I. Atrioventricular Nodal Reentrant Tachycardia: What every physician needs to know.

Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common form of paroxysmal supraventricular tachycardia (PSVT) encountered in clinical practice. It is responsible for approximately 60% to 70% of the paroxysmal forms of PSVT. AVNRT is generally a narrow complex tachycardia with rates of 120 to 240 bpm. It generally presents in the first 2 decades of life but can occur at any age, and sometimes has a bimodal distribution with the incidence peaking in the late teens and again in the early thirties. Gender expression is roughly 2:1 female to male.

Presentation may be subtle and nonspecific with the more common symptoms being palpitations, dizziness, and/or unexplained dyspnea. Other symptoms can be more severe and include chest pain often described as a fullness in the chest, neck, or throat associated with palpitations. Syncope can occur with AVNRT but this is uncommon. A key feature is abrupt onset and termination of the tachycardia and hence the signs and symptoms. The tachycardia can last minutes to hours and in extreme cases even days if not treated.

There is often no apparent precipitating cause of AVNRT. However, physiologically premature atrial contractions (PACs) and premature ventricular contractions (PVCs) precipitate AVNRT. Thus caffeine, tobacco products, alcohol, exercise, and/or emotional stress may increase the frequency of PACs and PVCs and therefore the frequency of AVNRT.

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The patient may have symptoms for years before the diagnosis is elucidated. Patients with AVNRT are often branded as having panic attacks or anxiety disorders due to the brief duration of the tachycardia. Often the patient’s presenting electrocardiogram (ECG) in the emergency department or clinician’s office is sinus rhythm or sinus tachycardia as the AVNRT has already terminated. A high index of suspicion must be maintained in determining the proper diagnosis in patients presenting with these symptoms.

Patients who have AVNRT generally have dual atrioventricular nodal physiology and the ability for a reentrant arrhythmia to occur involving the atrioventricular (AV) node and the perinodal tissue. Patients in general have a fast pathway in which normal conduction proceeds down during sinus rhythm.

However, patients with AVNRT have one or more slow pathways or additional circuits near the coronary sinus and connected to the AV node that are capable of electrical conduction. In the most common or “typical form” of AVNRT, patients become stuck in a reentrant loop with conduction proceeding down the slow pathway as the antegrade limb of the circuit and back up the fast pathway as the retrograde limb. Usually it is a properly timed premature atrial contraction (PAC) that initiates the typical form of AVNRT.

In the simplest model, unidirectional block occurs in the fast pathway after a PAC, and conduction proceeds down the slow pathway until it reaches the point of lower common pathway fusion where the two pathways join. At this point the conduction wavefront proceeds back up the fast pathway in a retrograde fashion and reentry ensues (Figure 1, Figure 2).

Figure 1.

Model of AVNRT.

Figure 2.

Model of AVNRT.

This is also referred to as the “slow-fast” form of AVNRT. In the less common ” fast-slow” form or atypical form of AVNRT, the conduction circuit proceeds in the reverse direction with the antegrade limb being the fast pathway and the retrograde limb of the reentrant circuit being the slow pathway.

II. Diagnostic Confirmation: Are you sure your patient has Atrioventricular Nodal Reentrant Tachycardia?

The history and 12-lead ECG are paramount in determining the diagnosis of AVNRT. Almost all of the patients who have this diagnosis will elicit one or more of the symptoms described above. It is important to obtain a 12-lead ECG at the time of presentation.

The ECG typically reveals a regular narrow complex tachycardia at rates of 120 to 240 beats per minute (Figure 3). Occasionally the ECG may show bundle branch block aberration (either right or left bundle) and appear as a wide complex tachycardia. While this is less common, it is certainly not rare.

Figure 3.

Typical AVNRT.

The most common form of AVNRT, the so-called typical AVNRT or “slow-fast” AVNRT, comprises over 95 % of cases of AVNRT. In this form the conduction circuit proceeds down the slow pathway as the antegrade limb of the circuit and back up the fast pathway as the retrograde limb.

The ECG of the typical form of AVNRT reveals a narrow complex tachycardia, with generally the P wave not being discernible and only QRS complexes seen to the untrained eye. However, often in precordial lead V1, and sometimes in leads II,III, and aVF, a retrograde P wave can be identified as a small terminal deflection or rSr’, indicating the near simultaneous contraction of the atrium and ventricle during this type of tachycardia.

A comparison ECG during sinus rhythm will not show the rSr’ morphology and P waves will be in the normal position relative to the QRS (Figure 4). The atypical form of AVNRT, the so-called “fast-slow” form, is seen in approximately 5% of cases. The ECG in this type of AVNRT is markedly different. The reason is that in this form of AVNRT the conduction circuit proceeds down the fast pathway and back up the slow pathway figuratively leading to a long delay in ventriculo-atrial activation. This is referred to as a long R-P tachycardia.

Figure 4.

Termination of AVNRT with loss of r prime.

The atria are also activated from caudal to cranial, making the P waves inverted in leads II, III, and aVF. When multiple slow pathways exist , a more rare type of AVNRT can occur. This is the “slow-slow” form of the tachycardia and uses separate slow pathways as the antegrade and retrograde limbs.

A. History Part I: Pattern Recognition:

The hallmark clinical features of AVNRT in decreasing order of prevalence are: palpitations, dizziness, dyspnea, chest pain or fullness, fatigue, and rarely presyncope or syncope. Patients with AVNRT often describe a fullness in their neck or throat as well, and this may be a reflection of the near simultaneous activation of the ventricle and the atrium.

Associated with the above symptoms can be increased frequency of urination. This is probably related to increased levels of atrial natriuretic peptide due to atrial stretch. Atrial stretch occurs due to altered hemodynamics, abnormal valve closure, increased heart rate, and an elevation of atrial pressure. In many patients, AVNRT can provoke significant anxiety.

This can be misdiagnosed as an anxiety/panic attack. Rarely, syncope can occur and this may be due to neurally mediated mechanisms and not just the tachycardia itself. Following termination of the arrhythmia, most patients are quickly relieved of symptoms but there is a subset of patients that are physically exhausted for hours to days.

B. History Part 2: Prevalence:

AVNRT occurs more commonly in females. There is a 2:1 gender bias. Familial predispositions have also been described. The triggers for typical AVNRT are usually premature atrial contractions and occasionally premature ventricular contractions.

Anything that increases the frequency of PACs, including aging, alcohol, tobacco products, adrenergic stimulating medications, hyperthyroidism, pregnancy, illness, emotional stress, and/or illicit drugs, can increase the frequency of AVNRT.

C. History Part 3: Competing diagnoses that can mimic Atrioventricular Nodal Reentrant Tachycardia.

The differential diagnosis for AVNRT include any regular narrow complex tachycardias, such as atrial flutter, atrial tachycardia, atrioventricular reentrant tachycardia using an accessory pathway (AVRT), junctional tachycardia, Mahaim-type left bundle branch block tachycardias, and sinus tachycardia. Atrial fibrillation at times, if it is rapid enough, can almost appear and feel regular, and in this case may rarely be confused with AVNRT.

Frequently, the symptoms of AVNRT can be mimicked by the more stable ventricular tachycardias (VT), such as fascicular ventricular tachycardia, ventricular outflow tract tachycardias, or even stable ischemic or nonischemic VTs. In most cases, AVNRT can be distinguished from those diagnoses listed above by ECG criteria, pharmacologic manipulation, and vagal maneuvers such as carotid sinus massage. The definitive test to sort out the mechanism of the arrhythmia is an electrophysiology study (EPS).

D. Physical Examination Findings.

Depending upon the individual’s hemodynamic response to AVNRT, the physical examination differs. Syncope or presyncope brought on by AVNRT most likely represents an episode of hypotension and resultant decreased cerebral perfusion. On examination, the patient may be cool, clammy, dyspneic, diaphoretic, as well as apprehensive.

Traumatic injury could be found. In most cases, patients do not present with syncope or presyncope. The symptoms are less severe, as are the physical findings. The typical patient is tachycardic with a pulse of 120 to 240 bpm and frequently cannon A waves are visualized in the neck.

Blood pressure is usually stable to mildly decreased upon presentation and the patient may be tachypneic. Many patients report an initial dizzy spell at the onset of AVNRT until physiologic changes occur to normalize their autonomic and hemodynamic response. The physical examination also changes depending upon the degree of stress and anxiety elicited by the arrhythmia.

Many patients are extremely apprehensive and anxious even, expressing a “sense of impending doom,” while others tolerate the arrhythmia with much less emotional involvement. Frequently, patients will develop polyuria during and post AVNRT.

E. What diagnostic tests should be performed?

In patients who are suspected of having AVNRT, it is important to obtain hard copy documentation of the arrhythmia. This is done ideally with a 12-lead ECG that is taken during the time that the arrhythmia is occurring. This can be obtained in the emergency department or the office setting.

Unfortunately, it is fairly common for the tachycardia to terminate prior to a 12-lead ECG being obtained. In this case, an event recorder should be ordered to try to capture the arrhythmia. Many times the event recorder will show the initiation of tachycardia and sometimes the termination of the tachycardia, which is very helpful in making in the diagnosis.

In the typical form of AVNRT, a PAC is often seen as the initiating event followed by a prolonged P–R interval and the onset of the tachycardia. A regular narrow complex tachycardia then ensues at 120 to 240 bpm. AVNRT usually terminates with a P wave that is buried within the QRS complex that may seen as a small notch at the terminal portion of the QRS as described above (see Figure 4).

If this is seen, it is more evidence that the presenting arrhythmia may be AVNRT. Once a supraventricular tachycardia has been diagnosed, an EPS can be performed to determine the exact mechanism of the tachycardia and if indicated catheter ablation may be chosen as an option for therapy and cure. The differential diagnosis of AVNRT includes other narrow complex tachycardias, such as orthodromic reciprocating tachycardia involving an accessory pathway or ectopic atrial tachycardia, which can be discerned at the time of electrophysiology study.

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

In some patients who have never had a prior episode of tachycardia or if the tachycardia frequency has increased dramatically, a thyroid profile, complete blood count (CBC), and/ or pregnancy test should be considered. Pregnancy tests should be done on women of child-bearing age prior to prescribing some antiarrhythmic medications or exposing them to the radiation of an electrophysiology study and/or catheter ablation.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

In patients who have evidence of congestive heart failure clinically and who develop suspected AVNRT, an echocardiogram should be performed if one has never has been obtained. In some patients who have been in tachycardia for hours, a slight elevation in troponin can be seen.

This may not reflect ischemic heart disease. Workup for ischemia should be based on risk factors and clinical suspicion. The 12-lead ECG during and post tachycardia can demonstrate ST and T wave abnormalities that usually don’t reflect ischemic heart disease. Again, the decision to pursue an ischemic workup should be based on clinical suspicion and risk factors, but in general it is not necessary.

At the time of EPS, the patient is paced at a stable atrial rate (usually a drive train of 8 beats at pacing rates of 100, 120, and 150 bpm) followed by the introduction of single PACs. The atrium-His (AH) interval, which is the time of conduction measured from the low right atrium through the AV node to the bundle of His, is then measured after each decrementing PAC is introduced.

PACs are generally introduced at decrementing 10 msec intervals, with measurement of the conduction time through the AV node and arriving at the bundle of His. The prolongation of the AH interval by 50 msec after introducing a PAC 10 msec earlier than the prior PAC defines the presence of fast pathway block, continued conduction down a slow pathway, and thus indicates dual nodal AV physiology. In some patients there can be multiple slow pathways.

At a critical AH delay or after an “AH jump,” an echo beat can often be seen, which is a single beat of AVNRT. In actuality, this represents antegrade conduction down the slow pathway with retrograde activation to the atrium via the fast pathway. Often at this point the tachycardia will continue with near simultaneous activation of the atrium and ventricle thus sustaining AVNRT (Figure 5, Figure 6, Figure 7, Figure 8).

Figure 5.

PAC introduced with conduction through fast pathway.

Figure 6.

AH jump with conduction through slow pathway with an echo beat.

Figure 7.

Another AH jump and hence second slow pathway with an echo beat.

Figure 8.

AH jump after a PAC with initiation of typical AVNRT.

III. Management

The management of AVNRT proceeds along two lines of therapy. One is empiric drug therapy and the other is catheter ablation for cure of the arrhythmia once acute management has been addressed.

Patients desiring drug therapy for suppressing of AVNRT should first receive oral beta-blockers or non–dihydropyridine calcium channel blockers. Digoxin can be used but it is not preferred due to lower efficacy and higher toxicity. In some cases where beta-blockers and calcium channel blockers are not effective in adequate control of the arrhythmia, type Ic, and occasionally type III, antiarrhythmics can be used. Amiodarone is not a preferred drug for the treatment of AVNRT.

For patients not desiring drug therapy or those who are drug intolerant, catheter ablation offers a cure rate in excess of 95% with low risk of complications and will be discussed below. For patients with hemodynamic compromise or syncope, catheter ablation is generally the preferred choice in therapy.

A. Immediate management.

The immediate management of AVNRT depends on the severity of symptoms and the patient’s hemodynamics. If there is hypotension and shock, sedation followed by urgent cardioversion according to ACLS guidelines must be performed. If the patient is relatively stable, vagal maneuvers such as carotid sinus massage, gagging, and Valsalva could be attempted.

Since this arrhythmia is AV node dependent, the goal of therapy is to change the AV nodal refractoriness or interrupt AV nodal conduction to terminate the tachycardia. Thus, the next step should be 6 to 18 mg of intravenous adenosine (although the authors prefer to start with 12 mg unless there is a central line in place) given through a large bore IV and immediately flushed with 30 ml of normal saline using a three-way stopcock so this can be done efficiently.

Sometimes there is termination followed by immediate return of the tachycardia even in AVNRT and in these patients, intravenous verapamil 5 to 10 mg slow push can be used. Diltiazem (20 mg IV as a loading dose following by 10 mg/min continuous infusion) can be used but it is less effective than verapamil. Intravenous beta-blockers ( metoprolol tartrate, esmolol ) can be used as an alternative to verapamil or diltiazem in patients who do not convert with or are intolerant to adenosine.

The authors prefer intravenous metoprolol tartrate (Lopressor) given at 5 mg increments every 5 minutes for a total dose of 15 to 25 mg. Blood pressure should be monitored during administration of verapamil, diltiazem, and beta-blockers.

As a reference, 10 mg of intravenous metoprolol tartrate is equivalent to roughly 25 mg orally. Also, the efficacy of adenosine in terminating AVNRT approaches 100% if adequate dosing is used, but adenosine should be administered with caution in patients with reactive airway disease (e.g., asthma, COPD). Verapamil is a better first line therapy In patients with reactive airway disease or prior known contraindication to adenosine.

Adenosine should not be used in patients who are concurrently taking theophylline as the adenosine receptor (A-1) is completely blocked by theophylline. Furthermore, dipyridamole is a potent agonist of adenosine and patients who are on this drug should not receive adenosine.

See Table 1.

Table 1.

Immediate Drug Management of AVNRT

B. Physical Examination Tips to Guide Management.

With acute pharmacologic management and if needed cardioversion of AVNRT, blood pressure, pulse, and oxygen saturation should be continuously monitored.

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

Patients desiring drug therapy for their arrhythmia should have an ECG periodically to determine the effects of the drugs on heart rate, P–R interval, QRS duration, and Q–T interval. If patients require a type III antiarrhythmic such as sotalol, in-hospital initiation is recommended with continuous telemetry monitoring to assess the Q–T interval and pro-arrhythmic effect.

Patients receiving type Ic antiarrhythmic drugs such as flecainide or propafenone should have periodic assessment of the P–R interval and QRS duration by ECG. If the 12-lead ECG suggests the possibility of structural heart disease, an appropriate workup should ensue. Baseline metabolic studies, CBC, and thyroid-stimulating hormone (TSH) level should be obtained at the time of the first episode.

D. Long-term Management.

The long-term management of AVNRT proceeds along two lines of therapy. One is empiric drug therapy, and the other is catheter ablation for cure of the arrhythmia once acute management has been addressed. Patients desiring drug therapy for suppression of AVNRT should first receive oral beta-blockers or non–dihydropyridine calcium channel blockers, such as verapamil or diltiazem.

Digoxin can be used but it is not preferred due to lower efficacy and higher toxicity. In some cases where beta-blockers and calcium channels blockers are not effective in adequate control of the arrhythmia, type Ic, and occasionally type III, antiarrhythmics can be used. Amiodarone is not a preferred drug for the treatment of AVNRT.

For patients not desiring drug therapy or those who are drug intolerant, catheter ablation offers a cure rate in excess of 95% with low risk of complications, and will be discussed below. For patients with hemodynamic compromise or syncope, catheter ablation is generally the preferred choice in therapy.

Once the patient has been treated acutely for AVNRT, a decision must be made regarding what is the next step in therapy. If this is the patient’s first event and symptoms have been minimal, perhaps no medical therapy is needed and observation may be adequate.

These patients should be taught vagal maneuvers. If patients have infrequent episodes of AVNRT, short-term therapy may be appropriate, such as oral beta-blockers or non–dihydropyridine calcium channel blockers at the onset to shorten the duration of the episode (Pill-in-the-Pocket).

For patients who require or desire medical therapy initially, oral long-acting verapamil, diltiazem, or beta-blockers, such as metoprolol or atenolol, are appropriate. Occasionally, patients who do not want catheter ablation require a type Ic antiarrhythmic drug, such as propafenone or flecainide.

If structural heart disease (coronary artery disease (CAD), valvular, etc.) is present and the patient still refuses catheter ablation, one may initiate a type III antiarrhythmic medication such as sotalol under a monitored situation. Class Ia drugs and amiodarone should generally be avoided.

If medications are not effective or not desired, then catheter ablation can be undertaken. Generally this can be done with radiofrequency energy (RF) or with the cryoablation technique but as a rule RF catheter ablation is more efficacious with less chance of recurrence and is generally the procedure of choice for ablation of AVNRT.

Recurrence rate with cryoablation is 9.4% versus only 4.4% with RF ablation. Complication of heart block with RF catheter ablation is less than 1% with ablation of the slow pathway, but with cryoablation it is even more rare.

Catheter ablation for therapy of AVNRT is generally done under conscious sedation in the electrophysiology laboratory. Four to eight French electrical catheters are used during the procedure, with catheters generally placed into the high right atrium, right ventricle, bundle of His area, and the coronary sinus from the femoral veins and sometimes the internal jugular and subclavian veins.

Standard and/or three-dimensional intracardiac mapping is used to localize vital structures, including the slow and fast pathways. Generally the target for ablation is the slow pathway of the AV node. It is usually located just to the right of the coronary sinus os in the 30- to 45-degree RAO position of the fluoroscope.

Generally a line of transection or series of lesions is made with the ablation catheter from the tricuspid valve to the coronary sinus os at the level of the low to mid coronary sinus os as a starting point. Application of RF energy at this site generally leads to destruction of the slow pathway and cure of AVNRT.

E. Common Pitfalls and Side Effects of Management

Physicians should be familiar with the side effects of medications that are used to treat AVNRT. This includes knowing and recognizing the side effects of beta-blockers, such as metoprolol and atenolol; calcium channel blockers, such as diltiazem and verapamil; the type Ic drugs, flecainide and propafenone; and type III antiarrhythmics such as sotalol.

Patients should be well informed of the risks and benefits of catheter ablation. The risks of catheter ablation include rare instances of heart block, bleeding, hematoma, infection, cardiac tamponade, pneumothorax, pericarditis, deep venous thrombosis, and pulmonary embolic events (see Table 2).

Table 2.n

Drug Interactions

What's the evidence for specific management and treatment recommendations?

Blomstrom-Lundqvist, C, Scheinman, CC, Aloit, EM. “ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias—executive summary: A report of the American College of Cardiology/ American Heart Association Task Force on practice guidelines and the European Society of Cardiology Committee for practice guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias)”. Circulation. vol. 108. 2003. pp. 1871

Blomstrom-Lundqvist, C, Scheinman, CC, Aloit, EM. “ACC/AHA/ESC Guidelines for the Management of Patients with Supraventricular Arrhythmias—Executive Summary”. October 2003.

Nakagawa, H, Jackman, W. ” Catheter ablation of paroxysmal supraventricular tachycardia”. Circulation. vol. 116. 2007. pp. 2465-78.

DRG Codes and Expected Length of Stay.

The diagnosis code for Paroxysmal Supraventricular Tachycardia and thus Atrioventricular Nodal Reentrant Tachycardia (AVNRT) is 427.0

Patients who present with an episode of AVNRT and are treated in the emergency department for immediate management may generally be discharged after a few hours. If drug therapy is chosen, calcium channel blockers and beta-blockers can be instituted as an outpatient.

Flecainide and propafenone can usually be instituted as an outpatient as well. If the patient requires a type III antiarrhythmic drug such as sotalol, the patient should be monitored on telemetry for five doses of the medications, which generally requires 21/2 to 3 days.

Patients undergoing uncomplicated catheter ablation therapy for treatment of AVNRT can generally be discharged 6 to 8 hours after the procedure while some practitioners prefer to keep the patient under observation for an overnight stay.