junctional tachycardia -...

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Junctional Tachycardia Mechanisms, Diagnosis, Differential Diagnosis, and Management By KENNETH M. ROSEN, M.D. IN THE ABSENCE of functioning anomalous connection between atria and ventricles, the A-V junction serves as the only link between these structures, allowing the atrial impulse to be transmitted to the ventricles. The A-V junction may be defined as consisting of the atrial approaches to the A-V node, the A-V node itself, and the penetrating portion of the His bundle. Total transection of the A-V junction at any point should produce A-V block, and stimulation in the presence of a normal His-Purkinje system should produce a narrow QRS. The electrophysiologic function of the A-V junction is primarily that of conduction. However, in addition, the A-V junction possesses intrinsic automaticity, allowing it to serve as a subsidiary pacemaker in the event of failure of proximal impulse formation or propagation. Under patholo- gic conditions, the A-V junction can serve as an ectopic pacemaker, or as a site of reentry. Electrophysiologic Considerations Experimental studies demonstrating automaticity in the A-V junction were extensively reviewed by Scherf and Cohen.1 Earlier workers produced A-V junctional escape rhythms after depressing sinus node function by various surgical, chemical, me- chanical, and thermal maneuvers. In addition, experimental A-V junctional rhythms were pro- duced by increasing sympathetic tone or by warming specific areas in the A-V junction. The site of origin in the A-V junction was determined by noting the timing of atrial and ventricular contrac- tion, and also by noting the initial sites of negativity with direct recording. Zahn suggested classification into upper, middle, and lower A-V nodal rhythms.2 In upper nodal rhythms, atrial contraction preceded From the Section of Cardiology, Department of Medicine, Abraham Lincoln School of Medicine, University of Illinois and Department of Cardiology, Hektoen Institute for Medical Research of the Cook County Hospital, Chicago, Illinois. Supported in part by Contract no. NIH 71-2478, Myocardial Infarction Program, National Heart and Lung Institute, National Institutes of Health. 654 ventricular contraction (fig. LA); in middle nodal rhythms, atria and ventricles contracted simultane- ously (fig. 1B); and, in lower nodal rhythm, ventricular contraction preceded atrial contraction (fig. IC). This classification has been useful descriptively, but is not accurate since it does not take into account variations in antegrade and retrograde conduction time.3 The recording of cellular action potentials from the specialized conduction system allowed a more direct approach to the determination of the nature and sites of cardiac automaticity. Automatic cells are characterized by the presence of slow depolari- zation during diastole (phase 4 diastolic depolariza- tion). Sinus node cells possess this characteristic as do other areas in the specialized conduction system where automaticity may be considered normally latent. Electrophysiologists have divided the A-V node into three regions based upon both anatomic location and on the characteristics of the recorded action potentials. These are the A-N region (atrionodal), the N region (nodal), and the N-H region (nodal-His). Diastolic depolarization has been definitely demonstrated in the N-H regions, possibly in the A-N regions, but not in the N region.4 Diastolic depolarization is also demon- strable in cells comprising the His bundle. A-V junctional rhythms due to enhanced automaticity may arise in one or more of the following areas: the A-N region, the N-H region, the coronary sinus, and the His bundle. The term A-V junctional rhythms is a more accurate description than A-V nodal rhythms,5 6 since these rhythms do not appear to arise in the N region of the A-V node. Diagnosis of A-V Junctional Rhythms If antegrade and retrograde conduction are intact, a beat arising from the A-V junction produces both a retrograde P wave and QRS of supraventricular configuration. The timing of this retrograde P wave in relation to the QRS is dependent upon the site of origin of the impulse, as well as the antegrade and retrograde conduction times.' 3 6 A beat arising in the proximal A-V Circulation, Volume XLVII, March 1973 by guest on July 2, 2018 http://circ.ahajournals.org/ Downloaded from

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Page 1: Junctional Tachycardia - Circulationcirc.ahajournals.org/content/circulationaha/47/3/654.full.pdf · Junctional Tachycardia Mechanisms, Diagnosis, DifferentialDiagnosis,andManagement

Junctional Tachycardia

Mechanisms, Diagnosis, Differential Diagnosis, and Management

By KENNETH M. ROSEN, M.D.

IN THE ABSENCE of functioning anomalousconnection between atria and ventricles, the A-V

junction serves as the only link between thesestructures, allowing the atrial impulse to betransmitted to the ventricles. The A-V junction maybe defined as consisting of the atrial approaches tothe A-V node, the A-V node itself, and thepenetrating portion of the His bundle. Totaltransection of the A-V junction at any point shouldproduce A-V block, and stimulation in the presenceof a normal His-Purkinje system should produce anarrow QRS.The electrophysiologic function of the A-V

junction is primarily that of conduction. However,in addition, the A-V junction possesses intrinsicautomaticity, allowing it to serve as a subsidiarypacemaker in the event of failure of proximalimpulse formation or propagation. Under patholo-gic conditions, the A-V junction can serve as anectopic pacemaker, or as a site of reentry.

Electrophysiologic ConsiderationsExperimental studies demonstrating automaticity

in the A-V junction were extensively reviewed byScherf and Cohen.1 Earlier workers produced A-Vjunctional escape rhythms after depressing sinusnode function by various surgical, chemical, me-chanical, and thermal maneuvers. In addition,experimental A-V junctional rhythms were pro-duced by increasing sympathetic tone or bywarming specific areas in the A-V junction. The siteof origin in the A-V junction was determined bynoting the timing of atrial and ventricular contrac-tion, and also by noting the initial sites of negativitywith direct recording. Zahn suggested classificationinto upper, middle, and lower A-V nodal rhythms.2In upper nodal rhythms, atrial contraction preceded

From the Section of Cardiology, Department of Medicine,Abraham Lincoln School of Medicine, University of Illinoisand Department of Cardiology, Hektoen Institute forMedical Research of the Cook County Hospital, Chicago,Illinois.

Supported in part by Contract no. NIH 71-2478,Myocardial Infarction Program, National Heart and LungInstitute, National Institutes of Health.

654

ventricular contraction (fig. LA); in middle nodalrhythms, atria and ventricles contracted simultane-ously (fig. 1B); and, in lower nodal rhythm,ventricular contraction preceded atrial contraction(fig. IC). This classification has been usefuldescriptively, but is not accurate since it does nottake into account variations in antegrade andretrograde conduction time.3The recording of cellular action potentials from

the specialized conduction system allowed a moredirect approach to the determination of the natureand sites of cardiac automaticity. Automatic cellsare characterized by the presence of slow depolari-zation during diastole (phase 4 diastolic depolariza-tion). Sinus node cells possess this characteristic asdo other areas in the specialized conduction systemwhere automaticity may be considered normallylatent.

Electrophysiologists have divided the A-V nodeinto three regions based upon both anatomiclocation and on the characteristics of the recordedaction potentials. These are the A-N region(atrionodal), the N region (nodal), and the N-Hregion (nodal-His). Diastolic depolarization hasbeen definitely demonstrated in the N-H regions,possibly in the A-N regions, but not in the Nregion.4 Diastolic depolarization is also demon-strable in cells comprising the His bundle. A-Vjunctional rhythms due to enhanced automaticitymay arise in one or more of the following areas: theA-N region, the N-H region, the coronary sinus, andthe His bundle. The term A-V junctional rhythms isa more accurate description than A-V nodalrhythms,5 6 since these rhythms do not appear toarise in the N region of the A-V node.

Diagnosis of A-V Junctional RhythmsIf antegrade and retrograde conduction are

intact, a beat arising from the A-V junctionproduces both a retrograde P wave and QRS ofsupraventricular configuration. The timing of thisretrograde P wave in relation to the QRS isdependent upon the site of origin of the impulse, aswell as the antegrade and retrograde conductiontimes.' 3 6 A beat arising in the proximal A-V

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JUNCTIONAL TACCRYCARDIA

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Figure 1

Three examples of paroxysmal junctional tachycardia demonstrating varyinig relstonships of P and QRS.(A) Retrograde P wave preceding the QRS ("upper nodal"). (B) P and QRS simtultaneous ("midnodal").(Ct) Retrograde P wiave following QRS ("lower nodal").

junction region is more likely to have a retrograde Pwave precedinig the QRS, while a beat arisingdistally is more likely to have a retrograde P wavefollowing the QRS.

If only antegrade conduction is intact, thenjunctional rhythms will be just characterized byQRS complexes. If retrograde conduction is intact,then juncti.onal rhythms wvlii produice retrograde Pwaves. Junctional impulses may also occur withouteither antegrade or retrograde conduction. Theseare electrocar-diographically silent unless they dis-turb impulse fornation or conduction in subsequentbeats.7 '

P-Wave Morphology

Typically, the P waves in junctional ihythms areinverted in leads II, III, and aVI,, and upright inlead aV1,. The P-wave amplitude in lead I is usuallysmall and of variable contour. The frontal axis ofthe P wave is generally between -60° and -80°. P-wave configuration in the precordial leads isvariable, with inverted P waves being noted inione, some, or all precoudial leads.Not all workers agree with this classical descrip-

tion of A-V junctional P waves. Moore et al.,studying P-wave morphology in dogs, suggestedCirculation, Volame XLVII, March 1973

that rhythms arising from the area of the coronarysinus or from the A-V node were characterized byupright P waves in leads II, III, and aVI.9 Waldoand co-workers, studying patients with A-V dissoci-ation developing during open-heart surgery, de-scribed junctional P waves which were diphasic(-/+) or predominantly (+) in leads II, III, andaVi,J'I In these cases, the initial negative portion ofthe P wave was often masked in the T wave, givingthe impression oni the surface electrocardiogramthat junctional P vaves were of antegrade con-tour.

Several specific categories of A-V junctionalrhythms have been designated based upon P-wavecontour and/or P-R interval. These include:(1) Coronary sinus rhythm, characterized by retro-grade P waves with normal P-R intervals.' Lancas-ter et al. and Lau et al., pacing the interior of thecoronary sinus, produced P waves conforming tothis description.'1- 12 Hovever, Waldo demonstra-ted that stimuilation of other atrial sites alsoproduced P waves of retrograde contour withnormal P-R intervals, which suggests that thisappearance was not specific for rhythms arisingfrom the coronary sinius.l" Thus, the use of the term,ccoronary sinus rhythm" is probably inappropriate.

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ROSEN

These rhythms could better be labeled as either in-ferior or low atrial rhythms. Some of these may arisein tissues of the A-V junction. (2) Left atrial rhythms,suspected to arise from specialized conductiontissue in the left atrium and characterized by P-wave inversion in V6.14 However, coronary sinuspacing produces P-wave inversion in V6, and leftatrial pacing may or may not produce a similarchange.11 12. 15 Because of this, the use of the term"left atrial rhythm" for rhythms characterized byretrograde P waves with additional P-wave inver-sion in V6 is probably inappropriate. These rhythmsshould be classified as either low atrial or A-Vjunctional. (3) Coronary nodal rhythm, character-ized by normal P-wave contour with short P-Rintervals.", 16 This rhythm has been suspected ofarising from the tail of the sinus node close to thecoronary sinus. Waldo was able to reproduce theelectrocardiographic pattern of coronary nodalrhythm by pacing a number of right atrialendocardial sites.'3 In addition, the presence ofaccessory conduction tracts bypassing the A-V nodecan allow the development of sinus rhythms withnormal P-wave configuration and short P-R inter-vals. The term "coronary nodal rhythm" is inaccu-rate, since these rhythms can either represent ectopicatrial rhythms arising from a number of sites, orsinus rhythm with bypass of the A-V node.

Part of the confusion regarding the various typesof A-V junctional P waves reflects changingconcepts regarding atrial depolarization. Currentevidence suggests that atrial depolarization is notradial, as originally proposed by Sir Thomas Lewis,but is asymmetric with internodal tracts playing asignificant role in the distribution of the atrialimpulse.'7 This implies that one cannot accuratelypredict the site of origin of an impulse by vectorialanalysis of the P wave. The difficulty is furthercompounded by the possible occurrence of conduc-tion lesions in the internodal tracts, which couldalter P-wave contour.'8 There is no information inman as to the specific alterations in P contourassociated with single or combined lesions in theinternodal tracts.

QRS MorphologyIn the absence of intraventricular conduction

defects, the QRS of a junctional beat is usuallynarrow, since the impulse arises above the branch-ing portion of the His bundle and is simultaneouslydistributed to both ventricles. In the presence ofintraventricular conduction defects, the QRS will beappropriately altered.

Junctional beats may occasionally manifest QRSabnormalities in axis and/or duration, not related topreviously existing conduction defects. This occursin several circumstances, namely: (1) When junc-tional premature beats follow long cycle lengths,the aberrant QRS in this circumstance reflectsfunctional bundle-branch block related to prolonga-tion of the refractory periods in the His-Purkinjesystem due to the preceding long cycle. (2) TheQRS may be aberrant when there are severalconsecutive junctional beats or for the totalduration of a junctional tachycardia. This canrepresent the perpetuation of a functional bundle-branch block due to repetitive concealed condue-tion,19 or it can represent rate-dependent bundle-branch block. (3) Aberrant QRS complexes mayoccur during a junctional escape rhythm.20 This canrepresent the effect of diastolic depolarization inone of the bundle branches with decreasedmembrane responsiveness in late diastole, or couldreflect either longitudinal dissociation in the Hisbundle or use of accessory pathways allowingasymmetric distribution of the cardiac impulse tothe ventricles. Studies utilizing the His bundlerecording technic suggest that many of the so-calledjunctional escape rhythms with aberrant conductionare really rhythms arising in the bundle branches ormore distal ventricular Purkinje system.2' In suchcases, the abnormal escape beats are preceded by Hpotentials with short H-V intervals, or have Hpotentials simultaneous or following the onset ofthe QRS. These H potentials are retrograde, thetiming in relation to the QRS depending upon thesite or origin of the escape beat and conductiontime antegrade to the ventricles and retrograde tothe His bundle.

Antegrade and Retrograde Conductionin Junctional Rhythms

Prolongation of either antegrade of retrogradeconduction from the site of impulse formation inthe A-V junction (first-degree block) will alter therelationship of retrograde P wave and QRS.Second-degree block between the A-V junctionalfocus and the atrium can occur.22 This may be oftype I (Wenckebach) with progressive R-P prolon-gation terminating in dropped retrograde P waves(fig. 2B). Type II retrograde block (Mobitz)without progressive R-P prolongation is less com-mon (fig. 2C).Antegrade conduction disturbance may also

complicate junctional rhythms. These can bedifficult to diagnose if they occur in the presence of

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JUNCTIONAL TACHYCARDIA

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Figuire 2Variationi of retrograde coniductioni with NPJT. (A) \NPJT weith intact retrograde conduiction. Note retro-grade P wave followinig every QRS. (B) NPJT with retrogradle Wenckebach periods. The R-P intervalgraduially increases from 0.16 to 0.20 sec during the first five QRS complexes. Retrograde block occuirsafter the sixth QRS, which is then followed by a sinuis escape and ventricular capture (C). The eight/iQRS is followed by a ftission P reeve (f), with fuision occuirring betwceen sinuis escape anid retrograde P. (C)NUJT wvith type II retrograde block. The first two QRS comnplexes ar.e followed by P waves with a fixedR-P interval. There is retrograde block after the third oRS, which then allows the sinus to escape withan antegrade P wave and ventricuilar capturewuith sinus escape and ventricuilar captures.

A-V dissociation since in these cases the conductiondisturbance does not affect the relationship of Pwaves and QRS, but only the periodicity of QRScomplexes.) 6 2 Antegrade Wenckebach periodsare associated with characteristic Wenckebachperiodicity, i.e., groups of QRS complexes withprogressively shortening R-R intervals followed bypauses which are less than the sum of twoconsecutive short cycles. Combiniations of antegradeand retrograde conduction disturbances may coexistin junctional rhythm giving rise to complex ar-rhythmias.22

Junctional tachycardia is one of the causesof A-V dissociation, the mechanism frequent-ly beiing a combination of both physiologicinterference in the A-V node between antegradesinus impulses and retrograde junctional impulses,anid also depression of conduction.5- In A-Vdissociation complicating junctional tachycardia,the atrial and ventricular rates are independent,with the ventricular rate being somewhat fasterthan the atrial (fig. 3B). A-V dissociation isfrequently incomplete with occasional ventricularcaptures from appropriately timed sinus beatsallowing antegrade conduction through the A-VCirculalion, Volume XLVII, March 1973

(C). Folowcing this sequiience, 2:1 retrogra(le block is noted

node (figs. 3B, C). The occurrence of capturesdepends upon the atrial and ventricular rate andthe A-V refractory period. Retrograde conduction ismore frequently impaired than antegrade conduc-tion in junctional tachycardia with A-V dissociation.This is niecessary, for if retrograde conduction werecompletely intact then junctional tachycardiashould be accompanied by 1:1 retrograde atrialcaptture (figs. 2A, 3A).

Junctional tachycardia with A-V dissociationoccturs with other supraventricular rhythms besidessinus rhythm, such as sinus bradyeardia, atrialfibrillation, atrial flutter, atrial tachycardia, or asecond junctional tachycardia characterized byretrograde P waves (fig. 3B, C, D).7 6 Theoccurrence of junctional tachycardia with addi-tional supraventricular tachycardia may be consid-ered a double tachycardia (fig. 3D).

In patients with sinus rhythm and junctionaltachycardia, A-V dissociation is frequently isorhyth-mic. In these instances, the ventricular rateapparently influences the atrial rate, with thedissociated sinus P wave fluctuating cyclically backand forth around the QRS complex. Waldo et al.,studying 11 patients with "isorhythmic dissociation"

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Figure 3

Nonlparoxy.smal junctional tachycardia (NPJT) with and without A-V dissociation. (A) NPJT with intactretrograde conduction. Note that as the A-V jurnctional pacemaker overtakes the sinus pacemaker, retro-grade P waves become apparent (last three complexes). A-V dissociation is present only for the two beatsbetween the three sinu1s captuires and the three retrograde capttures. (B) NPJT with incomplete A-V dis-sociationi. The sinuts rate is 100 beatslmin and the ventricular rate is 116 beatslmin. Atria and ventriclesare dissociated except for the eighth P wave which occu.rs at a time whern A-V junction is not refractorycaptturing the ventricles (C). (C) NPJT with incomplete A-V dissociation and sinus bradycardia. The atrialrate is SO/min while the ventricular rate is 72/min. The third and fifth P wave captures the ventricles.(D) Double tachycardia with NPJT at a rate of 84 beats/min, and PAT with an atrial rate of 150 beatslmin. Complete A-V dissociation is noted. QRS wideninig is due to preexistent conduction defect.

complicating open-heart surgery, suggested thatsynchronization of QRS and P resulted fromretrograde atrial capture from junctional beatsduiring the periods when junctional rate surpassedsinus rate.'. They further postulated that theretrograde P waves had either (-/+) polarity orpredominantly positive polarity simulating A-Vdissociation (as opposed to junctional rhythm withretrograde atrial capture). In their cases, the onlyperiod of true dissociation occurred in the transitionbetween sinus rhythm and junctional rhythm. Inour experience, the transition from antegrade toretrograde P waves in junctional rhythms hasgenerally been readily apparent (fig. 3A).Levy and co-workers proposed another mecha-

nism explaining isorhythmic A-V dissociation.23Based upon both clinical and experimental observa-tions, they suggested that isorhythmic dissociationreflected a biological feedback control system, withP-R interval determining stroke volume and bloodpressure. They demonstrated that increase in blood

pressure had an inverse effect on sinus rate, causingsinus slowing when the P-R interval becamehemodynamically optimal. This sinus slowing al-lowed the P wave to migrate back into the QRS atwhich point pr-essure fell and the sinus againaccelerated.

His Bundle Recording in the Diagnosisof Junctional Rhythms

The recording of His bundle potentials (H) withelectrode catheters passed to the right heart hasbeen helpful in the diagnosis of junctional rhythms.The presence of H potentials with normal orprolonged H-V intervals in front of either narrow orwide QRS complexes suggests that these complexesarise in or above the His bundle. The occurrence ofretrograde P waves, either in front or following theQRS, suggests A-V Junctional rhythm. Furtherconfirmation of the retrograde nature of P wavesmay be obtained by simultaneous recording ofbipolar atrial electrograms from the high and lowright atrium. A progression of atrial conduction

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from low to high suggests retrograde atrialdepolarization.

In atrial fibrillation, H potentials precede allconducted beats whether they propagate from theatrium or arise in the A-V junction. The diagnosis ofjunctional origin depends upon demonstration ofregular R-R intervals.

In A-V dissociation, A-V junctional beats arepreceded by H potentials with normal or prolongedH-V intervals without relationship to atrial activi-ty.

Paroxysmal Junctional TachycardiaParoxysmal supraventricular tachycardia (PSVT)

is characterized by the following: (1) abrupt onset(usually following a premature beat) and abrupttermination; (2) a ventricular rate usually between180 and 220 beats/min; the range of rates may be asslow as 100/min or as fast as 250/min; (3) thepresence of abnormal P waves (at identical rate) orabsent P waves; (4) QRS complexes of supraven-tricular origin which are usually narrow, althoughwith preexistent conduction defects or aberrantconduction may be wide; (5) the presence ofprecisely regular ventricular and/ or atrial com-plexes; and (6) either a complete lack of responseor abrupt termination with carotid massage.PSVT may be subdivided into paroxysmal atrial

tachycardia (PAT), in which P waves are abnormalbut not of retrograde contour and occur in rapidsuccession with a consistent relationship to QRS,and paroxysmal junctional tachycardia (PJT), inwhich there are retrograde P waves or no P waves(fig. 1).The differential diagnosis of PSVT includes:

(1) Sinus tachycardia. This arrhythmia can bediagnosed by noting the lack of paroxysmal onsetand termination, as well as slight slowing inresponse to carotid massage. (2) Atrial flutter with2:1 block, where one or both flutter waves areconcealed in the QRS and T. The demonstration offlutter depends upon transient increase in A-V blockwith vagal maneuvers allowing visualization offlutter waves, or by direct recording with atrialelectrograms or esophageal recordings of flutteractivity. (3) Atrial fibrillation with rapid ventricu-lar response. Slight variation in R-R intervalssuggest this arrhythmia. Demonstration of fibrilla-tory waves when the ventricular response is slowedby vagal maneuvers is also helpful. (4) Paroxysmalventricular tachycardia. This is always character-ized by QRS widening and usually by A-Vdissociation. The ventricular rate is not as preciselyCirculation, Volume XLVII, March 1973

regular as in PSVT. His bundle recordings may beuseful in the differentiation of PSVT and paroxys-mal ventricular tachycardia, with H potentialsbeing apparent before each QRS in the former.

Mechanisms of Paroxysmal A-V JunctionalTachycardiaPJT has generally been thought to be either due

to reentrant mechanism or to a rapidly firingectopic focus. "Reciprocating tachycardia" has beendesignated as a special type of PJT whereelectrocardiographic observations strongly supporta reentrant mechanism.24 These cases of PJT areinduced by atrial premature beats conducted slowlywith long P-R intervals. This premature P and QRSis then followed by a retrograde P wave (atrialecho) and then by a run of spontaneous QRScomplexes each followed by a retrograde P wave(fig. 4A). Patients with reciprocating tachycardiademonstrate ability for retrograde conduction andfrequently have atrial echoes without paroxysms oftachycardia.

It was postulated that functional dissociation ofthe A-V node into two pathways allowed thedevelopment of these reciprocating rhythms.25 Oneof these pathways was available for antegrade andthe other for retrograde conduction, thus setting upa circus movement. The premature beat inducingthe tachycardia was blocked in one pathway,which, during slow conduction in the otherpathway, recovered and was available for retro-grade conduction (fig. 5).Moe et al. reported a canine in which premature

atrial stimulation could reproducibly induce par-oxysms of PSVT.26 Janse et al.27 and Wit et al.28both demonstrated experimental models of PSVTusing isolated preparations of rabbit atria. Usingmicroelectrode recordings of A-V nodal actionpotentials, both groups were able to demonstrateevidence for A-V nodal reentry in the A-N regionduring induced episodes of PSVT.

Bigger and Goldreyer, studying six consecutivepatients with PSVT, demonstrated that spontaneousepisodes of tachycardia were each induced bypremature atrial contractions with slow conduction,and that these were followed by atrial echoes.29Timed premature atrial stimulation could reproducethe arrhythmias with demonstration of an echozone, an interval following the last normallyconducted P wave in which stimulation producedatrial echoes and often paroxysms of tachycardia.The echo zone occurred later than the atrialvulnerable period. They suggested that timing of

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Figure 4

PJT spontaneous and induced. Shown are leads I, II, III, V1, and HBE. Atrial electrograms are labeled Aand His bundle electrograms H. (A) There are two sinus beats followed by two atrial premature beats(APC). The second APC is conducted with a long A-H and is followed by an atrial echo and a run ofPJT. (B) PJT induced by atrial pacing. Atrial pacing spikes are labeled with arrows. Shown are fourpaced beats followed by a timed extra stimulus (EX) which is conducted with a long A-H and is followedby a run of PJT. Atrial echoes are present but masked in the ventricular electrogram. These were sub-sequently demonstrated with intraatrial recording.

retrograde P and QRS was a function of antegradeand retrograde conduction times. Frequently, theretrograde P and QRS were simultaneous. The rateof PSVT was related to A-V nodal refractoriness,the longer the refractory period the slower the rateduring the tachycardia. Capture of the atria withappropriately timed stimuli could convert thetachycardia by interrupting the circus movement.

Goldreyer and Damato, using the His bundlerecording technic, demonstrated that A-V nodaldelay was necessary for inducing the tachyarrhyth-mias.30 They noted that a critical degree of P-Hprolongation was necessary for induction of the

echo phenomenon. The necessary P-H prolongationcould be evoked by either premature atrialstimulation or during the course of pacing-inducedWenckebach periods. It seems likely that mostepisodes of PSVT are reentrant, with the site ofreentry being the A-V node (fig. 4A, B). We have,however, seen several examples of PSVT, whereA-V nodal reentry was apparently not involved. Inthese cases, the arrhythmia was provoked bypremature beats without A-V conduction delay,with all subsequent beats of the tachycardiaidentical to the initiating beat. The junctionalpacemaker manifested a warm-up phenomenon,

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Figure 5Ladder diagram demonstrating A-V nodal reentrant mechanism of PJT. An atrial premature beat with slowechanism of PJT. An atrial premature beat with slowlationship of retrograde P and QRS depends uponthe sites of reentry and the relative antegrade and retrograde conduction times.

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JUNCTIONAL TACHYCARDIA

with gradual acceleration of rate following initia-tion of the tachyarrhythmia (fig. 6). Carotidmassage produced conversion of the arrhythmia.Rapid atrial pacing was also followed by suppres-sion of the tachyarrhythmia, the duration ofsuppression being related to the duration of rapidpacing. Both the warm-up phenomenon andsuppression following cessation of pacing weresuggestive of a rapidly firing ectopic focus as causeof the tachycardia.

Therapy of PJT: Acute Attack

Since most episodes of PJT appear to reflect A-Vnodal reentry, therapy of the acute attack should bepredicated upon modification of properties of thecircus pathways permitting this arrhythmia. Prolon-gation of A-V refractory periods by vagal maneu-vers or antiarrhythmic medications appears to beeffective. It must be remembered that PJT is usuallyself-limited and well tolerated in the healthy heart.The presence of angina or congestive failure is anindication for emergency therapy.The specific therapeutic interventions effective in

the conversion of PJT include: (1) Vagal maneu-vers, such as carotid massage, performance of theValsalva maneuver, and eyeball pressure. Theintravenous administration of pressor agents, suchas Neo-Synephrine or Aramine, with production ofa vagal reflex may also produce conversion.Digitalization with increase of vagal tone mayinduce spontaneous conversion or enhance theeffectiveness of carotid massage. Administration ofacetylcholinesterase inhibitors such as Edrophoni-um or neostigmine may also be effective. (2)Antiarrhythmic drugs such as quinidine, procaineamide, diphenylhydantoin, and propranolol.31 It isdifficult to recommend one of these drugs asclearly superior to the others since good compara-tive studies of effectiveness in PJT are not available.

Propranolol is currently in vogue as the drug ofchoice. (3) Electrical means of conversion. DCcardioversion is generally successful in convertingPJT to sinus rhythm.32 Atrial pacing with deliveryof single or pairs of stimuli, or atrial pacing withfixed rates either slower or faster than thetachycardia, has been effective in conversion ofPJT, presumably by interruption of circus path-ways.33 Pacing technics can be coupled withrecording of atrial and His bundle electrograms,yielding diagnostically useful information. Wewould recommend the use of pacing for conversionof PJT in laboratories skilled in electrophysiologicprocedures, when simpler measures are ineffective.

Therapy: Prevention of Recurrences

Most attacks of PJT are sporadic, well tolerated,and self-limited. Patients can frequently be man-aged with reassurance alone and without recourseto antiarrhythmic regimens. In occasional cases,underlying preexcitation will be related to recurrenttachycardia. In these, therapy should be adminis-tered as recommended for Wolff-Parkinson-Whitesyndrome. The remainder of this discussion isdevoted to those patients with recurrent PJT, whereattacks are either frequent and/or distressing.The simplest management consists of chronic

administration of drug therapy. Success has beenreported with quinidine, procaine amide, proprano-lol, and oral diphenylhydantoin.24 31 Several work-ers have recommended combinations of antiar-rhythmic drugs. The sporadic occurrence of PJTmakes evaluation of the effectiveness of antiar-rhythmic regimens difficult.

In cases refractory to drug management, moreinvasive therapy may be attempted. Both chronicatrial and ventricular pacing have been utilizedsuccessfully in the prevention of recurrent PJT.34This therapy is most often indicated in patients

I ~ ~ ~ -60 0470 500 40 470 47

H BE

Figure 6

PJT apparently secondary to ectopic firing. The first APC is not conducted slowly, but induces a run ofPJT, with each P wave and QRS identical to the initiating APC. Note the gradual warm-up phenomenon(cycle lengths are listed in msec).

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where episodes of PJT complicate bradycardia.Chronic pacing should not be attempted unlesstemporary pacing has been successful.The carotid sinus stimulator has been used in the

management of intractable PSVT.35 The stimulatoris activated during paroxysms of tachycardia withconversion due to the vagal reflex produced.Giannelli has reported the surgical production ofheart block in a case of recurrent PSVT, withprevention of further episodes but with the need forpermanent pacing for control of bradycardia.36

In general, even the more difficult cases canusually be managed with chronic antiarrhythmictherapy. In resistant cases, pacing technics can beutilized.

Nonparoxysmal Junctional TachycardiaPick and Dominquez described nonparoxysmal

junctional tachycardia (NPJT), an arrhythmiacharacterized by a modest increase in ventricularrate, generally between 70 and 130 beats/min, anda lack of abrupt onset.37 NPJT usually occurs as amanifestation of digitalis intoxication, or in acutemyocardial infarction, or with acute rheumaticfever.37 38 We have seen several patients with heartdisease and NPJT where no precipitating causecould be demonstrated.The ventricular rate in NPJT is frequently only

slightly increased over the sinus rate. The presenceof physiologic interference, with or without associ-ated depression of retrograde conduction, predis-poses to A-V dissociation which is frequent.5 6,37A-V dissociation in NPJT is often incomplete, withcapture of the ventricles by sinus impulses that falloutside the A-V refractory period (fig. 3B). NPJTmay also occur with atrial fibrillation, flutter, oratrial tachycardia (fig. 2D)., 6 3 NPJT less com-monly occurs with intact retrograde conduction, orwith retrograde conduction with 2° retrogradeblock (fig. 2A-C).The diagnosis of NPJT depends upon the

demonstration of a gradual acceleration of junction-al pacemaker. The junctional beats may haveassociated retrograde P waves. More frequently, thediagnosis of NPJT is made in the presence of A-Vdissociation. In this latter case, the diagnosisdepends upon the demonstration of a series ofsupraventricular beats with regular R-R intervals,unrelated to the atrial rhythm. The periodicity ofthese regular R-R intervals is often disturbed by:(1) ventricular captures if A-V dissociation isincomplete (fig. 3B, C), (2) antegrade exit blockfrom the A-V junctional pacemaker producing

Wenckebach periodicity or sudden dropped beats,or (3) resetting of the A-V junctional pacemaker bypremature beats (concealed conduction) .5 22NPJT must be differentiated from A-V block,

since both arrhythmias may lead to A-V dissoci-ation. In addition, NPJT and A-V block maysometimes coexist. If A-V dissociation is demon-strated and the QRS is narrow, the diagnosis can beclarified by noting atrial and ventricular rates. Ifatrial rate is faster than ventricular rate, and thelatter rate is below 60 beats/min, then the diagnosisis A-V block with junctional escape. If atrial rate isfaster than ventricular rate, but the latter is above60 beats/min, then the rhythm is A-V block withsuperimposed NPJT. If the ventricular rate is fasterthan the atrial rate, then the rhythm is probablyNPJT. In this latter situation, the differentiationbetween physiologic interference and depressedA-V conduction is difficult.NPJT may be confused with accelerated idioven-

tricular tachycardia.39 40 Both rhythms behavesimilarly; however, the latter is always character-ized by aberrant QRS complexes. The difficulty liesin the differentiation of accelerated idioventriculartachycardia from NPJT with aberrant conduction.The presence of fusion beats supports the diagnosisof ventricular arrhythmia. Recording of His bundlepotentials may be useful in differentiating theserhythms.40

Mechanisms of NPJTNPJT appears to reflect an increase in A-V

junctional automaticity, which allows the A-Vjunction to become the dominant pacemakercontrolling the ventricles. Digitalis can enhancephase 4 diastolic depolarization in His-Purkinjecells. Several factors common to myocardial infarc-tion may also increase His-Purkinje automaticityincluding catacholamine release, ischemia, andstretch. It is not clear why an individual patientwith either digitalis intoxication or myocardialinfarction should develop NPJT due to enhancedHis bundle automaticity as opposed to a bundle-branch tachycardia or ventricular tachycardia aris-ing in the more distal His-Purkinje system. NPJTcould also reflect the development of automaticityin the N or A-N regions of the A-V node. There islittle experimental justification for proposing theformer site, but there is some evidence for the lattersite.The mechanisms allowing the development of

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producing PJT. Further work is necessary inunderstanding the mechanism of NPJT.

Management: NPJTNPJT usually occurs in the presence of organic

heart disease. The hemodynamic consequences ofthis rhythm are usually minimal, since the QRS issupraventricular and the ventricular rate is onlymodestly increased. The major disturbance reflectsonly a loss of atrial transport function.

Since NPJT is usually secondary to either digitalisintoxication or myocardial infarction, therapyshould be directed toward the primary problem. Inthe former case, digitalis should be discontinued,since NPJT may be a forerunner of a more seriousarrhythmia. Potassium can be administered if thepatient is hypokalemic. In acute myocardial infarc-tion, the arrhythmia is generally self-limited anddoes not necessitate therapy. If loss of atrialtransport function is hemodynamically troublesome,administration of atropine may restore sinus rhythmby increasing sinus rate and facilitating A-Vconduction. However, atropine can provoke a fasterNPJT, which could be deleterious.

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11. LANCASTER JF, LEONARD JJ, LEON DF, KROETZ FW,SHAVER JA: The experimental production of coronarysinus rhythm in man. Amer Heart J 70: 89, 1965

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KENNETH M. ROSENJunctional Tachycardia: Mechanisms, Diagnosis, Differential Diagnosis, and Management

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1973 American Heart Association, Inc. All rights reserved.

is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231Circulation doi: 10.1161/01.CIR.47.3.654

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