Atrioventricular nodal re-entrant tachycardia (AVNRT) is a regular, narrow-complex tachycardia with typical ventricular rates between 150-250 beats per minute (bpm). This arrhythmia often has an abrupt onset and termination. The terms paroxysmal supraventricular tachycardia or paroxysmal atrial tachycardia have been used to describe this entity, although such nomenclature is not considered to be accurate. AVNRT can last for just a few seconds to a few minutes at a time or can continue for days.

This tachyarrhythmia is due to the generation of a re-entrant current within the AV node, classically arising after conduction of a premature atrial contraction (PAC) to the AV node. The mechanism of disease involves dual AV nodal pathways. The most common dual pathways are the fast and slow pathways. If the fast AV pathway is in a refractory period at the moment of arrival of the PAC, the impulse will be conducted antegrade down the slow pathway.

As the impulse travels through the slow pathway, the fast pathway may recover from its refractory period. This allows for retrograde conduction through the fast pathway with subsequent retrograde atrial conduction and regeneration of the impulse down the antegrade slow pathway. In this manner, a re-entrant loop is created within the AV node.

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Symptoms often include palpitations, nervousness or anxiety. However, patients with underlying heart disease may have angina, heart failure, syncope, shock, and even asystole.

AVNRT often occurs in young adults who do not have structural heart disease and is more common in women than men. However, AVNRT does occur in those with known cardiac disease. There are no significant ethnic differences among those with AVNRT.

Consider other narrow complex tachycardias including atrial fibrillation, atrial flutter, atrial tachycardia, atrioventricular re-entrant tachycardia, junctional tachycardia, multi-focal atrial tachycardia, and sinus tachycardia. The specific electrocardiogram (ECG) pattern can distinguish AVNRT from other tachyarrhythmias.

Patients often display only tachycardia. However, hemodynamic compromise may be evident by hypotension, pulmonary crackles or jugular venous distension.

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None

An ECG is necessary for diagnosis. AVNRT is a regular, narrow-complex tachycardia with typical ventricular rates between 150-250 bpm. One should be particular suspicious of AVNRT if ventricular rates are between 180-200 bpm. A PAC often heralds the beginning of AVNRT. However, it is possible for AVNRT to occur after a PVC. P waves may not be visible or may occur at the end of the QRS complex. P waves can become buried within the QRS complex creating a pseudo r’ in V1 or a pseudo S in II, III, and aVF.

Cardiology consultation may be required for an electrophysiology study. This may be necessary for evaluation of dual AV node physiology and provides the potential for ablation of the arrhythmia.

Serum levels of cardiac enzymes and imaging such as echocardiography are often not needed for diagnostic evaluation of AVNRT. These tests are appropriate when concern for acute myocardial ischemia, heart failure or clinical decompensation is present.

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Initial nonpharmacologic therapies are an attempt to stimulate a vagal nervous response. These include carotid massage, exposure of the face to ice and performance of the valsalva maneuver. First-line pharmacologic therapy is adenosine administered as 6 milligrams (mg) intravenous (IV) and then 12mg IV if necessary. Remember to have atropine, pacer pads, and defibrillation equipment available as there is a possibility that significant bradycardia, asystole, or ventricular fibrillation may result after the administration of adenosine.

However, this risk is extremely small and should only occur in the setting of a non-AV accessory pathway. Calcium channel blocks such as verapamil and diltiazem and beta-blockers such as metoprolol are second line medications. Direct current (DC) cardioversion should also be considered if the patient has hemodynamic compromise or medications fail to control the arrhythmia. A synchronized DC shock of 10-50 joules should be sufficient.

Slowing of the heart rate on auscultation or resolution of jugular venous distension may be indications of successful treatment.

Continuous ECG monitoring should be utilized during management of AVNRT.

Some patients with recurrent episodes may require daily treatment with beta-blockers, calcium channel blockers or digoxin. Additionally, radiofrequency catheter ablation should be considered for patients with recurrent symptoms. The procedure is successful in over 95% of cases with very low likelihood of complications. Radiofrequency (RF) ablation may be preferred in most symptomatic patients and in those who do not wish to take or cannot tolerate medications. Patients should also avoid substances such as caffeine, coffee, tea, chocolate, and alcohol as they may precipitate episodes.

None

N/A

No change in standard management.

No change in standard management.

Caution with use of beta-blockers or calcium channel blockers in patients with systolic heart failure.

No change in standard management.

No change in standard management.

No change in standard management.

No change in standard management.

Caution with use of beta-blockers for patients with chronic obstructive pulmonary disease (COPD) or asthma.

No change in standard management.

No change in standard management.

No change in standard management.

Synchronized DC cardioversion for myocardial ischemia, heart failure, severe hypotension, or confusion due to arrhythmia.

1-3 days

Control of the arrhythmia for greater than 24 hours.

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Patients should follow-up with a cardiologist and/or cardiac electrophysiologist within 1-2 weeks of discharge if symptoms are recurrent. Otherwise, patients with rare, minimally symptomatic episodes should have initial follow-up within 4-6 weeks.

None

ECG

No specific placement considerations.

Excellent for most patients, especially if no chronic heart disease. For patients that undergo radiofrequency ablation, the cure rate is about 95%.

No specific core measures.

Bonow, RO, Mann, DL, Zipes, DP, Libby, P, Braunwald, E. “Braunwald's Heart Disease – A Textbook of Cardiovascular Medicine”. 2012.