Atrioventricular nodal reentrant tachycardia is the most common form of regular paroxysmal supraventricular tachycardia. Although it was classically described more often in the young and women, it can be detected at any age and sex. The overall prevalence of atrioventricular nodal reentrant tachycardia is 2–3 cases per 1000 persons. Atrioventricular nodal reentrant tachycardia is not usually associated with structural heart disease [5–7].

The reentrant circuit is confined not only in the compact AV node, but the perinodal atrial tissue has an important role too. Atrioventricular nodal reentrant tachycardia is related to the presence of two functionally and anatomically distinct AV nodal pathways (dual AV nodal pathways). The fast pathway, which conducts more rapidly (PR interval 100–150 ms and AH <220 ms) and has a long refractory period, appears to be located near the apex of Koch’s triangle. The slow pathway, which conducts more slowly (PR interval >220 ms) and has a short refractory period, extends inferoposterior to the compact AV node tissue and extends along the septal margin of the tricuspid annulus at the level of the coronary sinus. The fast pathway constitutes the normal, physiological, AV conduction axis [6].

AVNRT has been categorized into typical or atypical. This categorization is based on the retrograde limb of the circuit: if it is the fast pathway, it is defined typical; if it is the slow pathway, it is atypical. Typical atrioventricular nodal reentrant tachycardia is the more common type (90 %) and involves the slow pathway for antegrade conduction and the fast pathway for retrograde conduction (slow-fast variant). Atypical atrioventricular nodal reentrant tachycardia is less common (10 %) and includes fast-slow and slow-slow variants [6].

An atrial premature complex that is blocked in the fast pathway and is conducted through the slow pathway generally initiates typical AVNRT. If the fast pathway has recovered excitability, the impulse can conduct retrogradely over the fast pathway, resulting in an atrial echo. If the impulse reenters into the slow pathway, typical AVNRT may be initiated. Seldom it is initiated by a ventricular premature complex (Fig. 19.4).

Atypical AVNRT (fast-slow variant) initiates with a ventricular premature complex that is blocked in the fast pathway. The impulse then conducts to the atrium via the slow pathway and returns to the ventricle via the fast pathway. Seldom an atrial premature complex initiates tachycardia (Fig. 19.5).

In AVNRT, neither the atrium nor the ventricle has a critical role in the reentrant circuit [6].

AVNRT usually has a sudden onset and termination, without a warm-up period. Its symptoms include palpitations, neck pulsations, dizziness, and in some cases chest pain or dyspnea. Tachycardia can last a few minutes or hours, and the termination can be spontaneous or not. Sometimes precipitating factors (drugs, physical and psychological stress, menstruation, anemia, hyperthyroidism, etc.) can be found [5–7].

A 12-lead ECG is fundamental for the diagnosis. ECG, during AVNRT, shows in most cases a regular narrow QRS complex tachycardia; sometimes the QRS complex can be wide with the typical bundle branch block morphology (LBBB or RBBB). Rate of tachycardia is more often between 140 and 250 per minute. The AV relationship is practically in all cases 1:1. Atrial activation is concentric type because the retroconducted stimulus comes from the AV node, so the retroconducted P wave is narrow and negative in inferior leads. In typical AVNRT, the impulse conducts to the atrium via the fast pathway so the atrium and ventricle are activated simultaneously during tachycardia; the retrograde P wave is either hidden within the QRS or embedded in the terminal portion of the QRS, resulting in RP < PR (usually RP is less or equal to 70 ms) with pseudo-r waves in lead V1 and pseudo-s waves in inferior leads. Comparison with the QRS in sinus rhythm can help in identifying pseudo-r and pseudo-s waves. In atypical AVNRT, the conduction to the atrium is through the slow pathway; the atrium is activated late relative to the ventricle, so the retroconducted P wave is away from the previous QRS and it is near the following QRS (RP > PR) [6].

Invasive electrophysiological investigation (EPS) allows to detect the presence of dual AV nodal pathways, to induce and identify AVNRT (typical or atypical), and to perform catheter ablation of tachycardia. Dual pathway can be demonstrated with delivery of a premature atrial complex that results in a “jump” in AH conduction curve (defined as an increase >50 ms in AH interval with a 10 ms increase in atrial extrastimulus prematurity). This “jump” is due to antegrade block in the fast pathway with the conduction through the slow pathway. The electrophysiological characteristic of AVNRT is the concentric retrograde activation of the atrium, with a short ventriculoatrial (VA) interval or with a “A on V” (simultaneous activation of the atrium and ventricle) in typical AVNRT or with a long VA time in atypical (fast-slow) AVNRT [6].

Surface ECG can make differential diagnosis between AVNRT and the other narrow QRS complex tachycardia during tachycardia, by the induction and termination of tachycardia and by the response to vagal maneuvers [5].

ECG features to assess are shown in Fig. 19.6.

The response to vagal maneuvers or to adenosine can help to distinguish between the different types of supraventricular tachycardia. Gradual slowing then reacceleration of rate is typical of sinus tachycardia or focal atrial tachycardia. Sudden termination is typical of AVNRT and AVRT. Persisting tachycardia with transient high grade of AV block is typical of atrial flutter or atrial tachycardia [5].

Termination of tachycardia is due to block in slow pathway in AVNRT and in AV node in AVRT. Thus, typical AVNRT ends with a retroconducted P wave, atypical AVNRT ends with a QRS complex, and orthodromic AVRT ends with a retroconducted by accessory pathway P wave [5, 6].

Acute treatment: patients with hemodynamic compromise should be electrically cardioverted without delay. Usually, AVNRT does not cause significant hemodynamic compromise. Vagal maneuvers (Valsalva maneuver, dive reflex, carotid sinus massage) can be used to terminate the tachycardia. These maneuvers increase the vagal tone resulting in slow pathway conduction blockage. If vagal maneuvers are ineffective, medications known to prolong refractoriness of the slow pathway of the AVNRT circuit can be used. These agents include adenosine, calcium channel blocker (verapamil or diltiazem), and beta-blockers (metoprolol, atenolol, propranolol, esmolol). Intravenous administration of these drugs should be performed with continuous ECG monitoring. These agents are very effective in terminating the AVNRT [5, 6].