aberrant ventricular conduction escaped beats -...

Aberrant Ventricular Conduction of

Escaped Beats

Preferential and Accessory Pathways in the A-V Junction

By ALFRED PICK, IM.D.

Escape beats recorded in clinical electrocardiograms sometimes differ in contour and QRS dura-tion from conducted beats, and this in spite of their having a relatively short cycle length. This sug-

gests a location of the subsidiary pacemaker above the bifurcation of the common A-V bundle.While this, unlike other types of aberrant ventricular conduction, cannot be explained on a func-tional basis, recent investigations on the structure of the normal A-V junction suggest that "para-specific" A-V connections may act as preferential pathways to the ventricles in some A-V nodalescape beats. Difficulties and guides in differentiating A-V nodal from ventricular escapes undersuch circumstances are pointed out. On the basis of clinical, electrocardiographic and anatomicfacts such a normal preferential A-V conduction must be distinguished from an abnormal accessory

A-V conduction causing the pIe-excitation (Wolff-Parkinson-White) syndrome. However, the twomay occur in association.

W HEN consecutive atrial impulses failto stimulate the ventricles at anappropriate rate, subsidiary, ordi-

narily subdued, cardiac pacemakers will comeinto operation. First to escape under suchcircumstances are centers in the A-V junctionaltissues because this area has the ability tocreate impulses at a rate faster than pace-makers in the ventricles. Centers below thebifurcation of the common bundle will comeinto action when formation of impulses in theA-V junction is depressed, or conduction to theventricles of such impulses is prevented byinterference or block. It is generally acceptedthat the distinction between the two types ofectopic beats can be made in the electrocardio-gram on the basis of the length of their cycleand the contour of the QRST. Impulses arisingin junctional tissues above the bifurcation, in asupraventricular pacemaker, are expected totake over ventricular activation promptly, atrates between 40 and 50, and to produce ven-tricular complexes resembling beats of atrialorigin in all regards. Impulses originating

From the Cardiovascular Departnent, MedicalResearch Institute, Michael RZeese Hospital, Chi-cago, Ill.

This study was aided by the AMichael Reese Re-search Foundation and the Hibse Heart ResearchFund.

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below the bifurcation, in a ventricular pace-maker, appear tardily, at rates of 30 or less, andgive rise to aberrant ventricular complexes withprolonged QRS and abnormal ST-T contours.

In the following report several clinical recordsare presented showing escaped beats duringvarious abnormal rhythms in which the escapeorigin cannot be easily established on the basisof the above criteria. These are examples se-lected from many other instances encounteredin the course of the past years in routinetracings as well as during the study of simpleand complex forms of disturbances of rhythm.'Yet, despite this common occurrence, hardlyany mention of the problem can be found in theliterature.2' 3 It is the intent of this report: (1)to point out the varieties of contour deviationsoccurring in escapes of apparently supraven-tricular origin; (2) to call attention to difficul-ties and possibilities in determining, under suchcircumstances, the site of the ectopic subsidiarypacemaker; (3) to attempt an explanation ofventricular aberration in supraventricular es-capes by a mechanism which is comparable to,yet different from, that assumed to be in opera-tion in the pre-excitation syndrome.

MATERIAL AND METHODS

The material comprises selected electrocardio-grams of 11 different cases in whom escaped beatswere recorded as a consequence of various types of

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FIG. 1. Typical nodal escapes occurring during sinus bradyarrhythmia, and subsequent to a nodalpremature systole with retrograde A-V and aberrant ventricular conduction.

In the first half of the record broad and diphasic P waves are seen indicating irregular and slow(38-46) activity of the sinus node and an abnormal spread of its impulse through the atria. Theseimpulses are conducted to the ventricles at a P-R of 0.20 second, except the second which inter-feres with one from the A-V node escaping at a cycle length of 1.44 seconds (corresponding to a rateof 42). This nodal beat, apart from the short P-R distance, resembles precisely the conducted sinusbeats in contour and QRS duration. The fifth beat of the record is a premature systole of bizarrecontour. It is followed by a pause during which a P wave fails to appear at the anticipated time;instead a much earlier, inverted P is seen within the S-T of the premature systole, obviously causedby retrograde spread of the ectopic impulse to the atria. The last two ventricular beats are nodalescapes corresponding in timing and shape to the second beat of the record, and during this time nosign of atrial activity is seen. The sinus node appears to be in a depressed state subsequent to itspremature discharge by the retrograde ventricular impulse, but it is possible that retrograde P wavesare hidden within the QRS of the two nodal beats.At first glance, the contour of the premature systole suggests its origin in the ventricles. How-

ever, one would expect the subsequent nodal escape interval to be prolonged, as compared to theother escapes, by the retrograde conduction time of the ventricular impulse to the subsidiary A-Vnodal pacemaker. Since such prolongation does not occur, it must be concluded that the prematuresystole takes its origin within, or close to, the point of origin of the escaped beats, that is within theA-V node, and its bizarre contour is caused by aberrant ventricular conduction due to its early ap-pearance in the cycle, when some part of the ventricles is still in a refractory state. The close simi-larity of sinus and escaping nodal beats on the other hand indicates that both types of impulsesuse the same pathways in activating the ventricles-as is ordinarily the case.

disturbances of impulse formation or impulse con-duction. These records are grouped in figures 1through 5 according to the type and/or durationof QRS of the ectopic beats. A detailed analysisand interpretation of each tracing is presented inthe respective legends and the reasons are thereoutlined why the origin of the escapes was ascribedto areas above, or below, the bifurcation of thecommon A-V bundle, or could not be determined.Thus, figure 1 illustrates typical nodal escapes andtheir close similarity to conducted sinus beats incontrast to aberrant ventricular conduction of anodal beat occurring prematurely. In figure 2 fourcases are reproduced in which a supraventricularorigin of the escaped beats was postulated on thebasis of their normal QRS duration, in spite ofslight or marked differences in contour from thatof the conducted supraventricular beats. Figure 3exemplifies the problem in determining the originof escaped beats when promptness of their appear-ance does not conform with a marked contouraberration and a prolonged QRS duration. Identifi-cation of a ventricular escape on the basis of theoccurrence of ventricular fusion beats is demon-strated in figure 4 in two instances, one of whichshows evidence of parasystolic action of the ectopicpacemaker. Finally, in figure 5, a case of ventricularpre-excitation, escaped beats are seen which differin shape from both the normal and anomalousventricular complexes and suggest that various

pathways to the ventricles may be available toimpulses crossing the A-V junctional tissues fromabove and those arising within them. The physio-logic background and new anatomic data to beconsidered in the explanation of aberrant ventricularconduction of escape beats are pointed out below.

COMMENT

Ordinarily, aberration in the contour ofQRST complexes is the electrocardiographicmanifestation of the failure of supraventricularimpulses, traversing or initiated in the A-Vjunction, to complete ventricular activation viaordinary conduction pathways because part ofthese pathways is in a state of partial or com-plete refractoriness at the time of arrival of theimpulse. With normal or slow heart rates thishas to be ascribed to an abnormal prolongationof the refractory period, a block, somewhere inthe system of the two bundle branches. Whenaberration of the QRST complexes is limited tobeats with a short cycle it may be due entirelyto the operation of the normal refractory periodin some parts of the conduction system. Inabout 85 per cent of the beats affected by the

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FIG_. 2. Escapes with e contour but without QES prolongation. The four strips are recordsfrom different Ipatients.

In A, a/rial fibr.11itllotio is present with a slow venitricuilart rate averaging 55. There are two typesof ventricular comlplexes. The first three and the last, occurring at varying R-R intervals, relpresent,contdor/ald ariota inipolses. Tihe fourth1 to sixth beat, with a prominent S wave and a slightly higherT wave have the samne R B interval of 1.24 seconds (corresponding to a late of 48), the longest ofthe record. These evidently- are escaped beats. Their normal QRS of 0.08 second, equal to that of theconducted beats, idlicates t hat t heN- arise above the bifurcat ion of t he common A V bundle, p*+-sumnably in the A V node. Their differenit contour reveals ain .anomalous spread of the nodal impulstl.-esthrough the ventricles.

In B, similar caindit jul1s at prtsetlit during sintus ylo(rate 8S6) with a secoaLd degrot A.1V block,as in A. Again two types of ventricular complexes are seen. One type (the first, fourth anid last beats)has a constant relationship to P) waves (P BR 0.28 secondl) and relpresents cotitclued .sio us inipulses;the other ty~pe dliflers from the condlucted beats in having no S wave, a dlepressedl S-T anid a, lowercT wave. The P-It (listalLce of these lbeats is shorter and variable in cont tast, to that of the conductedbeats buat the R-R interval is .oilstantit (1.34 secondls) corresponding to a rate of 45. These are -s-

raped beats. Their supraventricular (nodal) origin is evidenced by the normal (0.08 second) QBSduration; however, .an.a'omalous vent ricular slreal is indicated byv the difference in contour as

compared with beats of sinuis origill.In C, a ease with a recent post erior wall infarction, the regular sequence of sinus lbeats (rate 68,

P I.0.18 second) is listurlel by a .entricular. pr>etatue ystsole (the fourth beat). The ensuing ven-tricular pause is less than compensatory, and is terminated by a beat (the fifth) occurring shortly(0.08 second) after a P' and (liffering in contour from the conducted beats by a smaller. Q, a largerR, and a less elevated S-T and a more inverted T-an escape beat. The escape, therefore, origi-niates above the bifurcation of the (amman bundle, but its imlpulse sp~read through the ventridlesis altered.

In D, a case of intraventricular block (QBS 0.14 second), an escaped beat (the fourth QRS) fol-lows a pause engendered by a nonronducted atrial preinature sy~stole; the lpremature (inverted)P wave is sulperimlposedl on the end of T of the third sinus beat. The ectopic atrial imllulse enteredand transienitly depressed the sinus node as evident from the prolongation of the first sinus cyclefollowing the pause. The escalpe beat which interferes with this sinus impulse differs from theconducted beats in having a normal (0.08 second) QBS duration. Its origin cannot be (definitelyestablished and two interpretations are possible. It may originate in the A-V node and its normalQRS duration could be attributed to recovery of intraventricular conduction during the ventricu-lar pause. Or it may originate inIthe ventricular septum below a blocking lesion of one of the bundlebranches; tinder these circumstances its impulse could reacthloboth bundle branches in atlout thesame time and tlitiscause shortening of QBS in contrast to the su)raventricular sinus beats. Thefirst interpretation appears to be the more likely one.


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FIu;. 3. e(atpl)('s with al)Crralit CoItour0 d11(l p)rolonged(l (2t S (oml)lexes Iecorl)tdliso ell Ol()I hreelifftere.t l)at ients.Record A_ starts anll(l eds withI a series of iegula..ti. simis l)eat s occurring at a rate of 94 and a P-R

of 0.24 seconl(l. In the mi(lele of the record the l' w aves (lisapIle)a)rI 10i1(1 three ventrniular beats withl)rolonge(l QItS (0.12 second() and an al)normal ST-T cootour occur at regular i It. i ot ervals of 1.08secotitis ((oriesl)oniding to a rate of 56). The last coincides with. a sinus 1P wave reappearing after3.44 seconds, .anl inoterval approaching the duration of five sinus cycl es. This suggests the presenceof an interi ltent S-.A block. The t hree al)errant ventricular heats evidently arle caused bI in)ilulsesof a stil)s(lidiyl).cey kll escap)ing dluring the attrial pause.

In B, during (tijialfibrillation, aitha veltliCular rate 7v0raging70, il e.h of the two leads oneheat is seen (liflerinig fromt the others in size, slllh)e and(2Q1S (dluration (().16 second). Both theseheats occur at the saeits( It- interval of 1.28 secon(ls, which is the longest of tll(e recor(l. Thlis il(li~cates their ectopfic origil illena escaping subsidiary )aceinaker.

Jll C, a (ase of se(ond (degee A-V block, regular P) waves cll l)e spaced throughout at a rat(e of 100.Of three successive P w aves, the first is followed b1 a QltS at a I -lt of 0.30 secon(l, thC second( ishlocked .an1d the third just )re(e(les a QRS at a P-It of 0.08 second. Thus, except at. the end of thestri), long vent ri(ular (ycles (1 .08 seconcls) .alt ernate with shorter ones (t).8t) se(oil(l)- a vent ric-lari bigeminy. The vent ricular l)eats are of t wo types. The one with the shorter It-It (an1(d long I1 It)}Ilts a slender Q(MS of (0.06 seconl (ldurationt; the other with the longer It-It (and short 1)l-I) consistsof a simaller It wa've of ().1() secon(l duhrat ion which is imore or less slurred in its uplstroke. In hoththe T wave is upright and of the samne size .aInd contour.. Superficially, intermittent occlrrenclle ot.an initiallv slurred It wave in Xassociation wsith .an abhnor.mallv short I'-it cold suggest ventricularpre-excitation (the Wolff-lP.akinlson Whiite syndrome), anomalous A-V conduct ion alternating withA-V conduct ion over normal pat hways at a Jersistent 3:2 A V ratio. If this were true, however., one

could exllect that : (1) variat ions in the (legree of slurring of It iIl the anomalous l)eat s would he as-

sociate(l with variations in their P-Ri interval airnd (2) secon(lary T-1wave chlanges would result fromthe operation of the ventricular pre-excitation. Since hoth these anticipated .alterations are, ab-XCIt it appears more likely that the anomalous beats represent, escaped heats of a subsidiarv pace-miaker interfering with the conduction of everv third sinus impulse with a resulting :3:1 A V con-

dluction ratio.In all three records, Q(RS l)rolongation of the escaped heats suggests their originl below the bifur-

cation of the common A V buln(lle. On the other hand the plroml)tness of their alpl)earance, at a ratearoundl 5(, is unuisutal for a true ventricular pacemaker but is common for escapes arising in the A Vjunction. In these three instances a distinction between nodal escapes with .I)errant conductionan1(d ventricular escapes is not possible (fig. 4).

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B

FIG. 4. Escape of a ventricular pacemaker demonstrated by the occurrence of ventricular fusionbeats. The two records are from different patients.

In A, during atrial fibrillation, three types of ventricular beats are seen. The first taype, with astrain pattern and QRS of 0.08 second duration (the second to fourth and the last beat), occurs atirregular R-R intervals at an average rate of 70; these are conduicted atrial impulses. The second taupe,similar in contour to the first but with QRS prolonged to 0.14 second aid the S-T more depressedand T more inverted (the second and third last beat), occurs at a cycle of 1.56 seconds, correspond-ing to a regular rate of 38; these are escaped beats of a subsidiary pacemaker. The third type, inter-mediate between the first two in QRS duration (0.10 second) and ST-T contour (the first and fifthbeat), has the same R-R interval (1.56 seconds) as the second t ype. These are rentricualar fuision beatsresulting from competition of a conducted atrial and an escaping ectopic impulse in activating theventricles. The interval separating the two fusion beats is not a multiple of the cycle length ofthe ectopic pacemaker, ruling out a parasystolic action of the latter.

In B, at a regular sinus rate of 95, the fundamental disturbance of rhythm is a 2:1 A-V block. Againthree types of ventricular complexes are seen. The first type with a P-R of 0.16 second and a patternof right bundle branch system block (QRS 0.12 second) (the fifth and sixth beat) represents (0o0-ducted sinus impulses. The second type, with a pattern of left bundle branch system block and a Q1tSprolonged to 0.12 second (the first beat) occurs at a foreshortened P-R and represents an escape of a

subsidiary pacemaker operating at a cycle length of 1.26 seconds, that is at, a rate slightly slower thanhalf the sinus rate. The other beats (the second, third and last) resemble in contour one or the otherof the two principal types but their QRS and/or T wave is smaller and their QRS duration shorter.These are ventricular fusion beats resulting from simultaneous invasion of the ventricles by the twotypes of impulses. Their variable contour reflects the relative amount of ventricular m}ocardliumactivated by each impulse and depends on the time relation of the ectopic impulse to a P wave. Thus,with t PH-R distance of less than 0.16 second, ventricular activation is dominated by. the ectopic im-pulse; with a P-It of 0.16 second the sinus impulse succeeds in "capturing" the ventricles to a greaterpart (or entirely). The interval between the third and the last beat of the record (both fusion beats)is 5.02 seconds, 0.02 second shorter than four times 1.26 seconds, the cy cle length of the ectopic pa e -

maker. Hence, continuous parasystolic operation of the subsidiary l)acemaker is suggested (wshichcould actually be proven in long strips).

In these two cases, the occurrence of ventricular fusion beats is the evidence for the location ofthe escaping ectopic pacemaker below the bifurcation of the common bundle. No competition foractivation of the ventricles is possible when sinus and ectopic impulses share a common pathwaythrough the A-V junction. In both these instances the aberrant contour of the escaped beats cantherefore be ascribed to an origin of the subsidiary impulses within the ventricles.

latter mechanism, a contour characteristic fora right-sided conduction defect develops.4

Aberration as encountered in escaped beatsand illustrated in figures 2 through 5 does notcomply with these criteria. Deviations in theirQRST contour cannot be attributed to theaction of the normal refractory phase of theconduction system considering the long cyclesof these beats. Nor, by the same token, is itpossible to invoke a latent abnormal intraven-

tricular conduction defect in all such cases. Theoperation of the normal or abnormal refractoryphase should become manifest in beats of thedominant rhythm rather than in the slowescape beats. Only in figure 2D is such anl inter-pretation feasible though another possibility isindicated in the legend. Furthermore, the typeof aberrant ventricular complexes in escapebeats does not correspond to that encounteredin ordinary instances of aberrant ventr icular

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FIG. 5. Escapes with aberrant ventricular conduction in ventricular pre-excitation (the Wolff-Parkinson-White syndrome). The four strips (all lead I) were recorded on different occasions in thesame patient. The time lines indicate 0.05 second.

In A, at a sinus rate of 51 and a P-R of 0.20 second, ventricular activation and deactivation takesplace in a normal fashion as indicated by the slender QRS of 0.08 second duration and the uprightT wave. In B, at a sinus rate of 60, ventricular pre-excitation is evident from the shortening of P-It(0.12 second) in association with the typical change in the QRST contour; a pronounced delta waveprolongs the QRS duration to 0.14 second and causes a secondary S-T depression and partial T in-version. In C, the sinus rate varies from 48 to 67 and the last, three beats show ventricular pre-excita-tion as in B. The first two differ from both the pre-excitation beats and the normal beats seen in A.There is a small Q wave, a notch near the top of R, and QRS measures 0.10 second while the ST-Tcontour is normal. Their R-R interval (1.27 seconds) is 0.05 second longer than the correspondingP-P interval and hence, their P-R distance differs by the same amount. These are escaped beats orig-inating in the A-V node. Their impulses prevent transmission of sinus impulses over normal as wellas anomalous A-V pathways with intermittent A Vir dissociation resulting. In D, A-V dissociationwas induced by carotid sinus pressure (indicated by arrows). The record start with a pre-excitationbeat. As the sinus rate progressively slows to 48, the A-V node escapes at, a regular rate of 53 tointerfere with five successive sinus impulses. A-V conduction with ventricular pre-excitation is re-ssumed in the last beat following restoration of the sinus rate to 58.The supraventricular (A-V nodal) origin of the escaped beats is inl(icated by their normal QRS

duration and by the presence of a small "septal" Q wave, like that seen in the normally conductedsinus beats. To account for the difference in contour of these two types of beats some anomalousspread of the nodal impulse in the ventricles must be postulated but differing from that occurringin the pre-excitation beats. It would, therefore, appear that in this case ventricular activation can

take place in three different ways: (1) entirely over ordinary A-V conduction pathways, resultingin beats with a normal P-R interval and QRST contour; (2) over an accessory A-V path, resulting inbeats with shortened P-R and pre-excitation contour and (3) over some preferential path, limitedto impulses originating in the A-V node and resulting in beats with slight QRS aberration.

conduction. When the QRS of escaped beats isabnormally prolonged and associated with sec-ondary ST-T alterations, the assumption of asupraventricular origin rests entirely on thepromptness of their appearance (fig. 3A andB). However, when both the QRS duration andST-T contour are normal, as in figure 2, theirorigin above the bifurcation of the commonbundle is almost certain.There are other possibilities to be considered

in an attempt to account for an aberrant con-tour of escaped beats. Thus, alterations in theshape of supraventricular beats are known tooccur subsequent to longer ventricular pauses

engendered by premature systoles, by a sec-ond degree A-V block, or occurring in atrialfibrillation and flutter.5-7 However, this type ofalteration, the cause of which is obscure,8 in-volves mainly the contour of the T wave andusually is restricted to the first beat after thepause. Where the phenomenon continues forseveral cycles an alternation of the T wave con-tour may be seen before it resumes its originalappearance.' 9 Contrariwise, in escaped beatsthe aberration involves primarily the QRScontour while the T wave may remain com-pletely unaltered, and this is maintained inconsecutive escapes. Normalization of the ven-

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tricular complex takes place abruptly, with thereappearance of the dominant rhythm. Anotherrare mechanism could be the operation of asupernormal phase of intraventricular conduc-tion.'0 This may perhaps apply to some specificcases but cannot generally account for a phe-nomenon occurring so commonly.

While, therefore, in the light of known nor-mal and abnormal cardiac physiology, it seemsimpossible to explain an aberrant contour ofsupraventricular escapes on a functional basis,anatomic background for a feasible interpre-tation has been provided by recent investiga-tions on the structure of the specific conductionsystem in the mammalian and human heart.The stimulus for the resumption of suchstudies were the doubts expressed by someworkers concerning the existence of a specificconducting system on the one hand, and theunsolved problem of ventricular pre-excitationon the other. The latest authoritative review ofthe subject by Lev, and his own careful investi-gations," leave no doubt about the validity ofour present concepts concerning a specificmuscle system joining atria and ventricles.But his studies also led to the recognition innormal fetal, newborn and young adult humanhearts of irregular communications of the A-Vnode, the common A-VI bundle and the be-ginning of the left bundle branch with ordinaryventricular myocardium, a confirmation of "par-aspecific fibers" described previously by Ma-haim12 and by others.'3 14 The demonstrationof these additional muscle bridges in the normalheart may in the future necessitate some re-vision of present views concerning the order ofventricular activation provided it could beproved that these fibers have a function ofconductivity, a very difficult task.But supposing that paraspecific fibers, like

ordinary specific fibers, do have the potentialproperty of transmitting impulses, their topicalrelation to nodal tissue could serve very well asa clue for certain hitherto unexplained observa-tions in clinical electrocardiograms and, inparticular, the phenomenon discussed in thisreport, namely, aberration of QRST limited toimpulses initiated by nodal or infranodal struc-tures. Confronting electrocardiographic facts,as illustrated in figures 1, 2, 3 and 5, with these

recently established histologic data, a hy-pothesis can be developed to account for theoccurrence of normal intravrentricular conduc-tion of A-V nodal impulses in somne, and more orless aberrant conduction in other instances. Allthat is required is the assumption that impulsesarising in peripheral portions of A-V junctionaltissue, in the vicinity of the point of origin ofparaspecific fibers, reach part of the ventricularmyocardium over preferential (paraspecific)pathways2 in contrast to impulses arising morecentrally in the A-V junction and traveling tothe ventricles over ordinary paths, like supra-nodal impulses (fig. 1). Depending on thelength, the course, and the point of insertionof such preferential pathways, and especiallytheir nearness to the ordinary A-V junction,the contour aberration of the resulting ectopicventricular complex would be more or lesspronounced and would vary from case to case(figs. 2, 3 and 5).

Conceivably such preferential pathwayscould operate even in the absence of paraspe-cific fibers if one assumes that the arrangementof conducting fibers in the lower A-V node andcommon A-V bundle is such as to determineimpulse distribution to specific limited parts ofthe ventricular myocardium an arrangementcomparable to that of the internal capsule ofthe brain. Prinzmetal and associates' havepostulated this to support their concept of"accelerated A-V conduction." Implication ofthe latter in the case of nodal escapes is un-necessary, since impulses initiated in distalparts of the A-V junction and proceeding overpreferential pathways at a normal speed couldreach one ventricle earlier than the other andthus cause aberrant ventricular complexes, incontrast to impulses arising higher up anddistributed simultaneously to both ventricles.

Evidently, if this concept is correct, presentcriteria for location of the origin of escape beats,whether above or below the bifurcation of thecommon A-V bundle, would require amend-ments and amplifications. Difficulties will arisein particular when escapes are encounteredconforming to idioventricular beats in QRSTcontour but not in timing (fig. 3). In such casesa retrograde P wave preceding the beats underquestion would favor their nodal origin. But

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this is seen only rarely in escaped beats"6 andcannot be expected in atrial fibrillation or in thepresence of A-V block, the two conditions inwhich escape of subsidiary centers is encoun-tered most commonly. As another point of dis-tinction, foreshortening of the first ectopic R-Rcycle may be used-since this occurs at theonset of nodal rhythms in contrast to idioven-tricular rhythms. But this criterion becomesapplicable only if escapes are repetitive (reveal-ing the true nodal interval) and is not observedinvariably in nodal rhythms; in fact depressionof nodal activity by preceding (conducted)impulses"7 may counteract the apparent abbre-viation of, and even prolong, the first R-R innodal rhythm. The most reliable criterion of anidioventricular origin of escapes is the findingof ventricular fusion beats (fig. 4), a principlealso valuable in the identification of ventricularparoxysmal tachycardia."' Obviously, when twosimultaneous heterogenetic impulses share theactivation of the ventricles at least one musthave been initiated beyond the bifurcation ofthe common A-V bundle.

If the concept of functioning short-cuts be-tween A-V junctional structures and the ven-tricular myocardium should turn out to bevalid, then such normal preferential pathwaysoperating in nodal escape beats must be distin-guished from abnormal accessory pathwaysoperating in the pre-excitation (Wolff-Parkin-son-White) syndrome. Data have been pre-sented in a recent report from this department19which strongly favor the latter mechaniismagainst all other invoked in the search for thecause of ventricular pre-excitation. There areseveral reasons to distinguish the two condi-tions. Aberrant conduction of escaped beats iscommon in clinical electrocardiography andbears no relation to the incidence of paroxysmalsupraveintricular tachycardia in contrast to thepre-excitation syndrome. Furthermore, pre-excitation beats typically reveal a distinct"anomalous component," the delta wave, andsecondary ST-T alteratioiis, in CoIntrast toaberrant supraventricular escapes. This is welldemonstrated in figure 3, where both types ofbeats occur side by side. In most instances, theelectrocardiographic pattern will permit thedifferential diagnosis but difficulties may arise

when the type of QRS aberration in escapebeats imitates the delta wsave of ventricularpre-excitation (fig. 3C).There is also reasonable anatomic back-

ground for a hypothesis ascribing the two typesof aberration of ventricular complexes to twodifferent types of anomalous A-V conductionpathways. Paraspecific fibers have been de-scribed as originating in the A-V node andproximal parts of the specific conduction sys-tem, and as maintaining a course close toordinary conduction pathways. Accessory mus-cular A-V bridges, on the other hand, demon-strated in a few completely and carefullyexamined cases with ventricular pre-excitation,were found remote from the A-V junction,bypassing the A-V node. Supposing that bothtypes of fibers have the function of coinductiv-ity, one might expect that nodal impulsesentering preferential, and perhaps soon rejoill-ing ordinary pathways in the ventricularseptum, should produce comparatively littlealterations of the ventricular complex in theelectrocardiogram compared with pre-excita-tion beats. In the latter, supraventricular imn-pulses traveling over abnormal accessory A-Vconnections would directly reach ventricularmyocardium of the free walls and hence causeprofound alterations in the sequence of ven-tricular activation and deactivation. C(on(eiv-ably normal preferential and abnormal acces-sory pathways could be inl action in the samecase as is suggested by the observation repro-duced in figure 3.

SUMIMARY AND) CON-CLUSION-S

(1) Alen aberrant QRST contour of escapebeats is commonly encountered in clinicalelectrocardiography. Selected examples are pre-sented, illustrating the problems of locating thesubsidiary pacemaker above or below the bi-furcation of the common bundle under suchcircumstances.

(2) Presentt criteria based on QRS (lurationand time of appearance of the escapes imay beunreliable in the differential diagnosis of supra-ventricular and ventricular subsidiary pace-makers. The latter can be diagnosed withcertainty when ventricular fusion beats arerecorded.

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7101IABRRANT VE'NTRICULAR COND)UCTION OF ESCA1PI') BEATS

(3) Aberrant conduction of supraventricular(nodal) escapes cannot be accounted for on afunctional basis. However, a background for afeasible interpretation is provided by recenthistologic studies of the A-V junction in thehuman heart. Paraspecific A-V connectionshave beeii demonstrated which conceivablycould represent preferential pathways for im-pulses initiated in proximal portions of thespecific system, in particular in the A-V node.

(4) On the basis of clinical, electrocardio-graphic and anatomnic facts, aberrant intraven-tricular conduction, supposedly effected by theoperation of such normal preferential A-Vconduction pathways, must be distinguishedfrom the mechanism of ventricular pre-excita-tion. The latter is to be ascribed to abnormalaccessory A-V bridges bypassing the A-V node.However, the two mechanisms need not bemutually exclusive.

(5) The presented concept of preferentialA-V conduction is hypothetical and needs ex-perimental or other confirmation.

SUMMARIO IN INTERLINGUA

(1) Un aberrante contorno QRST de pulsosescappate es de occurrentia commun in electro-cardiographia clinic. Es presentate exemplosseligite. Istos illustra le problemas del localisa-tion de centros subsidiari supra o infra lebifurcation del fasce commun.

(2) Le disponibile criterios, que es basatesuper le duration de QRS e le tempore quandole pulsos escappate se manifesta, non es semperdigne de confidentia in le diagnose differentialde centros subsidiari supraventricular e ven-tricular. In casos del registration de pulsosfusional ventricular, le diagnose de centrossubsidiari ventricular pote esser diagnosticatecon securitate.

(3) Le conduction aberrante de supraven-tricular (nodal) pulsos escappate non es ex-plicabile super un base functional. Tamen, lebase de un plausibile interpretation es providiteper recente studios histologic del junctionatrio-ventricular in le corde human. Para-specific connexiones atrio-ventricular essevademonstrate le quales poteva representar viaspreferential pro impulsos initiate in portiones

proximal del systema specific, particularmentein le nodo atrio-ventricular.

(4) Super le base de factos clinic, electro-cardiographic, e anatomic, le aberrante conduc-tion Mt raventricular (supponitemente afficiteper le functionamenito de tal normal viaspreferential de coniduction at rio-venitricular)debe esser distinguite ab le mechanismo depre-excitation ventricular. Iste ultime mecha-nismo es a ascriber a anormal pontes accessoriatrio-venitri(ular que non passa per le nodoatrio-venitricular. Sed le duo mechanismos nonse exclude mutualmente.

(5) Le hic-presentate concepto del (onduc-tion atrio-ventricular preferential es hypothetice require confirmnationes experimental o altere.

REFERENCES1 KATZ, L. N. AND PICK, A.: Clinical Electrocardi-

ography. I. Arirhythniias. Philadelphia, Lea andFebiger, 1956.

2 AND KAPLAN, L. G.: Unusual forms of rhythmsinvolving the A-V no(le. Amii. Heart J. 16: 694,1938.

3 HANG, W . AND LANGENDORF, R.: Auriculoven-tricular nodal escape in the presence of auricularfibrillation. Circulation 1: 931, 1950.

4GOUAUX, J. L. AND ASHMAN, R.: Auricular fibril-lation with aberration simulating ventricularparoxysmal tachycardia. Am. Heart J. 34: 366,1947.

SCHERF, 1).: Alterations in the form of the Twvave with changes in heart rate. Anm. Heart J.28: 332, 1944.

6 LEVINE, H., LOWN, B. AND STREEPER, R. B.The clinical significance of post-extrasystolicT wave changes. Circulation 6: 538, 1954.

7SCHERF, D. AND BLUMENFELD, S.: Variations ofform of T waves in auricular flutter and auricu-lar fibrillation, associated with changes of rate.Am. Heart J. 46: 543, 1953.

8 MANN, R. H. AND BURCHELL, H. B.: The signifi-cance of T waves inversion in sinus beats fol-lowing ventricular extrasystoles. Am. Heart J.47: 504, 1954.

9 LAUBRY, C. AND POUMAILLAUX, MX.: Lalternanceelectrique. Arch. mal. coeur. 23: 456, 1930.

10 SCHERF, 1).: Supernormal phase of intraventricu-lar conduction. Am. Heart J. 361: 621, 1948.

11 LEY, M1. AND LERNER, R.: The theory of Kent.A histologic study of the normal atrioventricularcommunications of the human heart. Circula-tion 12: 176, 1955.

12 LAHAIM,I.: Kent's fibers and the A-V paraspe-cific conduction through the upper connections

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of the bundle of His-Tawara. Akm. Heart .1.

33: 651, 1947.13 ROBB, .J. S. AND TURMAN, W. G.: Further con-

siderations of the Q-T interval. Am. J. M. Sc.214: 180, 1947.

14 KISTIN, A. D.: Observations on the anatomy ofthe atrioventricular bundle (bundle of His) andthe question of other muscular atrioventricularconnections in normal human hearts. Am.

Heart J. 37: 848, 1949.'5 PRINZMIETAL, N1., KENNAMER, R., CORDAY, E.,

OSBORNE, J. A., FIELDS, J. AND SMITH, L. A.:Accelerated Conduction. The Wolff-Parkinson-White Syndrome and Related Conditions.New York. Grune & Stratton, 1952.

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16 SCHOTrT, A.: Upper atrioventrieular nodal I)eatsprecipitated by ventricular extrasystoles withretrograde conduction. Brit. Heart J. 12: 247,1955.

17 PICK, A., LANGENDORF, R. AND KATZ, L. N.:D)epression of cardiac 1)acema-keirs by prenma-ture impulses. Aim. Heart J. 41: 49, 1951.

18 DRESSLER, W. AND ROESLER, H.: The occurrencein l)aroxysman.tl ventricular tachycardia of yen-triiular complexes transitional in shape tosino-o uiriculai l)eats. A litagnosti( aid. Aim.Heart J. 44: 485, 1952.

19 PICK, A. AND KATZ, L. N.: I)isturbances of im-pulse formation and conduction in the pre-excitation (WPW) syndrome their bearing onits mechanismn. Am. J. _Med. 19: 759, 1955.


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ALFRED PICKAccessory Pathways in the A-V Junction

Aberrant Ventricular Conduction of Escaped Beats: Preferential and

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1956 American Heart Association, Inc. All rights reserved.

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