Atrioventricular Nodal Reentry Tachycardia and Atrioventricular Reentry Tachycardia

AV nodal reentry tachycardia and AV reentry tachycardia are usually referred to as paroxysmal supraventricular tachycardias and are often seen in young patients with little or no structural heart disease, although a congenital heart abnormality giving rise to increased atrial pressure and dilatation (e.g., Ebstein’s anomaly, atrial septal defect, Fallot’s tetralogy) can coexist in a small percentage of patients with these arrhythmias.¹ The first presentation is common between age 12 and 30 years, and the prevalence is approximately 2.5 per 1000. Women are twice as likely as men to present with AV nodal reentry tachycardia.

Atrial Flutter and Fibrillation

Atrial fibrillation is the most common supraventricular arrhythmia, affecting 1% to 2% of the general population, especially the elderly. It is usually associated with cardiovascular pathologies, among which hypertension and congestive heart failure prevail.² About a third of patients, however, present with no underlying heart disease and are considered to have “lone” atrial fibrillation. The epidemiology of isolated atrial flutter is largely unknown and is believed to be in the range of 0.037% to 0.88% per 1000 person-years, but at least half these patients also have atrial fibrillation as a coexistent arrhythmia.

Atrial Tachycardia

Atrial tachycardia affects 0.34% to 0.46% of patients with arrhythmias and is common in younger individuals following surgical correction of congenital heart disease and in the elderly, in whom it often occurs in association with atrial fibrillation.

Other Supraventricular Tachycardias

Inappropriate sinus tachycardia and sinoatrial reentry tachycardia are less well-defined clinical and electrocardiographic entities, and their prevalence and associated conditions are not well appreciated. Sinoatrial reentry tachycardia is found incidentally in 1.8% to 16.9% of patients undergoing electrophysiologic study for other supraventricular tachyarrhythmias.

Narrow-Complex Tachycardias

The typical ECG feature is narrow QRS complexes less than 120 msec. In this case, the tachycardia is almost always supraventricular, and the differential diagnosis relates to its mechanism (Figure 78-2).

Figure 78-2 Differential diagnosis for narrow QRS complex (presumably supraventricular) tachycardias. Note that ventricular tachycardia may present with narrow QRS complexes (e.g., fascicular tachycardia). AV, atrioventricular; AVNRT, atrioventricular nodal reentry tachycardia; AVRT, atrioventricular reentry tachycardia.

Wide-Complex Tachycardias

The differential diagnostic features of wide-complex tachycardias favoring a supraventricular origin of the arrhythmia include, but are not limited to, preexistent bundle branch block; rate-dependent aberrancy; antidromic AV reentry tachycardia, when an accessory pathway conducts and excites the ventricles antegradely; and prominent electrolyte abnormalities (e.g., hypokalemia) or heart muscle disease (cardiomyopathy), all of which may result in QRS widening (Figure 78-3). If the diagnosis of supraventricular tachycardia cannot be proved, the patient should be treated as if ventricular tachycardia is present. Immediate direct-current (DC) cardioversion is the treatment for any hemodynamically unstable tachycardia.

Figure 78-3 Differential diagnosis for wide QRS complex tachycardias. AV, atrioventricular; AVRT, atrioventricular reentry tachycardia; BBB, bundle branch block; LBBB, left bundle branch block; RBBB, right bundle branch block; SVT, supraventricular tachycardia; WPW, Wolff-Parkinson-White; VT, ventricular tachycardia.

*Criteria for aberrancy: rate dependency, triphasic QRS complexes, rSR in V₁, with R >, QRS width < 140 msec, QRS deflections are discordant in precordial leads, absence of fusion and capture beats.

Mechanism

In AV nodal reentry tachycardia, there are two functionally and anatomically different pathways within the AV node: one is characterized by a short effective refractory period and slow conduction, and the other has a longer effective refractory period and faster conduction. In sinus rhythm, the atrial impulse that depolarizes the ventricles usually conducts through the fast pathway. If the atrial impulse (e.g., an atrial premature beat) occurs early, when the fast pathway is still refractory, the slow pathway takes over in propagating the atrial impulse to the ventricles; it then travels back through the fast pathway, which by then has recovered its excitability, thus initiating the most common “slow-fast,” or typical, AV nodal reentry tachycardia.

Electrocardiographic Presentation

In sinus rhythm, the ECG is usually normal unless other unrelated abnormalities are present. During AV nodal reentry tachycardia, the rhythm is regular, with narrow QRS complexes and a rate of 140 to 250 beats per minute. The atria are activated retrogradely, producing the inverted P waves in leads II, III, and aVF. Because atrial and ventricular depolarization occurs simultaneously, the P waves are often obscured by the QRS complexes and cannot be detected on the surface ECG (Figure 78-4, A). However, in about a third of cases of slow-fast AV nodal reentry tachycardia, a terminal positive deflection in lead aVR or V₁ (or both), imitating right bundle branch block or pseudo-S waves in the inferiorly oriented leads, may be present, reflecting retrograde activation of the atria. Tachycardia using these pathways in reverse (“fast-slow,” or long RP, tachycardia) is less common (5%-10% of cases).

Figure 78-4 A, Atrioventricular nodal reentry tachycardia, slow-fast type. Note narrow QRS complexes and absence of P waves. B, Atrioventricular reentry orthodromic tachycardia. Retrograde inverted P waves follow QRS complexes in leads II, III, and aVF. C, Atrioventricular reentry antidromic tachycardia with wide QRS complexes. Electrocardiogram during sinus rhythm with a QRS complex morphology identical to that seen during tachycardia may be helpful in the diagnosis. D, Atrial fibrillation in preexcitation syndrome with a fast ventricular rate response.

Accessory Pathways

AV reentry tachycardia occurs as a result of an anatomically distinct AV connection termed an accessory pathway, produced by incomplete separation of the atria and ventricles during fetal development. The most common AV accessory pathways (often called a Kent bundle) is located around the mitral or tricuspid annulus. In about 10% of cases, there are multiple pathways.

Accessory pathways are capable of conduction in either or both directions. Accessory pathways that are capable of antegrade conduction are referred to as manifest, demonstrating a delta wave during sinus rhythm when the atrial impulses conduct over the accessory pathway without encountering AV delay. The PR interval is short (<120 msec), and the QRS complex is wide; this occurs because the atrial impulse enters a nonspecialized ventricular myocardium, and depolarization progresses slowly at first, giving rise to the delta wave before it is overtaken by a depolarization wavefront propagating via the normal conduction tissue. An accessory pathway that is capable of only retrograde conduction is termed concealed and does not produce a short PR interval or a delta wave during sinus rhythm.

Mechanism and Electrocardiographic Presentation

The reentry circuit of orthodromic AV reentry tachycardia involves the AV node and an accessory pathway, with the impulses conducting from the atria to the ventricles over the AV node and traveling in the reverse direction through the accessory pathway (see Figure 78-4, B). In antidromic AV reentry tachycardia, the reentrant impulses conduct antegradely from the atria to the ventricles via an accessory pathway and retrogradely via the AV node or a second accessory pathway (see Figure 78-4, C). Antidromic AV reentry tachycardia is uncommon (<10% of cases). Atrial fibrillation is usually encountered in patients with antegradely conducting pathways (see Figure 78-4, D).

Acute Management

In an emergency, distinguishing between AV nodal reentry tachycardia and AV reentry tachycardia may be difficult, but it is usually not critical, because both tachycardias respond to the same treatment. If the patient is hemodynamically stable, vagal maneuvers including carotid sinus massage, Valsalva maneuver, and facial immersion in cold water (diving reflex) can terminate tachycardia in about 50% of patients (Box 78-1).^3,4 Commercially available gel packs can be used as cold compresses instead of facial immersion, but the most important element is wet nostrils and breath-holding.

Pharmacologic Termination

AV blocking agents such as adenosine, verapamil, diltiazem, and beta-blockers are effective in terminating both AV nodal reentry and AV reentry tachycardia (Table 78-1).¹

TABLE 78-1 Acute Pharmacologic Rate Control in Atrial Tachyarrhythmias

Adenosine

Intravenous (IV) adenosine is effective in diagnosing, rate slowing, and often terminating narrow-complex tachycardias.⁵ Adenosine usually terminates AV nodal reentry tachycardia and AV reentry tachycardia but rarely interrupts the atrial flutter circuit and does not suppress automatic atrial tachycardia; it can, however, produce high-degree AV block during which the tachycardia persists (Figure 78-5). It has no effect on most ventricular tachycardias. Adenosine is advantageous compared with verapamil because of its rapid onset and the absence of a negative inotropic effect in patients with poor left ventricular function and those with significant hypotension.

Figure 78-5 A, Adenosine usually terminates atrioventricular reentry tachycardias. B and C, It rarely interrupts the atrial flutter circuit or suppresses automatic focal atrial tachycardia but produces high-degree atrioventricular block during which the tachycardia persists.

Adenosine is administered as a very rapid 3- to 6-mg IV bolus; if this is ineffective, another 6- to 12-mg bolus can be given 2 to 5 minutes later. Adenosine is metabolized very quickly, with an effective half-life of 10 seconds. Adverse effects including dyspnea, facial flushing, and chest tightness are therefore short-lived, but in about 12% of patients, adenosine may shorten the atrial effective refractory period and provoke atrial flutter or fibrillation or accelerate conduction over the accessory pathway and produce a rapid ventricular response. In a proportion of patients, ventricular premature beats and nonsustained ventricular tachycardia may occur after the successful termination of supraventricular tachycardia.⁶ Some individuals, particularly heart transplant recipients, are unusually sensitive to adenosine and require a lower dose (1 mg).