Atrial fibrillation is characterized by an irregularly irregular atrial rhythm paired with tachycardia. Common symptoms include palpitations, weakness, dyspnea, and presyncope. Atrial fibrillation comes with a significant risk of atrial thrombi formation, which causes a considerable risk of embolic stroke. Diagnosis is byanalysis of ECG. Treatment involves ventricular rate control with drugs, rhythm control with cardioversionor drugs, and prevention of thromboembolism with anticoagulants.


Atrialfibrillation (AF) is a rapid, irregularly irregular heart rhythm. This chronic or paroxysmal arrhythmia ischaracterized by disorganized atrial electrical activation and uncoordinatedatrial contraction. Thereare several classifications of AF, identified by pattern of duration andfrequency of recurrences. AcuteAF is new onset, lasting less than 48 hours. This is in contrast to paroxysmal AF, whichlasts less than 48 hours but is recurrent. Paroxysmal AF will convert spontaneously backto normal sinus rhythm. Persistent AF lasts longer than 1 week, and requires treatment toconvert back to normal sinus rhythm. Permanent AF is an arrhythmia that cannot beconverted to normal sinus rhythm. Lone AF is found in patients under 60 years old without an identifiablecause.


Commoncauses of atrial fibrillation include hypertension, cardiomyopathy, mitral ortricuspid valvular disorders, hyperthyroidism, and binge alcohol drinking(sometimes known as "Holiday Heart"). Other less common causes include pulmonaryembolism, atrial septal and other congenital heart defects, COPD, myocarditis,and pericarditis.


Inthe past, rheumatic fever was considered the strongest predictor of AF risk. However, the disease only accounts for asmall minority of cases today. Leading predisposing factors are hypertension, coronary artery disease,and valvular heart disease.

The risk factorsassociated with atrial fibrillation are all conditions that can lead to atrialdilation or ventricular hypertrophy, as will be discussed in thepathophysiology. These riskfactors include hypertension, diabetes mellitus (because of its associationwith hypertension), left ventricle hypertrophy, coronary artery disease, congestiveheart failure, hyperthyroidism, rheumatic heart disease, binge drinking("Holiday Heart"), and a post-surgical state (specifically, any kind ofcardiothoracic surgery). There are no specific genetic factors predisposing one to atrialfibrillation.


Atrialfibrillation typically develops secondary to another disease state. These disease states cause an alteration inatrial chamber pressure, and this pressure fluctuation is associated withdevelopment of a dysrhythmia. The mechanism for development of AF is best illustrated through thefollowing example.

Uncontrolledsystemic hypertension can cause the left ventricle to become hypertrophic as itcompensates for increased vascular resistance. The relatively thin myocardium of the atriais sensitive to the increase in pressure and diminished ventricular chambervolume, leading to atrial dilation. Atrial dilation facilitates disorganized atrial conduction that leavesthe normal conduction pathway intermittently and circles back into theconduction pathway. Thisconduction is called a re-entry circuit. The underlying conduction abnormalities of AFare represented by this re-entry circuit.

Prolapsed mitralvalves can also cause AF. The prolapsed valve extends abnormally into the atria during ventricularcontraction. This allowsblood to flow backwards from the ventricle to the atrium. As blood from the ventricular contraction issent into the atrium, the atrium becomes distended, causing a re-entry circuit.


Themost important sign of atrial fibrillation is an irregularly irregular pulse,generally paired with tachycardia. Other signs and symptoms include heart failure, hypotension (due toreduced ventricular output), palpitations, lightheadedness, poor exercisecapability, fatigue dyspnea, angina, syncope or near syncope, stroke, andarterial embolization. Manyof these symptoms, such as syncope, lightheadedness, and fatigue, occur becausethe ventricular output is diminished.

However,it is important to note that atrial fibrillation is often asymptomatic. Patients could also present with symptoms ofacute stroke or of other organ damage due to a systemic embolus. A pulse deficit (where apical ventricularheart rate is faster than the rate palpated at the wrist) may be present. This occurs because left ventricular strokevolume is not always sufficient to produce a peripheral pressure wave at fastventricular rates.


The first step indiagnosis of atrial fibrillation is recognizing an irregularly irregular heartrate, frequently with tachycardia. Once arrhythmia is suspected, an electrocardiogram (ECG) is used to makea diagnosis. Positivefindings include the absence of P waves between the QRS complexes andirregularity in timing and morphology of the waves.

The R-R interval,or the time between QRS complexes, is an important structure in diagnosis ofAF. Confirming AF will showthe R-R interval as irregular on ECG. There may be other irregularrhythms that resemble AF on ECG, but these can be distinguished by the presenceof discrete P waves or flutter waves.

Another tool indiagnosing AF is the echocardiogram. The echocardiogram is important in detectingstructural heart defects, such as left atrial enlargement, left ventricularwall motion abnormalities suggesting past or present ischemia, valvulardisorders, and cardiomyopathy. An echocardiogram will also identify additional risk factors for stroke,such as atrial blood stasis or thrombus and complex aortic plaque. A spiral chest CT scan can be done ifpulmonary embolus is suspected. These tests are significant because AF can occur along with MI, stroke,or other cardiac events.

Lab tests that canbe done include a test for TSH (Thyroid Stimulating Hormone), T andT. High levels of these hormones can indicatehyperthyroidism.


Thereare several differential diagnoses of atrial fibrillation, including atrialflutter and multifocal atrial tachycardia. These cardiac arrhythmias are all verysimilar because they are all supraventricular tachycardias. Because the signs and symptoms are sosimilar, these arrhythmias can only be distinguished through skilled analysisof ECG results.

Atrialflutter is an abnormal atrial heart rhythm, usually associated withtachycardia. It mostcommonly occurs in patients with cardiovascular disease, but can occurspontaneously in those with otherwise normal hearts. It is typically an unstable rhythm and candegenerate into atrial fibrillation. There are several types of atrial flutter, asit can occur in the right or left atria and can travel in a clockwise orcounterclockwise circuit. For the purposes of this differential diagnosis, we will examinecounterclockwise right atrial flutter, which represents about 80% of all atrialflutter.

Typicalright atrial flutter has an atrial rate of 260 to 300 beats per minute, with aventricular response that is typically 130 to 150 beats per minute. Upon ECG, the P waves will produce a sawtoothappearance. This helpsdistinguish atrial flutter from atrial fibrillation.

Multifocal atrialtachycardia (MAT) is a rapid resting heart rate of 100 to 150 beats per minutewith at least 3 distinct P wave morphologies. It is the signature tachycardia seen inpatients with significant pulmonary disease. In MAT, the electrical impulse is generatedat different foci within the atria of the heart each time. The P-R intervals are variable due to aphenomenon known as wandering atrial pacemaker (WAP), as are the R-R intervals. The presence of an isoelectric baselinedifferentiates this arrhythmia from AF.

Differentialdiagnosis of atrial fibrillation extends beyond conditions that are verysimilar in mechanism to AF. The entire differential diagnosis of AF can be expressed in the mnemonic"Irregular P Waves", which stands for: Infarction (myocardial) /Intoxication,Rheumatic heart disease, Recent thoracotomy, Endocrine (hyperthyroidism),Geriatric, Unknown, Lung Disease (COPD), Atherosclerotic heart disease, Reducedoxygen (hypoxia), Pericarditis, Worry/stress, Atrial septal defect, Valvularlesion (mitral), Embolus (pulmonary), and Systemic arterial hypertension.


Treatmentof atrial fibrillation usually requires hospitalization, as a primarypractitioner or outpatient care center does not have the necessary resources. Once the cause of AF has beenmanaged (hypertension, hyperthyroidism, etc), treatment focuses on ventricularrate control, rhythm control, and prevention of thromboembolism.

Atrialfibrillation of any duration requires rate control, usually to fewer than 80beats per minute at rest. Rate control is needed to control symptoms and preventtachycardia-induced cardiomyopathy. In acute paroxysms of rapid rate (140 to 160beats per minute), intravenous AV node blockers are used. However, AV node blockers should not be used when an accessory AV pathway isinvolved (indicated by wide QRS duration); these drugs increase frequency ofconduction via the bypass tract, possibly leading to ventricular fibrillation.

If excesscatecholamines are suspected, mainly in patients with thyroid disorders orexercise triggered AF, beta blockers are used. Beta blockers of choice include metoprololand esmolol. Calciumchannel blockers, such as diltiazem and verapamil, are also effective. Digoxin is less effective than beta blockersor calcium channel blockers, but may be preferred if heart failure is present. These drugs all may be used forlong-term rate control.

When beta blockers,calcium channel blockers, and digoxin are ineffective, separately or incombination with one another, amiodarone may be required. Amiodarone is not preferred due to its sideeffects, which include hypothyroidism, hyperthyroidism, corneal micro-deposits,abnormal liver enzyme results, blue-grey discoloration of the skin, andinterstitial lung disease.

If the patientcannot take or is not responding to rate controlling drugs, radiofrequencyablation of the AV node is necessary. Ablation produces a complete heart block, anda permanent pacemaker needs to be inserted.

Restoration ofnormal sinus rhythm is indicated in AF to improve cardiac output. This can be achieved through drugs orsynchronized cardioversion. Synchronized cardioversion delivers a series of electrical shocks to theheart to bring it back to normal sinus rhythm. However, ventricular rate control must be thefirst priority. Beforecardioversion can be done, the patient must have a ventricular rate under 120beats per minute.

If atrialfibrillation has been present for over 48 hours, anticoagulation should be doneto reduce the risk of thromboembolism. Cardioversion always presents the risk ofthromboembolism. Anticoagulation with warfarin should ideally be maintained for at least3 weeks prior to cardioversion. Recurrence rate for AF is high, so anticoagulation should be continuedindefinitely. Cardioversionis most effective with lone atrial fibrillation, atrial fibrillation with areversible cause, and shorter term atrial fibrillation. As a general rule, the sooner AF is treated,the greater the chance of success.

Antiarrhythmics forconversion to normal sinus rhythm are defined by class: Class Ia(procainamide, quinidine, and disopyramide), class Ic (flecainide,propafenone), and class III (amiodarone, dofetilide, ibutilide, and sotalol). All are effective in 50-60% ofpatients, but adverse effects differ. Again, ventricular rate control is the firstpriority, so these drugs are not to be used until rate has been controlled viabeta blocker or calcium channel blocker. Antiarrhythmics can be used for long termmaintenance of sinus rhythm, with or without previous cardioversion.

Prevention ofthromboembolism is an important aspect of treating atrial fibrillation. Measures to prevent thromboembolism arerequired any time cardioversion is used and most of the time for long termtreatment. As mentioned,warfarin should be used for at least 3 weeks prior to cardioversion, andcontinued after for at least 4 weeks. In patients with recurrent paroxysmal,persistent, or permanent atrial fibrillation, anticoagulants should becontinued indefinitely. Warfarin is the drug of choice for anticoagulation. Aspirin is less effective, but may be used inpatients with no risk factors for thromboembolism (prolonged immobility, bonefracture, paralysis, varicose veins, obesity) or for those withcontraindications to warfarin.

Prevention ofthromboembolism is perhaps the most vital goal in treating atrial fibrillation. Twenty to thirty million Americans haveatrial fibrillation, which is likely associated with 15% of all ischemicstrokes, and 30% of those in the elderly. AF is not only dangerous in and of itself,but it is a major independent risk factor for all embolic strokes.


Preventionof atrial fibrillation can be achieved through use of multiple oralmedications. Oralanticoagulants (OAC), specifically warfarin, are the most common agent used toprevent AF. However, most providersagree that long term use of OAC is only indicated in patients with sustainedAF, not those with intermittent AF. Most patients are not given OAC because of potential contraindications,such as advanced age, low compliance, and risk of bleeding.

A new area ofresearch is aimed at the atrial remodeling theory (electrical, contractile, andstructural remodeling). Thistheory emphasizes that AF causes more AF. There is now evidence that ACE inhibitors cancontribute to atrial remodeling. An analysis of 374 patients enrolled in the Studies of Left VentricularDysfunction trial looked at the role of ACE inhibitors in AF prevention forpatients with left ventricular dysfunction. Enalapril was given to 186 patients, which188 received placebo. Aftera mean study time of 2.9 years, 55 patients had AF. However, only 10 patients with AF werereceiving enalapril, with other 45 patients in the placebo group.

Analysis showedthat enalapril was the strongest predictor of decreased AF risk. Though the exact mechanism in which ACEinhibitors decrease the risk of AF in patients with left ventriculardysfunction is unknown, most patients exhibiting AF also have other riskfactors for cardiovascular disease, including hypertension. ACE inhibitors are proven to be effective inthese patients.


1. Beers M, Porter R, Jones T. TheMerck Manual – 18 Ed. Merck; 2006.

2. Dambro M. 5-Minute Clinical Consult. Lippincott Williams & Wilkins; 2005.

3. Hewko C. Acuteischemic stroke-swift assessment and quick action produce optimal

outcomes. JAAPA. July 2004; 17:19-25.

4. Johnson J, Napier K. Atrial fibrillation: New theories, emerging treatments. JAAPA.

June 2005; 18: 20-22.

5. Prystowsky E, Waldo A. Atrial Fibrillation, AtrialFlutter, and Atrial Tachycardia.

Hurst's The Heart – 12 Ed.. New York:The McGraw Hill Company; 2008.

6. Schwarz B. AtrialFibrillation: Controlling the most common arrhythmia. JAAPA.

1999;10: 36.