in patients with known or suspected coronary
artery diseased referred for exercise testing. American Journal of Cardiology. 2010;1051207-1211.
40. Goto S, Bhatt DL, Röther J, Alberts M, Hill MD, Ikeda Y, et al. Prevalence, clinical
profile, and cardiovascular outcomes of atrial fibrillation patients with atherothrombosis.
American Heart Journal. 2008;156:855-863.
41. Anter E, Jessup M, Callans DJ. Atrial fibrillation and heart failure: treatment
considerations for a dual epidemic. Circulation. 2009;119:2516-2525.
42. Rosenthal L. McManus DD. Atrial fibrillation. eMedicine. June 1, 2010.
http://emedicine.medscape.com/article/151066-overview. Accessed July 9, 2010.
43. Fuster V, Rydén LE, Cannom DS, Crjins HJ, Curtis AB, Ellenbogen KA, et al.
ACC/AHA/ESC 2006 guidelines for management of patients with atrial fibrillation.
Circulation. 2006;114:e257-e354.
44. Rosenthal L. McManus DD. Atrial fibrillation. eMedicine. June 1, 2010.
http://emedicine.medscape.com/article/151066-overview. Accessed July 9, 2010.
45. Ogilvie IM, Newton N, Welner SA, Cowell W, Lip GY. Underuse of anticoagulants
in atrial fibrillation: a systematic review. American Journal of Medicine. 2010:123:638645.
46. Fuster V, Rydén LE, Cannom DS, Crjins HJ, Curtis AB, Ellenbogen KA, et al.
ACC/AHA/ESC 2006 guidelines for management of patients with atrial fibrillation.
Circulation. 2006;114:e257-e354.
47. Crandall MA, Bradley DJ, Packer DL, Asirvatham SJ. Contemporary management of
atrial fibrillation: Update on anticoagulation and invasive management strategies. Mayo
Clinic Proceedings. 2009;84:643-662.
48. Gladstone DJ, Bui E, Fang J, Laupacis A, Lindsay MP, Tu JV, et al. Potentially
preventable strokes in high-risk patients with atrial fibrillation who are not adequately
anticoagulated. Stroke. 2009;40:235-240.
49. Anter E, Jessup M, Callans DJ. Atrial fibrillation and heart failure: treatment
considerations for a dual epidemic. Circulation. 2009;119:2516-2525.
50. Crandall MA, Bradley DJ, Packer DL, Asirvatham SJ. Contemporary management of
atrial fibrillation: Update on anticoagulation and invasive management strategies. Mayo
Clinic Proceedings. 2009;84:643-662.
51. Crandall MA, Bradley DJ, Packer DL, Asirvatham SJ. Contemporary management of
atrial fibrillation: Update on anticoagulation and invasive management strategies. Mayo
Clinic Proceedings. 2009;84:643-662.
52. . Nottingham F. Diagnosis and treatment of atrial fibrillation. Journal of the American
Academy of Nurse Practitioners. 2010;22:280-287.
53. Abcede HG, Ovbiagele B. Update on antithrombotic therapy in atrial fibrillation.
Current Treatment Options in Cardiovascular Medicine. 2010;12:250-260.
54. Abcede HG, Ovbiagele B. Update on antithrombotic therapy in atrial fibrillation.
Current Treatment Options in Cardiovascular Medicine. 2010;12:250-260.
55. Ogilvie IM, Newton N, Welner SA, Cowell W, Lip GY. Underuse of anticoagulants
in atrial fibrillation: a systematic review. American Journal of Medicine. 2010:123:638645.
56. Walrave C, Hart RG, Singer DE, Laupacis A, Connolly S, Petersen P, et al.
Anticoagulants verus aspirin in nonvalvular atrial fibrillation: an individual patient metaanalysis. Journal of the American Medical Association. 2002;288:2441-2448.
57. Hart RG, Benavente O, McBride R, Pearce LA. Anti-thrombotic therapy to prevent
stroke in patients with atrial fibrillation: a meta-analysis. Annals of Internal Medicine.
1999;131:492-501.
58. Halbmayer WM, Haushofer A, Schön R, Fischer M. The prevalence of poor
anticoagulation response to activated protein C (APC resistance) among patients
suffering from stroke or venous thrombosis and among healthy subjects. Blood
Coagulation and Fibrinolysis. 1994;5:51-57.
59. Halbmayer WM, Haushofer A, Schön R, Fischer M. The prevalence of poor
anticoagulation response to activated protein C (APC resistance) among patients
suffering from stroke or venous thrombosis and among healthy subjects. Blood
Coagulation and Fibrinolysis. 1994;5:51-57.
60. Abcede HG, Ovbiagele B. Update on anti-thrombotic therapy in atrial fibrillation.
Current Treatment Options in Cardiovascular Medicine. 2010;12:250-260.
61. ACTIVE Writing Group of the Active Investigators. Connolly S, Pogue J, Hart RG,
Pfeffer M, Hohnloser S, Chrolavicius S, et al. Clopidogrel plus aspirin versus oral
anticoagulation for atrial fibrillation in the Atril fibrillation Clopidogrel Trial with
Irbesartan for prevention of Vascular Events (ACTIVE W). Lancet. 2006;367:1903-1912.
62. ACTIVE Investigators, Connolly S, Pogue J, Hart RG, Hohnloser S, Pfeffer M,
Chrolavicius S, et al. Effect of aspirin added to aspirin in patients with atrial fibrillation.
New England Journal of Medicine. 2009;360:2066-2078.
63. Singer DE, Albers GW, Dalen JE, Fang MC, Go AS, Halperin JL, et al. American
College of Chest Physicians: Antithrombotic therapy in atrial fibrillation: American
Colege of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition).
Chest. 2008;133:546S-592S.
64. Raghavan AV, Decker WW, Meloy TD. Management of atrial fibrillation in the
emergency room. Medical Clinics of North America. 2005;23:1127-139.
65. Crandall MA, Bradley DJ, Packer DL, Asirvatham SJ. Contemporary management of
atrial fibrillation: Update on anticoagulation and invasive management strategies. Mayo
Clinic Proceedings. 2009;84:643-662.
66. Crandall MA, Bradley DJ, Packer DL, Asirvatham SJ. Contemporary management of
atrial fibrillation: Update on anticoagulation and invasive management strategies. Mayo
Clinic Proceedings. 2009;84:643-662.
67. Kim SS, Knight BP. Electrical and pharmacologic conversion for atrial fibrillation.
Medical Clinics of North America. 2008;92:101-120.
68. Crandall MA, Bradley DJ, Packer DL, Asirvatham SJ. Contemporary management of
atrial fibrillation: Update on anticoagulation and invasive management strategies. Mayo
Clinic Proceedings. 2009;84:643-662.
69. Crandall MA, Bradley DJ, Packer DL, Asirvatham SJ. Contemporary management of
atrial fibrillation: Update on anticoagulation and invasive management strategies. Mayo
Clinic Proceedings. 2009;84:643-662.
70. Crandall MA, Bradley DJ, Packer DL, Asirvatham SJ. Contemporary management of
atrial fibrillation: Update on anticoagulation and invasive management strategies. Mayo
Clinic Proceedings. 2009;84:643-662.
71. Kalus JS. Pharmacotherapeutic decision-making for patients with atrial fibrillation.
American Journal of Health-System Pharmacy. 2010;67:S17-S25.
72. Pappone C, Augello G, Sala S, Gugliotta F, Vicedomini G, Gulletta S, et al A
randomized trial of circumferential pulmonary vein ablation versus antiarrhythmic drug
therapy in paroxysmal atrial fibrillation: the APAF Study. Journal of the American
College of Cardiology. 2006;48:2340-2347.
73. Lafuente-Lafuente C, Mouly S, Longás-Tejero MA, Mahé I, Bergmann JF.
Antiarrhythmic drugs for maintaining sinus rhythm after cardioversion of atrial
fibrillation: a systematic review of randomized controlled trials. Archives of Internal
Medicine. 2006;166:719-728.
74. Chung JWM. New and emerging antiarrhythmic and anticoagulant agents for atrial
fibrillation. American Journal of Health-System Pharmacy. 2010;67:S26-S34.
75. Allessie MA, Konigs K, Kirchoff CJ, Wijffels M. Electrophysiologic mechanisms of
perpetuation of atrial fibrillation. American Journal of Cardiology. 1996;77:10A-23A.
76. Nair GM, Nery PB, Diwakaramenon S, Healey JS, Connolly SJ, Morillo CA. A
systematic review of randomized trials comparing radiofrequency ablation with
antiarrhythmic medications in patients with atrial fibrillation. Journal of Cardiovascular
Electrophysiology. 2009;20:138-144.
76. Terasawa T, Balk EM, Chung M, Garlitski AC, Alsheikh-Ali AA, Lau J, et al.
Systematic review: comparative effectiveness of radiofrquency catheter ablation for atrial
fibrillation. Annals of Internal Medicine. 2009;151:191-202.
77. Crandall MA, Bradley DJ, Packer DL, Asirvatham SJ. Contemporary management of
atrial fibrillation: Update on anticoagulation and invasive management strategies. Mayo
Clinic Proceedings. 2009;84:643-662.
78. Chikwe J, Raikhelkar J, Filsoufi F, Fischer A. Current concepts in ablation of atrial
fibrillation. Seminars in Cardiothoracic and Vascular Anesthesia. 2009;13:215-224.
79. Chikwe J, Raikhelkar J, Filsoufi F, Fischer A. Current concepts in ablation of atrial
fibrillation. Seminars in Cardiothoracic and Vascular Anesthesia. 2009;13:215-224.
80. Prasad SM, Maniar HS, Camillo CJ, Schuessler RB, Boineau JP, Sundt TM 3rd, al.
The Cox maze III procedure for atrial fibrillation: long-term efficacy in patients
undergoing lone versus concomitant procedures. Journal of Thoracic and Cardiovascular
Surgery. 2003;126:1822-1828.
81. Khargi K, Hutten BA, Lemke B, Deneke T. Surgical treatment of atrial fibrillation: a
systematic review. European Journal of Cardiothoracic Surgery. 2005;27:258-265.
82. Gillinov AM, Bakaeen F, McCarthy PM, Blackstone EH, Rajeswaran J, Pettersson G,
et al. Surgery for paroxysmal atrial fibrillation in the setting of mitral valve disease: a role
for pulmonary vein isolation? Annals of Thoracic Surgery. 2006;81:19-26; discussion 2728.
83. Chikwe J, Raikhelkar J, Filsoufi F, Fischer A. Current concepts in ablation of atrial
fibrillation. Seminars in Cardiothoracic and Vascular Anesthesia. 2009;13:215-224.
84. Chikwe J, Raikhelkar J, Filsoufi F, Fischer A. Current concepts in ablation of atrial
fibrillation. Seminars in Cardiothoracic and Vascular Anesthesia. 2009;13:215-224.
85. Gillinov MA. Advances in surgical treatment for atrial fibrillation. Stroke.
2007;38:618-623.
86. Seifert PC, Collins J. Surgery for atrial fibrillation. AORN Journal. 2007;86:23-2339.