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Atrial Fibrillation

Amanda Ryan, D.O.

Cardiology FellowFrankford Hospitals

March 11th, 2008

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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'tpumped completely out of them, so it maypool and clot.

If a piece of a blood clot in the atria leaves theheart and becomes lodged in an artery in thebrain, a stroke results.

About 15 percent of strokes occur in people

with atrial fibrillation.

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Orderly Function

Orderly function of system is maintained:

by the domination of heart rate by a single pulse generatorknown as pacemaker

by the relatively fast & uniform conduction of electricalsignal via specialized conduction pathways

by relatively long & uniform duration of electrical signalrelative to its velocity of conduction through these pathways

these things assure uniform electrical excitation & contraction of the heart

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Define arrhythmia

Any disturbance in the normal sequenceof impulse generation & conduction in

the heart Arrhythmias may occur with or without

underlying heart disease.

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A normal heart beat

The electrical impulse begins at the sinus (or sinoatrial, SA) node, alsocalled the heart’s natural pacemaker. The SA node is a cluster of specialized cells, located in the right atrium. The SA node produces theelectrical impulses that set the rate and rhythm of your heartbeat. The

impulse spreads through the walls of the right and left atria, causingthem to contract, forcing blood into the ventricles.

The impulse then reaches the atrioventricular (AV) node, which acts asan electrical bridge allowing impulses to travel from the atria to theventricles. 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 intothe muscular walls of the ventricles and causes them to contract. Thiscontraction forces blood out of the heart to the lungs and body.

The SA node fires another impulse and the cycle begins again.

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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 passedMay be more than one of these things

happening at a time to create a particulararrhythmia

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Atrial fibrillation specifically Rapid discharging triggers or foci (rapid

discharge from musculature lining

thoracic veins - esp pulmonary veins)

Autonomic nervous system (maypromote trigger activity & modify the

substrate to facilitate arrhythmia) Substrate abnormalities that permit &

promote wavelet reentry

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History

Arrhythmias may or may not causesymptoms, when they do, common

complaints are: palpitations

lightheadedness

syncope shortness of breath

chest pain

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More history

Need to establish if there areprecipitating factors such as:

drinking coffee

smoking

exercise

emotional stress

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More history

Also need to identify if there aresymptoms of underlying disease that

may be associated with arrhythmias: heart failure

ischemic heart disease

thyroid disease

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RISK FACTORS FOR AFIB:

•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

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Medications

Thorough questions regarding use of stimulants (including OTC), and Rx

drugs that can contribute toarrhythmias such as: digitalis,theophylline, diuretics, beta blockers or

agonists, TCA’s, antihypertensives, anti-arrhythmic agents.

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Types of SVT

n Premature atrial contractions (PACs)

n Paroxysmal supraventricular tachycardia

(PSVT)

n Accessory pathway tachycardia (such as

Wolff-Parkinson-White syndrome)

n Atrial tachycardia

n Atrial fibrillation

n Atrial flutter

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Atrial Fibrillation

Rapid, uncoordinated generation of electricalimpulses by the atria

Triggered by a PAC that, by reentry, generatesmultifocal 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 concealedconduction of rapid impulses renders AV node

partially refractory.

Ventricular rate slower than atrial and is irregular

Untreated pts, usually 150-200 ventricular rate

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Atrial Fibrillation

May occur paroxysmally, often in young ptsassociated with caffeine, alcohol intoxication, PSVT’s,sinus tachycardia, stress, nicotine.

Most common arrhythmia encountered in practice,frequency increases with age.

10% of those over 65

Major noncardiac disease associated ishyperthyroidism.

Predisposing heart conditions

hypertension

atherosclerosis

rheumatic heart disease (esp. mitral valve involvement)

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RISK FACTORS FOR AFIB:

•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

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Reversible Risk Factors MI

Recent cardiac surgery

Thyroid dysfunction

Acute pulmonary disease

Pericarditis Myocarditis

Acute alcohol ingestion

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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 valvularheart disease are often symptomatic b/c of the lossof atrial “kick” to cardiac output, especially noted onexertion.

Irregularly irregular heartbeat and pulse withvariation of sounds on auscultation.

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Atrial Fibrillation

ECG shows rapid irregular fibrillatory atrialactivity with rates 300-500; no p waves are

present Ventricular rhythm is irregularly irregular

QRS usually normal

Most serious potential consequence iscardioembolic stroke

Asymptomatic pts at greatest risk fortachycardia-induced cardiomyopathy

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Distinguishing Afib on ECG A flutter has repetitive, stereotypical

undulations in baseline, resulting in

sawtooth pattern. MAT shows PAC’s with at least 3

different morphological types of P

waves that are distinguished from atrialfibrillation by presence of isoelectricbaseline between complexes.

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Wide QRS complex afib Presence of preexisting BBB

Aberrant conduction of a

supraventricular impulse (Ashmanphenomenon) - after a long RR intrevalan early atrial impulse is conducted

aberrantly b/c one BB is not fullyrecovered or is still partially refractory

Ventricular ectopy

Preexcitation

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Management

Hemodynamically stable pts in hospitalized setting,rate control is usually initial goal.

Hospitalized pts

diltiazem

digoxin

beta blockers

Amiodarone also good option - especially for thosewith borderline BP’s.

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More Management

Shock or severe hypotension - electrical cardioversionis treatment of choice, it is synchronized (on the R wave).

Usually start with 100-200J, can go to 360 if this isnot successful

Risk for thromboembolism exists, in controlledenvironment, 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.

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Subsequent management

Anticoagulation is indicated even in paroxysmal in pts who haveat 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 rhythmcontrol strategies.

Rate control options include digoxin, B-blocker, CCB

Most cardiologists believe, an initial attempt at cardioversionafter an appropriate period of anticoagulation should be tried at

least once.

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Facts about afib

only 25% of pts will remain in sinusrhythm on their own

up to 50% maintain sinus rhythm withlong-term antiarrhymic agents

The treatment decisions require risk-

benefit analysis. Refractory symptomatic afib -

radiofrequency AV node ablation &

permanent pacemaker

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AFFIRM >4000 pts >65 years of age

hx of afib + additional risk factors randomly assignedto rate vs rhythm control

mean follow up 3.5 yrs

Essentially no statistically significant difference inmortality, 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 withantiarrhythmics

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CHADS-2 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

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