WORKUP	Section 5 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography

Lab Studies:

• The history and physical examination findings guide laboratory studies. Asymptomatic hyperthyroidism, especially in elderly patients, can manifest with atrial fibrillation or flutter; therefore, obtain thyroid function tests. Hyperthyroidism is a rare cause of atrial flutter and should be excluded with blood testing.

Imaging Studies:

• Transthoracic echocardiography can be useful when evaluating underlying cardiac function. In addition, structural abnormalities, evidence of coronary artery disease, LV function, pericardial fluid, or evidence of LV thrombus can be sought.

• If immediate cardioversion is considered, TEE may be useful to help exclude thrombus from the left atrium or appendage.

Other Tests:

• Electrocardiography

• The common form of type I atrial flutter has sawtooth flutter (F) waves, best seen in leads II, III, and aVF, with atrial rates of 240-340 bpm and without an isoelectric interval between these F waves.

• The ventricular response may be regular or irregular.

• The ventricular rate is a fixed mathematical relationship of flutter waves and the resulting QRS complexes.

• Variable AV conduction can also be seen (commonly present with 2:1 or 3:1 AV conduction). With 1:1 AV conduction, hemodynamic collapse may occur.

• Morphology of the flutter wave can predict findings in the electrophysiology laboratory. A negative flutter wave in the inferior limb leads and a positive flutter wave in V₁ are highly predictive of a counterclockwise circuit; however, with positive flutter waves in the inferior limb leads and negative flutter waves in V₁, differentiating between clockwise type I atrial flutter and atypical forms of non–isthmus-dependent intra-atrial reentry is difficult.

Procedures:

• Catheter ablation

• Type I atrial flutter is a well-defined electroanatomic circuit and is amenable to cure with catheter ablation.

• Type II flutter is potentially curable with catheter-based techniques; however, this is more challenging.

• Catheter ablation represents a chance for long-term cure and must be weighed against other treatment options (long-term antiarrhythmic agents and anticoagulation).

• Consult with a cardiac electrophysiologist about this procedure.

• With current techniques, patients with Type I atrial flutter should expect a high rate of cure with catheter ablation.

• Cardioversion

• The timing of cardioversion depends on the hemodynamic need for sinus rhythm.

• Patients with chronic atrial flutter benefit from anticoagulation in the same manner as patients with atrial fibrillation.

	TREATMENT	Section 6 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography

Medical Care: General goals for the treatment of symptomatic atrial flutter are similar to those for atrial fibrillation and include (1) control of the ventricular rate, (2) termination of sustained episodes, (3) prevention and decreased frequency or duration of recurrent episodes, (4) prevention of thromboembolic complications, and (5) minimization of adverse effects from therapy. However, these goals can be modified for each patient. In an acute setting with pending hemodynamic collapse, follow the adult advanced cardiac life support algorithms for managing atrial fibrillation and flutter. Consider immediate electrical cardioversion for patients who are hemodynamically unstable.

• Ventricular rate control: Ventricular rate control is a priority because it may alleviate symptoms. Rate control is typically more difficult for atrial flutter than for atrial fibrillation.
  • Calcium channel blockers and beta-blockers
    • Ventricular rate control can be achieved with drugs that block the AV node. Intravenous calcium channel blockers (eg, verapamil, diltiazem) or beta-blockers can be used, followed by initiation of oral agents.

    • Hypotension and negative inotropic effects are concerns with the use of these medications.

    • A history of Wolff-Parkinson-White syndrome or evidence of ventricular preexcitation should be determined because agents that act exclusively at the level of the AV node may enhance accessory pathway conduction.

  • Vagal maneuvers: These can be helpful in determining the underlying atrial rhythm if flutter waves are not seen well.

  • Intravenous adenosine: This drug, administered as an intravenous push followed with an intravenous bolus with flush, can also be helpful in making the diagnosis of atrial flutter by transiently blocking the AV node.

• Termination of sustained episodes: After determining the patient's needs for anticoagulation and ventricular rate control, the issue of restoration of the sinus rhythm can be safely addressed.
  • Electrical cardioversion
    • The success rate of electrical cardioversion is higher than 95%.

    • Factors to consider include synchronization of shocks to R waves, adequate sedation, and electrode position (apex anterior, apex posterior, anteroposterior).

    • Atrial flutter generally requires less energy for conversion than atrial fibrillation, and as few as 50 joules may be necessary.

    • If cardioversion is not successful with one electrode configuration, switching may improve success. A second set of electrodes can be used with tandem or simultaneous shocks.

    • Biphasic external waveform may be more effective in restoring sinus rhythm.

    • A few points to remember about the cardioversion technique include a wide electrode separation in the anteroapex position, the application of pressure on paddles or electrodes to reduce thoracic impedance, and the placement of electrode patches under or lateral to the breasts in women.

  • Pharmacological cardioversion
    • Procainamide is effective for converting atrial flutter to sinus rhythm in 0-13% of patients.

    • Flecainide is effective in approximately 10% of patients.

    • Dofetilide is effective in 70-80% of patients.

    • Ibutilide is effective, converting recent-onset atrial flutter to sinus rhythm in 63% of patients with a single infusion.

    • Large single oral doses of type IC antiarrhythmic agents, such as propafenone (450-600 mg) or flecainide (200-300 mg), have also been shown to be effective in converting recent-onset atrial fibrillation to sinus rhythm. Their use in atrial flutter can be assumed to have at least equal success.

    • Oral amiodarone during the loading period (>1 mo) converted 18% of atrial fibrillations or flutters to normal sinus rhythms. Intravenous amiodarone is also effective in converting atrial flutter to sinus rhythm and in slowing the ventricular rate in patients with a rapid ventricular response.

  • Atrial overdrive pacing: This procedure can be performed invasively or through the use of a transesophageal electrode to pace the left atrium, with a success rate of approximately 50%.

  • Combination of the above treatments: Antiarrhythmic medication prior to electrical cardioversion or rapid atrial pacing has been shown to improve the rate of conversion to sinus rhythm.

  • Radiofrequency ablation: This treatment modality is not usually used in the acute setting.

• Prevention (decrease frequency or duration of recurrence episodes): After the initial episode is terminated and the underlying disease is treated, the patient may not need any further intervention except avoidance of the precipitating factor (eg, alcohol, caffeine). For atrial fibrillation, approximately 30% of patients remain in sinus rhythm at 1 year without antiarrhythmic therapy.
  • Antiarrhythmic agents
    • For more information on the use of antiarrhythmic agents, see Atrial Fibrillation. Data on the use of antiarrhythmic agents specifically for atrial flutter are limited. Most studies of antiarrhythmics agents and atrial fibrillation include some patients with atrial flutter (10-20%).

    • In general, the use of antiarrhythmic drugs in atrial flutter is similar to that of atrial fibrillation; however, with a high success rate and low complication rate, the use of radiofrequency ablation in atrial flutter makes this procedure a favorable option compared with lifelong antiarrhythmic drug therapy because fatal proarrhythmic events (even in healthy hearts) and organ toxicity may occur.

    • In general, antiarrhythmics used to treat atrial fibrillation have been shown effective in fibrillation or flutter during a 6- to 12-month follow-up. Considering the characteristic adverse effects of each antiarrhythmic agent, some guidelines are available regarding the choice of medication when taking into account the underlying cardiac pathology.

    • For patients without structural heart disease, class IC agents can be used safely.

    • For patients with LV hypertrophy without ischemia or conduction delay, class III agents, specifically sotalol, can be used.

    • For patients with an ischemic heart, sotalol or amiodarone can be used. Avoid class IC agents.

    • For patients with significant systolic dysfunction, amiodarone can be used, dofetilide may be used, and class IC agents should be avoided.

  • Radiofrequency ablation
    • Ablation or modification of the AV node with radiofrequency ablation and pacemaker implantation is a rarely used option and is only used when the arrhythmia is not suitable for curative ablation and other options have been exhausted.

    • For patients with recurrent symptomatic atrial flutter that is proven to be isthmus-dependent in the electrophysiologic laboratory, expect a success rate of higher than 90% with current technology.

  • Surgery: In patients who have atrial flutter and need cardiac surgery, modification of the atrial incision and creation of a cryothermal lesion, similar to the lesion created during radiofrequency catheter ablation, can be curative for atrial flutter and may prevent an incisional reentrant arrhythmia.

• Prevention of complications
  • Thromboembolic
    • Patients with atrial flutter are at increased risk of thromboembolic complications compared with the general population. Most clinicians anticoagulate patients with atrial flutter as they would patients with atrial fibrillation. Thus, use the same anticoagulation strategy used in patients with atrial fibrillation.

    • Unlike atrial fibrillation, atrial flutter has a regular pattern of atrial contraction. TEE data have demonstrated an organized sawtooth pattern of the left atrial appendage flow with alternating filling and emptying wavelets. No difference in the left atrial appendage function is observed compared with patients in sinus rhythm. Patients with both atrial flutter and atrial fibrillation have significantly decreased left atrial appendage function, more spontaneous echo contrast, and larger left atria and accompanying appendages.

    • Patients with atrial flutter and episodes of atrial fibrillation are at higher risk of thromboembolic events; however, determining whether episodes of atrial fibrillation are associated with episodes of atrial flutter is difficult.

    • A large retrospective review of patients in chronic atrial flutter revealed a 14% occurrence rate of thromboembolic events over 4.5 years, with half of these events being ischemic stroke. In another large cohort of patients with atrial flutter, the occurrence rate of embolic complications in patients with chronic or recurrent atrial flutter was 12%. For stroke, this risk is estimated at approximately one third of patients with nonrheumatic atrial fibrillation. Males with hypertension, structural heart disease, LV dysfunction, and diabetes may be at higher risk of thromboembolic complications. Interestingly, associated atrial fibrillation did not significantly increase the risk of the embolic complications.

    • Other reports have demonstrated thrombus in the left atrium appendage of patients with atrial flutter (as many as 43%). Most studies of non–anticoagulated patients with atrial flutter report a rate of 10-15% for patients with thrombus in the left atrium or left atrial appendage. Spontaneous echo contrast associated with increased risk of thromboembolism was found in 6-43% of patients with atrial flutter.

    • Postcardioversion thromboembolic events can complicate as many as 7.3% of procedures in patients who are not anticoagulated. These events occur within 3 days after the cardioversion; almost all occur within 10 days after the cardioversion.

    • In atrial fibrillation, postcardioversion stunning of the left atrial appendage is thought to contribute to thrombogenicity. This phenomenon may last as long as 4 weeks in patients with atrial fibrillation and may be related to how long patients have been in arrhythmia.

    • Stunning of the left atrial appendage also occurs following conversion from atrial flutter to sinus rhythm (electrical or spontaneous), although to a lesser degree. Left atrial and left atrial appendage function decrease immediately after conversion, and, in one study, spontaneous echo contrast was noted to develop within 5 minutes after conversion in 43% of patients. This is thought to be the source of emboli in patients whose TEE findings revealed no evidence of thrombus but who had a thromboembolic event after cardioversion.

    • In a study comparing left atrial appendage function before and after catheter ablation (immediate, 1 d, 1 wk, and 6 wk) of persistent atrial flutter, a significant increase in atrial standstill, decrease in left atrial appendage function, and new spontaneous echo contrast occurred after ablation. One patient formed a new left atrial appendage thrombus after ablation. Evidence of atrial stunning significantly improved after 1 week. Anticoagulation for at least 1 week is advocated after ablation of an atrial flutter that persists for more than 2 days.

    • Adequate anticoagulation, as recommend by the American College of Chest Physicians, has been shown to decrease thromboembolic complications in patients with chronic atrial flutter and in patients undergoing cardioversion.

  • Cardiomyopathy: Termination of long-standing atrial flutter with a rapid ventricular response has been reported to improve LV systolic function in patients without other known causes of dilated cardiomyopathy.

• Minimizing adverse effects of antiarrhythmic therapy: Because atrial flutter is a nonfatal arrhythmia, carefully assess the risks and benefits of drug therapy, especially with antiarrhythmic agents. A few points to remember that will help minimize the adverse effects include the following:
  • Avoidance of precipitating factor(s) or therapy of the underlying problem may be all that is needed to prevent recurrent episodes.

  • For patients with rare recurrence, cardioversion or medical, electrical, or rapid atrial pacing may be adequate.

  • Of antiarrhythmic agents, amiodarone is effective and is associated with a low proarrhythmic risk but may adversely affect multiple organs, including the skin, liver, lungs, and thyroid. Thus, sotalol would seem a reasonable choice of antiarrhythmic drug therapy for atrial flutter.

  • Radiofrequency ablation may be a preferred therapeutic choice. Although many patients who were treated with radiofrequency ablation subsequently developed atrial fibrillation after long-term follow-up (56% in one study), this procedure still represents a safe alternative to antiarrhythmic agents.

• Structural heart disease prior to atrial fibrillation and inducible atrial fibrillation after ablation predict a high risk of developing atrial fibrillation after successful atrial flutter ablation; however, successful atrial flutter ablation has been shown to eliminate or reduce the frequency of atrial fibrillation episodes.
  • Catheter ablation has been shown to significantly improve the quality of life in patients with atrial flutter.

  • The frequency of hospital admissions and emergency department visits and the number of antiarrhythmic drugs administered are decreased significantly after ablation.

  • Activity capacity significantly improves in patients with preexisting LV dysfunction.

  • In general, when atrial flutter persists for more than 48 hours, 4 weeks of adequate anticoagulation or TEE is needed before attempting cardioversion to sinus rhythm.

  • Thromboembolic complications occur spontaneously after cardioversion or ablation, and postconversion anticoagulation is recommended for a minimum of 4 weeks.

  • Use long-term anticoagulation for patients with persistent or paroxysmal atrial flutter. As with atrial fibrillation, keep the international normalized ratio (INR) at 2-3 to optimize the therapeutic effect and minimize the risk of bleeding.

Consultations: In general, consult a cardiologist and/or electrophysiologist because the use of antiarrhythmic drugs may be harmful and radiofrequency ablation may eliminate atrial flutter.

Diet: Any dietary recommendations should be appropriate for the underlying heart disease and other comorbidities (eg, diabetes).

	MEDICATION	Section 7 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography

Medications play a major role in the therapy of atrial flutter. Agents can be used to control the ventricular rate, terminate acute episodes, prevent or decrease the frequency or duration of recurrent episodes, and prevent complications. Various categories of drugs are used to treat atrial flutter. Drug initiation in an outpatient setting is generally accepted in patients without underlying structural heart disease who are in sinus rhythm. In addition, many specialists initiate outpatient drug therapy in patients with therapeutically anticoagulated atrial flutter who are awaiting outpatient electrical cardioversion in the near future. Regardless, close patient follow-up is mandated, with frequent ECG monitoring or transtelephonic monitoring for potential signs of proarrhythmia.

Drug Category: Atrioventricular nodal conduction blockers -- Used to slow ventricular response by slowing AV nodal conduction during atrial fibrillation or flutter. Also indicated for use in conjunction with class IA and IC antiarrhythmics, which slow atrial fibrillation/flutter rate and may cause more rapid ventricular response.

Drug Name	Propranolol (Inderal) -- Class II antiarrhythmic, nonselective, beta-adrenergic receptor blocker with membrane-stabilizing activity that decreases automaticity of contractions.
Adult Dose	1-3 mg (under careful monitoring) IV; not to exceed 1 mg/min to avoid lowering blood pressure and causing cardiac standstill Allow time for drug to reach site of action (particularly if slow circulation); administer second dose after 2 min prn; thereafter, do not administer additional drug in <4 h Do not continue doses after desired alteration in rate or rhythm achieved; switch to 10-160 mg PO bid
Pediatric Dose	2-4 mg/kg/d PO divided bid (1-2 mg/kg bid) IV use not recommended; however, for arrhythmias, 0.01-0.1 mg/kg, not to exceed 1 mg/dose, by slow push has been recommended; change to PO as soon as possible
Contraindications	Documented hypersensitivity; uncompensated congestive heart failure; bradycardia, cardiogenic shock; AV conduction abnormalities
Interactions	Coadministration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; withdraw drug slowly and monitor patient closely

Drug Name	Metoprolol (Lopressor) -- Selective beta1-adrenergic receptor blocker that decreases automaticity of contractions. During IV administration, carefully monitor BP, heart rate, and ECG.
Adult Dose	5 mg IV for 3 doses q2-5min; then up to 200 mg PO bid
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity, uncompensated congestive heart failure, bradycardia, asthma, cardiogenic shock, AV conduction abnormalities
Interactions	Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effects; toxicity may increase with coadministration of sparfloxacin, phenothiazines, astemizole (recalled from US market), calcium channel blockers, quinidine, flecainide, and contraceptives; may increase toxicity of digoxin, flecainide, clonidine, epinephrine, nifedipine, prazosin, verapamil, and lidocaine
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Beta-adrenergic blockade may reduce signs and symptoms of acute hypoglycemia and may decrease clinical signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; monitor patient closely and withdraw drug slowly; during IV administration, carefully monitor BP, heart rate, and ECG

Drug Name	Atenolol (Tenormin) -- Selectively blocks beta-1 receptors with little or no effect on beta-2 receptors.
Adult Dose	Up to 200 mg PO qd in divided doses (ie, 100 mg bid)
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity, congestive heart failure, pulmonary edema, cardiogenic shock, AV conduction abnormalities, and heart block (without a pacemaker)
Interactions	Coadministration with aluminum salts, barbiturates, calcium salts, cholestyramine, NSAIDs, penicillins, and rifampin may decrease effects; haloperidol, hydralazine, loop diuretics, and MAOIs may increase toxicity
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Beta-adrenergic blockade may reduce symptoms of acute hypoglycemia and mask signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism and cause thyroid storm; monitor patients closely and withdraw drug slowly; during IV administration, carefully monitor BP, heart rate, and ECG

Drug Name	Esmolol (Brevibloc) -- Excellent for use in patients at risk for experiencing complications from beta-blockade, particularly those with reactive airway disease, mild-to-moderate LV dysfunction, and/or peripheral vascular disease. Short half-life of 8 min allows titration to desired effect and quick discontinuation if needed.
Adult Dose	250-500 mcg/kg/min IV for 1 min loading dose followed by a 4-min maintenance infusion of 50 mcg/kg/min If adequate therapeutic effect not observed within 5 min, repeat loading dose and follow with maintenance infusion using increments of 50 mcg/kg/min (for 4 min); sequence may be repeated up to 4 times prn As desired heart rate is approached, omit loading infusion and reduce incremental dose of maintenance infusion from 50 mcg/kg/min to 25 mcg/kg/min IV or lower; interval between titration steps may be increased from 5-10 min if needed
Pediatric Dose	Not established; suggested dose is 100-500 mcg/kg IV administered over 1 min
Contraindications	Documented hypersensitivity, uncompensated congestive heart failure, bradycardia, cardiogenic shock, and AV conduction abnormalities
Interactions	Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effect; cardiotoxicity may increase when administered concurrently with sparfloxacin, astemizole (recalled from US market), calcium channel blockers, quinidine, flecainide, and contraceptives; toxicity increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Beta-adrenergic blockers may mask signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; symptoms of hyperthyroidism, including thyroid storm, may worsen when medication is abruptly withdrawn; withdraw drug slowly and monitor patient closely

Drug Category: Calcium channel blockers (nondihydropyridine) -- Effective for rate control.

Drug Name	Verapamil (Calan) -- Calcium channel blocker. Only nondihydropyridines are effective for rate control. During depolarization, inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium.
Adult Dose	5-10 mg IV; may repeat after 10 min; drip at 1 mg/min not to exceed 10 mg, then 120-480 mg/d PO
Pediatric Dose	<1 year: 0.1-0.2 mg/kg IV bolus over 2 min; if no response, repeat in 30 min 1-15 years: 0.1-0.3 mg/kg (ie, 2-5 mg) IV bolus over 2 min; single dose not to exceed 5 mg; if no response, repeat in 30 min; not to exceed total dose of 10 mg
Contraindications	Documented hypersensitivity, severe CHF, sick sinus syndrome or second- or third-degree AV block, hypotension (<90 mm Hg systolic)
Interactions	May increase carbamazepine, digoxin, and cyclosporine levels; coadministration with amiodarone can cause bradycardia and a decrease in cardiac output; when administered concurrently with beta-blockers, may increase cardiac depression; cimetidine may increase levels; may increase theophylline levels
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Hepatocellular injury may occur; transient elevations of transaminases with and without concomitant elevations in alkaline phosphatase and bilirubin have occurred (elevations have been transient and may disappear with continued verapamil treatment); monitor liver function periodically

Drug Name	Diltiazem (Cardizem) -- Only nondihydropyridines are effective for rate control. During depolarization, inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium.
Adult Dose	0.25 mg/kg IV over 2 min, then 0.35 mg/kg IV over 2 min, then 5-15 mg/h drip; then switch to 120-360 mg/d PO
Pediatric Dose	0.25 mg/kg IV bolus over 2 min; if necessary, repeat dose of 0.35 mg/kg IV bolus over 2 min, followed by continuous IV infusion of 10 mg/h, then switch to PO
Contraindications	Documented hypersensitivity; severe CHF, sick sinus syndrome, second- or third-degree AV block, hypotension (<90 mm Hg systolic)
Interactions	May increase carbamazepine, digoxin, cyclosporine, and theophylline levels; when administered with amiodarone, may cause bradycardia and a decrease in cardiac output; when administered with beta-blockers, may increase cardiac depression; cimetidine may increase levels
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in impaired renal or hepatic function, may increase LFT levels and hepatic injury may occur

Drug Category: Cardiac glycosides -- AV nodal blocking agents.

Drug Name	Digoxin (Lanoxin) -- Slows sinus node and AV node via vagomimetic effect and not very effective if sympathetic tone is increased. Generally not recommended unless depressed LV function is present.
Adult Dose	Loading dose: 1.5-2 mg PO/IV in divided dose over 1-2 d Maintenance dose: 0.25 mg PO/IV qd
Pediatric Dose	Premature neonates: 15-25 mcg/kg PO/IV divided into 3 or more doses (first dose equalling one half total dose), then remaining doses q6-8h; maintenance of 4-6 mcg/kg/d PO/IV divided bid Neonates: 20-30 mcg/kg PO/IV divided into 3 or more doses (first dose equalling one half total dose), then remaining doses q6-8h; maintenance of 5-8 mcg/kg/d PO/IV divided bid <2 years: 30-50 mcg/kg PO/IV divided into 3 or more doses (first dose equalling one half total dose), then remaining doses q6-8h; maintenance of 7.5-12 mcg/kg/d PO/IV divided bid 2-5 years: 25-35 mcg/kg PO/IV divided into 3 or more doses (first dose equalling one half total dose), then remaining doses q6-8h; maintenance of 6-9 mcg/kg/d PO/IV divided bid 6-10 years: 15-30 mcg/kg PO/IV divided into 3 or more doses (first dose equalling one half total dose), then remaining doses q6-8h; maintenance of 4-8 mcg/kg/d PO/IV divided bid >10 years: 8-12 mcg/kg PO/IV divided into 3 or more doses (first dose equalling one half total dose), then remaining doses q6-8h; maintenance of 2-3 mcg/kg/d PO/IV qd
Contraindications	Documented hypersensitivity, beriberi heart disease, idiopathic hypertrophic subaortic stenosis, constrictive pericarditis, carotid sinus syndrome
Interactions	Medications that may increase levels include alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone, propantheline, quinidine, diltiazem, aminoglycosides, oral amiodarone, anticholinergics, diphenoxylate, erythromycin, felodipine, flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline, tolbutamide, and verapamil Medications that may decrease serum levels include aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, oral colestipol, hydantoins, hypoglycemic agents, antineoplastic treatment combinations (including carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, and procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Hypokalemia may reduce positive inotropic effect of digitalis; IV calcium may produce arrhythmias in digitalized patients; hypercalcemia predisposes patient to digitalis toxicity; hypocalcemia can make digoxin ineffective until serum calcium levels are normal; institute magnesium replacement therapy in patients with hypomagnesemia to prevent digitalis toxicity; patients diagnosed with incomplete AV block may progress to complete block when treated with digoxin; exercise caution in hypothyroidism, hypoxia, and acute myocarditis

Drug Category: Antiarrhythmics -- Alter electrophysiologic mechanisms responsible for arrhythmia. Commonly used to prevent recurrences of atrial flutter. Currently, 5 drugs are approved by FDA for treatment of atrial flutter (ie, quinidine, flecainide, propafenone, sotalol, dofetilide); however, other antiarrhythmic agents are used in an off-label fashion with great clinical efficacy. Use antiarrhythmic agents with great caution because they can contribute to proarrhythmia, exacerbate a preexisting arrhythmia, or provoke a new arrhythmia. Proarrhythmia can be either bradycardic or tachycardic and atrial or ventricular. In addition, adverse effects can cause severe comorbidities and even death. Consultation with a cardiac electrophysiologist or knowledgeable physician is recommended prior to antiarrhythmic drug initiation. Finally, given current hospital constraints and pressure to initiate these agents in outpatient settings, carefully reconsider specific patient populations at low and acceptable risks for outpatient drug initiation.

Drug Name	Quinidine sulfate (Quinidex ER) -- Antiarrhythmic class IA. Maintains normal heart rhythm following cardioversion of atrial fibrillation or flutter. Depresses myocardial excitability and conduction velocity. Prior to administration, control ventricular rate and CHF (if present) with digoxin or calcium channel blockers. Concomitantly treat all patients treated with class IA agents with AV nodal blocking agents.
Adult Dose	300 mg PO q8-12h
Pediatric Dose	IR tab: 20-60 mg/kg/d (900 g/m2/d) PO divided doses q6h
Contraindications	Documented hypersensitivity; complete AV block or intraventricular conduction defects, patients presently taking ritonavir or sparfloxacin; prior thrombocytopenic purpura during administration
Interactions	Phenytoin, rifampin, and phenobarbital may decrease concentrations; toxicity increased when taken with ritonavir, sparfloxacin, beta-blockers, amiodarone, verapamil, cimetidine, alkalinizing agents, or nondepolarizing and depolarizing muscle relaxants; may enhance effect of anticoagulants
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in G-6-PD deficiency and patients with tendency to develop granulocytopenia; avoid use in myocardial depression, hepatic or renal insufficiency, and myasthenia gravis

Drug Name	Procainamide (Pronestyl) -- Antiarrhythmic class IA. Used for PVCs. Increases refractory period of atria and ventricles. Myocardial excitability reduced by increase in threshold for excitation and inhibition of ectopic pacemaker activity. Available IV and PO, making drug attractive for postoperative use. However, drug is a negative inotropic and must be used with care in patients with depressed LV function or CHF.
Adult Dose	1000-2500 mg PO q12h (based on body weight and normal renal function); alternatively, up to 18 mg/kg IV infusion over 1 h
Pediatric Dose	Not established; suggested dose 15-50 mg/kg/d PO divided q3-6h, not to exceed 4 g/d; alternatively, 3-6 mg/kg/dose IV infused over 5 min or 20-30 mg/kg/d IM divided q4-6h, not to exceed 4 g/d Maintenance: 20-80 mcg/kg/min IV administered as continuous infusion; not to exceed 100 mg/dose or 2 g/d
Contraindications	Documented hypersensitivity; patients diagnosed with complete heart block or second- or third-degree heart block, if a pacemaker is not in place; torsade de pointes; systemic lupus erythematosus
Interactions	Expect increased levels of procainamide metabolite NAPA in patients taking cimetidine, ranitidine, beta-blockers, amiodarone, trimethoprim, and quinidine; may increase effect of skeletal muscle relaxants (eg, quinidine, lidocaine) and neuromuscular blockers; ofloxacin inhibits tubular secretion of procainamide and may increase bioavailability; when taken concurrently with sparfloxacin, may increase risk of cardiotoxicity
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Monitor for hypotension; plasma concentrations and active metabolite, NAPA, may increase in renal failure; high or toxic concentrations may induce AV block or abnormal automaticity; caution in complete AV block, digitalis intoxication, organic heart disease, renal disease, and hepatic insufficiency; agranulocytosis reported at a rate of 0.5% with a 20-25% mortality; weekly CBC counts recommended for first 3 mo and regularly thereafter

Drug Name	Disopyramide (Norpace) -- Antiarrhythmic class IA. Strong negative inotropic agent with adverse anticholinergic effects. Generally not used often and can precipitate cardiogenic shock in patients with CHF and depressed LV function.
Adult Dose	150 mg PO q6h; not to exceed 1600 mg/d
Pediatric Dose	1-12 years: 6-20 mg/kg/d PO divided q6h
Contraindications	Documented hypersensitivity, history of complete heart block, sick sinus syndrome, cardiogenic shock
Interactions	Increases digoxin levels
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Metabolized in liver (45%); renally excreted unchanged 40-80%; dose adjustments necessary in liver disease, renal disease, and elderly persons; anticholinergic effects can cause urinary retention and blurred vision

Drug Category: Antiarrhythmics, class IC -- For use in patients with atrial flutter and SVT without structural heart disease. Use in conjunction with AV nodal blocking agents when administered to patients in atrial flutter because conversion to atrial flutter with 1:1 conduction (producing fast ventricular rates) is noted.

Drug Name	Propafenone (Rythmol) -- Treats life-threatening arrhythmias. Possibly works by reducing spontaneous automaticity and prolonging refractory period. Indicated for patients with AF and SVT without structural heart disease. Use in conjunction with AV nodal blocking agents when administered to patients in AF because conversion to AFL with 1:1 conduction (producing fast ventricular rates) is noted.
Adult Dose	150-300 mg PO tid
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity, bronchospastic disorders, conduction disorders, bradycardia, uncontrolled heart failure
Interactions	Decreases serum levels of rifampin; cimetidine, quinidine, warfarin, and beta-blockers may increase serum levels; dose-related increases in serum digoxin levels (35-85%) and effects of warfarin (25%)
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Use only for life-threatening arrhythmias; caution in patients with CHF, myocardial infarction, or hepatic or renal dysfunction

Drug Name	Flecainide (Tambocor) -- Treats life-threatening ventricular arrhythmias. Causes prolongation of refractory periods and decreases action potential without affecting duration. Blocks sodium channels, producing a dose-related decrease in intracardiac conduction in all parts of heart, with greatest effect on the His-Purkinje system (HV conduction). Effects on AV nodal conduction time and intra-atrial conduction times, although present, are less pronounced than on ventricular conduction velocity. Use in conjunction with AV nodal blocking agents when administered to patients in AF because conversion to AFL with 1:1 conduction (producing fast ventricular rates) is noted.
Adult Dose	50-150 mg PO bid
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity, third-degree AV block, myocardial depression
Interactions	Amiodarone, cimetidine, and digoxin may increase plasma concentrations; beta-adrenergic blockers, verapamil, and disopyramide may have additive inotropic effects when coadministered; ritonavir may increase cardiotoxicity
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Known to increase endocardial pacing thresholds; may suppress ventricular escape rhythms; exacerbates sick sinus syndrome and causes sinus pauses or sinus arrest; caution in renal or hepatic impairment

Drug Category: Antiarrhythmics, class III -- Class III drugs widely used in maintenance of sinus rhythm in patients with atrial flutter. Drugs may include amiodarone (Cordarone), sotalol (Betapace), ibutilide (Corvert), and dofetilide (Tikosyn).

Drug Name	Amiodarone (Cordarone), sotalol (Betapace), ibutilide (Corvert) -- dofetilide (Tikosyn) -- May inhibit AV conduction and sinus node function. Prolong action potential and refractory period in myocardium and inhibit adrenergic stimulation. Prior to administration, control ventricular rate and CHF (if present) with digoxin or calcium channel blockers. Alternatively, sotalol class III antiarrhythmic agent, which blocks K+ channels, prolongs action potential duration, and lengthens QT interval. Noncardiac selective beta-adrenergic blocker. Sotalol shown to be effective in maintenance of sinus rhythm, even in patients with underlying structural heart disease. Alternatively, ibutilide newer class III antiarrhythmic agent that may work by increasing action potential duration and thereby changing atrial cycle length variability. Mean time to conversion is 30 min. Two thirds of patients who converted were in sinus rhythm at 24 h. Ventricular arrhythmias occurred in 9.6% of patients and mostly were PVCs. Rate of torsades de pointes was <2%.
Adult Dose	Amiodarone: 400 mg PO tid for 7 d as loading dose, followed by weekly reductions with goal of lowest dose with desired therapeutic benefit; average maintenance dose is 200 mg/d PO Sotalol: 40-80 mg PO bid and increase dose gradually q2-3d to therapeutic goal of 120-160 mg PO bid Dofetilide: 125-500 mcg PO bid, depending on CrCl and QT prolongation Ibutilide <60 kg: 0.01 mg/kg IV over 10 min >60 kg: 1 mg IV over 10 min; second infusion of equal strength can be given 10 min after first prn
Pediatric Dose	Amiodarone: 10-15 mg/kg/d or 600-800 mg/1.73 m2/d PO for 4-14 d or until adequate control of arrhythmia attained Sotalol: Not established Dofetilide: Not established Ibutilide: Not established
Contraindications	Amiodarone: Documented hypersensitivity; complete AV block; intraventricular conduction defects; patients taking ritonavir or sparfloxacin Sotalol: Documented hypersensitivity; sinus bradycardia, second- and third-degree AV block, QT prolongation, renal impairment Dofetilide: Documented hypersensitivity; sinus bradycardia, second- and third-degree AV block, QT prolongation, renal impairment Ibutilide: Documented hypersensitivity, QT prolongation
Interactions	Amiodarone: Increases effects and blood levels of theophylline, quinidine, procainamide, phenytoin, methotrexate, flecainide, digoxin, cyclosporine, beta-blockers, and anticoagulants; cardiotoxicity increased by ritonavir, sparfloxacin, and disopyramide; coadministration with calcium channel blockers may cause additive effect and further decrease myocardial contractility; cimetidine may increase levels Sotalol: Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effect; cardiotoxicity may increase when administered concurrently with sparfloxacin, astemizole (recalled from US market), calcium channel blockers, quinidine, flecainide, and contraceptives; toxicity increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents Dofetilide: do not use concurrently with verapamil, ketoconazole, cimetidine, TMP-SMZ, megestrol, or prochlorperazine Ibutilide: Increases toxicity of quinidine and procainamide; concurrent administration with TCAs, phenothiazines, and astemizole may prolong QT interval; toxicity of digoxin increases when administered concurrently
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Amiodarone: Caution in thyroid or liver disease; rate of pulmonary fibrosis is 3-7% and is dose-related Sotalol: Beta-adrenergic blockade may decrease signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; withdraw drug slowly and monitor patient closely; caution in hypokalemia, peripheral vascular disease, hypomagnesemia, and congestive heart failure Dofetilide: monitor QTc, renal function, electrolytes, and heart rate; reduce dose (or discontinue) with renal dysfunction Ibutilide: Caution in renal or hepatic impairment

Drug Category: Anticoagulants -- Used to prevent thromboembolic complications.

Drug Name	Heparin -- Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not actively lyse but is able to inhibit further thrombogenesis. Prevents reaccumulation of clot after spontaneous fibrinolysis. Most data are related to use of unfractionated heparin. Low–molecular-weight heparin probably as effective but awaits results from clinical studies.
Adult Dose	60 U/kg IV initially, followed by maintenance infusion of 12 U/kg/h IV; target aPTT is 50-70 seconds
Pediatric Dose	50 U/kg IV initially, followed by a maintenance infusion of 15-25 U/kg/h IV; increase dose by 2-4 U/kg/h q6-8h prn, using aPTT results
Contraindications	Documented hypersensitivity, subacute bacterial endocarditis, active bleeding, history of heparin-induced thrombocytopenia
Interactions	Digoxin, nicotine, tetracycline, and antihistamines may decrease effects; NSAIDs, ASA, dextran, dipyridamole, and hydroxychloroquine may increase toxicity
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Bleeding; in neonates, preservative-free heparin is recommended to avoid possible toxicity (gasping syndrome) by benzyl alcohol, which is used as preservative; caution in severe hypotension and shock

Drug Name	Warfarin (Coumadin) -- Interferes with hepatic synthesis of vitamin K–dependent coagulation factors. Used for prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders. Tailor dose to maintain INR of 2-3.
Adult Dose	1-20 mg/d PO qd, adjust dose to desired INR (2-3) for nonvalvular atrial fibrillation/flutter
Pediatric Dose	0.05-0.34 mg/kg/d PO; adjust dose according to weight and desired INR
Contraindications	Documented hypersensitivity; severe liver or kidney disease; open wounds or GI ulcers; pregnancy, although AHA/ACC guidelines for pregnant patients with mechanical valves mention risk of thrombotic mechanical valve may be higher than risk of teratogenicity from warfarin
Interactions	Drugs that may decrease anticoagulant effects include griseofulvin, carbamazepine, glutethimide, estrogens, nafcillin, phenytoin, rifampin, barbiturates, cholestyramine, colestipol, vitamin K, spironolactone, oral contraceptives, and sucralfate Medications that may increase anticoagulant effects include oral antibiotics, phenylbutazone, salicylates, sulfonamides, chloral hydrate, clofibrate, diazoxide, anabolic steroids, ketoconazole, ethacrynic acid, miconazole, nalidixic acid, sulfonylureas, allopurinol, chloramphenicol, cimetidine, disulfiram, metronidazole, phenylbutazone, phenytoin, propoxyphene, sulfonamides, gemfibrozil, acetaminophen, and sulindac
Pregnancy	D - Unsafe in pregnancy
Precautions	Do not switch brands after achieving therapeutic response; caution in active tuberculosis or diabetes; patients with protein C or S deficiency are at risk of developing skin necrosis

	FOLLOW-UP	Section 8 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography

Further Inpatient Care:

• Base the decision to admit a patient with atrial flutter on hemodynamic considerations and the timing of cardioversion to sinus rhythm.

• For atrial flutter of less than 48 hours in duration, attempt cardioversion as soon as possible. Postconversion anticoagulation is usually unnecessary, although data from TEE studies indicate that postconversion anticoagulation a reasonable option.

• For episodes of atrial flutter of uncertain duration or greater than 48 hours, begin anticoagulation therapy. If cardioversion is needed sooner, anticoagulate patients with intravenous heparin and perform TEE as close to the time of cardioversion as possible. Patients still require anticoagulation for at least 4 weeks after cardioversion.

• If thrombus is observed or suspected based on TEE findings, delay cardioversion. Rate control and therapeutic anticoagulation is required for a minimum of 4 weeks.

• Cases have been reported of patients with atrial fibrillation who have experienced either a transient ischemic attack or stroke after cardioversion despite having no evidence of thrombus from the TEE. While atrial flutter is considered less thrombogenic than atrial fibrillation, neurological consequences can result from cardioversion.

• In patients with recurrent episodes of common type I atrial flutter that are not well-tolerated or in patients in whom adverse effects from medical therapy (rate control or antiarrhythmic drugs) have developed, offer electrophysiologic study with an eye toward radiofrequency catheter ablation. Given the high success rate and low complication rate, radiofrequency ablation is superior to medical therapy. The author believes the best plan is to offer radiofrequency ablation before antiarrhythmic medication.

• Consider inpatient initiation of long-term antiarrhythmic drugs, especially for patients with underlying structural heart disease or baseline prolonged QT interval. The risk of proarrhythmia is probably greatest during the first 24-48 hours after the initiation of antiarrhythmics, but lack of proarrhythmia during antiarrhythmic drug loading may yield a false sense of security because proarrhythmia is often not predictable. Pause-dependent torsades de pointes can occur after conversion to sinus rhythm.

Further Outpatient Care:

• Closely monitor the patient's anticoagulation therapy, with a target INR of 2-3. Take special care when additional medications (including antibiotics) are added because they may cause dramatic alterations in INR values.

In/Out Patient Meds:

• Anticoagulant therapy (ie, heparin and/or warfarin) is indicated, especially when the onset of atrial flutter is of more than 48 hours' duration or is uncertain.

• Patients need to maintain a therapeutic INR for 3 weeks prior to conversion and for at least 4 weeks after conversion to sinus rhythm.

• Long-term anticoagulation is recommended for patients with chronic atrial flutter.

• Anticoagulants are used to decrease thromboembolic complications.

• Preferred medications that slow AV node conduction include beta-blockers (eg, atenolol, metoprolol, propranolol) and calcium channel blockers (eg, verapamil, diltiazem).

• These medications are used to control ventricular rates.

• Also use these medications in patients who are taking class IA or IC antiarrhythmic drugs (to prevent rapid ventricular response, which can occur when the atrial rate is slowed).

• Antiarrhythmic drugs are indicated for the termination of acute episodes or the prevention of recurrent episodes.

• For atrial flutter, electrical cardioversion is effective and usually requires less energy than for atrial fibrillation.

• Catheter ablation offers a potential cure and may be safer than long-term use of an antiarrhythmic agent.

Complications:

• The major potential complication with atrial flutter (or atrial fibrillation) is neurologic insult, either transient ischemic attack or stroke. This risk can be minimized with proper anticoagulation. Consider patients with common Type I atrial flutter for catheter ablation to eliminate the need for long-term anticoagulation and antiarrhythmic medications.

Prognosis:

• Atrial flutter itself is not considered a life-threatening arrhythmia; however, uncontrolled ventricular rates can lead to impaired ventricular function. Additionally, patients with Wolff-Parkinson-White syndrome can develop life-threatening ventricular responses. Consider these patients for catheter ablation of their accessory bypass tract. Data from the Framingham study suggest that patients with atrial fibrillation do not live as long as patients without atrial fibrillation (ie, controls). No data are available on atrial flutter.

• The prognosis for patients with Type I atrial flutter who undergo catheter ablation is excellent, with a very low recurrence rate. The picture is not as clear for patients with both atrial flutter and atrial fibrillation. Some reports have documented fewer episodes of atrial fibrillation after successful flutter ablation, while others have not. Atrial fibrillation is thought to possibly be more responsive to antiarrhythmic agents after atrial flutter has been eliminated.

• Numerous reports indicate that patients with atrial fibrillation who are given class IC antiarrhythmic agents may convert to atrial flutter with faster ventricular rates. Thus, patients receiving type IC agents (flecainide) should also receive an AV nodal blocking drug such as a beta-blocker or calcium channel blocker.

Patient Education:

• Patient education regarding medications and diet is important.

• Patients taking warfarin should avoid major changes in their diet unless consulting with their physicians. Recall that warfarin inhibits vitamin K synthesis and that sources of vitamin K are green leafy vegetables. A sudden change to a diet high in vitamin K may increase the requirements for warfarin.

• For excellent patient education resources, visit eMedicine's Heart Center and Stroke Center. Also, see eMedicine's patient education articles Atrial Flutter, Heart Rhythm Disorders, Stroke, Supraventricular Tachycardia, and Palpitations.

	MISCELLANEOUS	Section 9 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography

Medical/Legal Pitfalls:

• Because data suggest that patients with atrial flutter may be at similar risk for neurologic events as patients with atrial fibrillation, considering anticoagulation in this patient population (at least until sinus rhythm is maintained) is a wise decision.

	PICTURES	Section 10 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography

Caption: Picture 1. Twelve-lead ECG of type I atrial flutter. Note negative “sawtooth” pattern of flutter waves in leads II, III, and aVF.
	View Full Size Image
Picture Type: ECG

	BIBLIOGRAPHY	Section 11 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography

• Aliot E, Denjoy I: Comparison of the safety and efficacy of flecainide versus propafenone in hospital out-patients with symptomatic paroxysmal atrial fibrillation/flutter. The Flecainide AF French Study Group [published erratum appears in Am J Cardiol 1996 Jul 1;78(1):1. Am J Cardiol 1996 Jan 25; 77(3): 66A-71A[Medline].
• Anderson JL: Acute treatment of atrial fibrillation and flutter. Am J Cardiol 1996 Oct 17; 78(8A): 17-21[Medline].
• Berger M, Schweitzer P: Timing of thromboembolic events after electrical cardioversion of atrial fibrillation or flutter: a retrospective analysis. Am J Cardiol 1998 Dec 15; 82(12): 1545-7, A8[Medline].
• Camm AJ, Obel OA: Epidemiology and mechanism of atrial fibrillation and atrial flutter. Am J Cardiol 1996 Oct 17; 78(8A): 3-11[Medline].
• Campbell RW: Atrial flutter. Eur Heart J 1998 May; 19 Suppl E: E37-40, E60-3[Medline].
• Chalasani P, Cambre S, Silverman ME: Direct-current cardioversion for the conversion of atrial flutter. Am J Cardiol 1996 Mar 15; 77(8): 658-60[Medline].
• Chang SL, Tai CT, Lin YJ, et al: The electroanatomic characteristics of the cavotricuspid isthmus: implications for the catheter ablation of atrial flutter. J Cardiovasc Electrophysiol 2007 Jan; 18(1): 18-22[Medline].
• Doni F, Staffiere E, Manfredi M, et al: Type II atrial flutter interruption with transesophageal pacing: use of propafenone and possible change of the substrate. Pacing Clin Electrophysiol 1996 Nov; 19(11 Pt 2): 1958-61[Medline].
• Dunn MI: Thrombolism with atrial flutter. Am J Cardiol 1998 Sep 1; 82(5): 638[Medline].
• Falk RH, Pollak A, Singh SN, Friedrich T: Intravenous dofetilid