ATRIAL FIBRILLATION

ATRIAL FIBRILLATION - Leonard Ganz, MD; Leonard S. Lilly, MD
BASICS
DESCRIPTION
• Chronic or paroxysmal arrhythmia is characterized by chaotic atrial electrical activity.
• Clinical pattern
- Paroxysmal AF (PAF)episodes are self-terminating.
- Persistentsinus rhythm can be restored through pharmacologic or direct current (DC) cardioversion
- Permanent sinus rhythm cannot be restored for meaningful period of time
• Electrophysiologic mechanism is most likely multiple re-entrant wavelets within the atria.
• In some patients, triggering premature atrial beats and/or bursts of tachycardia emanate from the pulmonary venous ostia or other sites.
• Because the atrioventricular node is bombarded with nearly continuous atrial electrical impulses, the ventricular response is irregular and usually rapid (may exceed 160 beats per minute).
• Symptoms vary from none to mild (palpitations, lightheadedness, fatigue, poor exercise capacity) to severe (angina, dyspnea, syncope). Symptoms are frequently more serious in patients with structural heart disease.
• In some patients with Wolff-Parkinson-White syndrome, atrial fibrillation may be extremely rapid and degenerate into ventricular fibrillation.
ALERT
Geriatric Considerations
Both the incidence of atrial fibrillation and the stroke risk of atrial fibrillation increase with age.
Pediatric Considerations
Uncommon in children with normal hearts; seen in congenital heart disease and in surgical repair.
Pregnancy Considerations
• Atrial fibrillation is unusual during pregnancy in the absence of structural heart disease.
• The use of digoxin is safe; beta-blockers, procainamide, and quinidine are probably safe. Limited information regarding calcium blockers
• The risk of fetal hemorrhage makes anticoagulation problematic; moreover, warfarin causes fetal anomalies. SC heparin is best choice if long-term anticoagulation is necessary.
• Direct current cardioversion does not harm fetus.
GENERAL PREVENTION
• Ethanol may trigger atrial fibrillation in some.
• In cardiomyopathy/heart failure, hemodynamic decompensation may trigger atrial fibrillation.
EPIDEMIOLOGY
• Incidence/prevalence increases with age.
• Predominant sex: Male > Female
Prevalence
• Estimated at 1 per 1,000 adults per year; estimated at 2-4% of adult population
• Approximately 2-4% of septuagenarians, 5-10% of octogenarians
RISK FACTORS
• Hypertension
• Diabetes mellitus
• Left ventricular hypertrophy
• Coronary artery disease
• Congestive heart failure
• Rheumatic heart disease
• Hyperthyroidism
• Post-surgical state (cardiothoracic surgery)
Genetics
There is no specific genetic pattern.
ETIOLOGY
• Hypertensive heart disease
• Valvular/rheumatic heart disease
• Coronary artery disease
• Acute myocardial infarction
• Pulmonary embolus
• Cardiomyopathy
• Congestive heart failure
• Infiltrative heart disease
• Pericarditis
• Ingestion (e.g., ethanol in "holiday heart")
• Hyperthyroidism
• Postoperative (e.g., cardiothoracic surgery)
• Sick sinus (tachy-brady) syndrome
• Idiopathic (including "lone" atrial fibrillation)
ASSOCIATED CONDITIONS
• Wolff-Parkinson-White syndrome
• Sick sinus syndrome
• Atrial flutter
- A related arrhythmia with regular atrial electrical activity, typical rate 250-350, manifested as sawtooth "flutter" waves on ECG. 2:1 or 4:1 conduction through the atrioventricular node to the ventricle is usual, so the pulse is frequently regular.
- Patients may have atrial fibrillation and flutter.
- Management for both arrhythmias is similar; atrial flutter is more difficult to control pharmacologically and more easily electrically cardioverted than is atrial fibrillation.
- Although atrial flutter alone may pose a lower a risk of thromboembolism than atrial fibrillation, guidelines for anticoagulation of atrial flutter and atrial fibrillation are the same.
- Radiofrequency catheter ablation to cure atrial flutter is widely applied.

DIAGNOSIS
SIGNS AND SYMPTOMS
• Irregular pulse
• Tachycardia
• Heart failure
• Hypotension
• Palpitations
• Lightheadedness
• Poor exercise capacity
• Fatigue
• Dyspnea
• Angina
• Near syncope/syncope
• Stroke
• Arterial embolization
History
• Palpitations, dyspnea, lightheadedness, etc.
• Cardiac risk factors common
Physical Exam
Irregularly irregular pulse, frequently tachcyardia
TESTS
• ECG is diagnostic; low amplitude fibrillatory waves without discrete P waves; irregularly irregular pattern of QRS complexes
• The Holter monitor and event monitor are helpful in diagnosing paroxysmal atrial fibrillation.
Lab
• TSH to screen for hyperthyroidism
• INR/PT in patients treated with warfarin
Imaging
• Chest x-ray for cardiopulmonary disease
• Echocardiogram for structural heart disease
• Spiral chest CT scan (or other tests such as D-dimer, ventilation-perfusion scan, or pulmonary angiography) if pulmonary embolus suspected
• Transesophageal echocardiography to detect left atrial appendage thrombus if cardioversion
Diagnostic Procedures/Surgery
• Evaluation for ischemia not generally indicated unless sign/symptoms are present
• Evaluation for pulmonary embolus not indicated unless signs/symptoms are present
Pathological Findings
• Atrial dilatation
• Atrial injury (chronic or acute)
• Atrial thrombus, especially in atrial appendage
• Sclerosis/fibrosis of sinoatrial node
• Coronary artery disease, valvular/rheumatic disease, cardiomyopathy, pulmonary embolus
DIFFERENTIAL DIAGNOSIS
• Multifocal atrial tachycardia
• Sinus tachycardia with frequent atrial premature beats
• Atrial flutter (see "Associated Conditions")
TREATMENT
STABILIZATION
• Inpatient if
- Significant symptoms
- Extremely rapid ventricular rate
- Initiating antiarrhythmic therapy
- Atrial fibrillation triggered by acute process (acute myocardial infarction, congestive heart failure, pulmonary embolus)
- High risk for stroke (rheumatic heart disease, prior transient ischemic attack/stroke)
• Outpatient management for low-risk patients
GENERAL MEASURES
• Avoid potential triggers.
- Avoid ethanol, caffeine, and nicotine.
- Manage underlying structural heart disease.
• Prevent complications.
- Anticoagulation to reduce the risk of embolic complications
- Antibiotic prophylaxis if atrial fibrillation is due to valvular heart disease
• Therapy strategies
- Ventricular rate control with atrioventricular nodal blocking agents
- Restore and maintain sinus rhythm with antiarrhythmic drugs.
- Nonpharmacologic therapies
Diet
As appropriate for underlying heart disease
Activity
• As tolerated
• When treated, minimal impairment in patients
ALERT
• Clinical risk factors for stroke
- Age >65
- Diabetes
- Hypertension
- History of stroke or transient ischemic attack
- History of congestive heart failure
• Echocardiographic risk factors for stroke
- Left atrial enlargement
- Mitral regurgitation
- Left ventricular dysfunction
Nursing
Monitor vital signs, symptoms
MEDICATION (DRUGS)
• Anticoagulation
- Unless contraindicated, patients with atrial fibrillation with any risk factors for stroke should receive warfarin to maintain an international normalized ratio of 2.0-3.0.
- Patients in whom warfarin is contraindicated should receive aspirin 325 mg/dayappropriate in low-risk patients (e.g., age 65 years with no risk factors for stroke).
- Paroxysmal atrial fibrillation treatment same as for chronic atrial fibrillation
• Routine use of antiarrhythmic drugs to maintain sinus rhythm has not proved beneficial. Antiarrhythmic drugs may be used when a specific indication for sinus rhythm maintenance exists.
• Control of ventricular rate:
- Beta-blockers (propranolol, metoprolol, atenolol, nadolol)
- Non-dihydropyridine calcium channel blockers (diltiazem and verapamil)
- Cardiac glycosides (digoxin), which might be less effective than other agents in controlling ventricular response
• Conversion to/maintenance of sinus rhythm
- DC cardioversion
- Antiarrhythmic therapy for chemical cardioversion and maintenance of sinus rhythm following cardioversion carries a risk of pro-arrhythmia.
- Ibutilide, an intravenous type III agent, for chemical cardioversion of atrial fibrillation and flutter of short duration (90 days)
- If duration of atrial fibrillation is >24-48 hours or unknown, treat with warfarin for 3 weeks before and 4 weeks after cardioversion. Or, once anticoagulation is established, perform transesophageal echocardiography. If no atrial thrombus, may cardiovert. Anticoagulation should be continued for 4 weeks thereafter.
- Long-term, and perhaps indefinite, anticoagulation should be considered.
• Chronic oral antiarrhythmic therapy to suppress atrial fibrillation recurrences
- Type IA (procainamide, disopyramide, quinidine)
- Type IC (flecainide, propafenone) in patients with structurally normal hearts or mild hypertensive heart disease
- Type III (sotalol, amiodarone, dofetilide)
• Acute therapy for hemodynamically compromised patients
- Heparin for anticoagulation
- IV beta or calcium channel blocker for control of ventricular rate
- Pharmacologic and/or direct current cardioversion
Contraindications
• Active bleeding precludes anticoagulation; the risk of bleeding is a relative contraindication to long-term anticoagulation.
• Warfarin is contraindicated in patients with a history of warfarin skin necrosis.
• Type IC drugs are contraindicated in patients with coronary artery disease and cardiomyopathy.
• Type IA drugs (sotalol, ibutilide, and dofetilide) should not be used in patients with torsade de pointes history.
Precautions
• With type IA drugs, the risk of torsade de pointes increases with the extent of QT interval prolongation (i.e., the QTc).
- Avoid other drugs that prolong QT interval, such as phenothiazines, tricyclic antidepressants, terfenadine, astemizole, and erythromycin.
- Avoid hypokalemia and hypomagnesemia.
- Torsade de pointes due to drug-induced long QT syndrome is said to be "pause dependent" as the risk increases with bradycardia, heart block, and sinus pauses.
• With type IC drugs, stress testing to exclude exercise-induced arrhythmia or QRS widening.
• With amiodarone, careful surveillance for hepatic, thyroid, pulmonary, skin, and ophthalmologic adverse effects is necessary.
• In many patients, adequate medical therapy of atrial fibrillation will cause bradycardia necessitating a permanent pacemaker.
Significant possible interactions
• Quinidine increases digoxin levels.
• Amiodarone increases digoxin levels and enhances effects of warfarin.
SURGERY
• Radiofrequency catheter ablation procedures to prevent atrial fibrillation recurrence in patients with both paroxysmal and persistent AF. Reserve catheter ablation for highly symptomatic patients who have failed drug therapy.
• Cardiac surgery (e.g., the "maze procedure") may be considered in severely symptomatic, medically refractory patients.
• Permanent dual chamber pacing may reduce the incidence of new onset atrial fibrillation and reduces the frequency of episodes of PAF in patients with sick sinus syndrome.
• Radiofrequency catheter ablation of atrioventricular node with pacemaker implantation in symptomatic medically refractory patients
• Consider implantable defibrillators to cardiovert atrial fibrillation in selected patients.
FOLLOW-UP
PROGNOSIS
• The stroke risk is low with anticoagulation.
• Atrial fibrillation increases the risk of morbidity and mortality, but prognosis is a function of underlying heart disease.
COMPLICATIONS
• Embolic stroke
• Peripheral arterial embolization
• Complications of pharmacologic therapy (bradyarrhythmias and torsade de pointes)
• Bleeding with anticoagulation
PATIENT MONITORING
• ECG/Holter to monitor rhythm
• Maintain INR at 2.0-3.0
• ECG to monitor QTc interval if on antiarrhythmic therapy
• Careful follow-up of antiarrhythmic drug
REFERENCES
1. ACC/AHA/ESC. Guidelines on the management of patients with atrial fibrillation. J Am Coll Cardiol. 2001;38:1231-1265.
2. Falk RH. Atrial fibrillation. N Engl J Med. 2001;344:1067-1078.
3. Prystowsky EN, Benson DW, Fuster V, et al. Management of patients with atrial fibrillation. Circulation. 1996;93:1262-1277.
4. Riley RD, Pritchell ELC. Pharmacologic management of atrial fibrillation. J Cardiovasc Electrophysiol. 1997;8:818-829.
MISCELLANEOUS
• Other notes: The risk of stroke is extremely low in young patients without structural heart disease, so called "lone atrial fibrillation."
• See also: Atrial Flutter