Supraventricular Tachycardia, Atrial Ectopic Tachycardia


Background: Atrial ectopic tachycardia (AET) is a rare arrhythmia; however, it is the most common form of incessant supraventricular tachycardia (SVT) in children. AET is believed to be secondary to increased automaticity of nonsinus atrial focus or foci. This arrhythmia, which is also known as ectopic atrial tachycardia or automatic atrial tachycardia, has a high association with tachycardia-induced cardiomyopathy. AET is often refractory to medical therapy and is not usually responsive to direct current (DC) cardioversion.

The diagnosis of AET is based on the presence of a narrow complex tachycardia (in the absence of aberrancy or preexisting bundle branch block) with visible P waves at an inappropriately rapid rate. The rates range from 120-300 and are typically higher than 200 bpm, although physiologic rates may be observed. The P wave axis is usually abnormal. Onset of the tachycardia occurs with a P wave identical to the subsequent P waves. The tachycardia may exhibit a “warming up,” which refers to a progressively shortening P-P interval for the first few beats of the arrhythmia. Similarly, a “cooling down” may be observed at its termination. First-degree atrioventricular (AV) block is typical and second-degree AV block is common. The tachycardia cycle length and degree of AV block are influenced by the autonomic tone.


Pathophysiology: Spontaneous depolarization is a phenomenon of automatic myocardium. The sinus node is usually the pacemaker of the heart because it has the most rapid spontaneous rate of firing. A small cluster of cells with abnormal automaticity is presumed to be responsible for AET. The conduction spreads from this cluster to the surrounding atrium and to the ventricles via the AV node. A conduction delay at the AV node often occurs, with most patients demonstrating first-degree AV block and some showing second-degree block.

Because AET often is incessant, tachycardia-induced cardiomyopathy is commonly observed. While the underlying mechanism of the development of cardiac dysfunction in the setting of chronic arrhythmias is unknown, numerous reports have documented improved cardiac function following ventricular rate control and treatment of the arrhythmia.



  • Internationally: Although the exact incidence is unknown and few large series exist, AET is reported to comprise 5-10% of pediatric SVTs. Estimates of the incidence of pediatric SVTs vary greatly, but AET likely occurs with an incidence of approximately 1 in 10,000 children.

Mortality/Morbidity: Tachycardia is generally well tolerated. Syncope is unusual, and cardiac arrest is rare, except when encountered as a complication of treatment. Tachycardia-induced cardiomyopathy is the most significant sequela of AET and may be insidious. The time to development is dependent on the rate and duration of the tachycardia, but dilatation may be present on initial presentation. This can also be reversed with successful treatment of the arrhythmia.

Age: The arrhythmia is predominantly observed in infants and children; this accounts for a peak of 11-16% of tachycardias for which a mechanism is determined in young childhood. The adult form of AET may have a different etiology and natural history than the pediatric form.



  • Although AET is occasionally encountered in patients following surgery for congenital heart disease, most patients have structurally normal hearts and are symptomatic.
    • Palpitations, chest pain, lightheadedness, presyncope, and dyspnea are the most common symptoms.
    • Asymptomatic or preverbal patients may be noted to be tachycardic or dyspneic on routine evaluation.
    • Exercise intolerance and congestive heart failure are late manifestations of secondary cardiac dysfunction.
  • The history must be sufficiently broad to rule out causes of persistently elevated heart rates, such as hyperthyroidism, anemia, or catecholamine-producing malignancy. The family history is rarely positive for AET.

Physical: The heart rate is elevated inappropriately for the degree of activity. If second-degree AV block is present, the heart rate may be irregular. The patient may be tachypneic. In advanced cardiomyopathy, pulses and perfusion are poor and evidence of cardiac enlargement is present. Hepatic and pulmonary congestion may be present.

Causes: AET is usually idiopathic. Occasionally, mycoplasmal or viral infections, such as respiratory syncytial virus, may trigger this arrhythmia, although more complex atrial tachycardias, such as chaotic atrial tachycardia, are more frequently found in this scenario. Atrial tumors have been reported to be associated with AET.


Atrial Flutter

Other Problems to be Considered:

The differential diagnosis for a narrow complex tachycardia is extensive, and the term SVT is nonspecific. Differentiation of automatic versus reentrant mechanisms may be determined by the presence of a warm-up or cool-down period at onset and termination and by the response to vagal maneuvers or adenosine. A right-sided AET focus in the presence of tachycardia-induced cardiomyopathy must be differentiated from idiopathic dilated cardiomyopathy with a secondary compensatory sinus tachycardia; the degree of dysfunction and heart rate are higher and second-degree AV block is more common in patients with AET. AET must also be differentiated from atypical AV node reentry, permanent junctional reciprocating tachycardia, and inappropriate sinus tachycardia; all 3 usually respond to adenosine with abrupt termination. Approximately one half of patients with AET demonstrate transient atrial slowing with adenosine, while the others demonstrate only transient AV block. Aberrantly conducting AET must be differentiated from ventricular tachycardia (VT).


Lab Studies:

  • Assess electrolyte levels, hematocrit levels, and thyroid function.
  • Consider thyroid studies or urine collections in some patients for assessment of possible pheochromocytoma.

Imaging Studies:

  • Perform echocardiography with focus on cardiac function and dimensions to rule out cardiomyopathy and associated congenital heart disease (CHD). The earliest manifestation of cardiomyopathy may be ventricular dilatation. A decreased shortening fraction follows. Reversal of these findings after treatment follows a reciprocal pattern. Diastolic function abnormalities may also occur in tachycardia-induced cardiomyopathy and may be the last parameter to correct after therapy.
  • Atrial angiography may occasionally be helpful as a roadmap during radiofrequency (RF) catheter ablation.

Other Tests:

  • During the arrhythmia in stable patients, 2-lead electrocardiography (ECG) is necessary.
    • Inspect the ECG for P wave axis and morphology, ventricular rate, and conduction block. Ectopic atrial tachycardia usually creates a P wave that is at least slightly different from sinus rhythm, first-degree AV block, and possible periods of second-degree AV block without termination of tachycardia.
    • To differentiate AET from sinus tachycardia secondary to cardiomyopathy, in 1990, Gelb and colleagues demonstrated that negative late terminal P wave forces in lead V2 occur more commonly in AET.
  • Patients should undergo Holter monitoring to determine the time spent in tachycardia and the ventricular rates. Holter monitoring is particularly useful to identify and analyze onsets and offsets of tachycardia.
  • Exercise testing may occasionally unmask an intermittent AET.


  • Although invasive studies are not usually necessary to make a diagnosis of AET, in some patients, an esophageal electrophysiology recording may be useful to assist confirmation of the diagnosis; the response to overdrive pacing can also be assessed. Many automatic foci transiently suppress when overdrive pacing is performed.
    • An invasive electrophysiology study can also be performed for these indications, but this is usually undertaken in patients undergoing attempt at RF ablation.
    • In patients with ectopic atrial tachycardias arising from the pulmonary veins, an esophageal recording may also be helpful in localizing the site of tachycardia.
  • The response of AET to adenosine may be persistence in the setting of AV block or a transient slowing of the tachycardia; it rarely terminates. DC cardioversion does not usually terminate the arrhythmia.
Histologic Findings: Endomyocardial biopsies often demonstrate vacuolized myocytes in the setting of tachycardia-induced cardiomyopathy.



Medical Care:

  • Acute AET
    • For patients presenting in cardiac arrest or with hemodynamic compromise, establish airway, breathing, and circulation (as is standard); provide appropriate monitoring; make sure that a defibrillator is available; and attempt conversion with a defibrillator if necessary.
    • Patients with AET may present with circulatory collapse similarly to patients with cardiomyopathy. Although these patients may benefit from afterload reduction and inotropy, primary therapy aimed at reversing their tachycardia usually is more successful.
    • Immediate rate control is desired in the child requiring significant intensive care unit support, including intubation. This can often be achieved without resorting to negative inotropic antiarrhythmic agents. Digitalization and the use of intravenous amiodarone may achieve rate control relatively quickly. An additional maneuver involves the use of atrial pacing (eg, esophageal, transthoracic, transvenous) to overdrive the atrial tachycardia to a point of consistent 2:1 AV block, thus lowering the ventricular response rate.
    • More frequently, patients are evaluated in the clinical setting, and hospitalization is often only necessary for initiation of certain antiarrhythmic medications.
  • Chronic AET


    • Three options are available for treatment of patients with AET, including medication to suppress the arrhythmia or control the ventricular response, surgery, or, more recently, RF ablation. Long-term oral medication is the mainstay of therapy in patients not undergoing RF ablation. Class IC and III antiarrhythmic agents are generally the most effective, and a staged approach is recommended. Medical therapy may be effective in as many as 75% of patients, but more than one medication is usually needed.


    • RF ablation has been very successful in curing AET, with success rates ranging from 75-100%. The complication rates are similar to other RF ablation procedures, with a higher risk of recurrence.

Surgical Care: Although surgical cryoablation has previously been used to treat patients with AET, this has been primarily supplanted by catheter RF ablation techniques. The encircling technique uses 2 catheters capable of delivering RF energy as mapping catheters, alternating the reference and roving catheters until no site provides an earlier signal than the reference. This early reference catheter is then used to deliver ablation.


Drugs with some effect in AET include digoxin (used predominantly for rate control), amiodarone, propafenone, moricizine, flecainide, procainamide, and esmolol. Only digoxin and oral amiodarone are devoid of negative inotropic effect. Adequate control may not require the complete abolition of all atrial ectopic beats or runs.

Drug Category: Antiarrhythmic agents -- These agents alter the electrophysiologic mechanisms responsible for arrhythmia.
Drug Name
Digoxin (Lanoxin, Lanoxicaps) -- Cardiac glycoside with direct inotropic effects in addition to indirect effects on the cardiovascular system. It 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. Used to control ventricular rate when administering propafenone, flecainide, or procainamide.
Adult Dose 0.125-0.375 mg PO qd
Pediatric Dose Digitalizing dose (administer one half of the total digitalizing dose [TDD] initially, then one fourth of TDD at 6- and 12-h intervals):
1 month to 2 years: 35-60 mcg/kg PO
2-5 years: 30-40 mcg/kg PO
5-10 years: 20-35 mcg/kg PO
>10 years: 10-15 mcg/kg PO
Maintenance dose: Use 25-35% of PO loading dose
Contraindications Documented hypersensitivity; beriberi heart disease; idiopathic hypertrophic subaortic stenosis; constrictive pericarditis; carotid sinus syndrome
Interactions Medications that may increase 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
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Hypokalemia may reduce positive inotropic effect of digitalis; IV calcium may produce arrhythmias in digitalized patients; hypercalcemia predisposes patients 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; patients with incomplete AV block may progress to complete block when treated with digoxin; exercise caution in hypothyroidism, hypoxia, and acute myocarditis
Drug Name
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.
Adult Dose Loading dose: 800-1600 mg/d PO in 1-2 doses for 1-3 wk, then 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, then 540 mg over next 18 h
Maintenance dose: 400 mg PO qd
Pediatric Dose Loading dose: 10-15 mg/kg/d or 600-800 mg/1.73 m2/d PO for 4-14 d or until adequate control of arrhythmia is attained, reduce to 5 mg/kg/d or 200-400 mg/1.73 m2/d for several wk (limited data available for IV loading dose)
Maintenance dose: 2.5 mg/kg/d PO or lowest effective dose following loading dose
Contraindications Documented hypersensitivity; complete AV block; intraventricular conduction defects
Interactions Increases effect and blood levels of theophylline, quinidine, procainamide, phenytoin, methotrexate, flecainide, digoxin, cyclosporine, beta-blockers, and anticoagulants; cardiotoxicity of amiodarone is increased by ritonavir, sparfloxacin, and disopyramide; coadministration with calcium channel blockers may cause an additive effect and further decrease myocardial contractility; cimetidine may increase levels
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Caution in breastfeeding women; caution in thyroid or liver disease; may cause proarrhythmic effect, optic neuritis, CNS toxicity, hypothyroidism, hepatotoxicity, interstitial pneumonitis, or pulmonary fibrosis
Drug Name
Esmolol (Brevibloc) -- Excellent drug for use in patients at risk of 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 for titration to desired effect and quick discontinuation if needed.
Adult Dose Loading dose: 250-500 mcg/kg/min IV for 1 min followed by a 4-min maintenance infusion of 50 mcg/kg/min IV; if adequate therapeutic effect (ie, decreased HR and BP) not observed within 5 min, repeat loading dose and follow with maintenance infusion using increments of 100 mcg/kg/min for 4 min; sequence may be repeated q5-10min, increasing maintenance infusion by 50 mcg/kg/min with each sequence; not to exceed 200 mcg/kg/min
Pediatric Dose Infants and children: Limited information available; suggested dose is 100-500 mcg/kg IV over 1 min initial; followed by 200 mcg/kg/min IV; titrate upward by 50-100 mcg/kg/min q5-10min until heart rate or BP decreases by >10%; typical dose 550 mcg/kg/min (range is 300-1000 mcg/kg/min)
Contraindications Documented hypersensitivity; uncompensated congestive heart failure; bradycardia; cardiogenic shock; AV conduction abnormalities
Interactions Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effect; cardiotoxicity 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
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Beta-adrenergic blockers may mask signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; symptoms of hyperthyroidism, including thyroid storm, may worsen when medication is abruptly withdrawn; withdraw drug slowly and monitor patient closely
Drug Name
Propafenone (Rythmol) -- Treats life-threatening arrhythmias. Possibly works by reducing spontaneous automaticity and prolonging refractory period.
Adult Dose 150 mg PO q8h initial; may increase q3-4d; not to exceed 300 mg q8h
Pediatric Dose Infants and children: Not established, the following doses have been suggested:
150-400 mg/m2/d PO divided tid/qid; may increase by 100 mg/m2/d q2-3d to achieve adequate control; not to exceed 600 mg/m2/d
Alternatively, 8-10 mg/kg/d PO divided tid/qid; may increase by 2 mg/kg/d to achieve adequate control; not to exceed 20 mg/kg/d
Contraindications Documented hypersensitivity; bronchospastic disorders; conduction disorders; bradycardia; uncontrolled heart failure; coadministration with ritonavir or amprenavir
Interactions Inhibits CYP2D6 and may decreases serum levels of isoenzyme substrates (eg, rifampin, cimetidine, quinidine, warfarin); inhibitors of CYP2D6 (eg, beta-blockers, amiodarone, paroxetine, fluoxetine, ritonavir), CYP1A2 (eg, cimetidine, ritonavir), or CYP3A4 (eg, amprenavir, ritonavir, erythromycin, amiodarone, fluoxetine) may increase blood levels
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Should only be used for life-threatening arrhythmias; caution in congestive heart failure, myocardial infarction, or hepatic dysfunction (adjust dose)
Drug Name
Moricizine (Ethmozine) -- Class I antiarrhythmic agent. Significantly prolongs conduction within atrium, AV node, and ventricular myocardium without affecting refractory periods. No direct effect on sinus node function.
Adult Dose 200 mg PO q8h; may increase by 150 mg/d q3d until adequate control achieved; not to exceed 900 mg/d
Pediatric Dose Not established, the following doses have been suggested:
200 mg/m2/d PO divided q8h; may increase by 100 mg/m2/d q2-3d to achieve adequate control; not to exceed 600 mg/m2/d
Contraindications Documented hypersensitivity; preexisting second- or third-degree AV block; right bundle branch block when associated with left hemiblock (bifascicular block) if pacemaker not in place; cardiogenic shock
Interactions Coadministration with drugs prolonging QT interval (eg, amiodarone, dofetilide, erythromycin, gatifloxacin) may increase risk of proarrhythmic effects
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions Caution in renal or hepatic disease (start dose at <600 mg/d), sick sinus syndrome, and CHF; reserve use for life-threatening arrhythmias; may show proarrhythmic effect, caution in electrolyte disturbances; common adverse effects include dizziness and headache
Drug Name
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 upon AV nodal conduction time and intra-atrial conduction times, although present, are less pronounced than on ventricular conduction velocity.
Adult Dose 100 mg PO q12h; may increase by 100 mg/d q4d until adequate response achieved; not to exceed 400 mg/d
Pediatric Dose 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: Typical dose is 3-6 mg/kg/d or 100-150 mg/m2/d PO divided tid
Contraindications Documented hypersensitivity; third-degree AV block; right bundle branch block when associated with left hemiblock (bifascicular block) if pacemaker not in place; cardiogenic shock
Interactions Beta-adrenergic blockers, verapamil, and disopyramide may have additive inotropic effects when administered with flecainide; may increase digoxin serum levels; CYP2D6 inhibitors (eg, ritonavir, amiodarone, cimetidine) may increase serum levels and cardiotoxicity
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Because of proarrhythmic effect and associated deaths, should only be used for life-threatening arrhythmias; caution in renal or hepatic impairment (adjust dose), CHF, and post-MI
Drug Name
Procainamide (Procan, Pronestyl) -- Class IA antiarrhythmic used for PVCs, ventricular tachycardias, and SVTs. Increases refractory period of the atria and ventricles. Myocardiac excitability is reduced by an increase in threshold for excitation and inhibition of ectopic pacemaker activity.
Adult Dose 0.5-1 g PO q6h (as SR)
Loading dose: 30 mg/min IV at continued infusion rates until arrhythmia is suppressed, patient becomes hypotensive, QRS widens 50% above baseline, or a maximum dose of 17 mg/kg is administered
Once arrhythmia is suppressed, may infuse at continuous rate of 1-4 mg/min
Pediatric Dose Not established; the following doses have been suggested:
15-50 mg/kg/d PO divided q3-6h; not to exceed 4 g/d
20-30 mg/kg/d IM divided q4-6h; not to exceed 4 g/d
Loading dose: 3-6 mg/kg/dose IV infused over 5 min; not to exceed 100 mg/dose; may repeat q5-10h to a maximum of 15 mg/kg per loading dose
Maintenance dose: 20-80 mcg/kg/min IV; not to exceed 2 g/d
Contraindications Documented hypersensitivity; complete heart block or second- or third-degree heart block if pacemaker not in place; torsade de pointes; systemic lupus erythematosus
Interactions Increased levels of procainamide metabolite NAPA when coadministered with 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; coadministration with sparfloxacin may increase risk of cardiotoxicity
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Monitor for hypotension; plasma concentrations of procainamide and active metabolite (NAPA) may increase in renal failure; high or toxic concentrations may induce AV block or abnormal automaticity; caution in complete AV block, digitalis intoxication, organic heart disease, renal disease, and hepatic insufficiency (adjust dose)



  • AET is one of the incessant tachycardias, which may become associated with myocardial dysfunction if the average ventricular rate remains elevated over a long term.


  • Several reports have documented the spontaneous remission of AET in the pediatric population and in young adults. This may occur in as many as one third of patients following withdrawal of medication.



Special Concerns:

  • Patients with AET should be monitored by a cardiologist.
  • RF ablation can be curative and performed with a high degree of success, a low complication rate, and a low recurrence rate.