Atrioventricular Nodal Reentry Tachycardia

Background

Atrioventricular nodal reentry tachycardia (AVNRT) is the most common type of reentrant supraventricular tachycardia (SVT). The substrate for AVNRT is the presence of dual AV nodal pathways that are bounded by Koch’s triangle – generally a slow and a fast pathway but sometimes two slow pathways.^{[1, 2]}  (See Etiology.)

Because of the abrupt onset and termination of the reentrant SVT, the nonspecific term paroxysmal supraventricular tachycardia (or even the misleading term paroxysmal atrial tachycardia [PAT]) has been used to refer to these tachyarrhythmias. With improved knowledge of the electrophysiology of reentrant SVT, greater specificity in nomenclature, based on the mechanism of reentry, has been possible. Such improved classification aids in the choice of appropriate therapies. (See Etiology, Prognosis, Treatment, and Medication.)

AVNRT is usually well tolerated, often occurring in patients with no structural heart disease.^[3] (See Prognosis, Presentation, and Workup.)

Patient education

Patients should be instructed on vagal maneuvers (Valsalva, diving reflex). These are used to try to terminate an episode of AVNRT. Patients with hemodynamic compromise or syncope should be instructed on avoiding activities that could be dangerous to them or to others (eg, driving, swimming) while the risk of an episode remains. Ablation obviates the need for long-term restriction.

For patient education information, see the Heart Health Center, as well as Supraventricular Tachycardia (SVT, PSVT).

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Etiology

The substrate for atrioventricular (AV) nodal reentry tachycardia (AVNRT) is anatomic. AVNRT occurs in young, healthy patients but also in those with chronic heart disease.

In patients with AVNRT, two pathways connect into the AV node and help form part of the reentrant circuit.^[4] In the majority of patients with AVNRT, antegrade conduction occurs over the slow pathway, and retrograde conduction occurs over the fast pathway during AVNRT. (See the image below.)

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Electrophysiologic mechanism of atrioventricular nodal reentry tachycardia (AVNRT).

In most patients with AVNRT, the tachycardia is initiated when an atrial premature complex is blocked in the fast pathway but can conduct via the slow pathway. Although many patients may have a dual pathway physiology, for AVNRT to occur, the fast pathway must have a longer refractory period antegrade than the slow conducting pathway.

In approximately 10% of patients, AVNRT is induced by premature ventricular stimulation. In addition to the typical mechanism of AV nodal reentry described above, atypical AV nodal reentry can occur in the opposite direction, with antegrade conduction in the fast pathway and retrograde conduction in the slow pathway. Less commonly, the reentrant circuit can be over two slow pathways, the so-called slow-slow AV nodal reentry. (See the images below.)

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Atypical atrioventricular nodal (AV) reentry tachycardia. Often, an inverted P wave is seen just before the QRS complex in leads II, III, aVF. This re....

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Typical atrioventricular nodal (AV) reentry tachycardia. In this electrocardiogram, the P wave appears immediately after or just within the QRS comple....

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Epidemiology

In the United States, atrioventricular nodal reentry tachycardia (AVNRT) occurs in 60% of patients (with a female predominance) presenting with paroxysmal supraventricular tachycardia (SVT), the other major types being bypass-mediated tachycardias and atrial tachycardias. SVT has a prevalence of 2.25 cases per 1000 in the general population and an incidence of 35 per 100,000 patients.^[5] Internationally, the occurrence of AVNRT is similar to that in the United States.

AVNRT may occur in persons of any age. It is common in young adults, but some patients do not present until their seventh or eighth decade or later.

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Prognosis

The prognosis for patients with atrioventricular nodal reentry tachycardia (AVNRT) is usually good in the absence of structural heart disease. Most patients respond acutely to vagal maneuvers or adenosine and long term to medications to prevent recurrence or to radiofrequency ablation, which is approximately 95% curative and has a low risk of complications. It is the preferred method of treatment for most patients.

Complications of AVNRT include hemodynamic compromise, congestive heart failure, syncope, tachycardia-induced angina, cardiomyopathy, myocardial ischemia, and myocardial infarction.

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History

Atrioventricular nodal reentry tachycardia (AVNRT) is typically characterized by an abrupt onset and termination. Episodes may last from seconds to minutes to days. In the absence of structural heart disease, it is usually well tolerated.

Common symptoms include the following:

• Palpitations
• Nervousness
• Anxiety
• Lightheadedness
• Neck pounding^[6]
• Neck and chest discomfort
• Dyspnea
• Polyuria - Can occur after termination of an episode (due to the release of atrial natriuretic factor)

AVNRT may cause angina or myocardial infarction in patients with coronary artery disease and may cause or worsen heart failure in patients with poor left ventricular function.

Syncope may occur in patients with a rapid ventricular rate or prolonged tachycardia due to poor ventricular filling, decreased cardiac output, hypotension, and reduced cerebral perfusion. Syncope may also occur because of transient asystole when the tachycardia terminates, due to tachycardia-induced depression of the sinus node.

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Physical Examination

The heart rate is usually rapid, ranging from 150-250 beats per minute (bpm). It is usually 180-200 bpm in adults; in children, the rate may exceed 250 bpm.

Cannon A waves can be seen in the neck due to simultaneous atrial and ventricular contraction.

Hypotension may occur initially or with rapid ventricular rates and prolonged episodes. Sometimes, initial hypotension evokes a sympathetic response that increases blood pressure and may terminate the tachycardia by an increase in vagal tone.

Rarely, signs of left heart failure may develop or worsen in patients with poor left ventricular function.

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Approach Considerations

Atrioventricular nodal reentry tachycardia (AVNRT) can be initiated by ectopic atrial or ventricular beats. Typically, it is initiated by atrial ectopic beats that block in the fast pathway and travel antegrade via the slow pathway. There is a "jump" in AV nodal conduction at tachycardia onset with retrograde activation, such that atrial activation is nearly simultaneous or just after the ventricular activation.

Sometimes, supraventricular tachycardia (SVT) due to AVNRT can present with a wide QRS due to underlying conduction system disease or aberration. A wide QRS tachycardia with a typical bundle branch block morphology during SVT due to aberration is not uncommon.

Occasionally, distinguishing ventricular tachycardia from SVT can be difficult, but in most instances this can be accomplished using the clinical scenario, the QRS morphology (owing to the frequent occurrence of the aforementioned typical bundle branch block), evidence for AV dissociation (this may be difficult if there is simultaneous activation), physical examination (including the presence of neck vein pulsations^[6] ), and lack of fusion and capture.

In patients with an otherwise normal heart, considering carotid massage or adenosine is reasonable unless the patient is hemodynamically unstable, in which case cardioversion may be required.

If the diagnosis is in question, an electrophysiologic study helps to distinguish the potential mechanisms for the tachycardia. Therefore, an electrophysiologic study may be indicated for a patient with a wide QRS complex tachycardia in whom the mechanism is not clear, and is also reasonable if the plan is to attempt to ablate the tachycardia and cure it.^[8]

Echocardiography

Echocardiography can be used to evaluate for the presence of structural heart disease.

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Electrocardiography

Electrocardiographic (ECG) evaluation usually reveals a supraventricular origin of QRS complexes at rates of 150-250 bpm and a regular rhythm. The QRS complex is usually narrow unless a conduction abnormality is present or is functionally induced (aberrancy) from the rapid heart rate or the abrupt change in rate. (See the images below.)

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Atypical atrioventricular nodal (AV) reentry tachycardia. Often, an inverted P wave is seen just before the QRS complex in leads II, III, aVF. This re....

View Image

Typical atrioventricular nodal (AV) reentry tachycardia. In this electrocardiogram, the P wave appears immediately after or just within the QRS comple....

P waves are not usually seen, because they are buried in the QRS complex. A pseudo R prime may be seen in V₁, or pseudo S waves may be seen in leads II, III, or aVF. The onset is abrupt, with an atrial premature complex that conducts with a prolonged PR interval. Atypical AV nodal reentry includes fast antegrade/slow retrograde conduction with a P wave before the QRS complex. Slow-slow AV nodal reentry can occur, with a P wave occurring in mid diastole.

The PR interval may shorten over the first few beats at onset, or it may lengthen during last few beats preceding termination of the tachycardia.

Abrupt termination occurs with a retrograde P wave, sometimes followed by a brief period of asystole or bradycardia.

Although atrioventricular nodal reentry tachycardia (AVNRT) is usually a short RP interval tachycardia (with the P wave buried in the QRS complex), rarely, retrograde conduction can occur via a slow pathway, producing a long RP tachycardia. The latter form of tachycardia is indistinguishable from automatic atrial tachycardia on the surface 12-lead ECG if it originates from the low posterior right atrial septal region, and there is A 1:1 AV conduction and AV reciprocating tachycardia if the retrograde concealed slow pathway is present near the os of the coronary sinus (which can cause permanent junctional reciprocating tachycardia [PJRT]). This is important to recognize. AVNRT and PJRT are usually fairly easy to cure with catheter ablation,^[9] whereas automatic atrial tachycardia may be more difficult to cure.

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Electrophysiology

Typical findings in atrioventricular nodal reentry tachycardia (AVNRT) on electrophysiologic studies include dual-node physiology, a discontinuous pattern of atrial-to-ventricular conduction reflecting the differing conduction properties of fast and slow antegrade conduction, and/or sustaining slow antegrade conduction, which mimics the superimposition of the P wave and QRS complex observed in the clinical arrhythmia. The most typical endpoint of ablation for AVNRT is modification or elimination of slow pathway conduction associated with inability to induce the arrhythmia.^[8]

During ventricular pacing, retrograde activation is through the AV node and is demonstrated by early atrial activation in the His bundle electrogram.

Atypical AVNRT has fast-activation antegrade through the AV node and slow-activation retrograde that allows early atrial activation to occur at a distinct time after the QRS complex and is earliest in the posterior septal right atrium. AV-reciprocating tachycardia (AVRT) causes eccentric retrograde atrial activation.

In some instances, if an accessory pathway is septal, retrograde activation can mimic retrograde atrial activation through the AV node. This can be distinguished using adenosine administration with ventricular pacing to assess ventriculoatrial conduction, and through the use of ventricular extrastimuli during tachycardia that allows for preexcitation of the atria once the His bundle is refractory. Other interventions during the electrophysiologic study may further distinguish AVNRT from AVRT (such as para-Hisian pacing), as well as determine if the tachycardia is atrial tachycardia, sinoatrial reentry, or ventricular tachycardia.

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Approach Considerations

Rest, reassurance, sedation, and/or vagal maneuvers may terminate an attack of atrioventricular nodal reentry tachycardia (AVNRT). The successful management of an acute attack, however, depends on the symptoms, the presence of underlying heart disease, and the natural history of previous episodes.

In the presence of a wide-complex tachycardia, the institution of therapy should always follow a careful review of the patient's prior cardiac history, including left ventricular function and previous electrocardiograms (ECGs), which are helpful tools for defining the origin of the arrhythmia (ie, supraventricular vs ventricular).

The use of calcium channel blockers is contraindicated in patients with tachycardias of ventricular origin and may cause hemodynamic compromise and death.

Vagal maneuvers

To terminate AVNRT, try vagal maneuvers (eg, carotid sinus massage, exposure of the face to ice water, Valsalva maneuver) before initiating drug treatment. These maneuvers can also be tried after each pharmacologic approach. Vagal maneuvers are unlikely to work and should not be tried if hypotension is present. Sometimes, putting the patient in the Trendelenburg position facilitates termination with a vagal maneuver.

Direct-current synchronized cardioversion

Direct-current (DC) synchronized cardioversion is used to terminate an attack if the patient has hemodynamic compromise or if drug conversion fails and the patient continues to be symptomatic. However, DC cardioversion is rarely necessary for AVNRT.

Competitive atrial or ventricular pacing may be used if DC cardioversion is contraindicated (eg, if high doses of digitalis have been administered).

Diet

No specific recommendations or restrictions are necessary, but some patients' episodes are exacerbated by caffeine, theophylline, or theobromine in selected foods (coffee, tea, or chocolate, respectively). Alcohol may also be a trigger.

Activity

Advise the patient to rest during tachycardia, preferably in a supine position.

Consultations

Consultations include the following:

• Cardiologist
• Electrophysiologist

Transfer

Transfer to a facility capable of performing electrophysiologic studies and radiofrequency ablation may be needed.

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Pharmacologic Therapy

Drugs that can be used to terminate an attack include adenosine, calcium channel blockers (eg, diltiazem, verapamil), beta-blockers, and digitalis.

Adenosine

Adenosine is the first-line drug used for termination of atrioventricular nodal reentry tachycardia (AVNRT). It is a potent purinergic blocker and generally blocks activation preferentially in the “slow pathway” of the AVNRT reentry circuit. In rare cases, the administration of adenosine may lead to atrial fibrillation or even asystole for a short period.

Adenosine administration should be given through a central, large bore intravenous (IV) needle, as it has a very short half-life. It should be followed by a saline flush and elevation of the extremity in which it is being injected. The initial dose is 6 mg followed by 12 mg and occasionally 18 mg. It should not be used in heart transplantation patients, it may be ineffective if given to a patient taking theophylline, and it may be potentiated by dipyridamole.

Verapamil

Intravenous verapamil 5-10 mg is effective to stop AVNRT and it may be better tolerated in some individuals than adenosine. Generally, adenosine is given as the initial therapy, but verapamil may be useful in patients who have recurrent episodes as there is a longer half-life. Intravenous verapamil may cause hypotension and bradycardia.

Diltiazem

Intravenous diltiazem can be effective to terminate AV nodal reentry supraventricular tachycardia but, in our experience, it is not recommended as the primary approach to stop AVNRT.

A 2017 emergency medicine review suggests that nondihydropyridine calcium channel blockers such as diltiazem and verapamil may be as effective as adenosine for converting narrow-complex tachycardia, particularly for refractory states, to sinus rhythm, and that no statistically significant difference exists in the conversion rate between these agents and adenosine (>90% conversion rate for both drug groups) (although adenosine is rapid acting).^[3] However, adenosine is associated with more negative short-term side effects. Hemodynamically unstable patients should undergo electrical cardioversion.^[3]

Intravenous beta-blockers

Intravenous metoprolol and esmolol parked potentially effective to terminate AVNRT particularly when it is sympathetically mediated but these are not generally used to treat AVNRT unless the other therapies are not available or there is reason to suspect that the patient has catecholamine mediated AVNRT and that it will recur early on. The dosing of metoprolol is 5-10 mg and the dosing of esmolol is 250-500 mcg/kg undiluted IV push.

Other acute therapies to stop AVNRT

Although there have been some recommendations to use IV amiodarone, propafenone, flecainide and other therapies, we do not recommend these therapies in patients who have known AVNRT, and we generally do not recommend these therapies for patients who have paroxysmal SVT that is suspected to be AVNRT.

Preventive therapy

Preventive therapy is needed for frequent, prolonged, or highly symptomatic episodes that do not terminate spontaneously or for those that cannot be easily terminated by the patient. Drugs that are used for prevention of recurrence include long-acting beta-blockers, calcium channel blockers, and digitalis alone or in combination. No comparative studies indicate that a calcium channel antagonist is preferable or superior to a beta-adrenergic blocker for long-term management.

Novel therapy

Etripamil is an investigational intranasal spray; 35-140 mg can convert 65-95% of SVT within 15 minutes compared to 35% of those receiving placebo. The safety and efficacy of this therapy based on the initial study suggests that self-administration of this therapy may be possible by patients but further real-life data may be necessary.^{[10, 11]} Such a therapy may be indicated in patients with frequent, recurrent, generally well-tolerated, SVT in patients who are not good candidates for ablation or who prefer not to undergo ablation. This therapy may also be useful in the acute setting in the hospital in lieu of intravenous adenosine. The advantages are that an intravenous line is not necessary and side effects are minimal.

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Radiofrequency Catheter Ablation

Radiofrequency catheter ablation^[9] of the reentrant circuit should be considered in patients who have frequent or highly symptomatic episodes, who do not want drug therapy, who cannot tolerate the drugs, or in whom drug therapy fails.

Radiofrequency catheter ablation is associated with cure rates of greater than 95%, with very low risk of atrioventricular (AV) block (< 1%) for patients with AV nodal reentry tachycardia (AVNRT).^[9] This is an invasive procedure in which catheter electrodes are placed percutaneously via central veins into the heart. Tachycardia can be initiated by pacing and by programmed electrical stimulation delivered from the atria or the ventricles.

An ablation catheter electrode can be placed in the location of the slow AV nodal pathway, with radiofrequency energy delivered via the catheter to interrupt conduction via this pathway and thus eliminate the circuit.

Cryoablation

Cryoablation has been increasingly used for treating AVNRT, with reported safety and efficacy,^[12] including in children.^{[13, 14]} One review of the literature concluded that cryoablation is safe and effective for AVNRT and is an option in patients for whom the avoidance of AV block is a priority, such as children and young adults.^[13] A more recent study also found cryoablation to be effective for 125 children with AVNRT (age >10 years), with comparable acute and mid-term follow-up success rates for both 6-mm and 8-mm tip catheters.^[14]

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Guidelines Summary

In 2015, American College of Cardiology, American Heart Association, Heart Rhythm Society (ACC/AHA/HRS)^[15] released guidelines for the management of supraventricular tachycardia which include specific recommendations for both acute and ongoing management of atrioventricular node reentry tachycardia (AVNRT). In August 2019, the European Society of Cardiology (ESC) in collaboration with the Association for European Paediatric and Congenital Cardiology (AEPC) released recommendations on the management of supraventricular tachycardia.^{[16, 17]} The European Heart Rhythm Association (EHRA) released recommendations in 2017.^[18] These guidelines are summarized in the following sections.

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2015 ACC/AHA/HRS guidelines for the management of supraventricular tachycardia (SVT)

Management of Acute Atrioventricular (AV) Nodal Reentry Tachycardia (AVNRT)

Vagal maneuvers and/or intravenous (IV) adenosine are the recommended initial treatments for acute AVNRT. (Class I; level of evidence B-R)

Additional recommendations for acute treatment when adenosine and vagal maneuvers are ineffective or contraindicated are summarized below.

Hemodynamically unstable patients

• Synchronized cardioversion (Class I; level of evidence B-NR)

Hemodynamically stable patients

• IV beta blockers, diltiazem, or verapamil (Class IIa; level of evidence: B-R)
• Oral beta blockers, diltiazem, or verapamil may be considered. (Class IIb; level of evidence: C-LD)
• Synchronized cardioversion when beta blockers, diltiazem, or verapamil are ineffective or contraindicated (Class I; level of evidence B-NR)
• IV amiodarone may be considered when other therapies are ineffective or contraindicated. (Class IIb; Level of evidence: C-LD)

The guidelines note that for rhythms that break or recur spontaneously, synchronized cardioversion is not appropriate.

Management of Ongoing AVNRT

Minimally symptomatic

Clinical follow-up without pharmacologic therapy or ablation is reasonable for minimally symptomatic patients with AVNRT. (Class IIa; level of evidence B-R)

Self-administered (“pill-in-the-pocket”) acute doses of oral beta blockers, diltiazem, or verapamil for patients with infrequent, well-tolerated episodes of AVNRT may be considered. (Class IIb; level of evidence C-LD)

Symptomatic

Catheter ablation of the slow pathway is the recommended initial treatment for ongoing management of symptomatic AVNRT. (Class I; level of evidence B-R).

Patients who are not candidates or prefer not to undergo catheter ablation should be treated with oral beta blockers, verapamil, or diltiazem (Class I; level of evidence B-R). If these agents are ineffective, additional treatment options include:

• ​Flecainide or propafenone in patients without structural heart disease or ischemic heart disease when class I therapies are ineffective or contraindicated. (Class IIa; level of evidence B-R)
• Oral sotalol, dofetilide, digoxin, or amiodarone for patients (Class IIb; level of evidence B-R)

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2019 ESC/AEPC Guidelines for the Management of Supraventricular Tachycardia

Supraventricular Tachycardia Clinical Practice Guidelines (2019)

Several changes from the previous guidelines (2003) include revised drug grades as well as medications that are no longer considered, and changes to ablation techniques and indications.^{[16, 17]} For detailed recommendations on specific types of SVTs, please consult the original guidelines as listed under the references.

Table. Medications, Strategies, and Techniques Specified or Not Mentioned in the 2019 Guidelines

View Table

See Table

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2017 EHRA Consensus Document on the Management of Supraventricular Arrhythmias

The European Heart Rhythm Association (EHRA) published its consensus document on the management of supraventricular arrhythmias, which has been endorsed by Heart Rhythm Society (HRS), Asia-Pacific Heart Rhythm Society (APHRS), and Sociedad Latinoamericana de Estimulación Cardiaca y Electrofisiologia (SOLAECE).^[18]  For detailed recommendations on specific types of SVTs, please consult the original guidelines as listed under the references.

Acute Management (without established diagnosis)

In the setting of hemodynamically unstable supraventricular tachycardia (SVT), synchronized electrical cardioversion is recommended.

In the setting of hemodynamically stable SVT, vagal maneuvers, preferably in the supine position, or adenosine are recommended. Intravenous (IV) diltiazen or verapamil, or beta blockers, may be considered.

AV Nodal Reentrant Tachycardia (AVNRT)

Acute therapy

• Valsalva maneuver, preferably in the supine position, is recommended.
• IV adenosine is recommended.
• Hemodynamically unstable patients in whom adenosine fails to terminate the tachycardia: Synchronized DC cardioversion
• In the absence of hypotension or suspicion of ventricular tachycardia or preexcited AF: IV verapamil or diltiazem
• Consider IV beta blockers (metoprolol or esmolol); or IV amiodarone; or a single oral dose of diltiazem and propranolol

Chronic therapy

• Symptomatic patients or patients with an implantable cardioverter-defibrillator: Catheter ablation for slow pathway modification
• Consider diltiazem or verapamil; or beta blockers
• Minimally symptomatic patients with infrequent, short-lived tachycardia episode: No therapy

AV Reentrant Tachycardia (AVRT) Due to Manifest/Concealed Accessory Pathways

Acute therapy

• First-line approach to terminate SVT: Vagal maneuvers (Valsalva and carotid sinus massage), preferably in the supine position
• To convert to sinus rhythm: Adenosine, but use with caution (it may precipitate AF with a rapid ventricular rate and even ventricular fibrillation)
• Hemodynamically unstable AVRT patients in whom vagal maneuvers or adenosine are ineffective or not feasible: Synchronized DC shock
• Patients with antidromic AVRT: Consider IV ibutilide, procainamide, propafenone, or flecainide
• Patients with orthodromic AVRT: Consider IV beta blockers, diltiazem, or verapamil
• Patients with preexcited AF: Potentially harmful drugs include IV digoxin, beta blockers, diltiazem, verapamil and, possibly, amiodarone

Chronic therapy

• Symptomatic patients with AVRT and/or preexcited AF: Catheter ablation of the accessory pathway
• Symptomatic patients with frequent episodes of AVRT: Consider catheter ablation of the accessory pathway
• Patients with AVRT and/or preexcited AF, but without structural or ischemic heart disease: Consider oral flecainide or propafenone, preferably in combination with a beta blocker
• Chronic management of AVRT in the absence of preexcitation sign on resting ECG: Oral beta blockers, diltiazem, or verapamil
• Oral amiodarone may be considered only among patients in whom other antiarrhythmic drugs are ineffective or contraindicated, and catheter ablation is not an option.

SVTs in Patients With Adult Congenital Heart Disease

For acute therapy for patients with hemodynamically stable AVNRT/AVRT, IV adenosine and atrial overdrive pacing (via esophagus or endocardial) may be considered.

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Resources

For more information, please see the following:

• 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia
• 2019 ESC/AEPC Guidelines for the Management of Supraventricular Tachycardia
• 2017 EHRA Consensus Document on the Management of Supraventricular Arrhythmias

Also see Medscape Drugs & Diseases topics Atrial Tachycardia, Atrial Fibrillation, and Atrial Flutter.

For more Clinical Practice Guidelines, please go to Guidelines.

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Medication Summary

Drugs used to terminate an acute episode of atrioventricular nodal reentry tachycardia (AVNRT) are given intravenously. These medications include the following:

• Adenosine (first line)
• Calcium channel blockers (eg, diltiazem, verapamil)
• Beta-blockers (eg, esmolol, propranolol, metoprolol, atenolol)
• Digitalis

Drugs used to prevent recurrences are given orally and include calcium channel blockers, long-acting beta-blockers, and digitalis.

As previously mentioned, the administration of adenosine or other AV nodal blocking agents may, in rare cases, lead to ventricular fibrillation or even asystole for a short time period.

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Adenosine (Adenocard)

• Dosing, Interactions, etc.

Clinical Context:  Adenosine transiently blocks conduction through the AV node. It can interrupt reentry pathways through the AV node and restore normal sinus rhythm in paroxysmal SVT, including paroxysmal SVT associated with Wolff-Parkinson-White (WPW) syndrome. Adenosine has a short half-life. It is the preferred medication for IV administration to terminate AVNRT because of its rapid metabolism and generally good safety profile.

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Digoxin (Lanoxin)

• Dosing, Interactions, etc.

Clinical Context:  Cardiac glycosides have direct and indirect inotropic effects on the cardiovascular system. Digoxin acts directly on cardiac muscle, increasing myocardial systolic contractions. Indirect actions result in increased vagal activity for any given increase in mean arterial pressure. Digoxin is administered intravenously to terminate an acute attack, but it has a delayed onset of action and is less effective than other therapies. The drug is given orally to prevent recurrence. IV digoxin has generally been supplanted by other medications.

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Class Summary

Antiarrhythmic drugs affect the electrophysiology of the pathways responsible for AVNRT.

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Diltiazem (Dilacor XR, Tiazac, Cartia XT, Cardizem)

• Dosing, Interactions, etc.

Clinical Context:  It is administered intravenously to terminate an acute attack, and orally to prevent recurrence.

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Verapamil (Calan, Covera-HS, Verelan)

• Dosing, Interactions, etc.

Clinical Context:  This is the second-line treatment for AVNRT after adenosine. Verapamil causes fewer adverse effects, is less expensive, and lasts longer; however, its action is not as rapid, and hypotension, bradycardia, and a negative inotropic effect may occur. The drug is good to use in lieu of adenosine if AVNRT recurs after termination.

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Class Summary

These drugs block the AV nodal pathways responsible for AVNRT (particularly, the slow pathway).

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Esmolol (Brevibloc)

• Dosing, Interactions, etc.

Clinical Context:  Esmolol's short half-life of 8 minutes allows for titration to the desired effect and quick discontinuation if necessary.

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Atenolol (Tenormin)

• Dosing, Interactions, etc.

Clinical Context:  Atenolol selectively blocks beta-1 receptors, with little or no effect on beta-2 types. Atenolol is excellent for use in patients at risk for experiencing complications from beta-blockade, particularly those with reactive airway disease, mild-to-moderate LV dysfunction, and/or peripheral vascular disease.

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Metoprolol (Lopressor, Toprol XL)

• Dosing, Interactions, etc.

Clinical Context:  Metoprolol is a selective beta-1 adrenergic receptor blocker that decreases the automaticity of contractions. During intravenous administration, carefully monitor blood pressure, heart rate, and ECG.

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Class Summary

These agents are used for AV nodal blockade.

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