tachycardia-dependent bradycardia-dependent intermittent ...tachycardia-dependent versus...

British Heart Journal, I972, 34, I67-I76.

Tachycardia-dependent versusbradycardia-dependent intermittentbundle-branch block

Nabil El-SherifFrom the Cardiology Department, Faculty of Medicine, Cairo University, Egypt, U.A.R.

Analysis of I6 cases with intermittent bundle-branch block showing rate-dependence revealed thepresence of 12 instances with tachycardia-dependent bundle-branch block, 3 with bradycardia-dependent bundle-branch block, and one instance showing both types at two different occasions.Tachycardia-dependent bundle-branch block was explained on the basis of cycle length-recoverytime relation and revealed a critical rate for normal intraventricular conduction. However, some

overlap in the RR cycles of normal and aberrant beats in the same record was frequently seen,

especially in the presence of atrialfibrillation. This was attributed to the sensitivity of the actionpotential duration of the diseased bundle to the possible cumulative effects of cycle length changes.On the other hand, the demonstration of bundle-branch block at widely varying heart rates inrecords taken on different occasions probably reflects the influence of slowly acting parameters.Bradycardia-dependent bundle-branch block was diagnosed whenever bundle-branch blockappeared on slowing of the heart rate or disappeared on its acceleration, and was best explainedon the basis of enhanced phase-4 depolarization of the bundle-branch system. The occasionaldemonstration of a paradoxical relation to cycle length changes under the influence of certainphysiological manoeuvres and/or pharmacological agents was explained by the role of these agentsin enhancing or depressing phase-4 depolarization.

Transient and intermittent conduction dis-turbances are more familiar at the atrioven-tricular (AV) junctional tissue as compared

z with the intraventricular conduction system.Though study of the electrophysiologicalcharacteristics of the conduction system atthe two sites may reveal some variations, yetthese are not at all sufficient to explain theobserved difference in the relative incidenceof the two conditions. The consideration ofat least two factors may be helpful in this con-cern. Firstly, autonomic control may beoperating in a good percentage of transientand intermittent AV blocks (though some ofthe organic affections of the region may betotally reversible). On the other hand, thepresence or otherwise of autonomic controlon impulse conduction in the bundle-branchsystem and its possible role is still contro-versial. Secondly, some of the disturbances ofimpulse conduction at the bundle-branchsystem may be either difficult to recognizefrom conventional cardiographic records ormay be partially or totally obscured by con-Rezeived 17 March 1971.

comitant disturbances at the AV conductionsystem.

Transient bundle-branch block is usuallydefined as an intraventricular conductiondefect that subsequently returns, if onlytemporarily, to normal conduction, whileintermittent bundle-branch block on theother hand is characterized in the same cardio-graphic record of complexes showing bundle-branch block and normally conducted beats(Bauer, I964). However, since some cases ofbundle-branch block may prove to be ratedependent (not considering for the momentother intricate factors) and since in many ofthese cases no attempt is usually taken to un-cover probable instances of normal intra-ventricular conduction (e.g. by inducing asufficient degree of bradycardia), it will behard sometimes to make a clear-cut distinc-tion not only between transient and inter-mittent bundle-branch block but even be-tween permanent and transient blocks. Infact, many cases of intermittent block areusually diagnosed from fortuitously obtainedcardiographic records and are rarely actively

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I68 Nabil El-Sherif

TABLE Pertinent data of (I6) cases of intermittent bundle-branch block

Case Age (yr) Diagnosis Conduction Rhythm Electrocardiogram showing normalNo. and sex defect* conduction

I 55 F Rheumatic mitral stenosis LBBB Atrial fibrillation; ventricular Left ventricular ischaemic patternand insufficiency ectopic systoles

2 55 F Diabetes Left anterior Sinus; supraventricular ectopic Normalhemiblock systoles and tachycardia

3 49 F Recent infarction; hyper- LBBB Sinus Extensive anterior injury patterntension; diabetes

4 I9 F Ostium secondum defect RBBB Sinus Right ventricular hypertrophy of rsR'pattern

5 55 F Hypertensive coronary LBBB Sinus Left ventricular ischaemic pattern;heart disease ? old anteroseptal infarction

6 26 M Ventricular septal defect; LBBB Sinus; supraventricular ectopic Left ventricular ischaemic patternsubacute bacterial endo- systolescarditis

7 48 F Rheumatic mitral insuffici- LBBB Atrial fibrillation Left ventricular hypertrophy andency ischaemic pattern

8 58 M Hypertensive heart disease LBBB Atrial fibrillation Left ventricular ischaemic pattern9 6i M Hypertensive coronary LBBB Sinus; ventricular ectopic systoles Left ventricular ischaemic pattern;

heart disease old inferior infarctionIO 65 F Recent infarction, diabetes LBBB Sinus; ventricular ectopic systoles Recent extensive anterior infarctionII 53 M Hypoxic cor pulmonale, RBBB Sinus; ventricular ectopic systoles Biventricular hypertrophy

hypertensionI2 57 F Diabetes RBBB Sinus; ventricular ectopic systoles Normal13 45 F Massive pulmonary RBBB Sinus arrhythmia; supraventricu- Normal

embolism lar ectopic systolesI4 52 M Coronary heart disease LBBB Sinus Incomplete LBBB; ? septal

infarctionI5 49 M Recent infarction LBBB Sinus Acute anterior injury patternI6 55 M Recent infarction RBBB (i) Sinus+ ventricular, ectopic Anterolateral injury pattern

systoles(2) Sinus

* Left or right bundle-branch block.t Obtained two weeks after the first record.

searched for. The situation is further compli-cated by the fact that records showing normalintraventricular conduction at a 'reasonable'heart rate may be masking a latent degree ofbundle-branch block which would only beuncovered by slight acceleration of the rateor other appropriate measures.Though many reports on both transient and

intermittent bundle-branch block have beenpublished and various studies have been con-ducted to elucidate the various factors con-trolling impulse conduction in the bundle-branch system, yet much controversy and agood deal of misconception still prevail. Thefollowing review represents a critical dis-cussion of the subject through the study of i6cases of intermittent bundle-branch blockobserved in the past 5 years (from JanuaryI965 to December I969) at Kasr El-AiniFaculty of Medicine of the Cairo University.

Subjects and methodsSixteen cases showing rate-dependent intermittentbundle-branch block were analysed. These includeI2 cases with tachycardia-dependent block, 3

cases with bradycardia-dependent block, and Icase showing both at different occasions (Table).In IO cases multiple records were usually analysedand the cases were followed for variable durationsup to 5 years. In these cases, the role of certainphysiological manoeuvres and/or pharmacologicalagents were repeatedly studied. The remaining 6cases (Cases 7 to I2) were found during a criticalreview of 50 consecutive cases of bundle-branchblock. Inthese cases, there were oneormorerecordsavailable for analysis but an effective follow-upwas usually lacking. In these 50, ectopic systoleswere present in I4 and atrial fibrillation in another6. In 4 records showing ectopic systoles and in 2others with atrial fibrillation, evidence of normalintraventricular conduction was seen in the beatsfollowing the compensatory pauses of the ectopicsystoles or the long RR intervals in atrial fibrilla-tion. On the other hand, no single evidence ofnormal intraventricular conduction was seen inthe 30 records showing regular sinus rhythm.This limited statistical survey stresses not onlythe high incidence of intermittent bundle-branchblock but more essentially the value of long RRcycles in revealing probable instances of tachy-cardia-dependent block. In the presence of ectopicsystoles or atrial fibrillation, fortuitously longRR intervals are usually seen. In their absence,however, other bradycardia measures, like caro-



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Tachycardia-dependent versus bradycardia-dependent intermittent bundle-branch block 169

Physiological manoeuvres and/or pharmacological agent applied

Carotid sinus compression, amyl nitrite; exercise; atropine, adenosinetriphosphate

Amyl nitrite

Exercise; atropine

Carotid sinus compression

Carotid sinus compression

Atropine

Carotid sinus compression, atropine(I) -

(2) Carotid sinus compression

Mechanism of bundle-branch block

Tachycardia-dependent







Tachycardia-dependentTachycardia-dependent

Tachycardia-dependentTachycardia-dependent

Tachycardia-dependentBradycardia-dependent

Bradycardia-dependent

Bradycardia-dependent(i) Tachycardia-dependent(2) Bradycardia-dependentt

tid sinus compression, should be consistentlyused.

Pertinent data of all the cases are summarized inthe Table, while illustrative examples of eachgroup will be critically analysed.

Tachycardia-dependent bundle-branchblockCase i A 55-year-old woman with rheumaticmitral stenosis and incompetence was first ad-mitted to hospital in January I965. Her cardio-graphic record revealed atrial fibrillation and'intermittent left bundle-branch block (Fig. i).The beats with normal intraventricular conduc-tion showed left ventricular ischaemic pattern.Records A to D in the figure are consecutive butnot continuous. Analysis of these records revealsthat long RR cycles favour normal intraventricu-lar conduction while short cycles end with aber-rant beats. There is a significant overlap of the'critical RR cycles for both types of conductionbetween 77 and 921 (heart rate of 65-78 beats aminute). However, slowing of the heart rate belowthe critical level induced by carotid sinus com-pression (record D) consistently resulted in nor-mal intraventricular conduction, while at higher1 All intervals are expressed in hundredths of a second.

rates induced by amyl nitrite inhalation (recordE), exercise, or atropine injection, left intraven-tricular aberrant conduction, was always observed.The effect of intramuscular injection of ioo mgadenosine triphosphate on the intraventricularconduction was repeatedly studied and was foundto lead to normal intraventricular conduction, butthis was always associated with slowing of theheart rate below the critical level. The patient wasfollowed for the next two years and intermittentleft bundle-branch block could always be seenbut the critical rate varied from 52 to 82 beats aminute in several occasions. There was, however,no specific pattern for the change in the criticalrate (in particular, no progressive decrease of thecritical rate was observed).

Comment This is a simple case of tachycardia-dependent left bundle-branch block of unusuallylong duration. It is interesting to observe boththe significant overlap of the critical RR cyclesfor both types of conduction in the same recordand the wide variation of the critical rate for nor-mal intraventricular conduction in records takenon different occasions.

Case 2 A 55-year-old diabetic woman was ad-mitted to hospital in September I966 with a



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170 Nabil El-Sherif

I_" 11 ~~t_t~ 111 - V1

V3 t VS_

(A) V _1521 56| 64

141 86 1 62 1 48 1 88 66 14S1 93 | 77 148 92 68 96 102

74 94 177 186 1 66 1 95 104 1 52 1841 64 1113 171 196 7174

78 84I 86 |8 I95 68 188 90 |92 179 103 193 164 87

{0 ) _-x

| 64 92 166 84 94 801 92 1120 87 1 95 12.0 150 919

C t

97 120j 108 j 128 128 134 135 127 112 1781

4 E) V6 AAAFIG. I Case I, tachycardia-dependent bundle-branch block, record (D) shows the effect ofcarotid sinus compression (CSC) while record (E) shows the influence of amyl nitrite inhalation.X represents ventricular ectopic systoles.

recent history of recurrent attacks of palpitation.The record in Fig. 2 was obtained at one sittingand was originally divided into two separatesheets that were remounted together with no lossof substance. Lead II shows sinus rhythm at a

FIG. 2 Case 2, tachycardia-dependent leftanterior hemiblock.

1401 68 60 60 1401 7.0 1381 74

401 70 1601 60 57 56 1 62 140136Vi

| 4, 68 1I40 72 56 57 1581

V2

1 1 581 58558 85 8 58

V3

rate of IOO beats a minute with normal intraven-tricular conduction (a QRS pattern with a dura-tion of o-o8 sec). There are multiple supraventri-cular ectopic systoles showing aberrant intra-ventricular conduction (an rS pattern with aduration of o-Ii sec). This pattern represents aleft anterior hemiblock (Rosenbaum et al., I969).In lead III, the first and third complexes representnormally conducted sinus beats, while the secondcomplex is an aberrantly conducted supraventri-cular beat. The fourth to eighth complexes areconducted sinus beats at a rate of 97 to I07 beatsa minute showing aberrant intraventricular con-duction of the same type seen in the ectopic beats(a left anterior hemiblock). The last two beats inlead III start a paroxysm of supraventriculartachycardia and are showing aberrant intraven-tricular conduction. In lead Vi, the first, third,and fifth complexes are normally conducted sinusbeats, the second and fourth complexes representaberrant conduction, as the last three complexesdo. Lead V2 shows sinus rhythm at a rate of 103beats a minute with aberrant intraventricularconduction. Lead V3 shows a paroxysm of supra-ventricular tachycardia at a rate of I36 beats aminute, with aberrant intraventricular conduc-tion. The paroxysm ends before the last beatwhich reveals normal intraventricular conduction.

Comment This is a simple case of tachycardia-dependent left anterior hemiblock. The caseshows the close similarity between tachycardia-dependent bundle-branch block and intraventricu-lar aberrant conduction of both supraventricularectopic systoles and tachyarrhythmias. This mayhelp to illustrate the fact that aberrant intra-



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Tachycardia-dependent versus bradycardia-dependent intermittent bundle-branch block 171

ventricular conduction of either an ectopic supra-ventricular beat showing a relatively long coup-ling interval or a supraventricular tachyarrhyth-mia with only moderate acceleration of the ratemay betray an underlying latent bundle-branchblock.

Case 6 A 26-year-old man known to have aventricular septal defect was admitted in Febru-ary I969 with the diagnosis of subacute bacterialendocarditis. His cardiogram showed sinus tachy-cardia (rate 120 beats a minute), grade I AV block,and a left ventricular ischaemic pattern. The re-

cord obtained 3 days later still revealed sinustachycardia (rate II0 beats a minute) and grade IAV block but showed left bundle-branch blockpattern. An attempt was made to uncover normalintraventricular conduction by inducing brady-cardia through carotid sinus compression (Fig. 3,records A and B). Record A shows left bundle-branch block for the first three beats followed bytwo beats with normal intraventricular conduction,then an escape rhythm occurs at a rate of 75 beatsa minute (this represents either an idioventriculartachycardia or an idiojunctional tachycardia withaberrant intraventricular conduction of classicalright bundle-branch block pattern). The escaperhythm ends by sinus capture of the ventriclewith normal intraventricular conduction thatcontinues for the next four beats before the re-sumption of aberrant intraventricular conductionin the last two beats. Record B reveals essentiallysimilar findings; however it is interesting to ob-serve that the five beats that represent the escape

rhythm in the middle of the record are all for-tuitously preceded by sinus P waves at practicallyconstant PR intervals. In records A and B, it isseen that normal intraventricular conductionoccurs at a critical RR cycle of 57 (heart rate I05beats a minute). This is best seen during the re-

turn of aberrant intraventricular conduction.Records C, D, and E were obtained one weeklater. The sinus tachycardia had disappeared butthe left bundle-branch block was still present ata heart rate of 88 to go beats a minute. Normalintraventricular conduction could still be easilyinduced either by holding the breath after deepinspiration (record C), or carotid sinus com-

pression (record D), or in the pause after anectopic supraventricular beat (record E). Inrecords C and D, normal intraventricular con-duction is seen to occur at a critical RR cycle of68 to 70 (heart rate of 85-88 beats a minute). Inrecord D, the escape rhythm, which occurs at arelatively slower rate of 68 beats a minute, endsby an early capture of the ventricle after an RRcycle of 6I that results in aberrant intraventricularconduction. The following sinus beats occurringat longer RR cycles reveal normal intraventricularconduction. The patient was successfully treatedfor the subacute bacterial endocarditis and hisrecords obtained one month later failed to showany evidence of left bundle-branch block at aheart rate of 130 beats a minute induced by amylnitrite inhalation.

Comment This is a classical case of tachycardia-dependent left bundle-branch block. It is interest-

FIG. 3 Case 6, tachycardia-dependent left bundle-branch block. Records A, B, and Dshow the effect of carotid sinus compression (CSC), while record C reveals the influence of deepinspiration, and record E the effect of a supraventricular ectopic systole (marked X).Note the occurrence of ectopic escape rhythm with right bundle-branch block pattern aftercarotid sinus compression.

(A) I

Ss601 62 160 61 80 I 80 80 80 1 79 1 79 1 79 63 159 5J5J56 56

(B) 1

1s4iS2[561 76 [ 8 717 791 79 78 177 0 65 59 57 57 54 52 53154I

VI} -(C) Inp

L 70 711 80 84 1 76_ 76 .76 74 J72 71 70 I70 68 1 68 68 169

70 170 72 76 76 192 8 188188 88I.O d 61 81 1831 83

(E) 1



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172 Nabil El-Sherif

VI 104 68 104 84 68

Ca)

VI ,

(b) 78 78 77 78 75 76 74

FI G . 4 Case 13, bradycardia-dependent right bundle-branch block.

ing to observe that left bundle-branch blockoccurred at widely varying heart rates in recordstaken on different occasions.

Bradyeardia-dependent bundle-branchblockCase 13 A 45-year-old woman with cancer ofthe body of the uterus was admitted to hospital inSeptember I966 for a hysterectomy. Her cardio-vascular system was clinically free and her pre-operative cardiogram was within normal limits.Nine days after operation the patient developedsevere dyspnoea with chest oppression and lower-ing of the blood pressure, and was diagnosed ashaving a massive pulmonary embolism. Thecardiogram taken on the same day showed sinustachycardia and complete right bundle-branchblock. Fig. 4 was recorded three days later andshowed intermittent bundle-branch block. Thetwo strips of lead Vi show four types of QRSpattern: (a) rS pattern with a duration of o-o8 secdenoting normal intraventricular conduction;(b) rs pattern with notched s wave and a durationof o o85 sec; (c) rsR' pattern with a duration ofo og sec (both the second and third patterns repre-sent incomplete right bundle-branch block;(d) rsR' pattern with a duration of O I3 sec repre-senting complete right bundle-branch block. Withthe exception of the first, third, and sixth beatsin strip Vi (a), which are ectopic supraventricularsystoles, all complexes are preceded by identicalP waves and constant PR intervals and representconducted sinus beats. Obvious variation in theRR intervals is seen in strip Vi (a), while sinusarrhythmia is seen in strip Vi (b). It is noted thatbeats with complete bundle-branch block followthe longest RR intervals, and beats with normalintraventricular conduction follow the shortestintervals, while beats with incomplete bundle-branch block occur at intermediate cycle lengths.A cardiogram taken on the next day revealed nor-mal intraventricular conduction.

Comment This is a classical case of bradycardia-dependent right bundle-branch block. The role ofthe acute but regressive right ventricular overloadin the genesis of the intermittent conduction dis-turbance is remarkable.

Case 14 A 52-year-old man was first seen inMarch I965 with a history ofmyocardial infarction

and with evidence of left ventricular failure. Hiscardiogram showed left bundle-branch block withsmall Q waves in the left surface leads suggestiveof septal infarction. The patient was repeatedlyseen later on and his cardiograms always showedbundle-branch block. During a last admission inMay I969, intermittent bundle-branch block wasobserved for the first time. There were frequentchanges from QRS complexes showing completeleft bundle-branch block with a duration of O I7sec to complexes showing incomplete left bundle-branch block and a duration of o II sec. Fig. 5shows instances of transition between the twotypes of intraventricular conduction. Lead Irecord (A) shows sinus arrhythmia with two beats

FIG. 5 Case I4, lead I in record (A) showstwo beats with left bundle-branch block duringthe slow phase of sinus arrhythmia. Record(B) shows the effect of atropine injection. Theobservation of both types of intraventricularconduction at widely varying heart rate repre-sents a bradycardia-dependent block. See textfor details.

(A)

76 174 172 76 j80 78 68 75 76

V1 m1

76 1 76 1 74 1 76 1 76 1 76 1 75 1 74

(B)

I

158 1 5958 56 1 58 158 158 1AVL

1 60 1 61 1 61 61 [ 61 56 1 60 | 58 | 59 | 59 |



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T intermittent bundle-branch block 173

showing complete bundle-branch block occurringduring the slow phase of the arrhythmia in themiddle of the strip. Lead Vi on the other handshows regular sinus rhythm with the shift fromcomplete to incomplete bundle-branch blockunaccompanied by change in the heart rate.Record (B) shows the effect of intravenous injec-tion of i mg atropine sulphate administered in thesame sitting. Atropine has resulted in sinus tachy-cardia; still however beats with incompletebundle-branch block could be observed at RRintervals of 56-6I (heart rate of 98-IO7 beats aminute).

Comment There are two interesting observationsin the case. Firstly, instances of incomplete leftbundle-branch block were only seen for the firsttime after four years from the first observation ofcomplete block. Secondly, the demonstration ofbundle-branch block during the slow phase ofsinus arrhythmia and the observation of bothtypes of intraventricular conduction at a widelyvarying heart rate represent bradycardia-depen-dent left bundle-branch block.

Case I6 A 55-year-old man was first seen inFebruary I967 with a history of recent myo-cardial infarction. His cardiogram showed com-plete right bundle-branch block with ST-Tchanges suggestive of recent anterolateral injurypattern. There were frequent ventricular ectopicsystoles that usually occurred in pairs. Record (A)in Fig. 6 was obtained shortly after admission. Inthe record, both the conducted sinus beat (strip(Via) and the junctional escape beat (strip Vib)

which follow the compensatory pause of thesecond ectopic systole reveal normal intraven-tricular conduction. The records under (B) wereobtained two weeks later. Strip Vi shows frequentspontaneous transition from a right bundle-branch block pattern to beats showing a slightdegree of incomplete right bundle-branch block(rSr'). The second to fourth strips show the effectof carotid sinus compression. In strip Vi, carotidsinus compression gives rise to a pause followedby a junctional escape beat which still revealscomplete bundle-branch block. This is followedby two junctional escape beats with normal intra-ventricular conduction before the resumption ofconducted sinus beats showing slight degree ofincomplete right bundle-branch block. Lead aVRshows nearly similar findings. In lead I on theother hand, immediately after carotid sinus com-pression there is a sinus beat with slight aberrantconduction followed by three junctional escapebeats all showing complete bundle-branch blockbefore the resumption of conducted sinus beatswith slight aberration at the end of the strip.

Comment The observation under record (A)where the compensatory pause after ventricularectopic systoles allows for functional recovery ofthe diseased bundle, represents a tachycardia-dependent bundle-branch block. On the otherhand, the findings in record (B) obtained twoweeks later, are more interesting: the persistenceof bundle-branch block in the beat immediatelyafter carotid sinus compression though precededby an RR interval which is longer than the inter-vals during the following sinus beats with normal

FIG. 6 Case I6, record (A) shows multiple ventricular ectopic systoles revealing atachycardia-dependent right bundle-branch block during an acute myocardial infarction. Record(B) obtained two weeks later shows the effect of carotid sinus compression (CSC) whichreveals a bradycardia-dependent bundle-branch block. See text for details.

(A)

VI a

V1b4i

(B)

103 j 96 l 100 | 105 | 96 ! 102 | 102 | 96 l 100 | 99

V,cont. TC.S.C.

AVR

bradycardia-dependentT"hycardia-dependent versus,

I A, J. -1 IV,-- ---y-



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174 Nabil El-Sherif

intraventricular conduction, and the demonstra-tion of a slow junctional rhythm with bundle-branch block, represent a bradycardia-dependentbundle-branch block. It is interesting to showthe operation of two different mechanisms ofintermittent bundle-branch block in the samecase on two different occasions.

DiscussionThe occurrence of bundle-branch block whena critical heart rate is exceeded is in accord-ance with known electrophysiological charac-teristics of the conduction system. Thus animpulse arriving to the bundle-branches at anRR interval shorter than its effective refractoryperiod will be either delayed or blocked. Thisis readily explained in terms of impulse spreadthrough incompletely repolarized fibres. How-ever, bundle-branch block developing at veryshort RR intervals (whether these are ob-served to occur once as in the case of an earlycoupled supraventricular ectopic systole orrepetitively as in the case of a supraventriculartachyarrhythmia) will be explained by the timenecessary for the physiochemical processes ofrecovery (Burch, I962) and will not be con-sidered pathological. The refractory periods ofthe specialized conducting system are knownto shorten with abbreviation of the precedingcycle length (Hoffman and Cranefield, I960;Linhart, Braunwald, and Ross, I965; Moe,Mendez, and Han, i965). Usually duringtachycardia, the functional refractory periodof the bundle-branch system shortens rela-tively more than that of the AV junctionaltissue and bundle of His, permitting after afew beats the passage through that bundle-branch system again (Moe et al., I965). Incertain instances, however, the impulse con-duction may be interfered with (delayed orblocked) at the AV junctional-bundle of Hislevel before reaching the bundle-branch sys-tem, which simply means a longer effectiverefractory period at the former regions. Thiswill help us to remember that disturbances ofconduction at the AV junctional-bundle ofHis level may completely mask significantdisease at the bundle-branch system. On theother hand, bundle-branch block observed tooccur at relatively long RR intervals is patho-logical and denotes abnormal prolongation ofthe effective refractory period of the bundle-branch system.The demonstration of a cycle length-

recovery time relation stimulated variousauthors to formulate the concept of criticalheart rate in intermittent bundle-branchblock. Some even suggested that the changefrom intermittent to permanent bundle-branch block might be effected through a

constantly decreasing critical heart rate untilsuch a time as the block was no longer revers-ible (Shearn and Rytand, I953). Much evi-dence however argues against incriminationof the heart rate as the sole determinant re-sponsible for intermittent bundle-branchblock. Thus, though in some records of inter-mittent bundle-branch block a critical RRcycle could be seen that varied for no morethan a few hundredths of a second, yet inother records more overlap could usually beseen. On the other hand, bundle-branch blockat widely varying heart rates may be observedin records taken on different occasions or inthe same record under the influence of avariety of physiological manoeuvres andpharmacological agents. These and similarobservations entailed the search of other fac-tors besides a critical rate that may influenceimpulse conduction in the bundle-branchsystem. Out of these factors, the effect of vagalimpulses and momentary changes in coronaryperfusion received much attention. Vagal im-pulses were thought to act on the conductionat the bundle-branch system in a similarfashion to its established role on conductionat the AV junctional tissue. Vesell and Lowen(I963) had critically discussed the subject;however, controversy prevails not only inrelation to clinical observations (Wilson,I915; Holzmann, I943; Katz and Pick, I956;Scherf, Blumenfeld, and Yildiz, I96I) buteven in experimental and anatomical studies(Mitchell, Brown, and Cookson, I953; Crane-field, Hoffman, and Paes de Carvalho, I959;Eliakim et al., I96I; Truex, I96I). The effectof momentary changes in coronary perfusionis even more controversial. Reduced bloodsupply to the bundle-branch system wasthought to act through local metabolic andphysico-chemical changes altering the trans-membrane ionic gradient, with secondaryprolongation of the refractory period (Veselland Lowen, I963).The presence of slight overlap of the RR

cycles of normal and aberrant beats in recordsshowing tachycardia-dependent bundle-branch block does not argue against the pre-sence of a cycle length-recovery time relation.This observation, which is more commonlyseen in the presence of atrial fibrillation (Fig.I), may reflect, in fact, the sensitivity of theaction potential duration of the diseasedbundle to the possible cumulative effects ofcycle length changes. Alteration in cyclelength results in altered cell action potential.It has been found that when the heart ratesuddenly changes, it may take several beatsbefore a constant action potential is achievedfor that rate (Hoffman and Cranefield, I960).



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Tachycardia-dependent versus bradycardia-dependent

In contrast to the slight overlap of the criticalRR cycle in the same record, the demonstra-tion of bundle-branch block at widely varyingheart rates in records taken on different occa-

sions probably reflects the influence of slowlyacting parameters, such as progressive or re-

gressive ischaemic changes, that may alter theaction potential duration of the diseasedbundle-branch system.On the other hand, it is interesting to ob-

serve that most of the reports that invokedvagal influence or momentary changes incoronary perfusion especially when certainphysiological manoeuvres or pharmacologicalagents were applied, had shown either bundle-branch block occurring at relative slowing ofthe heart rate or alternatively normal intraven-tricular conduction at relative acceleration ofthe rate. This situation, termed bradycardia-dependent bundle-branch block (signifying'slower' rather than 'slow' heart rate), findsa more ready explanation through the conceptof enhanced phase-4 depolarization. It isobvious that in the interpretation of recordsshowing bradycardia-dependent bundle-branch block, the abnormality cannot be ex-

plained on the basis of impulse spreadthrough incompletely repolarized fibres as inthe case of tachycardia-dependent bundle-branch block. It has been shown howeverthat a 'slower' ventricular rate may facilitatephase-4 depolarization of automatic cells.Sufficient reduction of the diastolic membranepotential will cause reduction in amplitudeand dv/dt of action potentials initiated inautomatic cells and alteration in conduction,ranging from simple slowing to decrimentalunidirectional and bidirectional block (Singer,Lazzara, and Hoffman, I967). The abnor-malities are comparable to those that occur ifthe impulse is conducted during repolariza-tion at corresponding level of membrane po-

tential (Kao and Hoffman, 1958; Van Dam,Moore, and Hoffmnan, I963). Agents andmeans that enhance or suppress phase-4 de-polarization in the human heart can conse-

quently induce or improve conduction abnor-malities caused by this mechanism (Singer etal., I967). Thus, some of the physiologicalmanoeuvres and pharmacological agents thatwere suggested to act through their influenceon a presumed vagal control on the bundle-branch system or through momentary changesin coronary perfusion can be more reasonablyexplained through their effect on phase-4depolarization. On these grounds, the bundle-branch block appearing after carotid sinuscompression in Case i6 (Fig. 6) can beexplained by vagal-induced AV slowing withjunctional escape rhythm which permitted

the exposure of occult diastolic depolariza-tion, the latter leading to impaired conductionin the corresponding bundle-branch. Theoccurrence of enhanced phase-4 depolariza-tion and bradycardia-dependent bundle-branch block in the case two weeks afterrecords showing tachycardia-dependent blockmay be related to variations in the blood sup-ply of the diseased bundle. On the other hand,atropine used in Case I4 had probably 'over-driven' the slow diastolic depolarizationpresent and in consequence bundle-branchblock appearing at a slow rate was replaced bya narrow QRS complex when the rate wasspeeded by this drug.

In spite of the previous considerations,bradycardia-dependent bundle-branch blockis still the subject of a good deal of miscon-ception. This has been recently outlined byMassumi (I968) who has only accepted 4cases from the earlier published reports(Dressler, I959; Wallace and Lazlo, I96I;Bauer, Julian, and Valentine, I956) to whichhe added another 4 cases of his own. However,3 of his cases (Cases 2 tO 4) represented equi-vocal examples. It is interesting to observethat in his second case the diagnosis of brady-cardia-dependent block was made on theassumption that the occurrence of six con-secutive escape beats, fortuitously precededby P waves, was highly improbable; in addi-tion, the QRS configuration was that of typi-cal right bundle-branch block. Both situationsare however illustrated in Fig. 3 record (B)in the presence of an unequivocal escaperhythm. This stresses the value of the analysisof long strips for correct interpretation ofcardiac arrhythmias. As a matter of fact, if theescape rhythm in our case and in the secondcase of Massumi were of junctional origin, theaberrant intraventricular conduction willrepresent a form of bradycardia-dependentbundle-branch block involving the rightbundle-branch system. The aberration ofjunctional escape beats can be generally ex-plained on the same lines as bradycardia-dependent block (Sarachek, I970). In ourcase, the left bundle will also reveal a tachy-cardia-dependent block.

ReferencesBauer, G. E. (I964). Transient bundle-branch block.

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(I965). Bundle-branch block in acute myocardialinfarction. British Heart3journal, 27, 724.

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Cranefield, P. F., Hoffman, B. F., and Paes de Car-valho, A. (I959). Effects of acetylcholine on singlefibers of the atrioventricular node. CirculationResearch, 7, I9.

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Moe, G. K., Mendez, C., and Han, J. (I965). AberrantA-V impulse propagation in the dog heart: A studyof functional bundle-branch block. CirculationResearch, I6, 26I.

Rosenbaum, M. B., Elizari, M. V., Levi, R. J., Nau,G. J., Pisani, N., Lazzari, J. O., and Halpern, M. S.(I969). Five cases of intermittent left anterior hemi-block. American Journal of Cardiology, 24, I.

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Scherf, D., Blumenfeld, S., and Yildiz, M. (I96I).Experimental study on ventricular extrasystolesprovoked by vagal stimulation. American HeartJournal, 62, 670.

Shearn, M. A., and Rytand, D. A. (I953). Intermittentbundle-branch block. Observations with specialreference to the critical heart rate. Archives of In-ternal Medicine, 9I, 448.

Singer, D. H., Lazzara, R., and Hoffman, B. F. (I967).Inter-relationships between automaticity and con-duction in Purkinje fibres. Circulation Research, 21,537.

Truex, R. C. (I96I). Comparative anatomy and func-tional considerations of the cardiac conductionsystem. In Symposium on the Specialized Tissues ofthe Heart, pp. 22 and 36. Ed. by A. P. de Carvalho,W. C. de Mello, and B. F. Hoffman. Elsevier Pub-lishing Company, New York.

Van Dam, R. T., Moore, E. N., and Hoffman, B. F.(I963). Initiation and conduction of impulses inpartially depolarized cardiac fibers. AmericanJour-nal of Physiology, 204, I133.

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Wallace, A. G., and Lazlo, J. (I96I). Mechanisms in-fluencing conduction in a case of intermittentbundle-branch block. American Heart journal, 6i,548.

Wilson, F. N. (19I5). A case in which the vagus influ-enced the form of the ventricular complex of theelectrocardiogram. Archives of Internal Medicine,I6, ioo8.

Requests for reprints to Dr. Nabil El-Sherif,Cardiology Department, Faculty of Medicine,Cairo University, Cairo, Egypt, U.A.R.



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