Supraventricular arrhythmias

Atrioventricular nodal reentry tachycardia and atrioventricular reentry tachycardia

AV nodal reentry tachycardia and AV reentry tachycardia are usually referred to as paroxysmal supraventricular tachycardias (SVTs). They 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 anomaly, atrial septal defect, Fallot tetralogy) can coexist in a small percentage of patients with these arrhythmias. 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%–2% of the general population, especially the elderly. It is usually associated with cardiovascular pathologies, among which hypertension and congestive heart failure prevail. About a third of patients, however, present with no underlying heart disease and are considered to have “lone” atrial fibrillation. The incidence of isolated atrial flutter is largely unknown and is believed to be in the range of 0.037%–0.88% per 1000 person-years, but at least half of these patients also have atrial fibrillation as a coexistent arrhythmia.

Atrial tachycardia

Atrial tachycardia affects 0.34%–0.46% of patients with arrhythmias. It is common in younger individuals after 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 characterized. Sinoatrial reentry tachycardia is found incidentally in 1.8%–16.9% of patients undergoing electrophysiologic studies for other supraventricular tachyarrhythmias.

Narrow-complex tachycardias

The typical ECG feature is narrow QRS complexes less than 120 ms. In this case, the tachycardia is almost always supraventricular, and the differential diagnosis relates to its mechanism ( Fig. 71.2 ).

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 ( Fig. 71.3 ). If the diagnosis of SVT 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.

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; the impulse 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 140–250 beats per minute. The atria are activated retrogradely, producing inverted P waves in leads II, III, and aVF. Because atrial and ventricular depolarization occur simultaneously, the P waves are often obscured by the QRS complexes and cannot be detected on the surface ECG ( Fig. 71.4 A). However, in about one-third of cases of slow-fast AV nodal reentry tachycardia, a terminal positive deflection may be present in lead aVR or V ₁ (or both), imitating right bundle branch block, or pseudo-S waves may be noted in the inferiorly oriented leads; these findings reflect retrograde activation of the atria. Tachycardia using these pathways in reverse (“fast-slow,” or long RP, tachycardia) is less common, occurring in 5%–10% of cases.

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 pathway (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 ms), and the QRS complex is wide; this occurs because the atrial impulse enters 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 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 Fig. 71.4 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 Fig. 71.4 C). Antidromic AV reentry tachycardia is uncommon (<10% of cases). Atrial fibrillation is usually encountered in patients with antegradely conducting pathways (see Fig. 71.4 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, the Valsalva maneuver, and facial immersion in cold water (diving reflex), can terminate tachycardia in about 50% of patients ( Box 71.1 ). Commercially available gel packs can be used as cold compresses instead of facial immersion, but the most important elements are wet nostrils and breath-holding.