eMedicine Specialties > Cardiology > Arrhythmias

Atrial Flutter: Treatment & Medication

Author: Lawrence Rosenthal, MD, PhD, Associate Professor of Medicine, Director, Section of Cardiac Electrophysiology and Pacing, Fellowship Director of Clinical Cardiac Electrophysiology, Department of Internal Medicine, Division of Cardiovascular Medicine, University of Massachusetts Memorial Medical Center
Coauthor(s): Cynthia Anne Ennis, DO, Electrophysiology Fellow, University of Massachusetts Medical Center
Contributor Information and Disclosures

Updated: Aug 3, 2009

Treatment

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) restoration of sinus rhythm, (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.

The main difference between atrial fibrillation and atrial flutter is that most cases of atrial flutter can be cured with radiofrequency ablation. In all available studies, catheter ablation is superior to rate control and rhythm control strategies with antiarrhythmic drugs.

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.

Restoration of sinus rhythm
After determining the patient's needs for anticoagulation and ventricular rate control, the issue of restoration of the sinus rhythm can be safely addressed.

  • Radiofrequency ablation
    • Radiofrequency ablation is often used as first-line therapy to permanently restore sinus rhythm. This procedure is often performed electively, rather than in the acute setting, to restore sinus rhythm.
    • 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 95% with current technology.
    • 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.
    • Type I atrial flutters (tricuspid valve isthmus dependent): Catheter ablation is typically an outpatient procedure. The procedure involves moderate sedation and accessing the femoral veins for catheter insertion. The diagnosis of atrial flutter is confirmed using pacing maneuvers and ablation is performed typically at 6:00 on the tricuspid valve isthmus. A line of block is required to interrupt the circuit. (see Media file 2). Postablation pacing maneuvers can confirm that the substrate required for the circuit has been modified. Recurrence is less than 5%. Postprocedure anticoagulation with warfarin is usually continued for 4-6 weeks.

    • Classic counterclockwise atrial flutter. This 3-d...

      Classic counterclockwise atrial flutter. This 3-dimensional electroanatomic map of the tricuspid value and right atrial show the activation pattern displayed in color format. Red is early and blue is late relative to a fixed point in time. Activation travels in a counterclockwise direction.

      [ CLOSE WINDOW ]
      Classic counterclockwise atrial flutter. This 3-d...

      Classic counterclockwise atrial flutter. This 3-dimensional electroanatomic map of the tricuspid value and right atrial show the activation pattern displayed in color format. Red is early and blue is late relative to a fixed point in time. Activation travels in a counterclockwise direction.

    • Type II atrial flutters (non—isthmus dependent): These circuits are amenable to catheter ablation, especially in centers with advanced mapping systems. The ablation procedure is similar but may involve additional mapping of the left atrium (via a trans-septal puncture). Success depends on localizing the circuit and creating a line of block that includes an electrically inert anatomic structure (ie, the mitral valve annulus). While success should approach 95%, recurrence is more common and may also require the use of antiarrhythmic agents for suppression.
  • 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 right anterior and left posterior position (sandwiching the atria) (the more traditional location of pad location [anterior and apical] will also work), 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
    • Flecainide2 is only effective in approximately 10% of patients.
    • Dofetilide3 is effective in 70-80% of patients. This drug should be initiated in an inpatient setting.
    • Ibutilide4,5,6,7 is effective, converting recent-onset atrial flutter to sinus rhythm in 63% of patients with a single infusion. This is the only agent available intravenously in the United States that can be used for cardioversion. This drug must be given in a monitored setting due to risk of QT prolongation and torsade de pointes. The patient should be monitored with continuous ECG monitoring for at least 4 hours after the 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.
    • Combination of the above treatments: Antiarrhythmic medication prior to electrical cardioversion has been shown to improve the rate of conversion to sinus rhythm.

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 amiodarone, can be used.
    • For patients with ischemic heart disease, 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.
  • 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. The anticoagulation strategy used for atrial fibrillation is also recommended for atrial flutter.
    • 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.
    • 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 cardioversion8 .
    • In atrial fibrillation, postcardioversion stunning of the left atrial appendage is thought to contribute to thrombogenicity.9 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. Always consider catheter-based ablation as first-line therapy prior to starting an antiarrhythmic agent. 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.
  • 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. Per guidelines, sotalol should be initiated in the inpatient setting.
  • Radiofrequency ablation is currently the 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.

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

Medications are usually used in the acute setting or in people who are not candidates for radiofrequency ablation. 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. 

Certain medications, such as initiation of sotalol and dofetilide, by guidelines should be administered in an inpatient setting as they can prolong the QT interval and be proarrhythmic. Regardless, close patient follow-up is mandated, with frequent ECG monitoring or transtelephonic monitoring for potential signs of proarrhythmia.

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.


Metoprolol (Lopressor)

Selective beta1-adrenergic receptor blocker that decreases automaticity of contractions. During IV administration, carefully monitor BP, heart rate, and ECG.

Adult

5 mg IV for 3 doses q2-5min; then up to 200 mg PO bid

Pediatric

Not established

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

Documented hypersensitivity, uncompensated congestive heart failure, bradycardia, asthma, cardiogenic shock, AV conduction abnormalities

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

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


Atenolol (Tenormin)

Selectively blocks beta-1 receptors with little or no effect on beta-2 receptors.

Adult

Up to 200 mg PO qd in divided doses (ie, 100 mg bid)

Pediatric

Not established

Coadministration with aluminum salts, barbiturates, calcium salts, cholestyramine, NSAIDs, penicillins, and rifampin may decrease effects; haloperidol, hydralazine, loop diuretics, and MAOIs may increase toxicity

Documented hypersensitivity, congestive heart failure, pulmonary edema, cardiogenic shock, AV conduction abnormalities, and heart block (without a pacemaker)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

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


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

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

Not established; suggested dose is 100-500 mcg/kg IV administered over 1 min

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

Documented hypersensitivity, uncompensated congestive heart failure, bradycardia, cardiogenic shock, and AV conduction abnormalities

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

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

Calcium channel blockers (nondihydropyridine)

Effective for rate control.


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

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

<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
>15 years: Administer as in adults

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

Documented hypersensitivity, severe CHF, sick sinus syndrome or second- or third-degree AV block, hypotension (<90 mm Hg systolic)

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

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


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

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

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

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

Documented hypersensitivity; severe CHF, sick sinus syndrome, second- or third-degree AV block, hypotension (<90 mm Hg systolic)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in impaired renal or hepatic function, may increase LFT levels and hepatic injury may occur

Cardiac glycosides

AV nodal blocking agents.


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

Loading dose: 1.5-2 mg PO/IV in divided dose over 1-2 d
Maintenance dose: 0.25 mg PO/IV qd

Pediatric

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

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

Documented hypersensitivity, beriberi heart disease, idiopathic hypertrophic subaortic stenosis, constrictive pericarditis, carotid sinus syndrome

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

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

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.


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

150-300 mg PO tid

Pediatric

Not established

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%)

Documented hypersensitivity, bronchospastic disorders, conduction disorders, bradycardia, uncontrolled heart failure

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Use only for life-threatening arrhythmias; caution in patients with CHF, myocardial infarction, or hepatic or renal dysfunction


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

50-150 mg PO bid

Pediatric

Not established

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

Documented hypersensitivity, third-degree AV block, myocardial depression

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

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

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).


Amiodarone (Cordarone)

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.

Adult

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

Pediatric

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

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

Documented hypersensitivity; complete AV block; intraventricular conduction defects; patients taking ritonavir or sparfloxacin

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in thyroid or liver disease; rate of pulmonary fibrosis is 3-7% and is dose-related


Sotalol (Betapace)

Class III antiarrhythmic agent, which blocks K+ channels, prolongs action potential duration (APD), and lengthens QT interval. Noncardiac selective beta-adrenergic blocker. Sotalol is shown to be effective in the maintenance of sinus rhythm, even in patients with underlying structural heart disease.

Adult

40-80 mg PO bid and increase dose gradually q2-3d to therapeutic goal of 120-160 mg PO bid

Pediatric

Not established

Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effect; cardiotoxicity of sotalol may increase when administered concurrently with sparfloxacin, calcium channel blockers, quinidine, flecainide, and contraceptives; toxicity of sotalol increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents

Documented hypersensitivity; sinus bradycardia, 2nd and 3rd degree AV block

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

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, congestive heart failure, and congestive heart failure


Ibutilide (Corvert)

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. The incidence of torsades de pointes was <2%.

Adult

<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

Not established

Ibutilide increases toxicity of quinidine, and procainamide; concurrent administration of ibutilide with tricyclic antidepressants and phenothiazines may prolong QT interval; toxicity of digoxin increases when administered concurrently with ibutilide

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in renal or hepatic impairment


Dofetilide (Tikosyn)

Recently approved by FDA for maintenance of sinus rhythm. Increases monophasic action potential duration, primarily due to delayed repolarization. Terminates induced re-entrant tachyarrhythmias (eg, atrial fibrillation/flutter, ventricular tachycardia) and prevents their reinduction.
Has no effect on cardiac output, cardiac index, stroke volume index, or systemic vascular resistance in patients with ventricular tachycardia, mild to moderate CHF, angina, and either normal or reduced LVEF. No evidence of negative inotropic effect.

Adult

125-500 mcg PO bid, depending on CrCl and QT prolongation

Pediatric

Not established

Coadministration with other Class III antiarrhythmic agents (eg, amiodarone, sotalol), may prolong QT interval and induce dangerous arrhythmias; other drugs that may prolong QT interval (eg, verapamil, gatifloxacin, erythromycin), may also increase risk for arrhythmia; drugs that decrease renal tubular excretion (eg, trimethoprim/sulfamethoxazole, triamterene, metformin) may interfere with dofetilide elimination and increase toxicity, CYP450 3A4 inhibitors (eg, ketoconazole) may elevate dofetilide serum levels; potassium depleting diuretics, digoxin, cimetidine, phenothiazines, prochlorperazine, amiloride, megestrol, and other antiarrhythmic agents may increase toxicity of dofetilide

Documented hypersensitivity; concomitant use of verapamil or the cation transport system inhibitor cimetidine, trimethoprim (alone or in combination with sulfamethoxazole), or ketoconazole; congenital or acquired long QT syndromes; severe renal impairment (CrCl <20 mL/min); prochlorperazine and megestrol coadministration; a baseline QT interval or QTc >440 ms (500 ms in patients with ventricular conduction abnormalities)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hypokalemia may increase risk for arrhythmias, maintain potassium levels within normal range prior and during administration to minimize risk of induced arrhythmia; CrCl calculation required for accurate dosing; continuous ECG monitoring must be performed to monitor QT interval changes; cardiac resuscitation equipment and personnel must be present

Antiarrhythmic agent, miscellaneous

Dronedarone is an antiarrhythmic agent with properties belonging to all 4 Vaughn-Williams antiarrhythmic classes.

Dronedarone (Multaq)

Blocks sodium channels, blocks beta1-adrenergic site, and alters adenyl cyclase generation (ie, negative inotropic effects); blocks potassium channels (eg, hERG) and therefore prolongs cardiac repolarization.
In a multinational clinical trial (n >4600), dronedarone reduced cardiovascular hospitalization or death from any cause by 24% compared with placebo.
Indicated to reduce risk for cardiovascular hospitalization in patients with paroxysmal or persistent atrial fibrillation (AF) or atrial flutter (AFL), with a recent episode of AF/AFL and associated cardiovascular risk factors (ie, age >70 y, hypertension, diabetes, history of CVA, LAD >50 mm or LVEF <40%) who are in sinus rhythm or who will be cardioverted.

Adult

400 mg PO bid with meals

Pediatric

Not established

CYP3A4 substrate, moderate CYP3A4 and CYP2D6 inhibitor; P-gP inhibitor
Avoid coadministration with CYP3A4 inhibitors (eg, itraconazole, azithromycin, erythromycin, grapefruit juice) that may decrease clearance and thereby increase dronedarone plasma levels (see Contraindications); avoid use with CYP3A4 inducers (eg, rifampin, carbamazepine) because of increased clearance and consequent reduction in dronedarone serum levels; use with other drugs that prolong QT interval (eg, phenothiazine, TCAs, macrolide antibiotics, class I and III antiarrhythmic agents) may cause life-threatening arrhythmias (see Contraindications)
When coadministered with P-gP substrates (eg, digoxin), P-gP substrate bioavailability may increase (consider discontinuing P-gp substrate or decrease P-gP substrate dose by 50%)
Coadministration increases serum levels of HMG-CoA reductase inhibitors (eg, atorvastatin), thereby increasing risk for adverse effects (eg, myopathy); monitor serum levels of CYP3A substrates with narrow therapeutic indexes (eg, sirolimus, tacrolimus) if coadministered
Coadministration with beta-blockers or calcium channel blockers requires lowered dose of these agents and dose should only be increased after ECG verification of tolerability

Documented hypersensitivity; severe heart failure (ie, NYHA class IV) or NYHA class II-III with recent decompensation requiring hospitalization or referral to heart failure program; second- or third-degree heart block or sick sinus syndrome (unless functioning pacemaker in place); bradycardia <50 bpm; QTc interval >500 milliseconds (coadministration with other drugs that prolong QT interval may cause torsade de pointes[en dash]type ventricular tachycardia); severe hepatic impairment; strong CYP3A4 inhibitors

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Boxed warning: May cause critical adverse reactions, including death, in patients with recent severe heart failure
Common adverse reactions include diarrhea, nausea, vomiting, fatigue, and asthenia; discontinue if new or worsening heart failure develops; monitor QT interval; hypomagnesemia and hypokalemia may increase risk for serious arrhythmic event

Anticoagulants

Used to prevent thromboembolic complications.


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

60 U/kg IV initially, followed by maintenance infusion of 12 U/kg/h IV; target aPTT is 50-70 seconds

Pediatric

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

Digoxin, nicotine, tetracycline, and antihistamines may decrease effects; NSAIDs, aspirin, dextran, dipyridamole, and hydroxychloroquine may increase toxicity

Documented hypersensitivity, subacute bacterial endocarditis, active bleeding, history of heparin-induced thrombocytopenia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

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


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

1-20 mg/d PO qd, adjust dose to desired INR (2-3) for nonvalvular atrial fibrillation/flutter

Pediatric

0.05-0.34 mg/kg/d PO; adjust dose according to weight and desired INR

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

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

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

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

More on Atrial Flutter

Overview: Atrial Flutter
Differential Diagnoses & Workup: Atrial Flutter
Treatment & Medication: Atrial Flutter
Follow-up: Atrial Flutter
Multimedia: Atrial Flutter
References
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Further Reading

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Keywords

atrial flutter, atrial flutter treatment, arrhythmia, atrial fibrillation, supraventricular tachycardia, SVT, congestive heart failure, CHF, ventricular tachycardia, VT, ventricular fibrillation, VF, coronary artery disease, CAD, thromboembolic stroke, percutaneous catheter-based techniques, congenital cardiac anomalies, hypertensive heart disease, chronic obstructive pulmonary disease, COPD, thromboembolic complications, cardiomyopathy, hypoxia, thyrotoxicosis, pheochromocytoma

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Contributor Information and Disclosures

Author

Lawrence Rosenthal, MD, PhD, Associate Professor of Medicine, Director, Section of Cardiac Electrophysiology and Pacing, Fellowship Director of Clinical Cardiac Electrophysiology, Department of Internal Medicine, Division of Cardiovascular Medicine, University of Massachusetts Memorial Medical Center
Lawrence Rosenthal, MD, PhD is a member of the following medical societies: American College of Cardiology, American Heart Association, and Massachusetts Medical Society
Disclosure: Nothing to disclose.

Coauthor(s)

Cynthia Anne Ennis, DO, Electrophysiology Fellow, University of Massachusetts Medical Center
Disclosure: Nothing to disclose.

Medical Editor

Alan D Forker, MD, Professor of Medicine, Program Director of Cardiovascular Fellowship, University of Missouri at Kansas City School of Medicine; Director, Outpatient Lipid Diabetes Research Center, MidAmerica Heart Institute of St Luke's Hospital
Alan D Forker, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, American Society of Hypertension, and Phi Beta Kappa
Disclosure: Research Grant Grant/research funds Hospital contracts to do research; I am a hospital employee with no personal profit; Speakers Bureau Honoraria Speaking and teaching

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Brian Olshansky, MD, Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine
Brian Olshansky, MD is a member of the following medical societies: American Autonomic Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American College of Sports Medicine, American Federation for Clinical Research, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, and New York Academy of Sciences
Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting; Reliant Grant/research funds Other; Novartis Honoraria Speaking and teaching; Novartis Consulting fee Consulting

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD, Professor of Medicine and Pharmacology, Director, Clinical Cardiac Electrophysiology Fellowship Program, Vanderbilt University School of Medicine; Chief, Department of Cardiology, Nashville Veterans Affairs Medical Center
Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association and North American Society of Pacing and Electrophysiology (NASPE)
Disclosure: Nothing to disclose.

 
 
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