Paroxysmal supraventricular tachycardias

The Journal of Emergency Medicine, Vol 14, No 1, pp 39-5 1, 1996 Copyright 0 1996 Elsevier Science Inc. Printed in the USA. All rights reserved 0736-4679/96 $15.00 + .OO ELSEVIER

SSDI 0736-4679(95)02061-6

Selected Topics: Cardiology Commentary

PAROXYSMAL Steven R. Lowenstein,

SUPRAVENTRICULAR

MD, MPH,**

TACHYCARDIAS

Blair D. Halperin, MD,t and Michael J. Reiter,

MD, PHDt

Divisions of *Emergency Medicine and tCardiology and SColorado Emergency Medicine Research Center, University of Colorado Health Sciences Center, Denver, Colorado Reprint Address: Steven R. Lowenstein, MD, MPH, University of Colorado Health Sciences Center, Division of Emergency Medicine, Box B-21 1, 4200 East Ninth Avenue, Denver, CO 80262

q Abstract-Paroxysmal supraventricular tachycardia (PSVT) is a distinct clinical syndrome. Most patients present with the abrupt onset of palpitations, dizziness, dyspnea, or chest pain. The electrocardiogram (ECG) demonstrates a fast heart rate (150-250 beats per min), a regular rhythm, and most often, a narrow QRS complex. The P wave is usually hidden within the QRS complex. PSVT is caused by reentry, and the tachycardias are classified, electropbysiologically, according to the anatomic location of the reentry circuit. Atrioventricular nodal reentry is the most common form of PSVT. In AV nodal reentry, there are two conducting pathways (alph and beta) that have different conduction times and refractory periods; both pathways are confined to the AV nodal and perinodal atria1 tissue. The other common form of PSVT, termed atrloventricular reciprocating tachycardia, depends on an anatomically distinct, or “accessory,” pathway that may conduct impulses between the atria and the ventricles, while bypassing the AV node. The two forms of PSVT may be distinguised in many casesby examining the 12-lead electrocardiogram. In the majority of cases of A-V nodal reentry, the atria and ventricles are depolarized simultaneously, and the P waves are hidden in the QRS complex. If the reentry circuit includes an accessory pathway, the P wave always follows the QRS, and usually the R-P interval exceeds70 msec. Several principles should guide the management of PSVT: (a) Unstable patients require emergent electrical cardioversion; (b) A 1Zlead ECG should be obtained immediately to confirm that the tachycardia has a nar-

RECEIVED: ACCEPTED:

row complex (ventricular tachycardia may masquerade as PSVT if only a single lead is examined); (c) Vagal maneuvers may be attempted (the Valsalva maneuver is safer and more efficacious, especially in the elderly); and (4) In most patients, adenosine is the first-line agent to treat PSVT. Contraindications to adenosine and drug interactions are noted in this article. In addition, the use of adenosine in wide complex tachycardias and the indications for admission and referral for electrophysiologic evaluation are discussed. 0 Keywords-supraventricular tachycardia; reentry; Wolff-Parkinson-White syndrome; adenosine

INTRODUCTION Eight years ago, an article in this journal reviewed the management of tachycardias (1). The differential diagnosis of wide-complex tachycardias was emphasized. In the present article, we discuss recent developments in the diagnosis and treatment of paroxysmal supraventricular tachycardia (PSVT), a common narrow-complex tachycardia. We emphasize the management of PSVT. Atria1 fibrillation, atria1 flutter, and multifocal atria1 tachycardia are mentioned only briefly. Although this article was written to highlight new discoveries in pharmacotherapy and electrophysiology,

Cardiology Commentary is coordinated by Steven R. Lowenstein, MD, SciencesCenter, Denver, Colorado 3 August 1994; FINAL SUBMISSION RECEIVED: 9 August 1995; 21 August 1995 39

MPH,

of the University of Colorado Health

S. R. Lowenstein et al.

40

readers are reminded of the importance of promptly evaluating each patient’s hemodynamic status.Patients who present with a faint or unobtainable pulse, hypotension, altered mentation, angina, or pulmonary edema require emergent electrical cardioversion. No diagnostic maneuversshould defer initiation of electrical therapy.

BASIC MECHANISMS OF SUPRAVENTRICULAR TACHYCAIWIAS Automaticity The two principal mechanisms of the genesis of cardiac dysrhythmias are enhanced automaticity and reentry (2,3). Automaticity is a normal property of some specialized cardiac cells; it is responsible for sinus node function and for the appearance of subsidiary (“escape”) pacemaker activity seen in atrial, A-V nodal, and His-Purkinje cells. Common automatic dysrhythmias include sinus tachycardia and multifocal atria1 tachycardia (2,4). Acute inferior wall myocardial infarction and digitalis toxicity often increase A-V nodal automaticity; the result is nonparoxysmal junctional tachycardia, another common automatic tachycardia.

Reentry Excluding sinus tachycardia, the vast majority of sustained supraventricular tachycardias are due to reentry (5). In the normal heart, conduction of electrical impulses proceeds rapidly and uniformly, from the sinus node, through the A-V node, to the specialized conducting tissues of the ventricles. Normal conduction depends upon electrical homogeneity: adjacent conducting pathways have similar refractory periods and conduction velocities. In contrast, in most patients who are prone to develop paroxysmal supraventricular reentrant tachycardia, two or more anatomically or functionally separateconducting pathways exist, which differ in refractoriness and conduction speed (Figure 1). During sinus rhythm, impulses conduct down both pathways but reach the His bundle or the ventricle via the rapid pathway. The electrocardiogram demonstrates only fast pathway conduction (the PR interval is less than .20 set) (6). A supraventricular tachycardia is initiated when a critically timed atrial premature contraction occurs and finds one pathway refractory. The impulse is then conducted down the nonrefractory pathway. If the first

Figure 1. Schematic illustrating development of A-V node reentry tachyoerdia. (A) Sinus beat in a patient with “dual AV nodal pathways.” Anterograde conduction occurs predominantly over the fast A-V nodal pathway. Conduction over the slowly conducting p&nodal pathway (afpha pathway) is not manifest, since the His-Purkinje system is refractory upon arrival of the activation over the slow pathway. (B) A-V node reentry tachycardia. Under appropriate conditions, a premature atrial contractfon may block in the fast pathway and will be conducted to the His-Purkinje system ovar the slow perinodal pathway. Upon arrival at the His-Purkinje system, activation may proceed both anterograde (to the ventricles via the His-Purkinje system) and retrograde over the fast A-V nodal pathways to the atrium and back to the proximal end of the slowly conducting pathway, initiating a reentry tachycardia.

pathway is capable of retrograde conduction and is now excitable, the impulse can travel back to its point of origin, thus completing the reentry circuits (2,5-7). It is the presence of at least two distinct pathways, with unidirectional block in one of them, that creates the potential for a reentrant (or “circus”) tachycardia (3,8). Conduction velocity in the anterograde limb

Supraventricular Tachycardia

must be slower than the refractory period of the return limb; the leading edge of the wavefront must always meet excitable tissue, or the tachycardia cannot be sustained (7,9). The two pathways that participate in a reentrant tachycardia may be anatomically distinct. One example is the accessory Kent bundle of the Wolff-Parkinson-White syndrome (10). Commonly, the two pathways cannot be distinguished anatomically, and in most patients with paroxysmal supraventricular tachycardia, the two pathways both lie within or near the AV node. The differentiation between automatic and reentrant tachycardias is important therapeutically. Supraventricular tachycardias due to reentry can be terminated with electrical cardioversion or pacing, whereas automatic tachycardias cannot. Reentry tachycardias involving the A-V node as part of the reentry circuit can also be terminated by vagal maneuvers.Vagal maneuvers usually induce A-V block in automatic tachycardias or reentry tachycardias confined to the atrium. Clues to the mechanism of the tachycardia may be found at the beginning or end of the tachycardia. Reentrant tachycardiasstart and stop abruptly, and often are initiated by a premature beat. In contrast, automatic tachycardias show rate variability. Rather than a sudden onset, they “warm-up” (the rate accelerates slightly during the first few beats of the tachycardia) (6,9). Automatic tachycardiasfrequently emerge as the normal sinus rate slows, with a relatively late tachycardia beat (Figure 2); they often end when the sinus rate accelerates. Unfortunately, the first clue to an automatic tachycardia may be its persistenceafter repeated attempts at cardioversion. CLASSIFICATION OF PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIAS Paroxysmal supraventricular tachycardia (PSVT) is a distinct clinical syndrome. Patients present with the

41

abrupt onset of palpitations, often with associatedchest pain, dizziness, dyspnea,or diaphoresis.The syndrome may appearat any age, although symptoms most often occur in healthy, young adults, precipitated by exercise or stress. The majority of patients are women (11). Frequently, patients may be aware that rest or vagal maneuvers (for example, breath holding or gagging) have terminated prior episodes. The PSVT syndrome includes several electrophysiologically distinct reentrant tachycardias. The tachycardias are classified according to the anatomic location of the reentry circuit.

A-V Nodal Reentry A-V nodal reentry is the most common causeof PSVT and accountsfor 40-60% of presentations(5,7,12,13). In A-V nodal reentry, the two pathways(called the alpha and beta pathways)have different conduction times and refractory periodsand are confined to the A-V nodal and perinodal atrial tissue.The tachycardiais precipitatedby a premature atrial beat, which is blocked in the fastconducting (but long refractory period) beta pathway. The atrial beat is conductedanterogradethrough the AV node via the slow (alpha) pathway; upon reaching the ventricle, it “reenters” back up the fast pathway. This common form of A-V nodal reentry, in which the slow pathway servesas the anterogradelimb, is often called a “slow-fast” tachycardia (7). If the onset of the tachycardia can be recorded, an abrupt increase in the PR interval is usually seen, as anterogradeconduction shifts from the fast to the slow pathway (12) (Figure 3). During the tachycardia, the rhythm is regular. The QRS complex is narrow, unless rate-dependent aberrancy or a preexisting bundle branch block is present. Usually, the heart rate is between 150 and 250 beats/min. The P wave is usually hidden within the QRS, becausethere is nearly simulta-

Figure 2. Ventricular rhythm originating from an automatic focus. The first two beats are ventricular (V), followed by a fusion beat (F), as the VT rate slows and the sinus rate accelerates slightly. Following seven beats of sinus, the ventricular rate accelerates. Two fusion beats are seen, followed by ventricular rhythm.

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neous activation of the atria and the ventricles. At times, a P wave can be seen on the terminal portion of the QRS complex, but the R-to-P interval is always very short (less than 70 millisec) (7,12) (Figure 4A). If P waves are seen, they are upright in lead V1 (“Pseudo R-waves”) and negative in leads 2, 3, and AVF (‘ ‘Pseudo S-waves”), indicating a low-to-high, superiorly directed, atria1activation sequence(5,6,13). Vagal maneuversresult in slight slowing (with persistenceof the tachycardia) or abrupt termination. Vagal maneuvers cannot cause A-V block with persistence of the tachycardia, becausethe A-V nodal conducting tissue is an integral part of the electrical circuit (6). A-V nodal reentry tachycardia is effectively terminated by intravenous adenosine,verapamil, or electrical cardioversion. Chronic therapy to prevent tachycardia is indicated in individuals with frequent symptomatic recurrences and is often initiated with diltiazem or verapamil, calcium channel blocking drugs that have significant antidromic effects on the A-V node (14).

S. R. Lowenstein et al.

interval less than 120 millisec; (b) a slurred QRS onset (delta wave); and (c) a QRS duration greater than 120 millisec (10). A reciprocating tachycardia is usually initiated by a premature atria1 beat. In most cases, the accessory pathway has the longer refractory period and is blocked. The PAC is conducted anterograde through the normal A-V node, and the accessory pathway is utilized in a retrograde direction, giving rise to a reentrant tachycardia with a normal QRS complex (Figures 4B, 4C, & 5). In approximately40-50% of individuals with PSVT, there exists an accessorypathway that is only capable of retrograde conduction. In sinus rhythm, there is no electrocardiographicevidenceof the pathway (it is ‘ ‘concealed”); however, it may participate in a tachycardia identical to that describedabove. In fact, patients with atrio-ventricular reentrant tachycardiascaused by concealed accessorypathways are more numerousthan are patients with the Wolff-Parkinson-White syndrome (WV

Atrio-Ventricular Reciprocating Tachycardia The second most common cause of PSVT, termed atrio-ventricular reciprocating tachycardia, dependson an anatomically distinct, or “accessory,” pathway. Patients with the Wolff-Parkinson-White syndrome are the most widely recognized. They have one or more accessoryconnections capable of conducting from the atrium to the ventricle. During sinus rhythm, anterograde conduction bypassesthe usual physiological delay of the A-V node and eccentrically and prematurely activates a part of the ventricle that is normally activated late. This accountsfor the characteristic electrocardiographic features during sinus rhythm: (a) a PR

In atrio-ventricular reciprocating tachycardias,as in A-V nodal reentry, the QRS is regular and normal in morphology, unlessa preexistingbundle branchblock or rate-dependentaberrantconductionis present.In reciprocating tachycardias,P-waves typically follow the QRS complex by 70 millisec or more (Figures4B & 4C). The P waves areupright in V, , and they are negativein leads 2, 3, and AVF, where they often notch or indent the T wave after eachQRS. The reasonfor this R-P relationship is easily understood.In A-V reciprocating tachycardia, unlike A-V nodal reentranttachycardia,the electricalcircuit includes a portion of the ventricle. After the wavefront has passedanterogradethrough the A-V node, it must traversea portion of the ventricle; only then can it accessthe accessorypathway that forms the retrograde limb of the tachycardiacircuit (9). Vagal maneuversresult in slight slowing or abrupt termination of the atrio-ventricular reciprocating tachycard&. Verapamil, adenosine,and cardioversionare appropriate for termination. Becauseof the involvement of an accessorypathway in the tachycardiacircuit, classIA antidysrhythmic agentsare also effective for termination or prevention. Atria1 Flutter

Figure 3. Paroxysmal supraventricular tachycardia secondary to A-V node reentry tachycardia. A premature atrial contraction (Arrow) after a sinus beat (SR) initiates tachycardia. An increase in the PR interval is seen in the last pretachycardia beat, as anterograde conduction shiis abruptly to the slow pathway.

Atria1 flutter and atrial fibrillation are also reentrant supraventricular tachycardias (6). In both, the reentry circuits reside completely within the atria. In atrial flutter, the atria1rate is typically 250 to 350 beats/min, but it may be slower in patients receiving antidysrhyth-

Supraventricular

Tachycardia

mic therapy. Typical flutter waves are seen in leads 2, 3, AVF, and Vi, and the ventricular rate is usually half the atria1 rate, due to 2: 1 block in the A-V node. Higher degrees of block, variable A-V block or, rarely, 1:l A-V conduction may be encountered. Vagal maneuvers or administration of adenosine or verapamil may increase the A-V block (but not terminate the tachycardia), causing a sudden drop in the ventricular rate and the appearance of flutter waves.

Atria1 Fibrillation Atria1 fibrillation is the most common reentrant tachycardia. In atria1 fibrillation, polymorphous reentrant circuits occur within the atrium and result in atria1 rates exceeding 350 beats/min (15), The ventricular rhythm is irregular. No atria1 activity is apparent on a surface ECG, although an esophageal lead may record rapid, irregular, sharp atria1 depolarizations.

MORE ON THE TACHYCARDIAS OF THE WOLFF-PARKINSON-WHITE SYNDROME The Wolff-Parkinson-White (WPW) syndrome is characterized by the presence of an accessory atrioventricular connection that is capable of anterograde conduction. As noted above, the most common tachycardia in patients with WPW is atrio-ventricular reciprocating tachycardia (7,lO). The QRS complex is usually narrow, because anterograde conduction proceeds through the normal A-V node. This tachycardia is commonly termed orthodromic reciprocating tachycardia. Antidromic reciprocating tachycardia occurs rarely in patients with WPW (7). Here, the circuit is reversed: the anterograde limb is the accessory pathway, and retrograde conduction occurs through the A-V node. This results in a wide-complex, regular tachycardia. Only patients with the WPW syndrome-not those with concealed accessory pathways-can develop antidromic reciprocating tachycardia. The morphology of the QRS complex in each of the 12 standard leads is identical to the delta wave morphology in the same lead during sinus rhythm (Figure 6). P waves may be seen before or after each QRS complex. Vagal maneuvers often will terminate an antidromic reciprocating tachycardia, since the A-V node is an obligatory part of the tachycardia circuit. In cases where anterograde conduction is occurring over the accessory pathway, intravenous verapamil and digoxin

43 should be avoided. It is often difficult to distinguish antidromic tachycardia from atria1 fibrillation or atria1 flutter with 2:l conduction. Both verapamil and digoxin may accelerate conduction over the accessory pathway (16- 19). Approximately 15% of tachycardias in patients with the Wolff-Parkinson-White syndrome are atria1 fibrillation. This tachycardia may be life-threatening. Because the accessory pathway can have a short refractory period and may be capable of rapid anterograde conduction, accelerated ventricular rates may result, with the potential to deteriorate into ventricular fibrillation (20). A rapid, irregular rhythm, with heterogeneity of QRS complexes (occasionally narrow. but frequently preexcited and wide) should alert the clinician to the possibility of atria1 fibrillation with preexcitation (6,7).

COMMON QUESTIONS ABOUT DIAGNOSIS AND TREATMENT 1. When a patient presents in stable condition and has a rhythm strip demonstrating a narrow-complex supraventricular tachycardia, what is thejrst step that should be taken? A 12-lead ECG should be obtained immediately to confirm that the tachycardia does, in fact, have narrow QRS complexes. Ventricular tachycardia may masquerade as a narrow-complex tachycardia if only a single lead is examined (21). 2. Should vagal maneuvers be attempted in the initial management of stable patients with PSVT.? Yes, probably. Vagotonic maneuvers, such as carotid sinus massage, the Valsalva maneuver, the headdown position, deep inspiration, and application of ice to the face can terminate episodes of PSVT (22,23). Success rates above 85% are often quoted (22-24). However, in most published studies, vagal maneuvers have been applied to highly selected patients-usually those with catheter-induced PSVT undergoing electrophysiologic testing in the laboratory (24). In these cases, vagotonic procedures are initiated almost immediately after induction of the tachycardia. In this artificial setting, even spontaneous reversion to sinus rhythm is very common. Indeed, when PSVT is induced artifically at the time of electrophysiologic study, the cumulative response rate to boluses of placebo is 16% (25). Patients with PSVT who present for care in emergency departments may have a more refractory dysrhythmia. Their tachycardia is usually of longer duration, is less likely to revert spontaneously, and may be

S. R. Lowenstein et al.

“pseudo AV Node

Reentry

Tachycardia.

retrograde Orthodromic

Reciprocating

Tachycardia,

R-prime” CL-490

msec.

RP

Interval-65

msec

P waves CL-390

meet.

RP

interval-115

msec

Figure 4(A and 6). Electrocardiograms of 2 types of paroxysmal supraventricular tachycardia illustrating utilii of the “R-P” relationship in distinguishing underlying mechanism. (A) A-V node reentry tachycardia. The activation of the vet’tttWea and atrla are near& simultaneous (R-P interval = 65 msec) and the P wave merges with the QRS complex. The cyds length of the tachycardia is 490 msec, corresponding to a rate of 122 beats/min. (B) Orthodromic reciproceting tacbycardia @iii&g a conce#ed atrioventricular accessory pathway. Note that activation of the atria follows ventricular a&vat&n by 115 meet. The cycle Ien@ is CW msec, equal to 154 beats/min.

Supraventricular

40 Hz

Tachycardia

25.0 mm/s

10.0 mm/mV

4 by 2.56 + 1 rhythm Id

MACVU 002C

12SLtm v260

Figure 4(C). This electrocardiogram was obtained in a 33-year-old man who presented with chest tightness and pa@itations. The ECG demonstrates atrio-ventricular reciprocating tachycardia. The P waves are negative in leads 2,3, and AVF, and are upright in lead V,, indiing a low-to-high, superiorly directed atrial activation sequence. The R-P interval is long (>70 msec), because the rebograde limb of the reentry circuit includes a portion of the ventricle. He converted spontaneously to a normal sinus rhythm. The 1Blead ECG in sinus rhythm was normal, suggesting a concealed accessory pathway. El-ologic studies were not performed.

more difficult to treat because of heightened sympathetic tone. In one recent emergency department study, 17 patients with PSVT were treated with carotid sinus massage,Valsalva maneuver, or a head-down tilt, singly and in combination; only 3 patients converted to sinus rhythm (24). Side effects of Valsalva maneuvers are seldom encountered. Occasionally, however, carotid sinus massage may provoke bradycardia or asystole in elderly patients who have sinoatrial conduction system disease. In addition, cerebrovascular accidents may follow carotid sinus massagein patients with carotid artery disease(26). In addition to its attendantrisks, carotid sinus massage is less effective than other vagal maneuvers. A recent study demonstratedthat the Valsalva maneuver was effective in terminating PSVT 3 times more often than right carotid sinus massageand 10 times more often than left carotid massage(27). These data (and a recent clinical decision model published by Grnato et al.) (24) suggestthat in young, healthy patients, vagotonic maneuversshould be tried, and that the Valsalva maneuver should be attempted first. In the elderly and

in otherswith cardiovasculardisease,carotid sinus massageis contraindicated.The Valsalva maneuvermay be attempted,followed by pharmacological treatment. 3. When a patient presents with PSVT, what are the best clues to the mechanism of the tachycardia? Speci&ally, how does one tell if an accessorypathway is present? An accessorypathway is a part of the tachycardia circuit in about 30% of casesof PSVT. The patient’s history is helpful if aware of an accessorypathway or the Wolff-Parkinson-White syndrome. If an electrocardiogram in sinus rhythm is available, it may demonstrate a short PR interval and a delta wave, confirming the diagnosis of WPW. A 12-leadECG should be performed if time permits. The most important electrocardiographic clues pertain to the timing of the retrograde activation of the atria (7). In the majority of cases of A-V nodal reentrant tachycardia, the atria and ventricles are depolarized simultaneously, and the P waves are hidden in the QRS complex. Occasionally, a P wave is seenafter the QRS, but the QRS-P interval is almost always less than 70 millisec. If the reentry circuit includes an accessory

S. R. Lowenstein et al.

46

HRA

-f-

Figure 5. A schematic diagram and corresponding ECG of the most common tachycardia in pat&tts with the Wolff-ParkinsonWhii syndrome: orthodromic reciprocating tachycardia. To illustrate the mechanism, we have Wized data from a whom pacing from the high right atrium (HRA) followed by an early atrial stimulus (3rd beat) inMates Who&on& tachycardia. The A-V node is represented by a circle, and the sinus node is labeled (SA). During slnus rhythm or atrial pacing (A, fiit two illustrated beats), the ventricular depolarization is a fusion of anterograde conduction over the atrioventricu+ar accessory pathway and the A-V node His-Purkinje system. Under appropriate conditions (e.g., a spontaneous or paoed premature atrial contraction) (PAC, third beat), anterograde block may occur in the accessory pathway, nonnafMng the Gf?S and setting up a reentry tachycardia (subsequent beats) that travels anterograde from the atrium through the A-V node and His-Purkinje system, to the ventricles. Retrograde conduction takes place over the accessory pathway (last 4 illustrated beats).

pathway (atrio-ventricular reciprocating tachycardia), the P wave always follows the QRS. Usually, the RP interval exceeds 70 millisec. Sustained aberration (more than 10 set) is uncommon in AV nodal reentrant tachycardia; its presence suggestsa bypass tract. The presence of QRS alternans also favors the diagnosis of atrio-ventricular reciprocating tachycardia incorporating a bypass track (12). 4. If a patient with PSVT is suspected of having WPW or another preexcitation syndrome, is it still safe to use intravenous verapamil?

If preexcitation is suspected,adenosine is a safer agent.Verapamil is contraindicated if the QRS is wide. 5. In stable patients with PSVT, should adenosine or verapamil be used first?

Verapamil and adenosine are equally effective in converting PSVT to sinus rhythm (25). Both agents have successrates greater than 90%. Yet, adenosine

is now the treatment of choice (11,28). Intravenous verapamil has three important disadvantages.First, it often causes hypotension, especially in patients with poor left ventricular function (29). Second,the half-life of intravenous verapamil is protracted; after a single intravenous dose of five milligrams, the physiological effects last 15-30 min. Third, verapamil can cause acceleratedconduction in accessorypathways. Often, these accessory pathways are not recognized before treatment begins. Adenosine is an endogenousnucleotide that is present in all body cells. Adenosine is rapidly degraded enzymatically or cleared from the circulation by vascular endothelial cells (28). After a bolus of adenosine, the half-life is approximately 6-10 set (25). Flushing, chest pain, and dyspneaoften occur after adenosineadministration, but thesediscomforts are brief (28). Similarly, if hypotension occurs, it lasts only a few seconds.

Supraventricular

Tachycardia

Figure 6. Antidromic reciprocating tachycardia in a patient with the WPW syndrome. (A) 1Blead ECG during sinus rhythm. Delta wave morphology is positive in leads I, II, aVL, V,-V,; the delta wave is negative in leads Ill, aVR, V,, and isoelectric in lead aVF. (B) ECG during antidromic tachycardia. Note similarity of QRS complex to delta wave morphology seen in sinus rhythm in each of the 12 leads.

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In contrast to verapamil, adenosine appears to be safe in patients who present with hypotension, in patients with heart failure, in those receiving concurrent beta-blocker therapy, and in those with accessory pathways (30,31). While acceleration of anterograde conduction in accessory pathways has been documented in electrophysiologic studies, this effect is extremely short-lived. Adverse effects of adenosine in patients with WPW have been reported on rare occasions (32); yet, adenosine is less likely to be deleterious than verapamil. Adenosine is not likely to be effective, nor is it recommended, in patients with preexcitation and atria1 fibrillation (32). The preferred emergency agent in such patients is procainamide. Intravenous beta-blockers are seldom indicated to manage PSVT; they may cause bronchoconstriction, hypotension, or cardiac dysfunction, and they are less effective than verapamil or adenosine. Intravenous digoxin has a delayed onset and is dangerous in the presence of accessory pathwaves. 6. How should adenosine be used for greatest eficacy and safety? What are the important contraindications and drug interactions? The initial dose of adenosine should be 6 mg intravenously. If the tachycardia persists, a second dose of 6 mg or 12 mg may be administered 1 to 2 min later (28,33). Adenosine must be administered as a rapid bolus through a large intravenous catheter placed in an antecubital or other proximal vein. Two drug interactions are noteworthy. First, theophylline is a potent adenosine receptor antagonist, and patients receiving theophylline may be refractory to adenosine. An opposite interaction has been observed with carbomazepine and dipyridamole; these agents prolong the half-life and physiological effect of adenosine. There are few medical contraindications to adenosine. However, adenosine may provoke bronchospasm and therefore should not be used in patients who are wheezing. Since adenosine administration frequently results in brief periods of bradycardia or asystole, this drug should be used cautiously in patients with sinus node dysfunction. One limitation of adenosine is its cost. One 6 mg dose costs $22 (wholesale price), compared to $3 for verapamil (5 mg). Another limitation of adenosine is its short half-life. In some patients (between 8 and 35% in one reported series), PSVT recurs within minutes of administration of adenosine. Verapamil may be needed to achieve long-lasting control (25,30,34,35). 7. How can adenosine be utilized in the diagnosis of narrow complex tachycardias? Adenosine has an obvious therapeutic role in PSVT.

S. R. Lowenstein et al.

In addition, adenosine may be useful in the differential diagnosis of narrow complex tachycardias. The effect of adenosine is highly specific for reentrant tachycardias that include the A-V node (36). Thus, as noted earlier, in A-V nodal reentry, the usual response to adenosine is abrupt termination of the tachycardia. Atrio-ventricular reciprocating tachycardias also cease after adenosine; however, since adenosine blocks the A-V node but not the bypass pathway, the first few sinus beats in the postconversion period often demonstrate marked preexcitation (delta waves). Indeed, some have advocated the administration of adenosine during sinus rhythm to uncover latent preexcitation (37). When adenosine is administered to patients with atria1 reentrant tachycardias, A-V block may be induced with continuation of the tachycardia (Figure 7). A similar response occurs if the presenting tachycardia is atria1 tachycardia, atria1 flutter, or atria1 fibrillation. 8. Can adenosine be used safely if the QRS complex is wide? Should it be used for diagnostic purposes? The vast majority of wide complex tachycardias are ventricular tachycardias (VT). In most series, 85% of patients with a wide complex tachycardia have VT; among patients with known coronary artery disease or congestive heart failure, this proportion rises to 95%. In most cases, the history and electrocardiogram provide robust clues to the diagnosis of ventricular tachycardia (l), and there is no reason to use adenosine where VT is highly likely. It is also well-established that administration of intravenous verapamil for patients with VT may cause catastrophic hemodynamic collapse (38-41). While the safety of adenosine in wide complex tachycardias has not been defined in large clinical trials, the brevity of its actions suggests an important theoretical advantage over verapamil. In several small studies, administration of adenosine in patients with VT did not cause adverse consequences (31,3335,42,43). The response to adenosine in ventricular tachycardia is variable. Many patients with VT have 1: 1 retrograde ventriculo-atria1 conduction. After adenosine, V-A conduction may be abolished, allowing AV dissociation, capture beats, or fusion beats to emerge. If seen, these responses confirm a ventricular origin of the wide complex tachycardia. Alternatively, there may be no response to adenosine, suggesting (but not proving) that the diagnosis is VT (42-44). 9. After treatment for PSVT, what is the likelihood of a recurrence of PSVT? What are the indications for long-term treatment, hospital admission, and referral? The reentrant tachycardias have been studied extensively in electrophysiology laboratories, but they have received little attention in ambulatory and emergency settings. Thus, there are few data available that de-

Supraventricular

Tachycardia

Figure 7. Intra-atrial reentry tachycardia. Note persistence of the atrial tachycardia administration of intravenous adenosine. (Strips are continuous).

scribe the natural history of PSVT. Sintetos et al. recently studied 34 patients who were referred for evaluation after one or more episodes of symptomatic PSVT (45,46). All patients were followed without treatment until the first tachycardia recurrence or for 90 days. Tachycardias were documented by telephone transmission. The rates of early recurrence were high: 20% of patients had a recurrence on the first or second followup day. Fifty percent of patients had their first recurrence before day 20, and 75% before day 36. At the end of the 90-day observation period, only 17% of patients had remained tachycardia-free. The median time to recurrence was 19 days, and the median duration of the first attack was 20 min. Of course, the patients in this series were highly selected; all were referred for study because of recurrent, symptomatic tachycardias, and many had underlying cardiac or pulmonary conditions. Therefore, these results may not reflect the natural history of PSVT among patients seen by emergency physicians. Nevertheless, these data indicate a variable natural history: although 1 patient in 5 had a recurrence in 48 hours, an equal proportion never had a recurrence in 90 days. Therefore, most patients should not receive treatment after a single episode of PSVT, until a period of outpatient observation demonstrates the frequency and severity of any recurrences.

during transient A-V block precipitated

by

Patients who have experienced a disabling episode of tachycardia (including syncope, angina, or severe hypotension) should be admitted to the hospital for an indepth evaluation. Other indications for hospitalization and electrophysiologic study include: uncertainty about the mechanism of the tachycardia (ventricular tachycardia or PSVT); suspicion of an accessory atrio-venticular connection; coronary artery or other structural heart disease; or, an episode of paroxysmal atria1 fibrillation in patients suspected of having an accessory pathway (6,47). If several recurrences have been documented, then referral is also indicated, because long-term treatment plans (including radio-frequency ablation, drug therapy, pacemakers, and surgery) are most easily accomplished after the site and electrical properties of the tachycardia circuit have been defined (7,47). The newest therapy, radio-ablation of accessory pathways, has a low risk of complications and a high rate of cure (48). 10. Are there any other reentrant PSVTs that the emergency physician should recognize? Although 90% of patients with PSVT have either dual A-V nodal pathways or atrio-ventricular accessory pathways, a minority of patients have reentry circuits confined to the atrium or the sinus node. In sinus node reentrant tachycardia, a P wave (with a morphology identical to that of the normal sinus P wave) precedes each QRS complex. The tachycardia is differen-

50

S. R. Lowenstein et al.

tiated from sinus tachycardia by its abrupt onset and termination (6). In addition, the clinical setting may raise the possibility of sinus node reentrant tachycardia: whereas sinus tachycardia occurs in response to acute volume depletion, pain, fever, hypoxia, or another physiological stress, sinus node reentrant tachycardia may be observed at rest. Intra-atria1 reentrant tachycardia is also characterized by a sudden onset and termination; here, the P wave is different from the P wave of sinus rhythm. Another electrocardiographic clue is observation of an unchanged tachycardia during episodes of A-V block. Pharmacologic A-V nodal blockade will not terminate

intra-atria1 reentry tachycardia, in sharp contrast to AV node reentry and reciprocating tachycardias. Both sinus node and atria1 reentrant tachycardias are uncommon, and both usually terminate spontaneously. Both tachycardias will respond to electrical cardioversion in emergent situations. When pharmacological treatment is required, sinus node reentrant tachycardia will usually respond to adenosine, calcium channel blockers, or beta blockers, the same agents that are effective in A-V node reentry. Intra-atria1 reentrant tachycardia will respond to agents that are used to treat atria1 flutter or fibrillation, including type IA antidysrhythmic agents.

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