AVNRT overview

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

AV nodal reentrant tachycardia is a type of tachycardia (fast rhythm) of the heart. It is one of several types of supraventricular tachycardia (SVT), and like all SVTs the electrical impulse originates proximal to the bundle of HIS. In the case of AVNRT, the electrical impulse originates in the AV node and the immediately surrounding tissue. AVNRT is the most common cause of supraventricular tachycardia.

Classification

There are several types of AVNRT. The "common form" or "usual" AVNRT utilizes the slow AV nodal pathway as the anterograde limb of the circuit and the fast AV nodal pathway as the retrograde limb. The reentry circuit can be reversed such that the fast AV nodal pathway is the anterograde limb and the slow AV nodal pathway is the retrograde limb. This, not surprisingly is referred to as the "uncommon form" of AVNRT. However, there is also a third type of AVNRT that utilizes the slow AV nodal pathway as the anterograde limb and left atrial fibers that approach the AV node from the left side of the inter-atrial septum as the retrograde limb. This is known as atypical, or Slow-Slow AVNRT.

Common AVNRT

In common AVNRT, the anterograde conduction is via the slow pathway and the retrograde conduction is via the fast pathway ("slow-fast" AVNRT). This accounts for 80%-90% of cases of AVNRT.

Because the retrograde conduction is via the fast pathway, stimulation of the atria (which produces the inverted P wave) will occur at the same time as stimulation of the ventricles (which causes the QRS complex). As a result, the inverted P waves may not be seen on the surface ECG since they are buried with the QRS complexes. Often the retrograde p-wave is visible, but also in continuity with the QRS complex, appearing as a "pseudo R prime" wave in lead V1 or a "pseudo S" wave in the inferior leads.

Uncommon AVNRT

In uncommon AVNRT, the anterograde conduction is via the fast pathway and the retrograde conduction is via the slow pathway ("fast-slow" AVNRT). Multiple slow pathways can exist so that both anterograde and retrograde conduction are over slow pathways. ("slow-slow" AVNRT).

Because the retrograde conduction is via the slow pathway, stimulation of the atria will be delayed by the slow conduction tissue and will typically produce an inverted P wave that falls after the QRS complex on the surface ECG.

AVNRT occurs when a reentry circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferiorly and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node. In the usual form of AVNRT, the conduction from the atrium to the ventricle is down the slow pathway, and the retrograde conduction from the ventricle to the atrium is up the fast pathway.

Pathophysiology

Premature Atrial Complex

The most common trigger for an episode of AVNRT is when an atrial premature complex (APC) approaches the fast pathway, and is blocked due to the longer refractory period of this pathway, and instead conducts down the slow pathway. As the impulse goes down the slow pathway, the fast pathway recovers, and allows the impulse to conduct backward or retrograde toward the atrium. It then re-enters the atrial entrance of the slow pathway and the cycle repeats itself.

Premature Ventricular Complex

The second most common mechanism whereby AVNRT is triggered is via the entry of a premature ventricular complex down either the slow conducting pathway (similar to a premature atrial complex above) or down the rapidly conducting pathway.

Epidemiology and Demographics

AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia and accounts for 60% to 70% of these cases.

Gender

The ratio of female to male involvement is 3:1.

Age

There is no age predilection.

Risk Factors

Underlying structural heart disease is generally absent. Often, there is no precipitant of an episode. Risk factors for precipitation of AVNRT include:

• Alcohol
• Caffeine
• Chocolate
• Hyperthyroidism
• Hypokalemia
• Hypomagnesemia
• Myocardial ischemia
• Psychological stress
• Tea
• Theobromine in foods like tea, coffee and chocolate
• Theophylline

Natural History, Complications and Prognosis

AVNRT starts and stops abruptly. Patients may develop syncope. The prognosis is good.

Natural History

The rhythm often ceases abruptly and spontaneously. An episode generally last seconds to hours.

Complications

• Some patients will develop syncope during episodes of AVRNT. The mechanism of syncope may be due to a reduction of cardiac output and hemodynamic compromise as a result of the short ventricular filling time or alternatively it may be due to transient asystole due to tachycardia-mediated suppression of the sinus node when the rhythm terminates. Those patients who do become symptomatic during episodes of AVNRT (i.e. have syncope) should avoid activities where the occurrence of hemodynamic compromise would endanger their safety or that of others (like driving).
• In patients with underlying ischemic heart disease, demand-related myocardial ischemia, angina and even myocardial infarction and/or congestive heart failure can occur.
• Tachycardia mediated cardiomyopathy may develop if the AVNRT is chronic and does not terminate.

Prognosis

AVNRT is rarely life threatening and in the absence of underlying structural heart disease, the prognosis is good. Radiofrequency ablation is curative in 95% of cases.

Diagnosis

Symptoms

The following symptoms may be present:

• Sudden onset and sudden offset of rapid palpitations is common
• Dizziness and rarely syncope, especially at the onset of the episode of tachycardia
• Neck "pounding" may occur as a result of the right atrium contracting against a closed atrioventricular valve and Cannon a waves and the simultaneous occurrence of the atrial and ventricular contractions.
• Chest pain and angina if the patient has ischemic heart disease
• Dyspnea
• Polyuria can occur after the episode breaks. It has been hypothesized that this is due to the release of atrial natriuretic peptide

Physical Examination

Pulse

The heart rate is typically regular and between 140-280 bpm. In adults the range is 140-250 bpm, but in children the rate can exceed 250 bpm.

Systolic Blood Pressure

• Hypotension may be present in some cases.

Neck

• Cannon a waves may be present in some cases

Lungs

• Rales may be present in some patients with congestive heart failure

Laboratory Findings

Depending upon the patient's history and demographics, the following laboratory studies should be considered:

• Thyroid function tests (TFTs) - an overactive thyroid may increase the risk of AVNRT
• Electrolytes - hypokalemia, hypomagnesemia may predispose to AVNRT
• Cardiac markers - if there is a concern that myocardial infarction (a heart attack) has occurred either as a cause or as a result of the AVNRT; this is usually only the case if the patient has experienced ischemic chest pain

Electrocardiogram

An electrocardiogram performed during the occurrence of symptoms may confirm the diagnosis of AVNRT.

Slow-Fast AVNRT (Common AVNRT)

• This form of AVNRT accounts for 80% to 90% of cases of AVNRT.
• The retrograde P wave that is conducted retrograde up the fast pathway is usually burried within the QRS but less frequently may be observed at the end of the QRS complex as a pseudo r’ wave in lead V1 or an S wave in leads II, III or aVF.

Fast-Slow AVNRT (Uncommon AVNRT)

• This form of AVNRT Accounts for 10% of cases of AVNRT
• In this form of AVNRT, the impulse is first conducted antegrade down the Fast AV nodal pathway and is then conducted retrograde up the Slow AV nodal pathway.
• In contrast to Common AVNRT, a retrograde P wave may be observed after the QRS complex before the T wave

Slow-Slow AVNRT (Atypical AVNRT)

• This form of AVNRT accounts for 1-5% of cases of AVNRT
• In this form of AVNRT, the impulse is first conducted antegrade down the Slow AV nodal pathway and retrograde up the Slow left atrial fibres approaching the AV node.
• The p wave may appear just before the QRS complex, and this makes it hard to distinguish the rhythm from sinus tachycardia.

Aberrant Conduction

It is not uncommon for there to be a wide QRS complex due to aberrant conduction due to underlying conduction system disease. This can make it difficult to distinguish AVNRT from VT. The distinguishing features include:

• AVNRT is associated with a QRS complex morphology resembles a typical bundle branch block
• AVNRT is not associated with AV dissociation where there is variable coupling of the p wave and the QRS complex
• AVNRT is associated with Cannon a waves
• AVNRT is not associated with capture beats or fusion beats
• AVNRT may convert with adenosine or vagal maneuvers

An electrophysiologic study may be needed to confirm AVNRT prior to ablation.

Holter Monitor / Event Recorder

If the patient complains of recurrent palpitations and no arrhythmia is present on the resting EKG, then a Holter Monitor or Cardiac Event Monitor should be considered.

Treatment

An episode of supraventricular tachycardia (SVT) due to AVNRT can be terminated by any action that transiently blocks the AV node. Various methods are possible.

Patient Position

Place the patient in a supine position to improve cerebral perfusion and reduce the odds of syncope. Placing the patient in Trendelenburg position may actually terminate the rhythm.

Vagal maneuvers

Some people with known AVNRT may be able to stop their attack by using various tricks to activate the vagus nerve. This includes carotid sinus massage (pressure on the carotid sinus in the neck), submersion of the face in ice water to trigger the diving reflex, putting the patient in Trendelenburg position or the Valsalva maneuver (increasing the pressure in the chest by attempting to exhale against a closed airway). Vagel maneuvers are contraindicated in the presence of hypotension.

Medication

Medical therapy can be initiated with drugs that slow AV nodal conduction:

First Line Therapy

Adenosine

Adenosine is generally considered first line therapy for AVNRT.

Treatment of AVNRT with adenosine can be complicated by:

• The development of shortness of breath due to bronchospasm
• In some cases there can be asystole which is transient given the short half life of adenosine
• Atrial fibrillation may be induced by adenosine administration
• Ventricular fibrillation is rarely induced by adenosine. When it does occur it is due to block of the AV node with rapid antegrade conduction of atrial fibrillation down the bypass tract. It is for this reason that defibrillation equipment be available.
• Adenosine should not be used in heart transplant patients
• Dipyridamole may potentiate the effect of adenosine
• Theophylline may reduce the effectiveness of adenosine

Administration:

• Place a large bore (18 gauge and larger) intravenous line
• The initial dose is 6 mg and this should be followed a saline flush with elevation of the arm to assure that the drug is infused
• If this is not effective, then 12 mg or 18 mg of adenosine can be admininistered

Beta blockers

A short acting beta-blocker such as esmolol (half life of 8 minutes) can be used to terminate an episode of AVNRT. Longer acting beta-blockers such as atenolol, metoprolol, and propranolol can also be used to reduce the risk of recurrent episodes. Atenolol may be preferable among patients with bronchospasm as it selectively blocks beta-1 receptors with little effect on beta- 2 receptors.

Second Line Therapy

Numerous other antiarrhythmic drugs may be effective if the more commonly used medications have not worked; these include flecainide or amiodarone. Both adenosine and beta blockers may cause tightening of the airways, and are therefore used with caution in people who are known to have asthma. Calcium channel blockers should be avoided if there is a wide complex tacycardia and the diagnosis of AVNRT is not clearly established in so far as calcium channel blockers should be avoided in ventricular tachycardia. If the diagnosis of AVNRT is established, then non-dihydropyridine calcium channel blockers (such as verapamil) may be administered to terminate the rhythm if other agents are not effective. Verapamil acts longer than adenosine and acts rapidly. Its administration can be complicated by hypotension, bradycardia and negative inotropic effects.

Cardioversion

In very rare instances, cardioversion (the electrical restoration of a normal heart rhythm) is needed in the treatment of AVNRT. This would normally only happen if all other treatments have been ineffective, or if the fast heart rate is poorly tolerated (e.g. the development of heart failure symptoms, hypotension (low blood pressure) or unconsciousness).

Electrophysiology and Radiofrequency Ablation

After being diagnosed with AVNRT, patients can also undergo an electrophysiology (EP) study to confirm the diagnosis. Catheter ablation of the slow pathway, if successfully carried out, and cures 95% of patients with AVNRT. The risk of complications is quite low. Ablation can be carried out in patients who do not want to take pharmacotherapy, in whom pharmacotherapy fails, or if the patient has side effects from pharmacotherapy.

Prevention

Triggers such as alcohol and caffeine should be avoided.

References