306 J AM CaLL CARDIOL1983;1:306-16

Electrocardiography of Arrhythmias: From Deductive Analysis toLaboratory Confirmation-Twenty-Five Years of Progress

CHARLES FISCH , MD, FACC

Indianapolis. Indiana

Before the advent of the microelectrode, His bundle re­cording and direct cardiac pacing, electrocardiographicinterpretation of arrhythmias in human beings was basedon presumed mechanisms derived by deductive analysis.This indirect approach was forced by the fact that thesurface electrocardiogram does not directly record thebehavior of the specialized tissue that is the site of origin

Although arrhythmias have been studied by a variety ofmethods (I) , none has approached the reliability of the elec­trocardiogram. Free of assumptions important in interpretingthe electrocardiographic waveforms relative to the QRS , STor T waves, the electrocardiogram of arrhythmias , with rareexceptions, closely reflects intracardiac event s. However,the probable mechanisms of arrhythmias must be largelyderived by the process of deductive analysi s. Thi s indirectapproach to the study of arrhythmias is due to the fact thatelectrocardiographic waves reflect the electrical behavior ofthe myocardial tissue while arrhythmias are caused by dis­turbances of impulse formation and conduction, or both, ofthe specialized tissue. As such, alterations in the propertiesof the specialized tissue are not reflected in the electro­cardiogram.

During the past 25 years, many of the basic concepts ofelectrocardiographic interpretation of arrhythmias that werederi ved by deductive reasoning have been confirmed ex­perimentall y. The advent of microelectrode and His bundlerecord ing techniques made it possible to record the electricalactivit y directly from the specialized tissue . In addition ,electrical pacing of the human heart and open heart surgerypermitting the stimulation of and direct recording from themyocardial surface provided the opportun ity to confirm inhuman subjects many of the electrophysiologic mechan ismsand properties previously recorded only in the experimentalanimal.

From the Krannert Institute of Cardi ology. Department of Medi cine.Indiana Univ ersity School of Medi cine. and the Veterans AdministrationMedical Center, Indianapolis. Indiana .

Addre ss for reprints; Charles Fisch, MD . Ind iana University Hospital.1100 West Michigan Street, Room 485W. Indianapol is . Indiana 46223 .

©1983 by the AmericanCollege of Cardiology

of most arrhythmias. In the past 25 years it has becomepossible to record directly from the specialized tissue.The result has been experimental confirmation of severalunderlying concepts of the electrocardiographic inter­pretation of arrhythmias and progress evidenced by theconversion of concept to fact.

Because a comprehensive review of the progre ss of thepast 25 years is beyond the scope of this presentation, theapproach will be to discuss selected arrhythmias. each rep­resenting a model of a different mechanism and all illus­trating the conversion of concept to fact. The specific mech­anisms to be discussed are the Ashman phenomenon ,concealed conduction. exit block and the role of the atriumin the perpetuation of reciprocating junctional tachycardia .

Ashman PhenomenonConduction fails or is delayed if a stimulus falls during theeffective or relative refractory period of recovery. When thestimulus falls during the relative or absolute refractory pe­riod of one of the bundle branches, unilateral delay or blockoccurs in that bundle branch . Important to the concept ofthe Ashman phenomenon is the knowledge that the durationof the refractory period depends in large measure on thelength of the immediately preceding cycle or cycles. Nor­mally, the refractory period shortens with acceleration ofthe heart rate and lengthens with deceleration of the heartrate . Therefore, in the presence of a fixed coupling of apremature excitation to the dom inant impulse, it is possibleto lengthen the refractory period sufficiently to induce ab­erration through prolongation of the preceding cycle. Thi sform of aberration . named by Lewis (2, 3). is referred to asthe Ashman phenomenon (4. 5). It has been demonstratedthat such aberration may persist over a number of cycles(see Concealed Conduction) . With rare exception, aberra­tion due to the Ashman phenomenon is of a right bundlebranch block configuration (6.7). The right bundle branch

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VI

Figure I. Ashman phenomenon illustrated in the elec­trocardiogram (upper panel) and confirmed by record­ing directly from the cell (lower panel). S = stimulus.

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block may be associated with left anterior divisional blockor, rarely , with left posterior divisional block .

Microelectrode techniques have made it possible to doc­ument the effect of sudden change s in cycle length on theduratio n of the transmembrane actio n potential, refractori­ness and conduction by direct cellular recordi ngs.

Figure I: intraventricular aberra tion (right bundle branchblock) due to the Ashman phenomenon. The two strips of theelectrocardiogram are part of a continuous record of lead YI . Thebasic rhythm is atria l tachycardia with Wen ckebach (type I) atrio­ventricular (AY) block . The long cycles of the Wenckebach se­quence are followed by one or more consecuti ve QRS complexeswith right bundl e branch block . The mechanism proposed to ex­plain the aberrancy of the first QRS co mplex is sudden prolongationof the transmembrane action potential and the refractory period ofthe right bundle branch . Aberrancy of the second QRS complexis discussed in connection with Figure 4 .

The validity of this extrapolation for the mechanism of aber­rancy was documented by recording directly fro m the cell as il­lustrated in the lower panel of Figure J. The regular basic cycle

length is interrupted by two premature stimuli (S ~ ). both coupledby the same interv al to the basic dr iving stimulus. The first S~

stimulates the cell after the tran smembrane action potential hasrecovered full y and result s in a norm al response . This action po­tent ial is then followed by a longer cycle that is terminated by aprolonged action potential. As a result. the second S~. althoughcoup led by the same interval to the basic cycle as the first S ~ .

stimul ates the cell before full recovery of exci tabilit y. and a re­duced takeoff pote ntial results in a slower upstroke of phase O.

decreased amplitude and shortened duration of the action potential.Such an action potential may cau se a slower propagation or failureof conduction.

When such events occur in the right bundle . right bundle branchblock may result. As indic ated. most instances of aberration dueto the Ashman phenomenon have a right bundle branch blockconfiguration probably because the normal refractory period of theright bundle exceeds that of the left bundle (8) . Con sequently .when pro longation of refractoriness due to a sudden change incycle length is "added" to the basic refractoriness of the twobundles. right bundle branch block is more likely to occur.

Concealed ConductionThe concept of concealed conduction emphasizes two factscentral to electrocardiograph ic analysis of arrhythmias: I )analysis of arrhythmias often depends on deductive reason­ing , and 2) the aim of such deducti ve reasoning is to definechanges in automaticity and conduction of the specializedtissue . This must be accomplished through analysi s of theelectrical potential generated by the myocardium as re­flected , in part. by the P and QRS waves . Therefore , con­cealed conduction is an ideal model for the study of theprinc iples governing the interpretation of complex arrhyth­mias. In 1894, some 9 year s before Einthoven introducedthe electrocardiogram, Englemann (9) working in Utrecht,defined concealed conduction and his definition still holdstrue today. By studying a hanging heart preparation he ob-

308 J AM COLL CARDIOL1983;1:306--16

-

FISCH

Figure 2. Concealed conduction responsiblefor paradoxical PR altemans in the electro­cardiogram (upper panel) is confirmed byrecording directly fromtheHisbundle (lowerpanel). BCL = basiccycle length.

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served that "every effective atrial stimulus, even if it doesnot elicit a ventricular systole prolongs the subsequent A­V interval. " In 1925, concealed conduction in the AV nodeof the animal was reported almost simultaneously by Lewisand Master (10), Drury (11), Ashman (12) and Scherf andShookhoff (13). Some 20 years later Langendorf, Pick andKatz (14-21) published an elegant series of papers applyingthis concept to human beings. Concealed conduction hasbeen observed in the sinoatrial node, the perinodal tissue,the atrium (22), the ventricular septum and the bundle branches(19,23). The concealing impulse may be normal in originor secondary to altered automaticity or reentry, and its con­duction may be anterograde or retrograde.

Although concealed conduction has been demonstratedexperimentally with pacing in human subjects (20), directlaboratory confirmation of the concept was made possibleby the advent of microelectrode (24) and His bundle re­cording techniques (25). Of the infinite number of electro­cardiographic manifestations of concealed conduction, AValtemans, concealed His bundle depolarization and con­cealed transseptal activation will be specifically discussed.

AV AlternansFigure 2: atrial tachycardia with 2:1 AV block and para­

doxical alternation of the PR interval in relation to the RPinterval. The accepted mechanism for this paradoxical alternationis concealed conduction of the blocked P wave (16). The PR

intervals of the conducted P waves in the electrocardiogram al­ternate between 0.30 and 0.20 second with a respective RP intervalof the conducted P waves of 0.47 and 0.36 second. The sequenceof a long RP and long PR interval alternating with a short RP andshort PR interval is contrary to expected physiologic behavior ofAV conduction. Further analysis reveals that the RP intervals ofthe respective blocked P waves measure 0.08 and 0.0 second.The RP interval preceding the P wave with a PR interval of 0.30second measures 0.08 second, the blocked P wave preceding theP wave with the PR interval of 0.20 second is buried within theQRS complex and its RP interval is 0.0 second.

The proposed mechanism-concealed conduction-is illus­trated with the aid of the Lewis diagram below the electrocardi­ogram. The diagram suggests that the blocked P wave with thelonger RP interval of 0.08 second penetrates deeply into the AVnode, delays conduction of the subsequent P wave and results inthe longer 0.30 second PR interval. In contrast, the P wave withan RP interval of 0.0 second is blocked high in the AV junctionand does not interfere with conduction of the subsequent P wavewhich is followed by the shorter, 0.20 second, PR interval.

The validity of this mechanism as an explanation for the par­adoxical alternation of the PR interval is proved in human beingsby recording directly from the His bundle (Fig. 2, lower panel).In this recording, the heart is paced at a basic cycle length of 350ms. For purposes of discussion, the stimulus (S) is equated withthe P and A waves of the electrocardiogram and the His bundleelectrogram, respectively. The electrocardiogram reveals that P2

with an RP interval of 450 ms is followed by a PR interval of 260ms, while P4 with an RP interval of 425 ms is followed by a PR

ELECTROCARDIOGRAPHY OF ARRHYTHMIAS J AM COLL CARDIOL1983;1:306-1 6

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Figure 3. Concealed junction al discharge manifest asa pseudo-Wenckebach type 1 AV block in the electro­cardiogram (top panel). The concept of concealedjunctional discharge is confirmed by recording directlyfrom the cell (middle panel) and from the His bundle(bottom panel). Abbreviations as in text and Figure2. (The middle panel was reproduced from Moore EN,Knoebel SB, Spear JR. Concealed conduction. Am JCardiol 1971;28:46. The upper and lower panels werereprinted from Fisch C, et al. [26], by permission ofthe American Heart Association , lnc.)

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interval of 190 ms. It is assumed that PI with an RP interval of100 ms penetrates into the junction to the level of the His bundle,delays AV conduction and prolong s the PR interval to 260 ms. Incontrast, P3 with a shorter RP interval of 75 ms is blocked in theAV node, fails to reach the His bundle and has a lesser impact onconduction of P4 , which is followed by a shorter PR interval of190 ms.

The assumption that deep penetration of PI is responsible forthe unexpect edly longer PR interval of P2 is also proved by re­cordin g directl y from the His bundle . and analysis is aided withthe Lewis diagram . AI reac hes the level of the His bundle and aHis potent ial is recorded . The refractoriness due to the deep pen­etration of AI delays the conduction of A2 , resulting in an AHinterval of 260 ms. Because of a shorter RP3 interval, A3 is blockedhigh in the AV node and does not reach the His bundle . A3 in­terferes less with conduction of ~ and, therefore , A, is followedby a short AH interval of 190 ms.

Concealed Junctional Discharge

Figure 3: pseudo-Wenckebach (type I) AV block due toconcealed junctional impulses. In the lower strip of the elec­trocardi ogram (aVF) (top panel ). the first two P waves are sinusin origin with a PR interv al of 0 .20 second. The third QRS complexis an interpolated junctional impulse with intraventri cular aber­ration due to the Ashman phenomenon. The subsequent sinusimpulse is conducted with a longer PR interval. This is followedby a second junctional premature complex with a normal QRScomplex and a fourth sinus impuls e with an even longer PR in-

terval. The third junctional impulse blocks conduction of the fifthsinus P wave and the sequence is repeated . The top row illustrate sgradual prolongation of the PR interval and ultimate failure of aP wave to conduct , which is indicative of Wenckebach (type I)AV block. If the interpolated jun ctional complexes in the secondrow are disregarded, an identical pattern of the AV conductionemerges . On the basis of such correlative extrapolation, the patternof AV conduction recorded in the upper row has been assumed toresult from repet itive concealed premature discharge of a junctionalpacemak er .

The validity of this assumption is proved in direct recordings,as illustrated in the middle panel. This record was obtained si­multaneously from the right atrium (RA), the His bundle (H) andthe right ventr icle (RV). The impul se generated by stimul ation ofthe right atrium is condu cted to the His bundle and the rightventricle . Preexcitation of the His bundle. indicated by the solidarrow, results in an action potential that fails to conduct either tothe right ventricle or to the right atrium and remains " concealed"within the His bundl e . The refractoriness that follows this pre­mature activation of the junctional tissue blocks the subsequentatrial impul se . Analy sis of the right ventricular electrogram sug­gests a Mobitz type II block. However , a correlation with therecording from the right atrium and His bundle indicates a pseudo­Mobitz type II block .

The bottom panel includes two His bundle electrograms (HE)and electrocardiographic leads I. II and Ill . In the electrocardi­ogram, the PR interval is prolonged from 225 to 275 ms and thethird P wave is blocked , indicating a Wenckebach type I AV block.

310 J AM COLL CARDIOL1983:1:30&-16

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VI

Figure 4. Concealed transseptal conduc­tion as the mechanism of perpetuation ofaberrancy illustrated in the electrocar­diogram (upper panel) andconfirmed byintracardiac electrophysiologic studies inhuman subjects (lower panel). Abbre­viations as in text.

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The respective AH intervals of the His bundle electrogram measure130 and 180 ms while the third A wave fails to conduct. A non­conducted premature His bundle discharge precedes both the de­layed AH interval and the blocked A wave. The temporal relationof the concealed His potential and the A wave (HA) explainsprolongation of the AH interval and block of conduction of thethird A wave. As the HA interval shortens from 530 to 485 ms,the third A wave arrives at an absolutely refractory junction andconduction fails. Recording from the His bundle also has dem­onstrated concealed His bundle discharge as the underlying mech­anism for a spectrum of bizarre AV conduction patterns (26).

Concealed Transseptal ActivationFigure 4: Ashman phenomenon with right bundle branch

block and concealed transseptal conduction. This electrocar­diogram (upper panel) and the one ilIustrated in Figure I wererecorded in the same patient. The basic rhythm is an atrial tachy­cardia with Wenckebach type I AV block. The aberrancy of thefirst QRS complex after the pause is due to the Ashman phenom­enon and persistence of the right bundle branch block is assumedto result from concealed transseptal activation of the right bundle(19).

Both mechanisms are illustrated with the aid of the diagram(below the electrocardiogram). The solid bar denotes the refractoryperiod, the dashed and dotted lines indicate the right and left bundlebranch, respectively. The refractory period is prolonged after thelong pause and blocks conduction in the right bundle (Ashmanphenomenon), The sinus impulse continues along the left bundle,crosses the septum, enters the right bundle and blocks conductionof the subsequent sinus impulse, thereby perpetuating the rightbundle branch block. An exact temporal relation between the con-

cealed transseptal conduction and the anterograde conduction ofthe sinus impulse is essential for the aberration to persist. If theconcealed transseptal conduction is delayed or the supraventricularimpulse or transseptal activation occurs prematurely, the right bun­dle branch may not be refractory and the impulse will propagatenormalIy. In the electrocardiogram in Figure 4, this critical relationis altered by the Wenckebach pattern of conduction which resultsin a gradual foreshortening of the RR interval.

The concept of concealed transseptal conduction is proved bydirect stimulation of the heart as is illustrated in the lower panel.The tracing ilIustrates a stimulus initiating reciprocating junctionaltachycardia with right bundle branch block aberrancy. Electro­cardiographic leads L II, Ill, VI and right atrial (RA), His bundle(HE) and coronary sinus (CS) electrograms are recorded. The atrialactivation is retrograde and indicated by the atrial potential firstrecorded in the coronary sinus. Excitation of the right ventricle(S). shortly before the expected activation by the transseptal im­pulse, terminates the concealed transseptal conduction and intra­ventricular conduction normalizes.

Figure 5: concealed transseptal activation recorded in anexperimental animal. Concealed transseptal activation, which maybe responsible for the aberrancy discussed, has been documentedin the experimental animal by recording directly from the bundlebranches (27). The tracings in Figure 5 were obtained simulta­neously from the surface (ECG), His bundle (HBE) and four sitesalong the right bundle (RB 1,2,4,5), left septum (LS), right (RV)and left (LV) ventricle. The path of impulse conduction is shownin the diagram. The anterograde activation initiated by SI conductsfrom the atrium (A) to the His bundle (H) and to sites RB I throughRB5 of the right bundle, respectively. The impulse generated byS2 is blocked between the His bundle and site RB I. with conduction

ELECTROCARDIOGRAPHY OF ARRHYTHMIAS J AM cou. CARDIOl1983:1:306-1 6

311

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Figure 5. Transseptal conduction from the leftbundle to the right bundle demonstrated by re­cording directly from the conduction system. ECG= electrocardiogram: other abbreviations as in text.(Reprint ed from Glassman RD. Zipes DP [27],by permission of the American Heart Association.

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moving along the left bundle; 30 ms later left ventricular deflection(LB) is recorded. The right bundle branch is activated in a ret­rograde manner from RB4 to RB I. Failure to register a deflectionat RBS is probably due to the deflection being obscured by theventricular complex.

Exit BlockThe presence of ex it block is ind icated by the failure of animpulse to propagate . This concept was first proposed to

explain the failure of a parasystol ic complex to bec omemanifest when the heart was no longer refractory (28). Sincethen it has been documented that all spontaneo us and art i­ficially induced impulses may manifest exit block (17 .29 ).Exit block du e to a path ophysiologic state can be assumed

onl y if the impulse fail s to conduct when the surrounding

myoc ardium is no longer refractory . Otherwise , failure to

propagate reflects ph ysiologic interference from refractor i­nes s. Experime ntal (30 ,31) and clinical ob servations (25 )

suggest that exit block results from delay or block of co n­

duction rather than from an abnormality of impulse format ion.

Exit block may be manifest as Wenckebach type I orMobitz type II AV block. Howe ver. a diagnosis of exit blockma y be impossible when the pattern of conduction distu r­ban ce fails to conform to either type I or type 11 block andthe PP or RR cycles are irregular.

Figure 6: atrial fibrillation, nonparoxysmal junctionaltachycardia and exit block. The electrocardiogram in Figure 6(lower panel) suggests atrial fibrillation with an irregular ventric­ular response . Measurement of the long cycles. however. revealsthat the cycles are equal in length and the pattern is repetitive(group beating). suggesting a mechanism other than simple atrialfibrillation. Further analysis discloses that the respective RR cyclesof each sequence beginning with the long interval are also similarin duration and that the RR intervals gradually shorten until thesequence terminates at the shortest cycle. The long cycle thatfollows is shorter than twice the length of the preceding cycle.The electrocardiogram. therefore. illustrates atrial fibrillation withnonparoxysmal junctional tachycardia and Wenckebach type I exitblock.

The concept of Wenekebach type I exit block fro m a junctionalfocus was confirmed by direct recording fro m the NH portion ofthe AV node (NH) and the His bundle (H), and is illustrated inthe upper panel of Figure 6. The impulse initiated in the NH fiberconducts with a progressively greater delay and ultimately fails toactivate the His bundle . The long HH interval that follows is shorterthan twice the length of the preceding shorter HH interval. Thepacemaker action potential is constant throughout. suggesting thatthe exit block is caused by altered conduction rather than an ab­normality of impulse formation.

Figure 7: ventricular tachycardia with exit block. The anal­ysis of the electrocardiogram begins with the part of the top tracingabove the Lewis diagram (A = atrium. J = junction, v = ventricle).The first QRS complex is sinus in origin with a right bundle branch

312

NH

H

J AM COLL CARDJOL1983 :1:30&--1 6

FISCH

Figure 6. Wenckebach type I exit blockfrom a junctional pacemaker illustratedin the electrocardiogram (lower panel)and confirmed by recording directly fromthe AV node in the His bundle (upperpanel). (Reprinted from Fisch C. et at.[30], with permission.)

block pattern. The sixth QRS complex is a ventricular fusioncomplex that confirms the ventricular origin of the tachycard ia.Beginning with the second QRS complex, the manifest interectopicQRS cycles measure 640. 640 ,400, 1.320,640. 320 and 400 rns,respecti vely. and the sequence is termin ated by a sinus complexwith right bundle branch block. The cycles of 400 , 320 and 400ms reflect a I: I exit from the ectopi c pacemake r with a changingconduction pattern . The presence of RR cycles equal in durationindicates group beating and suggests a common interectop ic de­nominator for this " irregular" ventricular tachycardia . The basicinterectopic interval can be estimated from analysis of the first two

manifest interectopic QRS complexes in the second row. The sumof the two manifest QRS cycles is I .280 ms and encompasses fourinterectopic intervals. By dividing 1.280 ms by 4. one obtains thetrue interectopic interva l of 320 ms. This estimate is supported bythe presence of two manifest QRS cycles of 320 ms in the upperrow. The difference in length between the manifest QRS cycles

Figure 7. Wenckebach type I exit block from a ventricular ectopic focusrecorded in the electrocardiogra m (upper panel ) and confirmed by stim­ulation and recording directly from the cell (lower panel ).

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ELECTROCARDIOGRAPHY OF ARRHYTHMIAS J AM COLL CARDIOL1983;1:306--16

313

Figure 8. Mobitz type II exit block from the ventricularfocus recorded in the electrocardiogram (lower panel) andconfirmed byrecording directly froma pacemaker andmyo­cardial cell (upper panel). (Reprinted from FischC, et at.[30), with permission.)

and the estimated true interectopic cycle of 320 ms is an estimateof the delay of conduction from the ectopic pacemaker.

The concept of exit block with a varying exit delay, with orwithout Wenckebach structure, has been confirmed by recordingdirectly from the respective cells and is illustrated in the lowerpanel. When the artificial stimulus is equated with an ectopicpacemaker cell, a latent period from the pacemaker to the myo­cardial cell, a 2:1 and 3:2 Wenckebach type 1 exit block is noted.Because the stimulus strength remains constant, the exit block isa function of altered conduction and not of a changing impulse.

Figure 8: ventricular tachycardia with exit block. The elec­trocardiogram (lower panel) illustrates ventricular tachycardia witha bigeminal rhythm and represents a section of long records thatconfirmed the ventricular origin of the arrhythmia. The longercycles are exactly twice the length of the shorter cycles, indicatingventricular tachycardia with a 3:2 Mobitz type II exit block.

The concept of ventricular tachycardia with exit block wasconfirmed by recording directly from the cell and is shown in theupper panel. The action potentials of an automatic Purkinje cellpacemaker and a distal myocardial cell, the latter responding pas-

sively to the pacemaker-initiated stimulus, are recorded. A constantrelation exists between the two action potentials except for inter­mittent failure of the distal cell to respond. The duration of thelonger cycles is twice the length of the shorter cycles, confirmingthe presence of Mobitz type II exit block. As noted in Figures 6and 7, the uniformity of the pacemaker transmembrane actionpotentials suggests that the exit block is a function of alteredconduction rather than of impulse formation.

The Role of the Atrium in MaintainingReciprocating Junctional Tachycardia

On the basis of animal studies it has been suggested that anatrial bridge is necessary for the maintenance of recipro­cating junctional (AV nodal) tachycardia (32-35). In humansubjects, however, electrocardiographic findings suggest thatthis is not necessarily the case (18).

Figure 9: reciprocating junctional tachycardia with occa­sional failure of the impulse to activate the atrium. All threeleads of the electrocardiogram were recorded simultaneously and

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314 J AM COLL CARDIOL1983:1 :306-16

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CFigure 10. Intracardiac atrial stimulation duringre-ciprocating junctional tachycardia in a patient con­firms that the atriumis not alwaysan essential com­ponentof the reentrant pathway.

are part of a long record reflecting the same sequence. The firstsinus P wave is followed by an interpolated junctional prematurecomplex with aberration. The subsequent atrial impulse is followedby a prolonged PR interval and a reciprocating junctional tachy­cardia. The retrograde atrial activation is seen as a negative P wavein leads II and III. Although retrograde conduction fails after thefifth QRS complex (arrow), the rhythmicity of the junctional tachy­cardia is undisturbed, indicating that the atrium was not part ofthe reentrant pathway. This assumption is confirmed by directintracardiac stimulation and is illustrated in Figure 10.

Figure 10: atrial pacing during a reciprocating junctionaltachycardia. Panel A includes electrocardiographic leads I, II,Ill, V, and right atrial (RA), His bundle (HBE) and coronary sinus(CS) electrograms. The first and second P waves are sinus in originwith an anterograde conducting pattern, as indicated by the earliestactivation recorded in the right atrial electrogram preceding the Awave of the His bundle. A premature atrial stimulus (S) initiateda reciprocating junctional (AV nodal) tachycardia with an RRinterval of 800 ms and retrograde AV conduction, represented bythe earliest activation of the coronary sinus electrode. In panel B,the atrium was stimulated prematurely by two consecutive stimuli(S" Sz), the S,Sz interval measuring 440 ms. Both stimuli elicitedan atrial response. Although retrograde atrial activation failed afterthe second and third junctional QRS complexes, the tachycardiacontinued uninterrupted. A similar sequence of events is recordedin panel C at an S,Sz interval of 400 ms. In panel D, with an S,Szinterval of 360 ms, the atrium failed to respond to Sz because thestimulus fell during the absolute refractory period. The failure of

the absolute refractory period of the atria to influence the junctionalrhythm indicates that an atrial bridge was not essential for main­tenance of the reciprocating tachycardia.

CommentsBy singling out representative clinical arrhythmias and theirexperimental electrophysiologic counterpart, an attempt wasmade to review the progress of the last 25 years duringwhich electrocardiographic concepts arrived at by deductiveanalysis became fact. Such an approach cannot be all in­clusive. The combination of cellular electrophysiology, car­diac pacing and intracardiac recording both confirmed thevalidity of many of the concepts and demonstrated the ex­istence in the human heart of various electrophysiologicphenomena previously described in the experimental ani­mal. In some instances the combined approach also eluci­dated the basic electrophysiologic mechanism responsiblefor these phenomena. An incomplete list of the conceptsand/or electrophysiologic phenomena include, in additionto the previously discussed aberration, concealed conduc­tion, exit block, the role of the atrium in the maintenanceof reciprocating junctional tachycardia, confirmation of thebypass concept of Wolff-Parkinson-White syndrome (36),reciprocation (37-40), supemormality of ventricular excit­ability and conduction (41,42), vulnerability (43), unidi­rectional AV conduction (44), levels of AV block (45,46),

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parasystoles (47), fusion complexes (48), overdrive depres­sion of impulse formation and conduction (49), the gapphenomenon as a possible mechanism of "supernormal"AV conduction (50,51) and the Wedensky (?) phenomenon(52,53) .

Among the concepts awaiting laboratory confirmation areprotection of a parasystolic pacemaker (54), intraventricularaberration due to acceleration of rate which appears at rel­atively slow heart rates, supernormality of AV conduction(55) and the mechanism of entrance and exit block. Withfurther refinement or the advent of experimental techniquesfor recording the behavior of the specialized conductingtissue (for example, computer-assisted recording of the Hisbundle potential from the body surfaces and the use ofmultiple electrodes to map the pathways of conduction),confirmation of a number of concepts and clarification oftheir electrophysiologic mechanisms can be anticipated.

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