eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Cardiology

Atrial Flutter

M Silvana Horenstein, MD, Consultant, Pediatric and Fetal Cardiac Diagnostic, Diagnostico Gineco-Obstetrico, PC; Associate Medical Director, Legacy Department, Best Doctors, Inc
Robert Murray Hamilton, MD, MSc, FRCPC, Section Head, Electrophysiology, Director, High-Risk Hereditary Heart Conditions Clinic, Labatt Family Heart Centre; Professor, Department of Pediatrics, Associate Scientist, Physiology and Experimental Medicine, The Hospital for Sick Children and Research Institute, University of Toronto, Canada

Updated: Sep 19, 2008

Introduction

Background

Atrial flutter is an electrocardiographic descriptor used both specifically and nonspecifically to describe various atrial tachycardias. The term was originally applied to adults with regular atrial depolarizations at a rate of 260-340 beats per minute (bpm). Historically, the diagnosis of atrial flutter was restricted to those patients whose surface ECG revealed the classic appearance of "flutter waves." This sharp demarcation is used less frequently in the current era.

In the fetus, atrial flutter is defined as a rapid regular atrial rate of 300-600 bpm accompanied by variable degrees of atrioventricular (AV) conduction block, resulting in slower ventricular rates.

When the atrial rate is such, normal AV nodes usually have a physiologic second-degree block, with a resultant 2:1 conduction ratio. In individuals with AV nodal disease or increased vagal tone, or when certain drugs are used, higher degrees of AV block may develop. In individuals with accessory AV nodal pathways, a 1:1 conduction ratio may occur, with resultant ventricular rates of 260-340 bpm, which can cause sudden death. A 1:1 conduction ratio may also occur when the atrial rate is relatively slow (eg, <340 bpm) during atrial flutter or when physiologic processes facilitate AV nodal conduction such that a rapid ventricular response can still result in sudden death.

Atrial flutter is infrequent in children without congenital heart disease. Patients who have undergone Mustard, Senning, or Fontan procedures are more prone to develop this arrhythmia because of atrial scars from surgery and right atrial enlargement, such as is found after the classic Fontan operation.

Similarly, patients who have undergone surgical repair of atrial septal defect, total anomalous pulmonary venous connection, and tetralogy of Fallot may later develop atrial flutter. Individuals with muscular dystrophies such as Emery-Dreifuss and myotonic dystrophy may also develop atrial flutter, as well as those with dilated, restrictive, and hypertrophic cardiomyopathies.

Pathophysiology

The pathophysiology of atrial flutter is a reentrant arrhythmia circuit confined to the atrial chambers. Such a circuit may be macroscopic and, therefore, amenable to mapping by techniques using standard electrophysiologic catheters or it may be microscopic and amenable to mapping only in the research laboratory using fine electrode arrays.

As a rule, atrial flutter originates in the right atrium, whereas atrial fibrillation, which is more frequent in adults, originates in the left atrium.

A flutter circuit typically surrounds an anatomical or functional barrier and includes a zone of slow conduction (or conduction over an extended circuit) and an area of unidirectional block, as required for reentry of all types. Frequently, a premature beat blocks one limb of the circuit and is sufficiently delayed in the other limb (while traversing around the anatomical or functional barrier) to allow for recovery from refractoriness in the first limb.

The reentrant circuits that occur in children with atrial flutter after congenital heart disease surgery are typically more variable than those in adults, who generally have atrial flutter confined to the tricuspid valve–coronary sinus isthmus (or isthmus-dependent flutter). The difference in children with congenital heart disease is believed to be secondary to abnormal atrial tissue that has been subject to chronic cyanosis, inflammation secondary to surgery, scarring, and increased wall stress in cases of enlarged atria. Such circuits may encircle anatomical barriers such as atriotomy scars or surgical anastomoses, and they may use areas of slow conduction along baffle limbs and other sites of injury in addition to the tricuspid valve–coronary sinus isthmus.

Sinus node dysfunction with bradycardia is generally present in many of these patients years after surgery. This is a contributing factor for development and maintenance of atrial flutter.

Frequency

United States

According to one study, 57% of patients with double inlet left ventricle who undergo the Fontan operation may be expected to present with atrial flutter or fibrillation 20 years after surgery.¹

International

• In one review, atrial flutter accounted for 26.2% of all cases of fetal tachyarrhythmias, and supraventricular tachycardia (SVT) accounted for 73.2%.²
• In an earlier population study of 3383 newborns by Southall and colleagues, only 1 newborn had atrial flutter.³ This likely underestimated the incidence of atrial flutter in utero because spontaneous conversion often occurs during birth and subsequent recurrence is uncommon.
• A long-term follow-up study into adulthood of patients undergoing the Mustard or Senning procedure for correction of D-transposition of the great vessels demonstrated SVT in 48%, of which atrial flutter was the most common type (73%).
• The mean annual incidence of new dysrhythmias (predominantly atrial flutter) after the Fontan operation is 5%.
• Arrhythmias accounted for 12.7% of pediatric cardiology consultations in a major pediatric academic medical center, of which atrial flutter was the second most common type.

Mortality/Morbidity

In patients who present with atrial flutter, morbidity and mortality largely depend on their age at presentation, cardiac anatomy (normal anatomy vs congenital heart disease), integrity and anatomy of the myocardial conduction system (normal sinus node vs sinus node dysfunction; AV block vs normal AV node, with or without accessory pathways), ventricular function, and availability of prompt recognition of the arrhythmia by the physician and initiation of adequate therapy.

• The fetus with atrial flutter may have significant morbidity and be at risk for mortality. According to one review, hydrops fetalis developed in as many as 40% of fetuses with atrial flutter. The mortality rate in these fetuses was 8%.²
• Mortality in newborns with atrial flutter is uncommon. Most patients remain in sinus rhythm following their initial conversion, and the need for antiarrhythmic prophylaxis in these patients during infancy is debated.
• In patients with postoperative atrial flutter that develops late following repair of congenital heart disease, the severity of presentation depends on the atrial flutter rate, conduction ratio, and presence of ventricular dysfunction. In patients who have undergone the Mustard procedure, Holter recordings incidentally capturing episodes of sudden fatality confirm that rapidly conducted atrial flutter is the dysrhythmia most frequently responsible for these fatalities. In contrast, patients who have undergone the Fontan procedure rarely die suddenly but frequently present with symptomatic atrial flutter. This may be caused by a relatively slower atrial flutter rate, a higher degree of AV conduction block, or both.
• When women with heart disease and arrhythmias reach childbearing age, arrhythmias can recur during pregnancy, significantly increasing the risk for the mother and fetus.
• Prolonged episodes of atrial flutter in asymptomatic or mildly symptomatic patients may be associated with development of atrial thrombi and although rarely in the congenital heart disease population, the possibility of thromboembolic events.

Sex

Following atrial septal defect repair, the prevalence of atrial flutter is higher in females (70.7%) than in males.

Age

As implied above, the prevalence and outcome of atrial flutter depend on the patient's age at presentation and associated causes.

• The fetus with atrial flutter may have associated mortality and risk for morbidity, as stated above. Because atrial flutter occurs mainly during the third trimester, the atrium is believed to reach a critical mass to support an intra-atrial macroreentry circuit at about 27-30 weeks' gestation.
• Atrial flutter in newborns requires immediate treatment, but this is unlikely to recur. Atrial flutter in children usually relates to repairs of congenital heart disease.
• Patients with Fontan repairs present with flutter either as children or as adults.
• Patients with repaired tetralogy of Fallot tend to present with atrial flutter as young adults.
• Because the Mustard and Senning procedures are now rarely performed, the cohort of patients with this substrate typically consists of older adolescents and adults.
• One study reported that the recurrence rate of atrial flutter and fibrillation in women with preexisting cardiac rhythm disorders during pregnancy was the highest of all the studied arrhythmias, reaching 52%.⁴

Clinical

History

Historical aspects of atrial flutter are important in designing a treatment plan, particularly in the setting of repaired congenital heart disease.

• The flutter may be perceived as a regular or irregular palpitation, the latter suggesting variable atrioventricular (AV) conduction.
  • The flutter may be associated with syncope, severe presyncope, or chest pain, suggesting either periods of 1:1 conduction ratio or associated ventricular dysfunction. Characterizing a history of previous self-terminating episodes is important.
  • Rare minimally symptomatic self-terminating episodes of atrial flutter are likely to require less treatment.
• The presence of associated sinus node disease with episodes of sinus bradycardia may provide an indication for pacemaker therapy, which also adds to the antiarrhythmic medical options for atrial flutter.
• Understanding the specific anatomy and surgical repair for each patient is important. Certain types of repair are more commonly associated with late atrial flutter than others.
  • In Fontan-type operations, atriopulmonary connections are associated with a risk of atrial flutter that is 2.5-fold higher than the total cavopulmonary connection.
  • Extracardiac Fontan repairs may have an even lower frequency of atrial flutter.
  • The type of repair may influence the technical approach to electrophysiological study, pacemaker placement, potential radiofrequency ablation therapy, or potential Fontan surgical revision. For example, patients who have the classic Fontan operation are amenable to ablation attempts of the atrial flutter in the electrophysiology laboratory because the right atrium can be approached via the inferior and/or superior vena cava. In addition, endocardial pacemaker leads can be inserted if the patient has sinus node dysfunction. However, patients who have an extracardiac Fontan repair in which the right atrium has been bypassed with a baffle require open-heart surgery if ablation is contemplated, which is performed at the time of their Fontan revision. In addition, only epicardial pacemaker leads can be placed in these patients.
• Several studies have shown that atrial flutter in the early postoperative period in patients who have undergone the Fontan operation predicts both early operative mortality and recurrence of the arrhythmia.
• In patients with congenital heart disease who have undergone surgery, episodes of atrial flutter have been shown to increase in frequency over time.

Physical

Physical examination in patients with atrial flutter should complement the history discussed above.

• The evaluation should assess the likely conduction ratio and rate of flutter and assess for signs of associated ventricular dysfunction or heart failure.
  • Depending on the ventricular rate and the individual's tolerance to that rate, symptoms may range from palpitations, dyspnea, presyncope, or syncope to sudden death.
  • If the ventricular response is rapid, atrial flutter may cause significant morbidity secondary to hemodynamic deterioration due to low cardiac output.
  • If the ventricular response is slow enough to permit a sustained arrhythmia, atrial thrombosis with consequent thromboembolism may result.
  • In patients who have undergone surgery for congenital heart disease, new onset of atrial arrhythmias such as atrial flutter may indicate elevated right atrial pressure and, thus, the need for surgery (eg, conduit obstruction in a patient with a Rastelli-type surgery).
• In patients who have undergone the Fontan, Mustard, or Senning operation, the presence of superficial venous collateralization suggests associated obstruction of major venous pathways, which may interfere with evaluation and management.

Causes

• Most fetuses and neonates with atrial flutter have structurally normal hearts. However, when atrial flutter is detected in a fetus, structural cardiac anomalies such as Ebstein anomaly of the tricuspid valve and AV septal defects should be ruled out because of a higher incidence of these defects.
• Some newborns and young children have associated conditions or anomalies that may predispose them to atrial flutter.
  • Atrial septal aneurysms appear to be associated with sustained atrial arrhythmias in newborns.
  • Restrictive cardiomyopathies are also associated with refractory atrial flutter.
  • In Costello syndrome, the dysmorphic appearance is also associated with a dysrhythmia characterized as chaotic atrial tachycardia, and this dysrhythmia may include long episodes of atrial flutter.
• Atrial flutter is not uncommon in the immediate postoperative period after congenital heart surgery.
• Surgery-induced inflammation of the pericardium, scarring, and volume overload may trigger atrial flutter.
• Case reports have linked atrial flutter to ingestion of herbal medicines and certain foods. These episodes had not recurred after avoidance of the triggers.
• Atrial flutter and atrial fibrillation have been related to obesity, alcohol consumption, and hyperthyroidism.
• One study reported that diabetes mellitus is a strong independent risk factor for development of atrial flutter and atrial fibrillation in adults.⁵

Differential Diagnoses

Supraventricular Tachycardia, Atrial Ectopic Tachycardia
Supraventricular Tachycardia, Atrioventricular Node Reentry
Supraventricular Tachycardia, Junctional Ectopic Tachycardia
Supraventricular Tachycardia, Wolff-Parkinson-White Syndrome
Ventricular Tachycardia

Other Problems to Be Considered

Atrial fibrillation
Chaotic atrial tachycardia

Workup

Laboratory Studies

• Optimize anticoagulation through monitoring of coagulation profiles in patients receiving heparin or warfarin. In patients with documented intracardiac thrombi, monitor for the presence of associated thrombophilia, as indicated.

Imaging Studies

• Consider transesophageal echocardiography in patients with associated structural or functional heart disease to ascertain the presence of intracardiac thrombi, myocardial dysfunction, or hemodynamically important residual structural defects that could predispose them to atrial flutter.
• Three-dimensional electroanatomical physiologic mapping of atrial arrhythmias is helpful, especially in patients who have undergone atriotomies because of the presence of multiple, extended, and/or complex reentry circuits.

Other Tests

• A 12-lead to 15-lead ECG is the mainstay of atrial flutter diagnosis.
  • A rapid atrial tachycardia with uniform P waves with flutter morphology and variable atrioventricular (AV) block indicates that atrial flutter or atrial ectopic tachycardia is present.
  • If the onset of tachycardia has been recorded, the absence of "warm-up" of the tachycardia cycle length makes atrial flutter the most likely diagnosis. Similarly, sudden termination of the tachycardia points to atrial flutter.
  • If the conduction ratio is consistently 1:1, the diagnosis is more difficult. The QRS complex may be aberrantly conducted at this rate, and a differential diagnosis of ventricular tachycardia must be considered.
  • With a 2:1 conduction ratio, every other flutter wave may be hidden within the QRS complex. In this case, the ECG findings often suggest a mild sinus tachycardia with first-degree AV block. Because adrenergic states that cause sinus tachycardia usually shorten rather than prolong the PR interval, the differential diagnosis of atrial flutter should be considered.
  • Assessment of heart rate or conduction ratio responses to vagal maneuvers or adenosine may be helpful.
  • According to one study, V1 was the most important ECG lead that aided diagnosis of the supraventricular tachycardia (SVT) mechanism; the study also reported that combining V1 with the inferior limb lead III increased the chances of identifying the SVT mechanism from 80% to 96%.⁶
• In patients with possible atrial flutter occurring early following repair of congenital heart disease, the use of temporary atrial wires is extremely helpful in diagnosis and therapy. Unipolar atrial wire recordings or bipolar recordings with a simultaneously recorded surface ECG can often be used to confirm a suspected atrial flutter with 2:1 conduction ratio by unmasking the second flutter wave.
• In patients without temporary atrial wires, the use of an esophageal electrode placed behind the left atrium is also extremely helpful for diagnosis and therapy. Bipolar recordings with a simultaneously recorded surface ECG can be optimized by advancing or withdrawing the electrode until the atrial electrogram is at its maximal size.
• Patients with modern atrial or dual-chamber pacemakers can provide a unipolar or bipolar atrial electrogram by telemetry from the device.
• Depending on the drug used, patients receiving antiarrhythmic therapy may benefit from the monitoring of specific drug blood levels and electrolyte and creatinine levels or ECG monitoring of the QTc (eg, class III agents).
• P-wave signal averaging using a specialized ECG has demonstrated some ability to differentiate adults who are likely to develop occurrences or recurrences of atrial fibrillation. This technique has been adapted to predict the occurrence of atrial flutter following the Fontan procedure.
• Electrical termination of atrial flutter and additional testing can be performed through atrial wires, esophageal electrodes, permanent pacing systems, or with an intracardiac electrophysiology study. These studies may identify whether an arrhythmia is reproducibly overdriveable, and invasive testing may help identify the specific arrhythmia circuit.

Procedures

• The reentrant arrhythmia circuit confined to the atrial chambers may be macroscopic and mappable using standard electrophysiologic catheters or it may be microscopic and mappable only in the research laboratory using fine electrode arrays.
• Postcatheterization precautions include hemorrhage, vascular disruption (if the patient underwent concomitant balloon dilation of a stenosed vessel), pain, nausea and vomiting, and arterial or venous obstruction from thrombosis or spasm.
• Complications include rupture of blood vessel, tachyarrhythmias, bradyarrhythmias, and vascular occlusion.

Treatment

Medical Care

• In children with atrial flutter, medical care should be broadly directed at the following:
  • Ensuring hemodynamic stability before, during, and after conversion to sinus rhythm
  • Minimizing influences favoring initiation or maintenance of atrial arrhythmias (eg, electrolyte disturbances, pericardial effusion, indwelling atrial lines or catheters)
  • Excluding or managing complications (eg, ventricular dysfunction, thromboembolic phenomena)
  • Restoring normal sinus rhythm as safely, expeditiously, and comfortably as possible
• Pace-termination of atrial flutter is best performed with a programmable stimulator that is capable of sensing atrial electrograms and delivering single, double, or multiple extrastimuli at adequate output and individually programmable cycle lengths down to 100 milliseconds.
  • Short discrete ramps or bursts of atrial stimuli are the most likely to produce a type I conversion of atrial flutter (immediate conversion to sinus rhythm), particularly if they can be delivered in or near the flutter circuit. If such a device is unavailable, a pacemaker capable of burst pacing at a specified rate may be used.
  • If pacing is performed via an esophageal electrode, the device should be capable of delivering stimuli at pulse widths of 9.9-20 milliseconds and outputs of 10-26 mA.
• R-wave synchronized cardioversion is the mainstay of therapy in patients who are unstable or if other therapies have failed.
  • In patients who are stable and have chronic atrial flutter, perform cardioversion only after documentation of freedom from intracardiac thrombi or following a 2-week course of anticoagulation. Cardioversion may be performed at increasing doses of 0.5 J/kg, 1 J/kg, 2 J/kg, and 4 J/kg, although newer biphasic waveform defibrillators may allow for lower energy applications.⁷  Ideally, place defibrillator paddles or pads in an anteroposterior configuration, with the apex paddle located over the mid sternum and the base paddle between the scapulae. An anesthesiologist usually administers a brief general anesthetic, except in truly emergent circumstances that mandate immediate cardioversion.
  • Hemodynamic instability requires immediate cardioversion as described above. However, if the patient is relatively stable, this state can be maintained by careful consideration of possible interventions. The patient should rest in a supine position without undue excitement or agitation. Consider digoxin if not already in use because it frequently increases the conduction ratio and decreases the ventricular rate. However, this effect usually takes many hours. Medications with the potential to slow the atrial rate without affecting the atrioventricular (AV) node should be used with caution because the conduction ratio often decreases to 1:1 AV association, resulting in a rapid ventricular rate and hemodynamic compromise.
  • Avoid adrenergic and atropinic agents during sedation or anesthesia for cardioversion. Ketamine is relatively contraindicated. Such agents may result in rapid 1:1 AV conduction, with resultant hemodynamic compromise. On the other hand, insufficient sedation during attempted esophageal overdrive pacing or a failed cardioversion may result in patient distress and 1:1 AV conduction ratio.
• Currently, radiofrequency catheter ablation appears to be somewhat effective in treating postoperative intra-atrial reentrant tachycardia in children. Because the flutter circuits and critical isthmuses are quite variable in these patients, mapping of flutter circuits may be enhanced by 3-dimensional electroanatomical display systems, identification of split potentials, and demonstration of concealed entrainment during pacing.

Surgical Care

• In patients with atrial flutter, surgical care may include one of the following procedures:
  • Correction of hemodynamic lesions, which may cause atrial volume loading
  • Specifically placed atrial incisions or cryoablation prophylactically to prevent atrial flutter (One study reported that a right-sided maze procedure in patients with atrial flutter or fibrillation undergoing congenital heart disease repair significantly reduced arrhythmia recurrence at a mean of 2.7 y after surgery.⁸ )
  • Empiric or map-directed lesions to eliminate documented atrial flutter and its circuits
• These surgeries include various modifications and updates to maze procedures and modifications of the Mustard and Fontan procedures.

Activity

• Aggressive strategies to convert atrial flutter and maintain sinus rhythm should be pursued in children.
• In rare cases of resistant chronic atrial flutter when only rate control can be accomplished, patients should avoid competitive sports. Also restrict the activities of patients likely to develop rapid conduction of intermittent acute episodes of flutter.

Medication

Drug therapy of atrial flutter in children can be classified under the 3 broad headings of ventricular rate control, acute conversion, and chronic suppression.

Digoxin is relatively safe for preventing rapid conduction of atrial flutter via the atrioventricular (AV) node to the ventricles, and some evidence indicates that this reduces symptomatology during flutter. Nevertheless, digoxin is unlikely to be particularly effective in the acute conversion or prevention of atrial flutter recurrence. It is devoid of negative inotropic effects (as is amiodarone) and is useful to control ventricular rate when using propafenone, flecainide, or procainamide.

Intravenous procainamide has been used with variable success to effect acute conversion of atrial flutter to sinus rhythm. Procainamide infusion should be preceded by digitalization to prevent procainamide-induced acceleration of AV node conduction to the ventricles.

The US Food and Drug Administration (FDA) has approved the novel Vaughan Williams class III agents ibutilide and dofetilide for acute conversion of atrial flutter and fibrillation. Both are more effective than other medications in converting atrial flutter, but their use is associated with QT prolongation with a nontrivial risk of induction of torsade de pointes polymorphic ventricular tachycardia. Clinical experience in adults is limited, and efficacy, dosing, and safety in children have not been established. Therefore, further drug information on this agent cannot be provided at this time.

Fetal atrial flutter is the second most common intrauterine tachyarrhythmia. Treatment is aimed at controlling ventricular rate and, thus, avoiding hydrops fetalis. First-line treatment is digoxin administered to the mother, which provides a conversion rate to sinus rhythm of 45-52%. In addition, its positive inotropic effect may be beneficial. Sotalol has also been used in numerous cases with success. Maternal drug levels were not reliable predictors of successful therapy.^9,10 Flecainide alone or in combination with digoxin is used as second-line treatment. Fetal atrial flutter in a structurally normal heart seldom recurs after conversion before or after birth, and postnatal suppressive antiarrhythmic therapy may not be necessary.

Flutter in patients with repaired or palliated structural congenital lesions is more likely to recur, and long-term antiarrhythmic therapy aimed at flutter suppression is often instituted after the first or the second flutter episode.

Vaughan Williams class IC (eg, flecainide, propafenone) or class III (eg, sotalol, amiodarone) agents have been prescribed with variable success. Some authors have cautioned against use of flecainide in this setting, but the data are equivocal. Combinations of agents occasionally succeed after failure of single-agent therapy. Use of antiarrhythmic agents other than digoxin for the long-term suppression of atrial flutter in sinus node disease (a frequent coexisting finding) is particularly controversial. In patients with atrial flutter who have had the Mustard procedure, treatment with quinidine was associated with case reports of sudden death. This resulted in the recommendation of antibradycardia pacing initiation before antiarrhythmic drug therapy in these patients. This recommendation has gradually broadened to encompass other antiarrhythmic agents in patients with other types of repaired congenital heart disease.

Rapid, consistent, and safe temporary ventricular rate control can be obtained in children with diltiazem.

Antibradycardia pacing may be directly advantageous in flutter suppression by reducing the frequency of flutter-inducing pauses and premature beats. It also provides a safety factor for more aggressive antiflutter drug therapy.

Antiarrhythmic agents

These agents alter the electrophysiologic mechanisms responsible for arrhythmia.

Digoxin (Lanoxin)

Cardiac glycoside with direct inotropic effects in addition to indirect effects on the cardiovascular system. Acts directly on cardiac muscle, increasing myocardial systolic contractions. Its indirect actions result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure.

Dosing

Adult

0.125-0.375 mg PO qd

Pediatric

10 mcg/kg/d (0.01 mg/kg/d) PO

Interactions

Medications that may increase serum digoxin levels include alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone, propantheline, quinidine, diltiazem, aminoglycosides, PO amiodarone, anticholinergics, diphenoxylate, erythromycin, felodipine, flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline, tolbutamide, and verapamil; medications that may decrease serum digoxin levels include aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, PO colestipol, hydantoins, hypoglycemic agents, antineoplastic treatment combinations (eg, carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid

Contraindications

Documented hypersensitivity; Wolff-Parkinson-White syndrome; tetralogy of Fallot (prerepair); beriberi heart disease; idiopathic hypertrophic subaortic stenosis; constrictive pericarditis; carotid sinus syndrome

Precautions

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 the positive inotropic effect of digitalis; IV calcium may produce arrhythmias in digitalized patients; hypercalcemia predisposes patient to digitalis toxicity, and hypocalcemia can make digoxin ineffective until serum calcium levels are within the reference range; magnesium replacement therapy must be instituted in patients with hypomagnesemia to prevent digitalis toxicity; AV block may progress to complete block when treated with digoxin; exercise caution in hypothyroidism, hypoxia, and acute myocarditis

Procainamide (Procanbid, Pronestyl)

Class IA antiarrhythmic used for PVCs. Increases refractory period of atria and ventricles. Myocardiac excitability is reduced by increase in threshold for excitation and inhibition of ectopic pacemaker activity.

Dosing

Adult

0.5-1 g PO q6h (as sustained release)
Loading dose: 30 mg/min IV at continued infusion rates until arrhythmia is suppressed, patient becomes hypotensive, QRS widens to 50% above baseline, or a maximum dose of 17 mg/kg is administered
Once arrhythmia is suppressed, may infuse at a continuous rate of 1-4 mg/min

Pediatric

Loading dose: 10 mg/kg IV over 20 min
Maintenance dose: 20-80 mcg/kg/min IV

Interactions

Can 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, 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

Contraindications

Documented hypersensitivity; complete heart block or second- or third-degree heart block if pacemaker is not in place; torsade de pointes; systemic lupus erythematosus

Precautions

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

Monitor for hypotension; plasma concentrations of procainamide and its 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

Propafenone (Rythmol)

Treats life-threatening arrhythmias. Possibly works by reducing spontaneous automaticity and prolonging refractory period.

Dosing

Adult

150 mg PO q8h initial; may increase at q3-4d; not to exceed 300 mg q8h

Pediatric

150-400 mg/m²/d PO divided tid/qid

Interactions

Decreases serum levels of rifampin; cimetidine, quinidine, warfarin, and beta-blockers may increase serum levels

Contraindications

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

Precautions

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

Only use for life-threatening arrhythmias; caution in patients with congestive heart failure, myocardial infarction, or hepatic or renal dysfunction

Amiodarone (Cordarone)

May inhibit AV conduction and sinus node function. Prolongs action potential and refractory period in myocardium and inhibits adrenergic stimulation.
Before administration, control ventricular rate and CHF (if present) with digoxin.

Dosing

Adult

Loading dose: 800-1600 mg/d PO in 1-2 doses for 1-3 wk, decrease to 600-800 mg/d in 1-2 doses for 1 mo
Alternatively, 150 mg (10 mL) IV over first 10 min, followed by 360 mg (200 mL) over next 6 h and then 540 mg over next 18 h
Maintenance dose: 400 mg/d PO

Pediatric

Loading dose: 5-15 mg/kg IV over 1 h; 10 mg/kg/d PO for 7 d
Maintenance dose: 5-15 mcg/kg/min IV; 5-7.5 mg/kg/d PO

Interactions

Increases effect and blood levels of theophylline, quinidine, procainamide, phenytoin, methotrexate, flecainide, digoxin, cyclosporine, beta-blockers, and anticoagulants; cardiotoxicity is increased by ritonavir, sparfloxacin, and disopyramide; coadministration with calcium channel blockers may cause an additive effect and decrease myocardial contractility further; cimetidine may increase levels

Contraindications

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

Precautions

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

Diltiazem (Cardizem)

AV nodal blocking agent. Administered IV temporarily (ie, <24 h) until definitive treatment can be initiated.

Dosing

Adult

0.25 mg/kg IV administered over 2 min initial, followed by a continuous IV infusion of 5 mg/h; typical dose is 5-10 mg/h; not to exceed 15 mg/h

Pediatric

0.25 mg/kg IV administered over 5 min initial, followed by 0.1 mg/kg/h

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 diltiazem levels

Contraindications

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

Precautions

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

Flecainide (Tambocor)

Treats life-threatening ventricular arrhythmias. Causes a 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 the heart with greatest effect on the His-Purkinje system (H-V conduction). Effects on AV nodal conduction time and intra-atrial conduction times, although present, are less pronounced than on ventricular conduction velocity.

Dosing

Adult

100 mg PO q12h; may increase by 100 mg/d q4d until adequate response achieved; not to exceed 400 mg/d

Pediatric

Initial dose: 1-3 mg/kg/d or 50-100 mg/m²/d PO divided tid; may increase gradually by 50 mg/m²/d q5d until adequate response achieved; not to exceed 8 mg/kg/d (200 mg/m²/d); children <6 mo initiate at lowest dose
Maintenance dose: 3-6 mg/kg/d or 100-150 mg/m²/d PO divided tid is typical dose

Interactions

Amiodarone, cimetidine, and digoxin may increase plasma concentrations; beta-adrenergic blockers, verapamil, and disopyramide may have additive inotropic effects when administered with flecainide; ritonavir may increase cardiotoxicity

Contraindications

Documented hypersensitivity; third AV block; myocardial depression

Precautions

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

Sotalol (Betapace)

Class III antiarrhythmic agent, which blocks potassium channels, prolongs action potential duration, and lengthens QT interval. Noncardiac selective beta-adrenergic blocker.

Dosing

Adult

80 mg PO bid, increase dose gradually q2-3d to 240-320 mg/d

Pediatric

Not established; the following doses have been suggested:
Initial: 200 mg/m²/d PO divided bid/tid; not to exceed 160 mg/d
Maintenance: 2-8 mg/kg/d (40-350 mg/m²/d) PO divided bid/tid

Interactions

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, astemizole, 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

Contraindications

Documented hypersensitivity; sinus bradycardia; second- and third-degree AV block

Precautions

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, 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 were mostly PVCs. The incidence of Torsades was <2%.

Dosing

Adult

<60 kg: 0.01 mg/kg IV infused over 10 min
>60 kg: 1 mg IV infused over 10 min

Pediatric

Not established

Interactions

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

Contraindications

Documented hypersensitivity

Precautions

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 because of delayed repolarization. Terminates induced reentrant tachyarrhythmias (eg, atrial fibrillation/flutter, ventricular tachycardia) and prevents their reinduction. Does not affect 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.

Dosing

Adult

The dose must be adjusted according to the CrCl and to the QTc; requires initiation in an inpatient monitored setting
Starting dose:
CrCl >60 mL/min: 500 mcg PO bid
CrCl 40-60 mL/min: 250 mcg PO bid
CrCl 20-40 mL/min: 125 mcg PO bid
CrCl <20 mL/min: Use contraindicated
If QTc has increased >15% or is >500 ms 2-3 h after administering first dose, decrease dose as follows:
Starting dose was 500 mcg PO bid: Reduce to 250 mcg PO bid
Starting dose was 250 mcg PO bid: Reduce to 125 mcg PO bid
Starting dose was 125 mcg PO bid: Reduce to 125 mcg PO qd
Discontinue if the QTc is >500 ms any time after the second dose

Pediatric

Not established

Interactions

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

Contraindications

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 (ie, CrCl <20 mL/min); prochlorperazine and megestrol coadministration; a baseline QT interval or QTc >440 ms (500 ms in patients with ventricular conduction abnormalities)

Precautions

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 reference range prior to and during administration to minimize risk of inducing 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

Follow-up

Further Inpatient Care

Thrombosis and thromboembolic events are recognized complications in patients with atrial flutter, particularly in the setting of repaired congenital heart disease.

• Patients with a history of symptoms suggesting subacute or chronic flutter (or those without symptoms in whom the onset of flutter cannot be identified) should undergo imaging studies to rule out intracardiac thrombi before proposed conversion of their rhythm. This is best performed with transesophageal echocardiography.
• Patients with identified thrombi or a history of chronic atrial flutter (>2 wk duration) should be treated with a period of anticoagulation (2-4 wk), if hemodynamically and symptomatically tolerated, before undergoing direct current (DC) cardioversion or other conversion of their rhythm.

Transfer

• As with most symptomatic arrhythmias, conversion should ideally be achieved before transfer, except in the case of a hemodynamically stable patient referred to an institution with clearly superior expertise and facilities for management of pediatric atrial flutter.

Deterrence/Prevention

• Atrial stretch, surgical scarring, and sinus node dysfunction all appear to play important roles in the development of atrial flutter in patients with congenital heart disease. The development of new surgical techniques to avoid atrial suture lines or dilatation and to prophylactically interrupt potential conduction isthmuses within the atria may reduce the frequency of this disorder in future surgical cohorts of patients with congenital heart disease. Efforts directed at sparing the sinus node during surgery, coupled with more aggressive pacing strategies in patients with sinus node dysfunction, could also play an important role in prevention of atrial flutter.

Complications

• Episodes of atrial flutter may be associated with low cardiac output, brain and other end-organ injury, and sudden or subacute death. Heart failure, thrombosis, and thromboembolism are other recognized complications.

Prognosis

• Neonatal atrial flutter is usually a self-limiting illness, requiring only conversion of the rhythm with esophageal atrial pacing or cardioversion. Incisional reentrant atrial tachycardia following complex atrial surgery in the repair of congenital heart disease may occur early in the postoperative period; this event is predictive of the occurrence of late postoperative flutter. The prevalence of atrial flutter in several classes of postoperative patients increases with the duration of follow-up care.

Patient Education

• For excellent patient education resources, visit eMedicine's Heart Center. Also, see eMedicine's patient education articles Atrial Flutter, Tetralogy of Fallot, and Supraventricular Tachycardia.

Miscellaneous

Medicolegal Pitfalls

• According to a legal precedent, patients with Mustard repair of transposition of the great vessels and sick sinus syndrome should not receive quinidine without a previously implanted pacemaker. However, quinidine is now recognized to have a detrimental adverse effect profile in general, and it is essentially no longer used in the treatment of rhythm disorders following congenital heart disease. Disagreement surrounds whether this recommendation should be extrapolated to other antiarrhythmics and other forms of repaired congenital heart disease.
• Patients who are treated with atrial antitachycardia pacing should undergo testing to confirm that their device is effective and not proarrhythmic.

Multimedia

Media file 1: Rhythm strip depicting lead II of a patient with atrial flutter with an atrial rate of 300 beats per minute (bpm). Atrioventricular conduction rate is variable at 2:1 and 3:1. Therefore, the ventricular rate ranges from 100-150 bpm.

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Keywords

atrial flutter, intra-atrial reentrant tachycardia, IART, incisional reentrant atrial tachycardia, IRAT, atrial reentry, auricular flutter, jugular embryocardia, supraventricular tachycardia, SVT, atrioventricular block, second-degree atrioventricular block, congenital heart disease, atrial septal defect, total anomalous pulmonary venous connection, tetralogy of Fallot, muscular dystrophy, Emery-Dreifuss dystrophy, myotonic dystrophy, cardiomyopathy, dilated cardiomyopathy, restrictive cardiomyopathy, hypertrophic cardiomyopathy, atrial fibrillation, sinus node dysfunction, hydrops fetalis, syncope, presyncope, pacemaker therapy

Contributor Information and Disclosures

Author

M Silvana Horenstein, MD, Consultant, Pediatric and Fetal Cardiac Diagnostic, Diagnostico Gineco-Obstetrico, PC; Associate Medical Director, Legacy Department, Best Doctors, Inc
M Silvana Horenstein, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and American Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Robert Murray Hamilton, MD, MSc, FRCPC, Section Head, Electrophysiology, Director, High-Risk Hereditary Heart Conditions Clinic, Labatt Family Heart Centre; Professor, Department of Pediatrics, Associate Scientist, Physiology and Experimental Medicine, The Hospital for Sick Children and Research Institute, University of Toronto, Canada
Robert Murray Hamilton, MD, MSc, FRCPC is a member of the following medical societies: American Heart Association, Canadian Cardiovascular Society, Canadian Medical Association, Canadian Medical Protective Association, Cardiac Electrophysiology Society, Heart Rhythm Society, Ontario Medical Association, Pediatric Electrophysiology Society, Royal College of Physicians and Surgeons of Canada, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Medical Editor

Charles I Berul, MD, Associate Professor of Pediatrics, Harvard Medical School; Senior Associate, Department of Cardiology, Children's Hospital of Boston
Charles I Berul, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, Heart Rhythm Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Alvin J Chin, MD, Professor of Pediatrics, Division of Cardiology, The Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine
Alvin J Chin, MD is a member of the following medical societies: American Association for the Advancement of Science and American Heart Association
Disclosure: Nothing to disclose.

CME Editor

Gilbert Herzberg, MD, Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College
Gilbert Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Chief Editor

Steven R Neish, MD, SM, Director of Pediatric Cardiology Fellowship Program, Associate Professor, Department of Pediatrics, Baylor College of Medicine
Steven R Neish, MD, SM is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and American Heart Association
Disclosure: Nothing to disclose.

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