Part II: Management, Complications, and Disposition
Author: Donald A. Moffa Jr., MD, Associate Staff, Emergency Medicine, Cleveland Clinic Foundation, Cleveland, OH.
Peer Reviewers: Corey M. Slovis, MD, FACP, FACEP, Professor of Emergency Medicine and Medicine; Chairman, Department of Emergency Medicine, Vanderbilt University School of Medicine; Medical Director, Nashville Fire Department EMS, Nashville, TN; Stephen W. Smith, MD, Faculty Emergency Physician, Hennepin County Medical Center, Minneapolis, MN.
In general, the approach to managing patients with atrial fibrillation (AF) must be systematic and account for a variety of possible complications. The initial approach to the patient with AF is no different from other emergencies. The emergency physician (EP) should assess the patient’s airway, respiratory, and cardiovascular status, looking for signs of shock or pulmonary edema. The EP should perform a quick pulse check or apical auscultation, looking for regularity of pulse and cardiac rhythm. An irregular pulse may signify the presence of AF. Confirmation by electrocardiogram (ECG) and cardiac rhythm monitoring should follow. While addressing the "ABCs," the EP should consider the acuity of the arrhythmia and whether it contributes to the presenting symptoms, while considering the effects of any underlying conditions.
The EP must determine how and when to treat AF. It is entirely possible that therapeutic (or even spontaneous) cardioversion of AF of any duration may cause a thromboembolism and stroke. (See Figure 1.) First, ventricular rate must be controlled. This alone may improve the patient’s symptoms and hemodynamics and may provide enough time for elective cardioversion. Emergency electrical cardioversion may be necessary when the patient shows signs of any organ dysfunction such as pulmonary edema with hypoxemia, hypotension with neurological deficits, or acute cardiac ischemia with chest pain.1 Unfortunately, it sometimes is impossible to determine how "recent" recent-onset AF truly is when the patient presents in extremis, needing emergency cardioversion. Whether the patient has had adequate anticoagulation becomes a moot point in this situation. In this case, and when the AF is believed to have persisted for more than 48 hours, it is reasonable to give an intravenous (IV) heparin bolus and begin an infusion at the time of electrical cardioversion, although cardioversion should not be delayed to begin anticoagulation.2 The EP may consider IV heparin or full-dose subcutaneous low molecular weight heparin (enoxaparin) for stable patients in AF of unknown duration.3
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Early restoration of sinus rhythm in patients with acute onset AF prevents atrial remodeling, lowers thromboembolic risk, and may improve cardiac performance.4 Cardioversion can be performed electrically and externally; internally (by the cardiologist in the catheterization laboratory); or by pharmacological means using IV or oral routes.2 In the ED, cardioversion generally is limited to emergent, external, transthoracic means and to IV cardioverting medications (such as ibutilide) when restoration to normal sinus rhythm is less imperative in the stable patient. Delaying cardioversion in the hemodynamically stable patient affords time to search for underlying conditions, such as hyperthyroidism, electrolyte imbalance, or myocardial ischemia, that may have caused the arrhythmia. It also offers the dysrhythmia the chance to revert spontaneously to normal sinus rhythm, since approximately one-half of acute-onset AF cases convert within 24-48 hours.5 AF may terminate once the underlying conditions that caused it are corrected. With these strategies and considerations in mind, the final part of this two-part series outlines this evidence-based approach to patient management.—The Editor
Control of Ventricular Rate
Controlling ventricular rate response during AF may be all that is required to alleviate the patient’s symptoms and prevent a tachycardia-induced cardiomyopathy.
For many patients, particularly those with few symptoms, rate control and anticoagulation may be appropriate therapy.6
Medications for Rate Control. Medications that suppress conduction and prolong refractoriness in the AV node, particularly class IC (i.e., flecainide and propafenone) and class III antiarrhythmics (i.e., amiodarone, sotalol, ibutilide, and dofetilide) in the Vaughan-Williams classification,7 frequently are used to control ventricular rate, control symptoms, and improve hemodynamics during AF.8 In the absence of significant symptoms, the EP should avoid IV medications to control ventricular rate because of their potential to cause hypotension, impair left ventricular function, and precipitate congestive heart failure (CHF).8 The EP may substitute oral medications instead. For those patients in whom the AF causes significant symptoms, IV medications, such as the calcium channel blockers verapamil and diltiazem or the beta-blockers metoprolol or esmolol, offer effective rate control. (See Table 1.) IV procainamide is the drug of choice if rapid conduction is over an accessory pathway, as in Wolff-Parkinson-White syndrome (WPW). Beta-blockers are effective in patients with thyrotoxicosis, poor left ventricular ejection fraction, heart failure, and in conditions of increased sympathetic tone. (It is wise to avoid beta-blockers in patients with bradycardia, heart block, or severe bronchospastic disease.)
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Digoxin is first-line treatment only in patients with CHF secondary to impaired systolic ventricular function, but its therapeutic effect may take 60 minutes, achieving full effect by six hours and making it a poor choice for acute rate control.8-10 Combination therapy with digoxin, calcium channel blockers, and beta-adrenergic blockers may be needed to control rapid and tenacious ventricular response in some patients who do not respond to single agent therapy.8 For example, the combination of IV diltiazem and digoxin results in better ventricular rate control with fewer rate fluctuations than that achieved by IV diltiazem alone.11
Cardioversion
Restoring sinus rhythm may improve symptoms and hemodynamics and has been shown to increase cerebral blood flow, cardiorespiratory function, and exercise tolerance.8,12 Approximately one-third of patients who present with chronic AF have had prior pharmacological cardioversion.13 The EP immediately should cardiovert the hemodynamically unstable patient with synchronized direct-current (DC) electrical shock (100-200 J) while monitoring the patient for potential pro-arrhythmia.14 Hemodynamically stable and asymptomatic patients who have AF for an unknown duration or more than 48 hours should either: 1) receive anticoagulation for three weeks prior to electrical or pharmacological cardioversion and for four weeks after cardioversion; or 2) receive IV heparin and subsequent transesophageal echocardiography to assess for atrial thrombi. If no thrombi are present, the patient may be cardioverted and then treated with warfarin for four weeks thereafter.8,15,16
When considering pharmacological cardioversion, the physician should choose antiarrhythmic medications according to the patient’s concomitant illnesses; medications used; and renal, hepatic, and cardiovascular function.8 One should choose the lowest initial drug dose to achieve therapeutic effect and titrate upward. Drugs such as verapamil, diltiazem, propranolol, esmolol, and digoxin used for acute rate control rarely terminate new onset AF. Drugs that can terminate AF include quinidine, procainamide, disopyramide, propafenone, sotalol, flecainide, and amiodarone. Antiarrhythmic drugs other than class III may increase defibrillation thresholds, whereas some drugs, including ibutilide and digoxin, may reduce defibrillation thresholds.2 One should consider chemical cardioversion using ibutilide for the first event if the arrhythmia is well-tolerated.2 A single dose of a class IC drug (i.e., flecainide or propafenone) after rate control may be used for patients with structurally normal hearts but who have frequent episodes of paroxysmal AF.2 Recurrent AF likely will require maintenance drug therapy. In this case, procainamide is an option since it can be used intravenously for cardioversion, as a continuous maintenance infusion, and orally for outpatient therapy.2
Considerations for Electrical Cardioversion. Electrical external thoracic cardioversion has a 70-90% success rate in converting AF to sinus rhythm.22,23 The recurrence rate of AF after successful DC cardioversion is higher in patients who have a longer history of AF.24 DC shock should be synchronized to the QRS to avoid shocking on the T-wave, which can precipitate ventricular fibrillation.2 Defibrillation patches should be positioned in the anterior-posterior position to minimize defibrillation energy requirements and to increase the chance of success.2 Current recommendations advise an initial shock energy of 100 J,6 followed by 200 J if necessary.25 It has been reported that fewer shocks and less total energy are required when the initial shock energy is 360 J, which achieves normal sinus rhythm in greater than 90% of cases.6 Cardioversion of AF frequently requires multiple shocks and at least 300 J of total energy.1 Some studies report that chronic AF resistant to conventional low energy DC cardioversion has been cardioverted successfully using 720 J shocks delivered externally to the thorax by two external defibrillators simultaneously.26 Compressing the chest or pressing paddles closer to the chest during cardioversion reduces thoracic impedance and improves success rate.6 Biphasic waveform defibrillators decrease the energy required for atrial defibrillation.1 Internal electrical cardioversion is an option for the cardiologist and utilizes either high energy (up to 200-400 J) delivered between a right atrial cavity electrode and body surface patch or lower energy (2-20 J) delivered between right atrium and coronary sinus electrodes.2 Failed cardioversion may be due to elevated defibrillation thresholds associated with atrial remodeling, atrial disease, high thoracic impedance, or drug effects.2
Pharmacologically Augmented Electrical Cardioversion. Providing controlled sedation for the patient undergoing electrical cardioversion is humane. It sometimes is prudent to premedicate with an antiarrhythmic drug before cardioversion to prevent immediate recurrence of AF after electrical cardioversion.6 Here, calcium channel blockers may be useful, considering the putative role of calcium overload in AF.6 Pretreatment with 1 mg ibutilide IV improves transthoracic cardioversion in AF.27 However, ibutilide should be avoided in patients who have ejection fractions less than 20% because of the likelihood of causing polymorphic ventricular tachycardia.27 (The EP should have IV magnesium sulfate and a cardiologist on hand in anticipation of torsade de pointes when using ibutilide.)
Pharmacological Cardioversion. Recent-onset AF, absence of CHF, and lack of concomitant digoxin use are factors that bode well for the pharmacological conversion of the arrhythmia.28 Pharmacological cardioversion is effective in up to 70% of patients.2 Spontaneous conversion frequently occurs after the antiarrhythmic drug used is metabolized.8 Pharmacological cardioversion of acute-onset AF is most effective with the class III agent ibutilide and the class IC medications flecainide and propafenone.29 Class IC drugs are the least proarrhythmic and least organ toxic of the antiarrhythmics. Oral Class IC medications are ideal for the patient who has infrequent paroxysmal AF, has no ischemic or structural heart disease, and achieved quick rate control with prior episodes (i.e., fewer than 2-6 hours).2 Digoxin and diltiazem are not effective in converting AF to sinus rhythm.2,5,30
Pro-arrhythmia is the most significant risk of antiarrhythmic therapy. Arrhythmias include various bradycardias and ventricular tachyarrhythmias, in particular torsade de pointes. Antiarrhythmic medications should be used in a monitored setting, and underlying hypokalemia, hypomagnesemia, or bradycardia should be corrected before giving the medications.2 Factors that enhance the risk of torsade de pointes include left ventricular hypertrophy, a dilated left ventricle, a prolonged baseline QT interval, and female gender.2 Torsade de pointes can occur in patients given ibutilide and in those without structural heart disease when class IA drugs or sotalol are used.31
Organ toxicities, including thrombocytopenia, agranulocytosis, lupus erythematosus, and pulmonary fibrosis, are other risks of antiarrhythmic therapy. Organ toxicity is less likely to occur with propafenone, flecainide, disopyramide, and sotalol.31
Specific Medications for Cardioversion. (See Table 2.)
Class III Antiarrhythmics. IV ibutilide may be used in hemodynamically stable ED patients with acute-onset AF. Ibutilide (1 mg IV)32 cardioverts up to 61% of patients with atrial flutter and approximately one-third of patients with AF within 90 minutes,33,34 although cardioversion generally takes 30-60 minutes.2 The conversion rate for AF rises to 47% when patients are given two doses of ibutilide 10 minutes apart.32 The ideal patients for IV ibutilide are those with acute-onset AF, infrequent paroxysmal AF without the need for maintenance antiarrhythmic therapy, and those not taking medications that prolong the QT interval.35 Cardioversion with ibutilide is not affected by enlarged left atrial diameter, presence of valvular heart disease, or the use of concomitant medications (i.e., beta-adrenergic blocking agents, calcium channel blocking agents, or digoxin). The EP should monitor the patient who receives ibutilide for at least four hours (or at least as long as it takes for the QT interval to return to normal, usually within 1-3 hours) since one of the most frequent adverse events is polymorphic ventricular tachycardia in up to 8% of patients.33,36
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Dofetilide is a class III antiarrhythmic that is available in the United States only in oral form. Like ibutilide, dofetilide is significantly more effective in cardioverting atrial flutter than AF (75% vs 22%) and carries the same risks of ventricular pro-arrhythmia.37 The EMERALD (European and Australian Multicenter Evaluative Research on Atrial Fibrillation Dofetilide) and SAFIRE-D (Symptomatic Atrial Fibrillation Investigation and Randomized Evaluation of Dofetilide) studies showed that oral dofetilide 0.5 mg twice daily for three days was effective in cardioverting AF to normal sinus rhythm in 32% and 29% of patients, respectively.35 Treatment must be initiated in the hospital with three days of cardiac monitoring.38 Dosage is adjusted to the length of the QTc interval, creatinine clearance, and the presence of heart failure or recent myocardial infarction.38 Dofetilide can be given with digoxin and beta-blockers, but other antiarrhythmic drugs and drugs that interfere with renal excretion or metabolism of dofetilide should be avoided.38 If AF is associated with severe heart failure or myocardial infarction, dofetilide and amiodarone are safe for cardioversion, and dofetilide may be considered as the first-choice treatment.38
Although amiodarone is less effective for cardioverting AF than class IC drugs,2 high-dose amiodarone (30 mg/kg PO) in a single dose will convert 50% of patients to normal sinus rhythm within eight hours, and 87% within one day.39 Lower conversion rates are observed in patients with hypertension, ischemic heart disease, CHF, and in patients with left atrial diameter greater than 45 mm, an ejection fraction less than 45%, or significant mitral regurgitation.40,41 IV amiodarone may cause hypotension, sinus node suppression, and, rarely, torsade de pointes.2
IV sotalol is not available in the United States, but it has been shown to convert acute-onset AF to normal sinus rhythm in one-half of patients.42 Oral sotalol (120 mg bid for 2 days) is more effective for adrenergically mediated paroxysmal AF than for vagally mediated AF (71% vs 36% conversion).43 Because of the risk of ventricular arrhythmia (5.8%), significant bradycardia (16.7%), and prolonged QTc interval (6.7%), patients started on sotalol should be monitored in the hospital.44
Class IA Antiarrhythmics. Procainamide often is used intravenously for termination of AF because it is highly effective (approximately 70% conversion rate) and may be continued orally, which is especially attractive in postoperative patients who develop AF.2,45 Procainamide is the treatment of choice for WPW. Procainamide is loaded 50 mg/min IV to a maximum of 20 mg/kg until the arrhythmia is suppressed, hypotension occurs, or the QRS widens by 50%.10
As with procainamide, hypotension is the main adverse effect of IV quinidine, and if it is used at all (more likely by the cardiologist than the EP), it is given as oral quinidine gluconate 300 mg every three hours for a total loading dose of 900 mg.2 Quinidine’s anticholinergic effect may increase AV nodal conduction, causing an increased ventricular rate, and should be administered only after giving agents such as calcium channel blockers or beta-blockers that slow AV nodal conduction when treating atrial flutter to prevent 1:1 AV nodal conduction and an accelerated ventricular response.2
Disopyramide (200 mg orally every 4-6 hours with a maximal dose of 800 mg daily) will terminate acute-onset AF in 92% of patients within 24 hours.46 This regimen may offer a safe and effective means for treating paroxysmal AF out of the hospital. Because of its negative inotropy and anticholinergic activity, disopyramide may cause torsade de pointes, sinus node suppression, and atrial flutter with 1:1 AV conduction.2 It should be avoided in patients with heart failure, glaucoma, myasthenia gravis, and urinary retention.47
Class IC Antiarrhythmics. IV flecainide (not available in the United States) will successfully cardiovert acute-onset AF in 76-93% of patients.48-51 Oral flecainide may be used, although the mean time for cardioversion is twice that of IV flecainide (110 minutes vs 52 minutes).52 Propafenone (600 mg PO) or flecainide (300 mg PO) may be used for single-dose cardioversion.53 Life-threatening ventricular tachydysrhythmias are associated with rapid dose escalations, coexisting ventricular dysrhythmias, or left ventricular dysfunction.
Complications of Cardioversion. The major risk of cardioversion (whether electrical, chemical, or spontaneous) is thromboembolism, associated with a 5.4% risk of stroke in the absence of prior anticoagulation.54 Even if AF lasts fewer than 48 hours, there is a 0.8% risk of thromboembolism from cardioversion.55,56
Acute pulmonary edema is uncommon, but if it does occur, half of the cases occur within three hours of cardioversion, and it is wise to observe the recently cardioverted patient during this time. It is believed that pulmonary and/or coronary artery emboli from the resumption of right atrial mechanical activity may be pathogenic factors of pulmonary edema after cardioversion.57
It is highly unlikely that electrical cardioversion causes damage to the myocardium. Therefore, the EP must suspect and search for antecedent coronary ischemia or myocardial infarction that may have precipitated the AF when cardiac troponin T is elevated.58
DC cardioversion in the presence of digoxin toxicity may trigger ventricular dysrhythmias. If digoxin toxicity is suspected and cardioversion is emergent, lidocaine may be used to decrease the risk of ventricular dysrhythmias.2
Choosing the Method for Cardioversion. The decision of when and by what means to cardiovert AF is one that the EP must make based on the patient’s acute physical condition (whether hemodynamically and neurologically stable or not); the patient’s underlying medical illnesses and factors that may have precipitated the AF (cardiac ischemia, myocardial infarction, thyrotoxicosis, electrolyte imbalance); and the EP’s knowledge and familiarity with the medications and tools at his or her disposal. Electrical cardioversion is the proven leader in restoring normal sinus rhythm and is the treatment of choice for the unstable patient, but the patient receiving this therapy will be subject to deep sedation, possible anesthetic side effects, and possible airway compromise. Medical cardioversion, on the other hand, is relatively slow, should not be used for the hemodynamically unstable patient, and may induce arrhythmias. Either treatment may liberate a thromboembolic clot. Therefore, a physical examination must be performed before and after cardioversion to assess for signs of neurological disability.
Maintenance of Sinus Rhythm
Once the patient is cardioverted, the EP must decide whether and how to prevent AF from recurring. Antiarrhythmic drugs (See Table 2) are chosen based on the patient’s medical condition, side effect profile, and whether the patient is at risk for recurrence of the dysrhythmias. The first episode of AF in an otherwise healthy individual who has been cardioverted successfully does not require maintenance antiarrhythmic therapy. The efficacy of maintaining normal sinus rhythm for all available oral agents is approximately 50% at six months.31 Beta-blockers such as atenolol may reduce the frequency of symptomatic paroxysmal AF (by preventing tachycardia) but may not prevent AF from recurring.59
For patients with lone AF or hypertension, the cardiologist may consider propafenone, flecainide, sotalol, disopyramide, dofetilide, or amiodarone. For patients with CAD but without CHF, sotalol, dofetilide, amiodarone, or disopyramide are preferred. For patients with CHF or a left ventricular ejection fraction less than 35%, dofetilide or amiodarone are the drugs of choice.1 The EP should consult the cardiologist prior to committing the patient to long-term antiarrhythmic therapy.
Anticoagulation and Prevention of Thromboembolism
Why Anticoagulation Is Important. AF in the absence of rheumatic valvular disease carries a five- to sevenfold increased risk of ischemic stroke.60 Most ischemic strokes associated with AF, particularly in women, are cardiogenic and probably due to embolism of stasis-induced thrombi formed in the left atrium and the left atrial appendage.8,61,62 A newly formed thrombus may take more than two weeks to become anchored to the atrial myocardium.24 Patients with nonrheumatic AF who have had recent cerebral vascular events have approximately 12% per year risk of recurrent stroke.63 Anticoagulation with warfarin, maintaining an international normalized ratio (INR) between 2.0 and 3.0, reduces the risk of stroke by two-thirds, which is comparable to primary prevention.63 In patients who have contraindication to anticoagulation, aspirin, although less effective, is a reasonable alternative.63 Clopidogrel, an anti-platelet agent with proven benefit in preventing recurrent cerebral ischemic events in patients with cerebral vascular disease, has not yet been recommended for stroke prophylaxis in patients with AF.64
The annual risk of major hemorrhage (intracranial hemorrhage or major bleeding requiring two units of packed red blood cell transfusion) in patients treated with warfarin is low, approximately 1.3%.65 Warfarin decreases the risk of stroke by 68% in patients with chronic AF with virtually no increase in the frequency of major bleeding. Patients with AF who are younger than 65 years without a history of hypertension, previous cerebral vascular event, or diabetes are at very low risk of stroke even when not anticoagulated. In these patients, aspirin may be the only drug prescribed by some.60,65
The Stroke Prevention in Atrial Fibrillation II (SPAF-II) study compared warfarin with aspirin for prevention of ischemic stroke and systemic embolism in two parallel trials, comparing patients 75 years or younger with patients older than 75, but the result was not conclusive. SPAF-II found that warfarin may be more effective than aspirin for stroke prevention in patients with AF, but the absolute reduction from warfarin was small. Older patients, whether treated with warfarin or aspirin, and younger patients treated with aspirin had a low risk of stroke. In the older group, the rate of all strokes (ischemic or hemorrhagic) with residual deficit was 4.3% per year with aspirin and 4.6% per year with warfarin.66 Younger patients without risk factors had a low rate of stroke when treated with aspirin.66 These investigators suggest that the patient’s age and inherent risk factors for thromboembolism should be considered when choosing the type of antithrombotic prophylaxis.66 Current, accepted risk factors are shown in Table 3.1,67
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Anticoagulation Guidelines. There are two alternative approaches to anticoagulation: 1) anticoagulate with warfarin to achieve an INR of 2.0-3.0 for at least three weeks, then cardiovert the patient; or 2) cardiovert the patient guided by TEE if sufficient anticoagulation is not achieved. (See Table 4.) Use anticoagulation before, during, and after TEE. Anticoagulation should continue for a minimum of 3-4 weeks after cardioversion for either of these approaches. The cardiologist will consider continuing anticoagulation longer than this period, since the greatest likelihood for recurrence of AF is in the first three months after cardioversion.1 Patients younger than age 65 who have no risk factors for stroke (as described above) or patients who have major risk factors for anticoagulation (i.e., fall risk) may be given aspirin.67
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Considerations for Coexisting Illnesses Complicating Atrial Fibrillation
Wolff-Parkinson-White Syndrome. Patients with AV reentry, especially those with WPW, can sustain a very rapid ventricular response, typically greater than 250 beats per minute,1 via conduction over an accessory pathway. Syncope, ventricular fibrillation, or sudden death can occur. These patients often will require aggressive, immediate ventricular rate control, cardioversion to normal sinus rhythm, and subsequent radiofrequency catheter ablation of the accessory pathway.8 (See Table 5.) Hemodynamically stable patients may not require emergency electrical cardioversion. Digoxin, calcium channel blockers, and beta-adrenergic blockers typically are ineffective in blocking conduction over an accessory pathway and, paradoxically, may enhance conduction, resulting in hypotension and cardiac arrest. IV procainamide is the treatment of choice in treating rapid ventricular response and cardioverting AF in patients with WPW.
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Neurogenic AF. There are vagally mediated and adrenergically mediated forms of AF. The vagally mediated form of AF characteristically occurs in men rather than women (approximately 4:1); in patients 40-50 years of age; presents as lone AF with little tendency for chronic AF; occurs during the night, during rest, after eating, or with absorption of alcohol; and usually occurs after a preceding progressive bradycardia.68 Beta-blocking drugs and digoxin may increase the frequency of AF.68 Vagally mediated AF may be treated with anticholinergic drugs such as disopyramide, flecainide, or quinidine.31
The adrenergic form of AF occurs less frequently than the vagally mediated form, usually occurs during the daytime, often is preceded by exercise or emotional stress, commonly is associated with polyuria, and typically occurs with a specific sinus rate, often near 90 beats per minute. This form of AF is treated with beta-blocking drugs.68
Thyrotoxicosis. Thyrotoxicosis, fever, acute gastrointestinal bleeding, or a hyperadrenergic state may cause a resting ventricular rate faster than 150 beats per minute in the absence of preexcitation. The individual patient’s clinical presentation, signs, and symptoms should guide the search for an underlying cause of the tachycardia.1
A beta-blocker such as esmolol most effectively controls the ventricular rate in patients with thyrotoxicosis.8,10 The thionamides propylthiouricil (PTU) and methimazole (Tapazole) may be given to the patient to reduce the formation and release of thyroid hormone.69 The doses are PTU (200-250 mg) or methimazole (20 mg) PO or PR every four hours.69 Iodine preparations and lithium carbonate (300 mg every six hours initially) block the release of preformed thyroid hormone from stores in the colloid space, and iodine inhibits conversion on T4 to T3.69 The oral contrast agent iopanic acid (Telepaque) contains 108 g iodine/3 g dose and is the iodine preparation of choice.69 The dose is 1 g of iopanic acid every 8 hours for 24 hours, then 500 mg twice daily.69 Lugol’s iodine or a saturated solution of potassium iodide (SSKI), 4-8 drops PO every 6-8 hours, also may be used.69
Left Ventricular Hypertrophy. Patients with left ventricular hypertrophy (LVH) are at risk for AF because hypertrophic hearts are associated with increased action potential duration and tend to have early after-depolarizations. Patients with LVH may be at increased risk for torsade de pointes. In the absence of ischemic heart disease (or strain pattern on ECG) and in the absence of a conduction delay, class IC agents (i.e., flecainide and propafenone) are first-line therapy.31
Ischemic Heart Disease/Myocardial Infarction. According to the Cardiac Arrhythmia Suppression Trial (CAST), class IC antiarrhythmic use for ventricular arrhythmias after myocardial infarction is associated with increased mortality.70 Therefore, their use is unwise in the setting of myocardial ischemia or infarction. Dofetilide, sotalol, and amiodarone, however, are safe in post-myocardial infarction patients who have AF.31,38,71
Congestive Heart Failure/Left Ventricular Dysfunction. When AF and CHF are present together, the treatment of each individually may exacerbate the other, rendering neither with adequate therapy. Both must be treated simultaneously. Digoxin, beta-blockers, or calcium channel blockers may be used for ventricular rate control, but calcium channel blockers, in particular, may decrease cardiac output by a negative inotropic effect on the heart.8 Contrary to a once widely held belief, long-term beta-blocker use in systolic dysfunction heart failure has been shown to slow the clinical progression of the disease and reduce mortality.14 Carvedilol, bisoprolol, and metoprolol CR/XL are the three beta-blockers that have shown positive effects in patients with stable moderate heart failure (New York Heart Association [NYHA] class II, III).14
For long-term therapy, amiodarone reduces the mean ventricular rate during AF in patients with CHF by 20% at two weeks, 18% at six months, and 16% at one year.72 Class IC drugs are contraindicated in patients with CHF.31 Oral dofetilide significantly reduces the incidence of hospitalization for worsening CHF and may convert AF to normal sinus rhythm.73
Post-surgical AF. AF is the most common dysrhythmia following cardiac surgery, with an incidence of 5-40%, usually occurring within the first week after surgery.31 Age, cardiomegaly, left atrial enlargement, multiple bypass grafts, long cross-clamp times, presence of pericardial effusion in patients undergoing valve replacement, and withdrawal of beta-blockers prior to surgery are all factors that predispose the patient to AF after surgery.31 Procainamide is appealing for treating AF in this circumstance because it can be started as an IV infusion and continued orally for two or three months after discharge.31
Brady-Tachy Syndrome. Reducing AV nodal conduction by pharmacological means or by nodal ablation followed by permanent pacemaker implantation often is required to control ventricular rate in patients with brady-tachy syndrome.8 Beta-blockers (with or without digoxin) may provide effective ventricular rate control in patients with brady-tachy syndrome as an alternative to standard AV nodal blocking drugs plus a pacemaker.31 Sotalol or amiodarone will depress AV nodal conduction, and the patient may not require additional medications to prevent AF recurrence.8 Provisions for temporary cardiac pacing should be arranged with the cardiologist before attempting to cardiovert or slow the ventricular rate in patients with suspected brady-tachy syndrome.2
Exercise-induced AF. The AV node of patients with exercise-induced AF is very sensitive to autonomic influences. In these patients, digoxin may be useful for slowing the ventricular rate at rest, but it does not provide adequate rate control during exercise.8 A beta-blocker is a better choice for rate control. Propafenone and sotalol have some beta-blocking properties and the ability to maintain normal sinus rhythm, and the cardiologist may consider using them for long-term rate control in patients with exercise-induced AF.31
Nonpharmacological Therapy for Persistent AF. Methods for controlling ventricular rate in patients with AF focus on ablating conduction through the AV node and include surgical cryoablation, catheter ablation with DC shocks, intra-coronary ethanol infusion, and radiofrequency catheter ablation.8 Of these, radiofrequency catheter ablation is the technique most commonly used, although there is no evidence that this specific technique influences survival in patients with AF.
The Maze Procedure. In the maze procedure, long incisions are made in both atria, creating paths or mazes in atrial tissue that channel sinus node impulses to the AV node, thereby preventing adjacent atrial tissue from conducting fibrillatory waves while still maintaining atrial contractility.8 Both atrial appendages are excised in an attempt to reduce the potential space where thrombi form, and the pulmonary veins, where ectopic foci often are located, are isolated.31 Indications for the maze procedure include: 1) failed medical therapy with respect to symptom control or prevention of recurrent embolic events; 2) combination with other surgical interventions; and 3) failed AV nodal ablation and medical therapy.31 The maze procedure is 84-98% successful, and 71-91% of patients will not require pharmacological therapy after this operation.18 Surgical mortality is approximately 3%.31 Complications of surgery include sinus node dysfunction requiring pacemaker placement, bleeding requiring reoperation, and interruption of atrionatriuretic factor production, which may result in edema.31
Endocardial Radiofrequency Catheter Ablation. AV nodal ablation and permanent pacemaker implantation may provide symptomatic relief in some patients whose symptoms have not improved after adequate trials of antiarrhythmic medications. Exercise tolerance and quality of life improve in patients with either paroxysmal or chronic AF after this procedure.8 Endocardial radiofrequency catheter ablation creates long, linear lesions in the atria, which effectively isolates large areas of the atria, thereby preventing chaotic conduction of atrial impulses in much the same way as the maze procedure does.8
When to Call the Cardiologist
The EP should call the cardiology consultant early if he or she feels uncomfortable treating the patient with AF, especially when deciding to pharmacologically cardiovert, anticoagulate long-term, or begin antiarrhythmic medications in an otherwise hemodynamically stable patient. The cardiology consultant will be of little use, however, when faced with an emergency cardioversion. It is likely that the cardiologist will admit the patient with new onset AF, although some patients who are rate-controlled and don’t have signs of cardiopulmonary or neurological compromise sometimes are discharged on anticoagulation with prompt cardiology follow-up. At the very least, the cardiologist can help arrange proper outpatient referral.
Patient Disposition
In general, patients who present with acute-onset AF of fewer than 48 hours’ duration who convert either spontaneously or by electrical means in the ED, provided they are hemodynamically stable and without other conditions requiring emergency attention, may be discharged without anticoagulation. Patients given IV ibutilide and who convert to normal sinus rhythm should be monitored for four hours or until their QTc intervals, if prolonged, return to baseline. Magnesium sulfate should be kept on hand to treat torsade de pointes if it occurs. Outpatient antiarrhythmic therapy should be considered for patients suspected of having frequent episodes of paroxysmal AF. Patients with acute-onset AF who fail to convert within a reasonable time in the ED should be admitted to a monitored bed in either the hospital or the observation unit, depending on what the clinical circumstances allow. IV heparin anticoagulation should be started in this situation. However, there is growing interest in the use of low molecular weight heparin for anticoagulation in those patients with acute-onset AF who are undergoing TEE and elective cardioversion.74,75
Conclusions and Future Considerations
Although AF is rarely a lethal arrhythmia, its presence is felt along a spectrum of symptoms from annoying palpitations to devastating cardiopulmonary collapse. It is, therefore, imperative that the EP consider the following four areas in treating the patient with AF: 1) control of ventricular rate; 2) cardioversion to sinus rhythm; 3) maintenance of sinus rhythm; and 4) anticoagulation. The patient’s presenting symptom complex, underlying medical conditions, likelihood of arrhythmia recurrence, and experience of the clinician will guide decisions in each of these areas.
Better techniques for detecting the underlying cause of AF or its likelihood of recurrence are being developed in the field of PC-based analysis of P-wave variance and spatial analysis of the cardiac cycle on ECG.19 Intracardiac ultrasound is used to help locate critical endocardial structures for radiofrequency catheter ablation. Using this technique reduces the fluoroscopy time needed for an ablation procedure and helps detect thrombus or pericardial effusion.20 Permanent pacing may prevent AF, and bi-atrial pacemakers now are being used to help coordinate atrial contractility.
References
1. Falk RH. Atrial fibrillation. N Engl J Med 2001;344(14):1067-1078.
2. Costeas C, Kassotis J, Blitzer M, et al. Rhythm management in atrial fibrillation—with the primary emphasis on pharmacological therapy: Part 2. Pacing and Clinical Electrophysiology 1998;21(4 Pt 1):742-752.
3. Falk RH. Atrial Fibrillation. In: Rakel RE, et al. eds. Conn’s Current Therapy. 53rd ed. Philadelphia: WB Saunders; 2001:276-280.
4. Thamilarasan M, Klein AL. Transesophageal echocardiography (TEE) in atrial fibrillation. Cardiology Clinics 2000;18:819-831.
5. Falk RH, Knowlton AA, Bernard SA, et al. Digoxin for converting recent-onset atrial fibrillation to sinus rhythm: A randomized, double-blind trial. Ann Intern Med 1987;106:503-506.
6. Wyse DG. Initial energy for electrical cardioversion of atrial fibrillation—is more better? Am J Cardiol 2000;86(3):324-325.
7. Vaughan Williams EM. A classification of antiarrhythmic actions reassessed after a decade of new drugs. J Clin Pharmacol 1984;24: 129-147.
8. Prystowsky EN, Benson DW Jr, Fuster V, et al. Management of patients with atrial fibrillation. A Statement for Healthcare Professionals. From the Subcommittee on Electrocardiography and Electrophysiology, American Heart Association. Circulation 1996; 93(6):1262-1277.
9. Segal JB, McNamara RL, Miller MR, et al. The evidence regarding the drugs used for ventricular rate control. J Fam Pract 2000;49(1): 47-59.
10. Fulton S, Jackimczyk KC. Antidysrhythmics. Emergent. Emerg Med Clin North Am 2000;18(4):655-669.
11. Wattanasuwan N, Khan IA, Mehta NJ, et al. Acute ventricular rate control in atrial fibrillation: IV combination of diltiazem and digoxin vs. IV diltiazem alone. Chest 2001;119(2):502-506.
12. Schimpf R, Omran H, Jung W, et al. Hemodynamic and cardiorespiratory function following internal atrial defibrillation for chronic atrial fibrillation. Am J Cardiol 1999;83(12):1633-1637.
13. Levy S, Maarek M, Coumel P, et al. Characterization of different subsets of atrial fibrillation in general practice in France: The ALFA study. The College of French Cardiologists. Circulation 1999; 99(23):3028-3035.
14. Diller PM, Smucker DR. Cardiovascular disease: Management of heart failure. Primary Care: Clinics in Office Practice 2000;27(3): 651-675.
15. Laupacis AA, Albers G, Dunn M, et al. Antithrombotic therapy in atrial fibrillation. Chest 1992;102(suppl 4):426S-433S.
16. Manning WJ, Silverman DI, Keighley CS, et al. Transesophageal echocardiography facilitated early cardioversion from atrial fibrillation using short-term anticoagulation: Final results of a prospective 4.5-year study. J Am Coll Cardiol 1995;25:1354-1361.
17. Salerno DM, Anderson B., Sharkey PJ, et al. Intravenous verapamil for treatment of multifocal atrial tachycardia with and without calcium pretreatment. Ann Intern Med. 1987;107(5):223-228.
18. Cox JL, Canavan TE, Schuessler RB, et al. The surgical treatment of atrial fibrillation II. Intraoperative electrophysiologic mapping and description of the electrophysiologic basis of atrial flutter and atrial fibrillation. J Thorac Cardiovasc Surg 1991;101:406-426.
19. Andrikopoulos GK, Dilaveris PE, Richter DJ, et al. Increased variance of P wave duration on the electrocardiogram distinguishes patients with idiopathic paroxysmal atrial fibrillation. Pacing Clin Electrophysiol 2000;23(7):1127-1132.
20. Lesh MD, Kalman JM, Karch MR, Use of intracardiac echocardiography during electrophysiologic evaluation and therapy of atrial arrhythmias. J Cardiovasc Electrophysiol 1998;9(8 Suppl):S40-S47.
21. de Paola AA, Veloso HH. Efficacy and safety of sotalol versus quinidine for the maintenance of sinus rhythm after conversion of atrial fibrillation. SOCESP Investigators. The Cardiology Society of São Paulo. Am J Cardiol 1999;84(9):1033-1037.
22. Lown B, Amarasingham R, Neuman J. New method for terminating cardiac arrhythmias use of synchronized capacitor discharge. JAMA 1962;182:548-555.
23. Van Gelder IC, Crijns HJ, van Gilst WH, et al. Prediction of uneventful cardioversion and maintenance of sinus rhythm from direct-current electrical cardioversion of chronic atrial fibrillation and flutter. Am J Cardiol 1991;68:41-46.
24. Wijffels MC, Kirchhof CJ, Dorland R, et al. Atrial fibrillation begets atrial fibrillation: A study in awake chronically instrumented goats. Circulation 1995;92:1954-1968.
25. Burdick W. Chapter 10: Carotid Sinus Massage and Cardioversion. In: Roberts: Clinical Procedures in Emergency Medicine, 3rd ed. Philadelphia: WB Saunders; 1998:173-185.
26. Saliba W, Juratli N, Chung MK, et al. Higher energy synchronized external direct current cardioversion for refractory atrial fibrillation. J Am Coll Cardiol 1999;34(7):2031-2034.
27. Oral H, Souza JJ, Michaud GF, et al. Facilitating transthoracic cardioversion of atrial fibrillation with ibutilide pretreatment. N Engl J Med 1999;340(24):1849-1854.
28. Zaqqa M, Afshar H, Rasekh A, et al. Predictors of conversion to sinus rhythm using ibutilide for atrial fibrillation or flutter. Am J Cardiol 2000;85(1):112-114.
29. Reiffel JA. Drug choices in the treatment of atrial fibrillation. Am J Cardiol 2000;85(10A):12D-19D.
30. Wang HE, O’Connor RE, Megargel RE, et al. The use of diltiazem for treating rapid atrial fibrillation in the out-of-hospital setting. Ann Emerg Med 2001;37(1):38-45.
31. Kassotis J, Costeas C, Blitzer M, et al. Rhythm management in atrial fibrillation—With a primary emphasis on pharmacological therapy: Part 3. PACE 1998;21:1133-1142.
32. Stambler BS, Wood MA, Ellenbogen KA, et al. Efficacy and safety of repeated intravenous doses of ibutilide for rapid conversion of atrial flutter or fibrillation. Circulation 1996;94:1613-1621.
33. Ellenbogen KA, Stambler BS, Wood MA, et al. Efficacy of intravenous ibutilide for rapid termination of atrial fibrillation and atrial flutter: A dose-response study. J Am Coll Cardiol 1996;28(1):130-136.
34. Domanovits H, Schillinger M, Thoennissen J, et al. Termination of recent-onset atrial fibrillation/flutter in the emergency department: A sequential approach with intravenous ibutilide and external electrical cardioversion. Resuscitation 2000;45(3):181-187.
35. McClellan KJ, Markham A. Dofetilide: A review of its use in atrial fibrillation and atrial flutter. Drugs 1999;58(6):1043-1059.
36. Capucci A, Villani GQ, Aschieri D, at al. Effects of Class III drugs on atrial fibrillation. J Cardiovasc Electrophysiol 1998;9(8 Suppl): S109-S120.
37. Bianconi L, Castro A, Dinelli M, et al. Comparison of intravenously administered dofetilide versus amiodarone in the acute termination of atrial fibrillation and flutter. A multicentre, randomized, double-blind, placebo-controlled study. Eur Heart J 2000;21(15):1265-1273.
38. Torp-Pedersen C, Brendorp B, Kober L. Dofetilide: A class III anti-arrhythmic drug for the treatment of atrial fibrillation. Expert Opinion on Investigational Drugs 2000;9(11):2695-2704.
39. Peuhkurinen K, Niemela M, Ylitalo A, et al. Effectiveness of amiodarone as a single oral dose for recent-onset atrial fibrillation. Am J Cardiol 2000;85(4):462-465.
40. Cotter G, Blatt A, Kaluski E, et al. Conversion of recent onset paroxysmal atrial fibrillation to normal sinus rhythm: The effect of no treatment and high-dose amiodarone. A randomized, placebo-controlled study. Eur Heart J 1999;20(24):1833-1842.
41. Kreiss Y, Sidi Y, Gur H. Efficacy and safety of intravenous amiodarone in recent-onset atrial fibrillation: Experience in patients admitted to a general internal medicine department. Postgrad Med J 1999;75(883):278-281.
42. Peters FP, Braat SH, Heymeriks J, et al. Treatment of recent onset atrial fibrillation with intravenous sotalol and/or flecainide. Netherlands Journal of Medicine 1998;53(3):93-96.
43. Yesil M, Bayata S, Postaci N, et al. Cardioversion with sotalol in selected patients with vagally and adrenergically mediated paroxysmal atrial fibrillation. Angiology 1999;50(9):729-733.
44. Chung MK, Schweikert RA, Wilkoff BL, et al. Is hospital admission for initiation of antiarrhythmic therapy with sotalol for atrial arrhythmias required? Yield of in-hospital monitoring and prediction of risk for significant arrhythmia complications. J Am Coll Cardiol 1998;32(1):169-176.
45. Mattioli AV, Lucchi GR, Vivoli D, et al. Propafenone versus procainamide for conversion of atrial fibrillation to sinus rhythm. Clin Cardiol 1998;21(10):763-766.
46. Kishikawa T, Maruyama T, Kaji Y, et al. Effects of oral repetitive loading of disopyramide on acute-onset atrial fibrillation with concurrent monitoring of serum drug concentration. Int J Cardiol 1998;68(1):57-62.
47. Lampert R, Ezekowitz MD. Heart failure in the elderly: Management of arrhythmias. Clin Geriatr Med 2000;16(3):593-618.
48. Crozier IG, Ikram H, Kenealy M, et al. Flecainide acetate for conversion of acute supraventricular tachycardia to sinus rhythm. Am J Cardiol 1987;59:607-609.
49. Crijns HJ, Wijk van LM, van Gilst WH, et al. Acute conversion of atrial fibrillation to sinus rhythm: Clinical efficacy of flecainide acetate. Comparison of two regimes. Eur Heart J 1988;9:634-638.
50. Suttorp MJ, Kingma JH, Lie-A-Huen L, et al. Intravenous flecainide versus verapamil for acute conversion of paroxysmal atrial fibrillation or flutter to sinus rhythm. Am J Cardiol 1989;63:693-696.
51. Suttorp MJ, Kingma HJ, Jessurun ER, et al. The value of class IC antiarrhythmic drugs for acute conversion of paroxysmal atrial fibrillation or flutter to sinus rhythm. J Am Coll Cardiol 1990;16: 1722-1727.
52. Alp NJ, Bell JA, Shahi M. Randomised double-blind trial of oral versus intravenous flecainide for the cardioversion of acute atrial fibrillation. Heart 2000;84(1):37-40.
53. Sage JI, Van Uitert RL. Risk of recurrent sroke in patients with atrial fibrillation and non-valvular heart disease. Stroke 1983;14:537-540.
54. Bjerkelund CJ, Orning OM. The efficacy of anticoagulants therapy in preventing embolism related to DC cardioversion of atrial fibrillation. Am J Cardiol 1969;23:208-215.
55. Silverman DI, Manning WJ. Role of echocardiography in patients undergoing elective cardioversion of atrial fibrillation. Circulation 1998;98:479-486.
56. Weigner M, Caulfield T, Canias P, et al. Risk of clinical thromboembolism associated with cardioversion to sinus rhythm in patients with atrial fibrillation lasting less than 48 hours. Ann Intern Med 1997;126:615-620.
57. Upshaw CB Jr. Hemodynamic changes after cardioversion of chronic atrial fibrillation. Arch Intern Med 1997;157:1070-1076.
58. Greaves K, Crake T. Cardiac troponin T does not increase after electrical cardioversion for atrial fibrillation or atrial flutter. Heart 1998;80(3):226-228.
59. Falk RH. Atrial Fibrillation. In: Rakel RE, Bope ET, eds. Conn’s Current Therapy: Latest Approved Methods of Treatment for the Practicing Physician. Philadelphia: WB Saunders Co.; 2001:279.
60. The Stroke Prevention in Atrial Fibrillation Investigators. Stroke Prevention in Atrial Fibrillation Study: Final results. Circulation 1991;84:527-S39.
61. Miller VT, Pierce LA, Feinberg WM, et al. For the Stroke Prevention in Atrial Fibrillation Investigators. Differential aspects of aspirin vs. warfarin on clinical stroke types in patients with atrial fibrillation. Neurology 1996;46:238-240.
62. Stroke Prevention in Atrial Fibrillation Investigators. A different effect of aspirin for prevention of stroke in atrial fibrillation. Journal of Stroke and Cerebral Vascular Diseases 1993;3:181-188.
63. Koudstaal PJ, Koudstaal A. Secondary stroke prevention in atrial fibrillation: Indications, risks, and benefits. J Thromb Thrombolysis 1999;7(1):61-65.
64. Albers GW, Amarenco P, Easton JD, et al. Antithrombotic and thrombolytic therapy for ischemic stroke. Chest 2001;119 (1 Suppl):300S-320S.
65. Atrial Fibrillation Investigators. Risk factors for stroke and efficacy of antithrombotic therapy in atrial fibrillation. Arch Intern Med 1994;154:1449-1457.
66. McBride R, Chesebro JH, Wiebers DO, et al. Warfarin versus aspirin for prevention of thromboembolism in atrial fibrillation: Stroke Prevention in Atrial Fibrillation II Study. Lancet 1994; 343:687-691.
67. Laupacis A, Albers G, Dalen JE, et al. Antithrombotic therapy in atrial fibrillation. Chest 1998;114:Suppl:579S-589S.
68. Coumel P. Neurogenic and humoral influences of the autonomic nervous system in the determination of paroxysmal atrial fibrillation. In: Atteul P, at al, eds. The Atrium in Health and Disease. Mount Kisco, NY: Futura Publishing Co; 1989:213-232.
69. Ringel MD. Management of hypothyroidism and hyperthyroidism in the intensive care unit. Crit Care Clin 2001;17(1):59-74.
70 . Cardiac Arrhythmia Suppression Trial (CAST) Investigators. Preliminary report: Effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction. N Engl J Med 1989;321:406-412.
71. Julian DG, Prescott RJ, Jackson FS, et al. Controlled trial of sotalol for one year after myocardial infarction. Lancet 1982;1:1142-1147.
72 . Deedwania PC, Singh BN, Ellenbogen K, et al. Spontaneous conversion and maintenance of sinus rhythm by amiodarone in patients with heart failure and atrial fibrillation: Observations from the veterans affairs congestive heart failure survival trial of antiarrhythmic therapy (CHF-STAT). The Department of Veterans Affairs CHF-STAT Investigators. Circulation 1998;98(23):2574-2579.
73. Torp-Pedersen C, Moller M, Bloch-Thomsen PE, et al. Dofetilide in patients with congestive heart failure and left ventricular dysfunction. Danish Investigations of Arrhythmia and Mortality on Dofetilide Study Group. N Engl J Med 1999;341(12):857-865.
74. Murray RD. Potential clinical efficacy and cost benefit of a transesophageal echocardiography-guided low-molecular-weight heparin (enoxaparin) approach to antithrombotic therapy in patients undergoing immediate cardioversion the atrial fibrillation. J Am Soc Echocardiogr 2001;14(3):200-208.
75. Camm AJ. Atrial fibrillation: Is there a role for low-molecular-weight heparin? Clin Cardiol 2001;24(3 suppl):I15-I19.
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