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

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).

Atrial Pacing

In patients with implantable devices, antitachycardia pacing facilities can be used to terminate the arrhythmia. However, there is also a risk of inducing atrial fibrillation with a rapid ventricular response in a patient with an antegradely conducting accessory pathway.

Long-Term Management

Patients with AV nodal reentry tachycardia and AV reentry tachycardia should be referred to a cardiologist for electrophysiologic evaluation and long-term management. Both pharmacologic and nonpharmacologic alternatives, including ablation of an accessory pathway, are widely available.

Atrial Flutter

Electrocardiographic Presentation

Atrial flutter is usually an organized atrial rhythm with an atrial rate typically between 250 and 350 beats per minute. In the more common counterclockwise flutter, F waves are negative in leads II, III, aVF, and V_5-6 and positive in leads V_1-2 (Figure 78-7, A). Typical clockwise atrial flutter is characterized by positive F waves in leads II, III, and aVF and negative waves in leads V_1-2.

Figure 78-7 A, Typical counterclockwise atrial flutter. F waves are negative in leads II, III, aVF, and V_5-6 and positive in leads V_1-2. B, Atrial flutter with 1 : 1 atrioventricular conduction and a ventricular rate of 270 beats per minute in a patient treated with flecainide. C, Atrial fibrillation with fast, uncontrolled ventricular rates.

Treatment with propafenone, flecainide, and amiodarone to prevent recurrent atrial fibrillation without adding an AV blocking agent (beta-blocker or nondihydropyridine calcium antagonist) can organize the arrhythmia into typical atrial flutter with AV conduction of 1 : 1 or 2 : 1, producing a ventricular rate response of 150 beats per minute or higher (see Figure 78-7, B). The probability of 1 : 1 conduction is increased in the presence of an accessory pathway with a short effective refractory period.

Atrial Fibrillation

Acute Management

Acute therapy for atrial flutter and atrial fibrillation depends on the clinical presentation. Emergency electrical cardioversion is indicated for patients with hemodynamic collapse and progressively deteriorating left ventricular systolic function.

Pharmacologic Cardioversion

If the arrhythmia is hemodynamically stable and is of recent onset, pharmacologic cardioversion can be effective.

Flecainide and Propafenone

Pharmacologic cardioversion of atrial fibrillation can be accomplished with the IC class of antiarrhythmic drugs—flecainide and propafenone administered orally as a single dose of 300 and 600 mg, respectively (Table 78-2).² Placebo-controlled randomized studies show an efficacy rate of 60% to 80% between the third and eighth hour after drug ingestion.^9,10 Both oral and IV routes of administration are equally effective, although with IV injection, restoration of sinus rhythm can be achieved more quickly.

TABLE 78-2 Antiarrhythmic Drugs for Pharmacologic Conversion of Atrial Tachyarrhythmias

Flecainide is given as a slow IV injection of 2 mg/kg over 10 to 30 minutes, up to the maximum dose of 150 mg. Propafenone is administered as a slow IV injection of 1.5 to 3 mg/kg, up to 300 to 600 mg. Because these drugs can significantly slow the atrial rate (from 300-350 beats/min to 200 beats/min), which may result in 1 : 1 AV conduction, beta-blockers or calcium antagonists with negative dromotropic effects on AV node conduction (verapamil, diltiazem) should be used concomitantly Other cardiovascular effects include reversible QRS widening and (rarely) left ventricular decompensation. Because of the negative inotropic effect, they are contraindicated in patients with severe structural heart disease and a poor ejection fraction.

Class IC drugs are usually ineffective for the conversion of atrial flutter, because they slow conduction within the reentrant circuit and prolong the flutter cycle length but rarely interrupt the circuit. These drugs pose the risk of increased (e.g., 2 : 1 or 1 : 1) AV conduction. Reported efficacy rates are as low as 13% to 40% with IV flecainide and propafenone.

Ibutilide

The class III agent, ibutilide, is administered IV as a 10-minute injection of 1 to 2 mg and is particularly effective in terminating atrial flutter, with a success rate of about 60%. Its administration may be associated with excessive QT interval prolongation, however, because of the rapid delayed rectifier potassium current (I_Kr) blockade and the risk of torsades de pointes.^11,12 It is less effective in atrial fibrillation. Higher doses of ibutilide administered as two successive infusions of 1 mg are usually required to terminate fibrillation. The advantage of ibutilide is that it may be effective in the conversion of arrhythmias of up to 30 days’ duration, but the success rate drops significantly to 20% to 30%. The safety of ibutilide in patients with poor left ventricular function is unknown.

Amiodarone

Amiodarone administered IV at a dose of 5 mg/kg for 1 hour, followed by an infusion of 20 mg/kg over 24 hours, is effective in converting both atrial fibrillation and flutter, but the effect is significantly delayed.^13,14 However, because of its ability to control the ventricular rate, a low likelihood of torsades de pointes, and the absence of a negative inotropic effect, amiodarone can be used safely in patients with significant structural heart disease and those who are critically ill.

Procainamide and Sotalol

Procainamide administered as a slow IV injection of 1000 mg over 20 to 30 minutes, followed if necessary by an infusion of 2 mg/min over 1 hour, converts atrial flutter or fibrillation of less than 48 hours’ duration, but its efficacy is limited in longer-lasting arrhythmias.¹⁵ It is less effective than propafenone, flecainide, and ibutilide.

Sotalol is not indicated for the pharmacologic cardioversion of atrial flutter or fibrillation because its efficacy does not exceed 11% to 13%; however, it may satisfactorily control the ventricular rate.

Vernakalant

This drug is given by a short IV infusion (3 mg/kg over 10 minutes). If after a 15-minute waiting period the arrhythmia persists, a second infusion of 2 mg/kg may be given over 10 minutes. In recent-onset atrial fibrillation (<72 hours), about 50% of cases will terminate on average 12 minutes from the start of the first infusion. Vernakalant may be given to patients with underlying structural heart disease but not to patients with grade II/IV congestive heart failure. Proarrhythmia is uncommon, but hypotension and posttermination bradycardia may occur.¹⁶

The choice of an antiarrhythmic agent for cardioversion is illustrated in Figure 78-8.

Figure 78-8 Choice of antiarrhythmic for pharmacologic cardioversion of atrial fibrillation.

Anticoagulation

Anticoagulation is imperative if the arrhythmia persists for more than 24 to 48 hours or if its duration is unknown. Atrial flutter and atrial fibrillation pose similar risks of thromboembolism, and the same criteria for anticoagulation should be applied in patients with either arrhythmia. In hemodynamically stable arrhythmias of more than 48 hours’ or of unknown duration, rate control and 3 weeks’ anticoagulation with warfarin (International Normalized Ratio 2.0 to 3.0) should be considered before any intervention (electrical or pharmacologic cardioversion, catheter ablation).¹⁷

Transesophageal Echocardiography–Guided Cardioversion

If, for any reason, deferral of cardioversion is not indicated, the transesophageal echocardiography–guided approach, with short-term anticoagulation with low-molecular-weight heparin, is a safe and effective alternative.¹⁸ It may be clinically beneficial in patients with recent-onset arrhythmias or in individuals at high risk of bleeding complications during prolonged anticoagulation therapy.¹⁹ Compared with unfractionated heparin, low-molecular-weight heparin therapy does not involve prolonged IV administration or laboratory monitoring and therefore has the potential to greatly simplify cardioversion-related anticoagulation therapy in low-risk individuals. Postcardioversion anticoagulation should be considered if atrial fibrillation has been present for 48 hours or more, or if thromboembolic risk factors are present (Table 78-3).^17,20

TABLE 78-3 Risk Stratification and Indications for Anticoagulation in Atrial Fibrillation and Flutter

INR, International Normalized Ratio.

Modified from Straus SE, Majumdar SR, McAlister FA. New evidence for stroke prevention: scientific review. JAMA 2002;288:1388-95.

Mechanism

The mechanism of atrial tachycardia is attributed to enhanced automaticity, triggered activity, or intraatrial reentry. Macroreentrant atrial tachycardia often occurs after surgery for congenital heart disease. Focal atrial tachycardia typically originates along the crista terminalis in the right atrium, in the pulmonary veins in the left atrium, or around one of the atrial appendages.

Electrocardiographic Presentation

The heart rate varies from 120 to 250 beats per minute, P waves precede the QRS complex, and PP intervals are regular (see Figure 78-5, B). The PR interval is linked to the rate of tachycardia and is longer than in sinus rhythm at the same rate. P wave morphology is usually different from that during sinus rhythm and depends on the site of origin. Left atrial tachycardia presents with the negative P waves in leads I, aVL, V₅, and V₆. Automatic atrial tachycardia may present as an incessant variety, leading to tachycardia-induced cardiomyopathy

Atrial Tachycardia With Atrioventricular Block

Tachycardia with AV block occurs commonly in patients with organic heart disease, and in 50% to 75% of cases, it is due to digitalis toxicity (Figure 78-9). Digoxin-specific antibody fragments are available for the reversal of life-threatening overdosage.

Figure 78-9 Atrial tachycardia with varying atrioventricular block due to digitalis toxicity.

Multifocal Atrial Tachycardia

This tachycardia presents as rapid, irregular atrial activity with discrete P waves of varying morphology and is considered a transitional rhythm between atrial tachycardia and fibrillation. However, it may occur in patients with chronic severe pulmonary disease as a result of theophylline or β-agonist overdose. Elimination of the causative factor may reduce the need for antiarrhythmic therapy. IV verapamil can accomplish rate control.

Acute Management

DC cardioversion converts atrial tachycardia based on the reentry mechanism or triggered activity, but it may not terminate automatic tachycardia. Similarly, atrial overdrive pacing may slow the tachycardia rate but seldom suppresses the automatic focus.

It is generally accepted that beta-blockers and calcium antagonists, particularly verapamil, can either terminate the tachycardia or produce rate control. Adenosine can terminate atrial tachycardia, but the most common response to adenosine is to create AV block and thereby reveal the unaffected tachycardia (see Figure 78-5, B and C).

Flecainide, propafenone, sotalol, and amiodarone are effective in converting the arrhythmia. If tachycardia occurs as a result of digitalis intoxication, therapy includes the cessation of digoxin and IV administration of potassium.

Long-Term Management

Patients with atrial tachycardia should be referred to a cardiologist because the arrhythmogenic focus can be found and ablated in up to 86% cases.