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Supraventricular Tachycardia, Junctional Ectopic Tachycardia
Article Last Updated: Aug 3, 2007
AUTHOR AND EDITOR INFORMATION
Section 1 of 11  
Author: M Silvana Horenstein, MD, Director, Pediatric Cardiology, Department of Pediatrics, Division of Pediatric Cardiology, Hospital Italiano (Mendoza, Argentina)
M Silvana Horenstein is a member of the following medical societies: American College of Cardiology
Coauthor(s):
Robert Hamilton, MD, Section Head, Electrophysiology, Division of Cardiology, Professor, Department of Pediatrics, The Hospital for Sick Children and University of Toronto, Canada
Editors: Charles Berul, MD, Assistant Professor, Department of Pediatrics, Harvard Medical School; Senior Associate, Department of Cardiology, Children's Hospital of Boston; Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc; Hugh D Allen, MD, Professor, Departments of Pediatrics and Medicine, Ohio State University College of Medicine and Public Health; Gilbert Herzberg, MD, Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College; Stuart Berger, MD, Professor of Pediatrics, Division of Cardiology, Medical College of Wisconsin; Chief of Pediatric Cardiology, Medical Director of Pediatric Heart Transplant Program, Medical Director of The Heart Center, Children's Hospital of Wisconsin
Author and Editor Disclosure
Synonyms and related keywords:
supraventricular tachycardia, junctional ectopic tachycardia, JET, junctional automatic tachycardia, Coumel's tachycardia
Background
Junctional ectopic tachycardia (JET) is characterized by rapid heart rate for a person's age that is driven by a focus with abnormal automaticity within or immediately adjacent to the atrioventricular (AV) junction of the cardiac conduction system (ie, AV node–His bundle complex). It does not have the features associated with reentrant tachycardia (eg, AV node reentry) because this tachycardia does not respond to a single extrastimulus and does not convert with programmed stimulation or cardioversion, it may (or may not) have ventriculoatrial (VA) dissociation, and administration of adenosine results in VA dissociation without termination.
JET primarily occurs in 2 forms: idiopathic chronic junctional ectopic tachycardia is observed in the setting of a structurally normal heart, and transient postoperative junctional ectopic tachycardia occurs following repair of congenital heart disease. In addition, nonparoxysmal junctional tachycardia, which is a related but rare pattern of arrhythmia, can be observed in the setting of digoxin toxicity.
Pathophysiology
The pathophysiology of JET is unclear. Postoperative JET is associated with manipulation within the crux of the heart. It is believed to be secondary to trauma and/or inflammation of the conduction tissue.
As implied by the synonym junctional automatic tachycardia, the mechanism may be automaticity. Others have suggested that triggered activity is responsible for this disorder.
The location of the responsible tissue probably is truly ectopic to the primary conduction pathway of the AV junction because JET has been treated successfully by the application of radiofrequency catheter lesions without the production of AV block. Intracardiac mapping shows a normal heart volume interval and VA dissociation, or VA association if VA conduction is present.
Junctional acceleration, albeit at a lesser rate than typical JET, is a recognized phenomenon during and following radiofrequency energy delivery for modification of slow pathway conduction in the therapy of AV node reentry.
Histamine, eosinophil cation protein, or other products of mast cell, eosinophil, or basophil degranulation that are liberated in response to cardiopulmonary bypass have been implicated in the genesis of transient postoperative JET. The relative levels of various cytokines may also play a role. Low magnesium levels have been noted in children who develop JET following cardiopulmonary bypass surgery.
Frequency
United States
Postoperative JET occurred in 5.6% of 594 patients who underwent cardiac operation.
International
In one series, postoperative JET was identified in 7.5% of young patients undergoing Fontan procedures. In another series, postoperative JET requiring intervention was identified in 1.5% of infants undergoing the arterial switch procedure. JET is one of the rarest forms of supraventricular tachycardia in infants.
Mortality/Morbidity
Although not a frequent type of arrhythmia, JET is one of the most serious and difficult to treat supraventricular tachycardias. Rare case reports have suggested that JET may be associated with progression to complete AV block. This does not appear to be the case in postoperative JET, and it has not been the author's experience in the rare cases of idiopathic JET.
- Postoperative JET is usually transient and begins upon rewarming the patient. Its morbidity and mortality relates to the fact that it occurs at an extremely vulnerable period following cardiac surgery, when nodal inflammation and/or ischemia may be present and ventricular function is often diminished. The additional insults of poor ventricular filling because of tachycardia and the loss of AV sequential contraction are considered to contribute significantly to morbidity and mortality. However, if the JET rate is not too fast, or is somewhat faster than the sinus node rate, it can be well tolerated until JET subsides spontaneously.
- In a large series of patients with postoperative JET, dopamine use and an age less than 6 months were associated with the development of this tachycardia. However, only 39% of patients required intervention.
- Congenital JET occurs in neonates and infants as an incessant tachycardia that usually results in tachycardia-induced cardiomyopathy.
- Mortality in these patients has been reported to be as high as 34% and may occur secondary to congestive heart failure, sudden onset of ventricular fibrillation, sudden evolution to paroxysmal complete atrioventricular block, and as result of proarrhythmic effect of drug therapy and medical interventions.
Age
- Congenital JET is presumed to be present from birth but may not be identified until months or years later.
- Postoperative JET most commonly occurs in younger patients (as stated above, it was found to occur more frequently in patients younger than 6 mo), but is also known to occur in teenagers and adults after cardiopulmonary bypass surgery.
History
In general, postoperative JET occurs in the hospital with rapid hemodynamic instability, whereas congenital JET may have a more insidious course before producing signs of congestive heart failure.
- Postoperative JET usually begins 6-72 hours following cardiopulmonary bypass surgery for repair of congenital heart lesions. It is usually identified during monitoring in the intensive care unit. A fall in blood pressure and cardiac output usually occurs concomitantly.
- The onset of congenital JET is often insidious. The clinical presentation of congenital JET may occur from birth to age 4 weeks. However, sporadic cases of intrauterine tachycardia have been reported in infants who presented with JET at birth. Prolonged moderate tachycardia may not be recognized until myocardial dysfunction and signs of congestive heart failure ensue. Heart rate variability is decreased; the heart rate is very regular except for occasional sinus capture beats.
Physical
Patients with congenital JET present with moderate tachycardia and signs of congestive heart failure. If VA dissociation has occurred, which is usually the case, cannon waves may be present in the jugular venous pulse and the intensity of the first heart sound is variable.
Causes
The speculative causes of postoperative JET are discussed in Pathophysiology. The one fairly uniform finding is a preceding cardiopulmonary bypass surgery.
- The cause of congenital JET is unknown. A family history of JET has been reported in 50-55% patients.
- Postoperative JET occurs more often after tetralogy of Fallot repair. It has been associated with resection of muscle bundles, increased traction through the right atrium for relief of right ventricular outflow tract obstruction, and with higher bypass temperatures.
- The nonparoxysmal form of junctional tachycardia, which may be a triggered arrhythmia, is observed following digoxin overdose.
Atrial Flutter
Supraventricular Tachycardia, Atrial Ectopic Tachycardia
Supraventricular Tachycardia, Atrioventricular Node Reentry
Supraventricular Tachycardia, Wolff-Parkinson-White Syndrome
Other Problems to be Considered
Permanent junctional reciprocating tachycardia
Lab Studies
- In patients with postoperative JET, assess serum magnesium levels, electrolyte levels, and lactate concentration.
- In patients with other forms of JET, assess serum magnesium, electrolytes, and digoxin levels.
Imaging Studies
- Chest radiography: Chest radiography is used to assess for ventricular dilatation and dysfunction (when signs of pulmonary edema are present) in all patients with JET.
- Echocardiography:
- Transthoracic echocardiography is also used to assess for ventricular dilatation and dysfunction in all patients with JET.
- Transthoracic echocardiography and transesophageal echocardiography may be used to assess for significant postoperative residual hemodynamic abnormalities in patients with postoperative JET.
- Rarely, cardiac catheterization is required in postoperative JET to assess for significant postoperative residual hemodynamic abnormalities.
Other Tests
- Electrocardiography is the single most important test in all forms of JET. Diagnosis of JET is based upon the following:
- QRS morphology is similar to sinus or atrial-conducted beats.
- JET usually starts gradually (ie, has a "warm-up" pattern).
- In junctional rhythm with 1:1 retrograde VA conduction, ventricular rate is equal to the atrial rate.
- In junctional rhythm with retrograde VA dissociation, an irregular ventricular rate may be observed when appropriately timed atrial impulses conduct to the ventricles.
- An exception to these last two described patterns occurs rarely, when both JET and complete heart block are present.
- Adenosine: The response to adenosine can also be used to identify whether the atrium or junction are driving the rhythm; however, this should be performed with care if the patient is severely ill. For example, in JET with 1:1 VA conduction, JET may be difficult to distinguish from other forms of supraventricular tachycardia with AV conduction. In this case, intravenous adenosine may be given to block VA conduction and, thus, help visualize atrial nonparticipation.
Procedures
- In postoperative patients, the use of atrial wire recordings to assess P wave timing can facilitate determination of the diagnosis.
- In some patients with 1:1 AV or VA association, whether the rhythm is being driven by the atrium or junction may be unclear.
- If this occurs, pacing the atrium faster than the intrinsic rhythm and then identifying the origin of the first escape beats following termination of pacing may be helpful.
- In JET with 1:1 VA conduction, an atrial premature beat introduced immediately before the expected atrial depolarization does not conduct retrogradely because the origin of the intrinsic atrial depolarization is from retrograde conduction of the JET. However, if it were an atrial tachycardia with first-degree AV block (ie, with 1:1 AV association) a timed atrial premature beat would advance (ie, make it appear earlier in the electrogram) the next ventricular and atrial depolarizations. This would prove that ventricular depolarizations are being conducted from atrial depolarizations and not vice versa.
Histologic Findings
Histological studies have shown His bundle degeneration, Purkinje cell tumors, and fibroelastosis.
Medical Care
Congenital JET is usually treated initially with antiarrhythmic therapy, with the choice of medication guided by the degree of coexisting ventricular dysfunction. The most appropriate management of asymptomatic infants with "slow" JET (ie, 150 bpm) is debatable. However, these asymptomatic patients should have close monitoring. Numerous therapeutic options have been used for the treatment of postoperative JET, including the following:
- Some propose that management of symptomatic infants with slow JET should consist of digoxin to control symptoms of cardiac failure and antiarrhythmic drugs to control the ventricular rate of the arrhythmia. However, caution should be exerted, because development of ventricular fibrillation or faster tachycardia (£400 bpm) during progressive digoxin loading has been described in patients with congenital JET and severe cardiac failure.
- Propafenone has also been effective in preventing or controlling JET in some neonates, especially neonates with slower ventricular rates (approximately 170 bpm).
- Amiodarone may successfully control ventricular rate. Furthermore, the combination of amiodarone and an Ic antiarrhythmic drug can be used to reduce the dose of amiodarone.
- A recent multicenter study has shown that success of intravenous amiodarone is dose-related. However, so are its side effects. Therefore, the dose-related risks should be taken into account when treating children with incessant arrhythmias.
- True drug-refractory JET is very rare. Therefore, in patients who fail to respond to a single drug regimen, a second antiarrhythmic agent with different electrophysiological effects may be added.
- Controlled hypothermia has been relatively effective in reducing JET rate in early postoperative patients. These patients are often intubated and can be effectively paralyzed, sedated, and cooled. Other traditional approaches include increase of ventricular preload and reduction of inotropic agents (which are also usually chronotropic) as much as possible.
- The use of atrial or AV sequential pacing can help to restore AV sequence and cardiac output once the JET rate is reduced.
- Multiple antiarrhythmic agents have been used and are considered somewhat effective in postoperative JET.
- Occasionally, atrial high-rate pacing to the point of 2:1 AV block can provide a controlled ventricular response while continuing to suppress the JET focus. This finding suggests a relatively high insertion site of the JET focus into the AV conduction system.
- Ventricular paired pacing, with or without additional atrial pacing, has been used in rare cases when patients have not responded to other therapies. This technique is potentially dangerous and requires essentially constant monitoring and adjustment by personnel who are extremely familiar with electrophysiologic procedures. During ventricular paired pacing, electrolytes and antiarrhythmic medications should be administered by constant infusions only.
- A recently published small-case series advocates for radiofrequency catheter ablation for JET, if antiarrhythmic drug therapy has failed. Success was achieved safely by plotting the entire His-bundle using a modern navigation system that would permit marking the spot of earliest retrograde conduction during tachycardia, and, later, empirically ablating that spot during sinus rhythm.
Surgical Care
The primary functions of surgical care in postoperative JET are to correct major residual defects that may be contributing to morbidity, to ensure that atrial-based pacing can be achieved, and to provide extracorporeal life support (ie, extracorporeal membrane oxygenation [ECMO]) if required.
The mechanism of JET is not well understood, and identifying a specific pharmacologic agent to target the disorder is difficult. Because some experimental forms of junctional tachycardia exhibit a triggered mechanism induced by digoxin toxicity, avoiding digoxin seems reasonable. Nevertheless, digoxin is frequently used in the treatment of JET without apparent adverse effect but with questionable efficacy. Ventricular dysfunction is often prominent in patients with postoperative and congenital JET; thus, calcium channel blockers are usually avoided because of their negative inotropic effects. One case report has documented use of calcium channel blockers with apparent effectiveness. Drugs effective against automatic tachycardias appear to be effective in the treatment of congenital and postoperative JET. Congenital JET has been successfully controlled with amiodarone, propafenone, or cautious combinations of both medications. Postoperative JET has been successfully controlled with amiodarone, propafenone, procainamide, or moricizine (discontinued from market in July 2007). Propranolol or sotalol have also been used in the therapy of these rhythm disorders.
Drug Category: Antiarrhythmic agents
These agents alter the electrophysiologic mechanisms responsible for arrhythmia.
| Drug Name | Amiodarone (Cordarone) |
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| Description | May inhibit AV conduction and sinus node function. Prolongs action potential and refractory period in myocardium and inhibits adrenergic stimulation.
Before administration, control the ventricular rate and CHF (if present) with digoxin. |
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| Adult Dose | 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 IV (200 mL) over next 6 h, then 540 mg IV over next 18 h
Maintenance dose: 400 mg/d PO |
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| Pediatric Dose | Loading dose: 10-15 mg/kg/d PO 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 weeks; limited data available for IV loading dose
Maintenance dose: 2.5 mg/kg/d PO or lowest effective dose following loading |
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| Contraindications | Documented hypersensitivity; complete AV block; intraventricular conduction defects |
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| 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 |
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| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus
|
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| Precautions | Caution in breastfeeding women, thyroid, or liver disease; may cause proarrhythmic effect, optic neuritis, CNS toxicity, hypothyroidism, hepatotoxicity, interstitial pneumonitis, or pulmonary fibrosis |
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| Drug Name | Propafenone (Rythmol) |
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| Description | Treats life-threatening arrhythmias. Possibly works by reducing spontaneous automaticity and prolonging refractory period. |
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| Adult Dose | 150 mg PO q8h initial, may increase at q3-4d; not to exceed 300 mg q8h |
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| Pediatric Dose | Infants and children: Not established, the following doses have been suggested:
200-300 mg/m2/d PO divided tid/qid, may increase by 100 mg/m2/d q2-3d to achieve adequate control; not to exceed 450 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 |
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| Contraindications | Documented hypersensitivity; bronchospastic disorders; conduction disorders; bradycardia; uncontrolled heart failure; coadministration with ritonavir or amprenavir |
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| 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 |
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| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus
|
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| Precautions | Should only be used for life-threatening arrhythmias; caution in congestive heart failure, myocardial infarction, or hepatic dysfunction (adjust dose) |
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| Drug Name | Moricizine (Ethmozine) |
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| Description | Discontinued in July 2007 because of diminished market demand. Class I antiarrhythmic agent. Significantly prolongs conduction within the atrium, AV node, and ventricular myocardium without affecting their refractory periods. No direct effect on sinus node function. |
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| Adult Dose | 200 mg PO q8h, may increase by 150 mg/d q3d until adequate control achieved; not to exceed 900 mg/d |
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| 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 |
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| 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 |
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| Interactions | Coadministration with drugs prolonging QT interval (eg, amiodarone, dofetilide, erythromycin, gatifloxacin) may increase risk of proarrhythmic effects |
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| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
|
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| 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 |
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| Drug Name | Procainamide (Procan, Pronestyl) |
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| Description | Class IA antiarrhythmic used for PVCs, ventricular tachycardias, and supraventricular tachycardias. 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. |
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| Adult Dose | 0.5-1 g PO q6h (as SR)
Loading dose: 30 mg/min IV as continuous infusion 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 a continuous rate of 1-4 mg/min |
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| 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
Alternatively, 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 20 min; not to exceed 100 mg/dose; may repeat q5-10min to a maximum of 15 mg/kg per loading dose
Maintenance dose: 20-80 mcg/kg/min IV; not to exceed 2 g/d |
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| Contraindications | Documented hypersensitivity; complete heart block; second- or third-degree heart block if pacemaker not in place; torsade de pointes; systemic lupus erythematosus |
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| 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 and may increase bioavailability; coadministration with sparfloxacin may increase risk of cardiotoxicity |
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| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus
|
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| 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) |
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| Drug Name | Propranolol (Inderal) |
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| Description | Class II antiarrhythmic nonselective beta-adrenergic receptor blocker with membrane-stabilizing activity that decreases automaticity of contractions. |
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| Adult Dose | 1-3 mg IV (under careful monitoring); not to exceed 1 mg/min to avoid lowering blood pressure and causing cardiac standstill; allow time for drug to reach site of action (particularly if slow circulation); administer second dose after 2 min prn; thereafter, do not administer additional drug in <4 h
Do not continue IV doses after desired alteration in rate or rhythm achieved; switch to PO ASAP; 10-30 mg PO tid/qid (usual); alternatively, administer total daily dose as SR product qd |
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| Pediatric Dose | 0.5-1 mg/kg/d PO divided q6-8h initially; titrate upward q3-5d prn; typical dose is 2-4 mg/kg/d; not to exceed 16 mg/kg/d or 60 mg/d; in older children, total daily PO dose may be administered as SR product qd
0.01-0.1 mg/kg IV administered over 10 min; not to exceed 1 mg (infants) and 3 mg (children) |
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| Contraindications | Documented hypersensitivity; uncompensated congestive heart failure; bradycardia; cardiogenic shock; AV conduction abnormalities |
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| Interactions | Coadministration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase |
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| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus
|
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| Precautions | Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; withdraw drug slowly and monitor closely |
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| Drug Name | Sotalol (Betapace) |
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| Description | Class III antiarrhythmic agent, which blocks potassium channels, prolongs action potential duration (APD), and lengthens QT interval. Noncardiac selective beta-adrenergic blocker. |
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| Adult Dose | 80 mg PO bid and increase dose gradually q2-3d to 240-320 mg/d |
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| Pediatric Dose | Not established; the following doses have been suggested:
Initial: 200 mg/m2/d PO divided bid/tid; not to exceed 160 mg/d
Maintenance dose: 2-5 mg/kg/d PO divided bid/tid |
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| Contraindications | Documented hypersensitivity; sinus bradycardia; second- and third-degree AV block; prolonged QT |
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| 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 |
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| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
|
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| 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; slower dose titration and lower maintenance doses required in renal impairment |
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| Drug Name | Atenolol (Tenormin) |
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| Description | Selectively blocks beta1-receptors with little or no effect on beta2 types. |
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| Adult Dose | 50 mg PO qd; may increase to 100 mg/d |
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| Pediatric Dose | 0.8-1.5 mg/kg PO qd; not to exceed 2 mg/kg/d |
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| Contraindications | Documented hypersensitivity; congestive heart failure; pulmonary edema; cardiogenic shock; AV conduction abnormalities; heart block (without a pacemaker) |
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| Interactions | Coadministration with aluminum salts, barbiturates, calcium salts, cholestyramine, NSAIDs, penicillins, and rifampin may decrease effects; haloperidol, hydralazine, loop diuretics, and MAOIs may increase toxicity of atenolol |
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| Pregnancy | D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
|
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| 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 an IV, carefully monitor BP, heart rate, and ECG |
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Prognosis
- Spontaneous resolution of congenital JET has been observed in up to one third of patients who reach age one year. Patients who continue to experience JET may do so at slower rates.
- Curative attempts with radiofrequency catheter ablation therapy are probably warranted in patients with uncontrolled JET or if their size and age is sufficient to minimize procedural risks. Nevertheless, permanent AV block is a significant potential risk in the ablation of congenital JET.
- Postoperative JET usually subsides after 36 hours without recurrence.
Patient Education
Medical/Legal Pitfalls
- Failure to identify JET in a neonate with potential for developing tachycardia-induced cardiomyopathy and sudden death.
- Failure to promptly identify postoperative JET with development of rapid hemodynamic compromise and death.
| Media file 1:
Lead II rhythm strip of a surface ECG from a patient with postoperative JET. Atrial activity (P) is marked with blue lines and ventricular rhythm (QRS) is marked in red. Note a narrow QRS due to its origin at the junction. Dissociation between atrial and ventricular rhythm can be seen: for QRS complexes following the P waves the PR interval would be exceedingly short to allow conduction, and some P waves fall after the QRS. |
 |  View Full Size Image | |
Media type: Rhythm Strip
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Supraventricular Tachycardia, Junctional Ectopic Tachycardia excerpt Article Last Updated: Aug 3, 2007
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