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Atrial Fibrillation

Amanda Ryan, D.O. Cardiology Fellow Frankford Hospitals March 11th, 2008

Atrial Fibrillation Facts

Atrial fibrillation is a disorder found in about 2.2 million Americans. During atrial fibrillation, the atria quiver instead of beating effectively. Blood isn't pumped completely out of them, so it may pool and clot. If a piece of a blood clot in the atria leaves the heart and becomes lodged in an artery in the brain, a stroke results. About 15 percent of strokes occur in people with atrial fibrillation.

Orderly Function

Orderly function of system is maintained:

by the domination of heart rate by a single pulse generator known as pacemaker by the relatively fast & uniform conduction of electrical signal via specialized conduction pathways by relatively long & uniform duration of electrical signal relative to its velocity of conduction through these pathways these things assure uniform electrical excitation & contraction of the heart

Define arrhythmia

Any disturbance in the normal sequence of impulse generation & conduction in the heart Arrhythmias may occur with or without underlying heart disease.

A normal heart beat

The electrical impulse begins at the sinus (or sinoatrial, SA) node, also called the hearts natural pacemaker. The SA node is a cluster of specialized cells, located in the right atrium. The SA node produces the electrical impulses that set the rate and rhythm of your heartbeat. The impulse spreads through the walls of the right and left atria, causing them to contract, forcing blood into the ventricles.
The impulse then reaches the atrioventricular (AV) node, which acts as an electrical bridge allowing impulses to travel from the atria to the ventricles. There is a short delay before the impulse travels on to the ventricles.

From the AV node, the impulse travels through a pathway of fibers called the HIS-Purkinje system. This network sends the impulse into the muscular walls of the ventricles and causes them to contract. This contraction forces blood out of the heart to the lungs and body.
The SA node fires another impulse and the cycle begins again.

Mechanisms of Arrhythmia

3 basic causes
suppression or enhancement of initiation or propagation of action potential ectopic pacemaker activity reentry of action potential into a pathway through which its already passed May be more than one of these things happening at a time to create a particular arrhythmia

Atrial fibrillation specifically

Rapid discharging triggers or foci (rapid discharge from musculature lining thoracic veins - esp pulmonary veins) Autonomic nervous system (may promote trigger activity & modify the substrate to facilitate arrhythmia) Substrate abnormalities that permit & promote wavelet reentry


Arrhythmias may or may not cause symptoms, when they do, common complaints are:

palpitations lightheadedness syncope shortness of breath chest pain

More history

Need to establish if there are precipitating factors such as:

drinking coffee smoking exercise emotional stress

More history

Also need to identify if there are symptoms of underlying disease that may be associated with arrhythmias:

heart failure ischemic heart disease thyroid disease


Increased age Coronary heart disease (including myocardial infarction) High blood pressure Abnormal heart muscle function (including congestive heart failure) Disease of the mitral valve Hyperthyroidism or overdose of thyroid medication Pericarditis Pulmonary embolism Chronic lung diseases (emphysema, asthma, COPD) Alcoholism Stimulant drug use such as cocaine or decongestants Recent heart or lung surgery Congenital heart disease


Thorough questions regarding use of stimulants (including OTC), and Rx drugs that can contribute to arrhythmias such as: digitalis, theophylline, diuretics, beta blockers or agonists, TCAs, antihypertensives, antiarrhythmic agents.

Types of SVT
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Premature atrial contractions (PACs) Paroxysmal supraventricular tachycardia (PSVT) Accessory pathway tachycardia (such as Wolff-Parkinson-White syndrome) Atrial tachycardia Atrial fibrillation Atrial flutter

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Atrial Fibrillation

Rapid, uncoordinated generation of electrical impulses by the atria Triggered by a PAC that, by reentry, generates multifocal impulses at a rate of 300-500/minute These impulses enter AV node randomly; b/c of slower rate of conduction of AV node & b/c concealed conduction of rapid impulses renders AV node partially refractory. Ventricular rate slower than atrial and is irregular Untreated pts, usually 150-200 ventricular rate

Atrial Fibrillation

May occur paroxysmally, often in young pts associated with caffeine, alcohol intoxication, PSVTs, sinus tachycardia, stress, nicotine. Most common arrhythmia encountered in practice, frequency increases with age. 10% of those over 65 Major noncardiac disease associated is hyperthyroidism. Predisposing heart conditions

hypertension atherosclerosis rheumatic heart disease (esp. mitral valve involvement)


Increased age Coronary heart disease (including myocardial infarction) High blood pressure Congestive heart failure Obstructive sleep aprea Disease of the mitral valve Hyperthyroidism or overdose of thyroid medication Pericarditis Pulmonary embolism Chronic lung diseases (emphysema, asthma, COPD) Alcoholism Stimulant drug use such as cocaine or decongestants Recent heart or lung surgery Congenital heart disease WPW syndrome

Reversible Risk Factors

MI Recent cardiac surgery Thyroid dysfunction Acute pulmonary disease Pericarditis Myocarditis Acute alcohol ingestion

Atrial Fibrillation

Palpitations & fatigue are most common symptoms If ventricular response is fast, pts often complain of feeling strange, weak, or faint. Those with heart failure, ischemic CM, or valvular heart disease are often symptomatic b/c of the loss of atrial kick to cardiac output, especially noted on exertion. Irregularly irregular heartbeat and pulse with variation of sounds on auscultation.

Atrial Fibrillation

ECG shows rapid irregular fibrillatory atrial activity with rates 300-500; no p waves are present Ventricular rhythm is irregularly irregular QRS usually normal Most serious potential consequence is cardioembolic stroke Asymptomatic pts at greatest risk for tachycardia-induced cardiomyopathy

Distinguishing Afib on ECG

A flutter has repetitive, stereotypical undulations in baseline, resulting in sawtooth pattern. MAT shows PACs with at least 3 different morphological types of P waves that are distinguished from atrial fibrillation by presence of isoelectric baseline between complexes.

Wide QRS complex afib

Presence of preexisting BBB Aberrant conduction of a supraventricular impulse (Ashman phenomenon) - after a long RR intreval an early atrial impulse is conducted aberrantly b/c one BB is not fully recovered or is still partially refractory Ventricular ectopy Preexcitation


Hemodynamically stable pts in hospitalized setting, rate control is usually initial goal. Hospitalized pts diltiazem digoxin beta blockers Amiodarone also good option - especially for those with borderline BPs.

More Management

Shock or severe hypotension - electrical cardioversion is treatment of choice, it is synchronized (on the R wave). Usually start with 100-200J, can go to 360 if this is not successful Risk for thromboembolism exists, in controlled environment, can do TEE to look for clot (esp. in LA appendage), but if unstable, benefits outweigh risks. If this fails, may load with IV ibutilide or IV
procainamide, then retry.

Subsequent management

Anticoagulation is indicated even in paroxysmal in pts who have at least 1 risk factor for stroke - CHADS criteria (CHF &/or CAD, HTN, Advanced Age, DM, prior stroke). Goal INR 2-3. In those with lone afib, Aspirin alone is accetable for anticoag. Can undergo electrical or chemical cardioversion - medication options ibutilide, amiodarone, propafenone (normal heart), sotalol, flecainide. AFFIRM & RACE trials indicated rate control with long-term anticoagulation was associated with same outcomes as rhythm control strategies. Rate control options include digoxin, B-blocker, CCB Most cardiologists believe, an initial attempt at cardioversion after an appropriate period of anticoagulation should be tried at least once.

Facts about afib

only 25% of pts will remain in sinus rhythm on their own up to 50% maintain sinus rhythm with long-term antiarrhymic agents The treatment decisions require riskbenefit analysis. Refractory symptomatic afib radiofrequency AV node ablation & permanent pacemaker


>4000 pts >65 years of age hx of afib + additional risk factors randomly assigned to rate vs rhythm control mean follow up 3.5 yrs Essentially no statistically significant difference in mortality, stroke, quality of life or development of HF Rhythm control trend towards higher mortality & hospitalizations Sinus rhythm was associated with improved survival, offset by decreased survival associated with antiarrhythmics


Congestive heart failure hypertension advanced age (>75) diabetes mellitus stroke or TIA (2 points) Annual stroke rate is 1.2% with CHADS score 0; risk increases to 44% with 6