Brevibloc

Narrow-complex tachycardia is a frequent reason patients present to an emergency department or to a primary care physician. An understanding of the pathophysiology of the different forms of narrow-complex tachycardia is important for both acute and chronic management. With this knowledge, the physician can better identify patients who have a life-threatening problem that requires further evaluation by a subspecialist.

The terms "paroxysmal atrial tachycardia" and "supraventricular tachycardia" are often applied to a heterogeneous group of arrhythmias that vary in mechanism and location. Paroxysmal atrial tachycardia is a diagnosis that is frequently used in the clinical setting of narrow-complex tachycardia. Imprecise use of this term can hinder efforts to make a more specific diagnosis and select the most appropriate therapy.

The pathophysiology, diagnosis and treatment of various forms of narrow-complex tachycardia are reviewed in this article. Clues to look for during clinical examination and on the electrocardiogram (ECG) are also discussed.

Mechanisms

The characteristics of the different types of narrow-complex tachycardia are summarized in Table 1, and a schematic representation of the location of these arrhythmias is shown in Figure 1. The mechanism of an arrhythmia has important implications for therapy.

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The mechanisms of tachyarrhythmias are primarily automatic and reentrant. An automatic focus is best thought of in terms of a single point, like a radio tower. Triggered by a variety of factors (Table 2), an automatic focus initiates and sustains the tachyarrhythmia. The focus may be affected by a number of autonomic and metabolic factors, but no loop circuit is required for impulse propagation. Reentry is defined by a loop circuit consisting of pathways with varying conduction velocity and refractoriness (Figure 2).

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Many of the tachyarrhythmias discussed in this article are confined to the atrial tissue, with the atrioventricular (AV) node serving its normal function of conducting from the atrium to the His-Purkinje system. However, in nonparoxysmal junctional tachycardia, the permanent form of junctional reentrant tachycardia, AV nodal reentrant tachycardia and AV reentrant tachycardia, the AV node usually serves as one limb of the tachycardia circuit.

Sinus Tachycardia

Sinus tachycardia rarely results in heart rates of greater than 180 beats per minute. However, rates of more than 200 beats per minute have been seen in healthy adults and children.[1,2]

A sinus tachycardia can occur during pregnancy, or it can be produced by a number of metabolic and disease states, including hyperthyroidism, pheochromocytoma, dehydration, stimulant excess and fever. These conditions should be excluded before a primary cardiac diagnosis, such as sinoatrial nodal reentry, intra-atrial reentry or automatic atrial tachycardia, is considered. Inappropriate sinus tachycardia may require treatment with beta-adrenergic blocking agents.

Atrial Fibrillation

Atrial fibrillation is the most common supraventricular arrhythmia in clinical practice, and it is also the most difficult to treat. In patients with this condition, the arrhythmia may appear to be regular if the ventricular response is fast. Vagal maneuvers, such as Valsalva's maneuver, carotid sinus massage or the diving reflex, often slow the heart rate enough to unmask the uneven baseline and irregular ventricular response.

If vagal maneuvers are unsuccessful in the acute setting, the administration of 6 to 12 mg of adenosine (Adenocard) by intravenous push will produce an AV nodal block of sufficient duration to confirm or exclude atrial fibrillation. Verapamil (Calan, Isoptin) may also be used, but it has a longer half-life than adenosine and is more likely to produce hypotension.

Digoxin (Lanoxin) may be used acutely to slow the heart rate, but its peak action does not occur until four hours after it is administered. Other agents may be more useful if rate control is needed sooner. Esmolol (Brevibloc), an intravenously administered beta[1]-selective blocking agent with a short half-life, has been effective in acutely controlling the ventricular response and aiding in the conversion to normal sinus rhythm.[3] Intravenous diltiazem (Cardizem) is also efficacious for rate control, but other agents are required to achieve sinus rhythm.[4]

Intravenously administered procainamide is very useful for acute therapy, while orally administered procainamide is effective for chronic therapy. In the acute setting, procainamide not only decreases atrial automaticity but also slows AV nodal conduction, as opposed to other class Ia drugs, such as quinidine (Quinaglute) and disopyramide (Norpace), which are vagolytic and may enhance AV nodal conduction[5] (Table 3). Class Ic drugs, specifically propafenone (Rythmol) and flecainide (Tambocor), are effective for chronic therapy. Early experience with moricizine (Ethmozine) and sotalol (Betapace) has also been favorable. Amiodarone (Cordarone) is very efficacious in the treatment of atrial fibrillation, but toxicity tends to limit its long-term use.

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In chronic, persistent atrial fibrillation, AV nodal ablation and ventricular rate-responsive pacing provide near-normal hemodynamics and exercise capacity while eliminating the risk of drug toxicity.

Atrial Flutter

Atrial flutter is currently believed to be a right atrial macroreentrant tachycardia, with the left atrium uninvolved in the tachycardia circuit. An area of slowed conduction has been found in the posteroseptal area of the right atrium. Recently, reports have been published describing treatment success with radiofrequency catheter ablation to this area.[6] Typical atrial flutter has an atrial rate of 250 to 350 beats per minute. This tachycardia is characterized by sawtooth F waves that are negative in leads II, III and AVF and well seen in leads [V.sub.1] and [V.sub.2]. The vagal or pharmacologic maneuvers noted in the discussion of atrial fibrillation may be necessary to slow ventricular response and better visualize atrial activity. Neither a rhythm strip nor a monitor may optimally demonstrate atrial activity. Therefore, a 12-lead ECG should be obtained.

Atrial flutter may be treated with class Ia or Ic drugs. Beta blockers or verapamil may slow AV conduction and control the ventricular response.

Antitachycardia atrial pacing may occasionally be efficacious. Other nonpharmacologic treatments include mapping and radiofrequency catheter ablation in the right atrium, AV nodal catheter ablation and permanent ventricular pacing for rate control, and atrial surgery.[7]

Paroxysmal Atrial Tachycardia

Paroxysmal atrial tachycardia, usually accompanied by 2:1 AV block, is thought to be a result of triggered automaticity. The most common clinical scenario is one in which digitalis toxicity produces delayed after-depolarizations (Figure 3).

This arrhythmia has become less common as the use of digitalis has decreased. However, one study[8] found that in 50 percent of cases, paroxysmal atrial tachycardia resulted from structural heart disease in the absence of digitalis.

It is important to examine the 12-lead ECG closely. Special attention should be given to leads II, III, AVF and [V.sub.1]; lead [V.sub.1] may have the blocked P wave buried in the complex, resulting in a pseudo-right bundle branch block pattern (Figure 4). Verapamil is useful if therapy is required.

Multifocal Atrial Tachycardia

Multifocal atrial tachycardia is an irregular atrial tachycardia. This arrhythmia usually occurs in adults over 50 years of age who have an acute noncardiac illness, most commonly exacerbation of chronic obstructive pulmonary disease.[9,10]

On the ECG, multifocal atrial tachycardia is characterized by an atrial rate of 100 to 150 beats per minute and by the presence of at least three different P-wave morphologies. The baseline is isoelectric, and the P-P interval is irregularly irregular.

Evidence suggests that multifocal atrial tachycardia also may be caused by triggered automaticity, since this arrhythmia is frequently associated with hypoxemia, beta-adrenergic stimulation, hypokalemia and digitalis therapy. The response of this tachycardia to magnesium and verapamil and its lack of response to class Ia drugs support this hypothesis.[11,12]

A continuous verapamil infusion titrated to the desired rate results in excellent control, with little or no hypotension in ventilated and perioperative patients.

Nonparoxysmal Junctional Tachycardia

Nonparoxysmal junctional tachycardia is a relatively uncommon arrhythmia that is most likely caused by enhanced automaticity. The ventricular rate is 70 to 120 beats per minute, and the impulse arises from within the AV node. Previous reports[13,14] have associated this arrhythmia with digitalis administration, cardiac surgery and acute myocardial infarction. More recently, an association with amyloidosis and congenital heart disease has been reported.[15]

In nonparoxysmal junctional tachycardia, the ECG may show AV dissociation or retrograde P waves inverted in leads II, III and AVF (Figure 5). If therapy is required, verapamil is the drug of choice. Beta blockers may also be efficacious.

Permanent Form of Junctional

Reentrant Tachycardia

The permanent form of junctional reentrant tachycardia is a reentrant arrhythmia with a ventricular rate of 130 to 200 beats per minute. The antegrade limb of the arrhythmia is the AV node, and the retrograde limb is a concealed paraseptal accessory pathway. The heart rate during tachycardia varies with the autonomic tone and may temporarily respond to beta-adrenergic blocking agents, procainamide or verapamil. However, the arrhythmia usually resumes and is frequently refractory to drug therapy

Patients often present with a tachycardia-induced cardiomyopathy.[16] This arrhythmia may be cured with either radiofrequency catheter ablation or surgery.[17,18]

AV Reentrant Tachycardias

Depending on the ECG findings, AV reentrant tachycardias have also been known as Wolff-Parkinson-White syndrome (short PR interval, delta wave and other ECG abnormalities) and Lown-Ganong-Levine syndrome (short PR interval only). However, anatomic definitions are changing, and it is best to think in terms of AV nodal reentry and AV reentry using an accessory pathway, rather than Lown-Ganong-Levine syndrome and Wolff-Parkinson-White syndrome, respectively.[19,20] AV reentry using an accessory pathway requires the ventricle as a limb of the tachycardia circuit.

AV NODAL REENTRY

AV nodal reentrant tachycardia is probably the most common of the narrow-complex tachycardias often grouped under the term "paroxysmal atrial tachycardia." The onset is usually in childhood or adolescence. This tachycardia occasionally presents later in life.

Like most paroxysmal tachycardias, AV nodal reentrant tachycardia is described as the sudden onset of rapid, regular palpitations lasting seconds to hours. In most cases, the palpitations cease suddenly. The occurrence of symptoms such as dizziness, near-syncope and syncope depends on the rate of the arrhythmia, which may reach 270 beats per minute in adolescents and young adults.

The usual anatomy in AV nodal reentrant tachycardia consists of a normal AV node and His-Purkinje system plus a "slow" pathway of decrementally conducting tissue that appears to lie posterior in the AV septum near the ostium of the coronary sinus, to run along the tricuspid ring and to insert in the His bundle.[19]

In classic antegrade-slow, retrograde-fast tachycardia (Figure 2), a premature beat is unable to conduct down the normal "fast" pathway, but is able to conduct down the "slow" pathway. The beat then conducts back up the "fast" pathway, initiating the tachycardia, which tends to have a long PR interval and a short R-P' interval, where P' is the retrograde-conducted P wave.

On the ECG, the atrial premature beat conducts with a long PR interval compared with baseline. In tachycardia, the P wave is usually buried in, just preceding or just after the QRS complex.

For acute therapy, AV nodal reentrant tachycardia responds well to vagal maneuvers, adenosine, verapamil or beta-blocking agents. For chronic therapy, digoxin, verapamil, beta blockers and class Ia and Ic drugs are quite effective.

Radiofrequency catheter ablation is safe and effective and has become the treatment of choice in patients with drug intolerance or recurrent arrhythmias, as well as in young patients facing long-term drug therapy and potential problems in qualifying for insurance.

AV REENTRY USING AN ACCESSORY PATHWAY

AV accessory conducting pathways, which predispose to reentrant tachycardia, lead to a phenomenon known as preexcitation. The term "preexcitation" refers to premature electrical activation of the ventricular myocardium via an anomalous accessory pathway

Preexcitation is observable on one to three per 1,000 routine ECGS.[21] Preexcitation may be quite obvious, based on the presence of a short PR interval (less than 0.12 seconds), large delta waves and broad, bizarre QRS complexes. More often, however, the findings are subtle and may be apparent only intermittently As many as 40 percent of persons with AV reentrant tachycardia have accessory pathways that may only conduct retrograde; in such cases, no surface ECG evidence of preexcitation will be present.

The accessory pathway, or Kent bundle, consists of myocardium (not specialized conduction tissue) that remains at birth after the formation of the annulus fibrosus normally severs any connection between the atria and the ventricles in utero. The primary care physician has to decide whether the pathway is potentially life-threatening in the patient with preexcitation. That is, if the patient goes into atrial fibrillation, will the accessory pathway conduct antegrade fast enough to produce ventricular fibrillation?

The following findings can suggest a more "benign" pathway: (1) minimal preexcitation on a surface ECG; (2) intermittent preexcitation from beat to beat on a single ECG or from visit to visit on serial tracings, and (3) the absence of symptoms. The literature to date suggests that no therapy is needed for completely asymptomatic patients who have preexcitation on a surface ECG; instead, these patients should be followed and evaluated further if symptoms occur.

If the patient has intermittent preexcitation or minimal preexcitation, a more benign pathway is suggested, and the primary care physician may be comfortable prescribing a trial of drug therapy for recurrent tachycardia. The medications that tend to be best tolerated in adolescents and young adults are digoxin, verapamil, beta blockers, disopyramide and flecainide.

Digoxin and verapamil should be used with extreme caution, because they tend to slow AV nodal conduction, and in the event of atrial fibrillation, they may preferentially direct impulses down the accessory pathway at a more rapid rate. Beta blockers are probably a better first choice, because they not only slow AV nodal conduction but they also slow conduction of the impulse through the atrial tissue and the ventricular myocardium.

If the initial drug therapy fails, the patient should consider undergoing an electrophysiologic evaluation and radiofrequency catheter ablation before embarking on a lifetime of antiarrhythmic drug therapy. Likewise, if the patient has a potentially life-threatening pathway, there is no reason for the physician to wait for drug therapy to fail before referring the patient for definitive therapy.

Intra-atrial Reentry

and Sinoatrial Nodal Reentry

Intra-atrial reentry and sinoatrial nodal reentry are rare arrhythmias that most often present as a paroxysmal sustained tachycardia with a rate that is usually less than 250 beats per minute. Structural heart disease is frequently present, and patients often have a history of atrial surgery for closure of an atrial septal defect or correction of transposition of the great vessels.[24] Controversy presently exists as to whether the sinoatrial node is truly a participant in the reentrant circuit or whether it is simply intra-atrial r-eentry near the sinoatrial node.[25]

Intra-atrial reentry and sinoatrial nodal reentry usually originate in the right atrium and are recognized electrocardiographically by a normal P-wave morphology and axis (upright in the inferior leads and in lead I, biphasic or negative in lead V[1]). The PR interval is also normal (0.12 to 0.20 seconds), and it increases with increasing atrial rates, because the AV node is not part of the circuit. This finding may help differentiate intra-atrial reentry and sinoatrial nodal reentry from AV reentry, in which the R-P' interval is usually constant.

Therapy is initially pharmacologic, because these arrhythmias usually respond to class la drugs, such as quinidine, procainamide or disopyramide. Class Ic drugs, such as flecainide or propafenone, also may be useful.

If medical therapy fails, many surgical techniques have been successful in curing intra-atrial reentry and and sinoatrial nodal reentry.[26,27] Antitachycardia pacing is frequently efficacious. The use of radiofrequency catheter ablation in the treatment of these arrhythmias has been reported.[28,29]

Automatic Atrial Tachycardia

Automatic atrial tachycardia is an uncommon clinical entity that may be repetitive or continuous. The repetitive form is often seen in the absence of structural heart disease. However, the continuous form is more commonly associated with other abnormalities, such as an atrial septal defect, and patients may be very symptomatic.[30]

If the arrhythmia is not controlled, a tachycardia-induced cardiomyopathy may develop, and congestive heart failure may occur. Any other of the continuous tachyarrhythmias described in this article may produce a similar long-term clinical picture.

The P-wave morphology in automatic atrial tachycardia may be very similar to, or even identical to, the sinus P wave. Therefore, it sometimes can be difficult to differentiate this arrhythmia (Figure 6) from sinus tachycardia.

Automatic atrial tachycardia also may be misdiagnosed as atrial flutter when the atrial rate approaches 250 beats per minute. However, the onset is distinctive electrocardiographically, because the first P wave in the tachycardia has the same morphology and PR interval as the subsequent tachycardia beats. Since this is an automatic arrhythmia, a "warm-up" phenomenon may occur, with the first few beats being slower than the stable tachycardia.

Automatic atrial tachycardia responds poorly to the usual class Ia drugs. Class Ic drugs, such as flecainide and propafenone, and Class HI drugs, such as amiodarone, are more efficacious. Beta blockers may be useful in slowing the tachycardia rate. Moricizine may be effective in treating this arrhythmia.[31] Antitachycardia pacing is not helpful.

Radiofrequency catheter ablation has shown promise in the treatment of this unusual tachycardia,[32] and it is probably the best option if drug therapy fails. Long-term success has been achieved with surgical resection of the tachycardia focus after atrial mapping.[33]

Final Comment

Although the clinical presentation and the ECG hold clues to a specific tachycardia, the features of the various narrow-complex tachycardias frequently overlap and the findings may be subtle (Table 4 on the following page). If initial drug therapy is unsuccessful, the diagnosis should be reconsidered before another medication is selected. Electrophysiologic studies can be very helpful in identifying the specific tachycardia and determining the appropriate therapy.

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With the advent of radiofrequency catheter ablation, it is now possible to cure many forms of narrow-complex tachycardia. In this procedure, catheters are usually placed in the high right atrium, the right ventricular apex, the His bundle area and the coronary sinus in order to map the tachycardia, as in a routine electrophysiologic study. Next, a catheter, which usually has a deflectable large tip, is advanced through the vein or the femoral artery to the site of the abnormal conduction. Radiofrequency energy is then delivered through the tip of the catheter, which makes a small superficial burn, up to 4 mm in diameter, on the endocardial surface. Many arrhythmias that were previously treated medically or that required surgery are now amenable to treatment with catheter ablation. In most cases, patients require less than a 48-hour hospital stay.[34] Radiofrequency catheter ablation has been shown to be efficacious in the treatment of AV nodal reentry, AV reentry using an accessory pathway and the permanent form of junctional reentrant tachycardia. This procedure has also shown promise in the treatment of automatic atrial tachycardia and intra-atrial reentrant tachycardia and atrial flutter.

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Management of cardiac arrhythmias: the nonpharmacologic approach. Philadelphia: Lippincott, 1987:304-39. [19.] Hazlitt HA, Jackman WM, Beckman KJ, McClelland JH, Wang X, Moulton KP, et al. Direct recordings of slow pathway activation in patients with atrioventricular nodal reentrant tachycardia. Circulation 1991;84(Suppl 2):931. [20.] Murdock CJ, Leitch JW, Klein GJ, Guiraudon GM, Yee R, Teo WS. Epicardial mapping in patients with "nodoventricular" accessory pathways. Am J Cardiol 1991;68:208-14. [21.] Gallagher JJ, Pritchett EL, Sealy WC, Kasell J, Wallace AG. The preexcitation syndromes. Prog Cardiovasc Dis 1978;20:285-327 [22.] Farshidi A, Josephson ME, Horowitz LN. Electrophysiologic characteristics of concealed bypass tracts: clinical and electrocardiographic correlates. Am J Cardiol 1978;41:1052-60. [23.] Klein Gj, Yee R, Sharma AD. Longitudinal electrophysiologic assessment of asymptomatic patients with the Wolff-Parkinson-White electrocardiographic patteRN. 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MICHAEL C. GIUDICI, is director of cardiac electrophysiology at St. Luke's Regional Heart Center in Davenport, Iowa. After receiving his medical degree from the University of Iowa College of Medicine, Iowa City, he completed a residency in internal medicine and a fellowship in cardiology at Thomas Jefferson University Hospital, Philadelphia. Dr. Giudici subsequently completed a fellowship in interventional cardiology and electrophysiology at the University of Missouri-Columbia Hospitals and Clinics.

TAMRA J. GUMPERT, C.C.R.N. is a cardiovascular nurse/specialist in the cardiac catheterization laboratory at St. Luke's Regional Heart Center.

LISA L. HEATHNUN, R.T.R. is a cardiovascular specialist and an advanced cardiac life support instructor at St. Luke's Regional Heart Center.

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