etiology right bundle-branch block in patients undergoing ... fileetiology of right bundle-branch...

Etiology of Right Bundle-Branch Blockin Patients Undergoing Total Correction

of Tetralogy of FallotBy HENRY GELBAND, M.D., ALBERT L. WALDO, M.D., GERARD A. KAISER, M.D.,

FREDERICK 0. BOWMAN, JR., M.D., JAMES R. MALM, M.D.,AND BRIAN F. HOFFMAN, M.D.

SUMMARYThe electrocardiographic (ECG) pattern of right bundle-branch block (RBBB) oc-

curs routinely in patients after open-heart surgery for tetralogy of Fallot (TF). Todetermine the etiology of the RBBB pattern, 14 patients with TF, seven with ventricularseptal defects (VSD), and one with pulmonary stenosis (PS) were studied duringand after cardiac surgery. Bipolar electrograms from 10 selected right ventricular epi-cardial sites were recorded simultaneously with an ECG. Records were obtained beforeand immediately after vertical right ventriculotomy, after infundibular resection, andafter repair of a ventricular septal defect (VSD). The vertical ventriculotomy alonewas always associated with significant prolongation of the time of epicardial activationonly to the recording sites lateral to the incision with prolongation of the QRScomplex by an average of 39 msec, and with the appearance of an RBBB ECGpattern. Infundibular resection and VSD repair were not associated with any changesin the electrophysiologic parameters measured. A retrospective analysis of 251 patientswith TF, VSD, and PS revealed a 100% incidence of RBBB pattern in the electrocardio-grams of only those who had undergone ventriculotomy. It can be concluded that theRBBB pattern seen postoperatively in patients with TF is due to changes in rightventricular activation secondary to the vertical ventriculotomy.

Additional Indexing Words:Vertical ventriculotomyRight ventricular activation timeSpecialized conduction system

T HE electrocardiographic pattern of rightbundle-branch block (RBBB) invariably

follows total surgical correction of tetralogy ofFallot (TF).1 4 However, to date there is nodirect physiologic evidence concerning theetiology of this RBBB pattern. RBBB has also

From the Departments of Pharmacology andSurgery, The College of Physicians and Surgeons ofColumbia University, and the Surgical Service, ThePresbyterian Hospital, New York, New York.

Supported in part by research grant HE 12738 fromthe National Heart and Lung Institute, U. S. PublicHealth Service. Work was performed during Dr.Gelband's tenure as Special Postdoctoral ResearchFellow (HE-42457) from the National Heart andLung Institute and during Dr. Waldo's tenure as aJohn Polachek Medical Research Fellow. Dr. Waldo

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Congenital heart diseaseCardiac surgery

been noted after surgical correction of ventric-ular septal defects (VSD )4-6 and infundi-bular pulmonic stenosis (PS ) 7 Investigatorshave attributed the RBBB pattern observedfollowing surgical repair of VSD to operativetrauma to the right main bundle branch.6 The

and Dr. Kaiser are Otto G. Storm Established Investi-gators, American Heart Association.

Dr. Gelband's present address: Department ofPediatrics, University of Miami School of Medicine,Miami, Florida.

Address for reprints: Albert L. Waldo, M.D.,Department of Pharmacology, College of Physiciansand Surgeons of Columbia University, 630 West 168thStreet, New York, New York 10032.

Received June 22, 1971; accepted for publicationAugust 3, 1971.

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ETIOLOGY OF RBBB

etiology of this electrocardiographic patternfollowing correction of PS was thought to bedue to infundibular resection of the subpul-monic area with interruption of distal ramifi-cations of the right bundle branch.7 However,Coggin and associates, in a publishedabstract,8 suggested that the RBBB seenfollowing VSD repair was not due to traumato the main right bundle branch but was adirect result of interruption of the peripheralventricular conduction system secondary tothe right ventriculotomy.

It had been assumed from electrocardio-graphic observations, from the clinical studieson other forms of congenital heart disease justcited,4- and because the anatomic course ofthe right bundle branch9' 10 is similar in TFand VSD, that the RBBB pattern observedpostoperatively in TF was most likely due tosurgical trauma to the proximal right bundlebranch.11 12 Because no physiologic data areavailable concerning the etiology of the RBBBpattern observed postoperatively in TF tosupport the conclusions drawn from theanatomic and clinical studies, and becauseright ventriculotomy, infundibular resection,and direct closure of the VSD have all beenimplicated in the etiology of the RBBB, andall are necessary in the surgical repair of TF,we have conducted a systematic physiologicinvestigation to determine which is the primefactor in the genesis of this electrocardio-graphic manifestation.

MethodsAll patients were studied during cardiac

surgery. The experimental protocol varied slightlyfor each patient and was determined by thenature and requirements of the surgical proce-dure. A summary of pertinent clinical data on the22 patients studied is provided in table 1. Theages of the patienits studied ranged from 3 to 19years, the mean age being 9 years. All patientsunderwent cardiovascular catheterization andcardiac angiography prior to surgery. Fourteenipatients had TF, seven had VSD, and one patienthad infundibular and pulmonary valve stenosis.Of the seven patients with VSD, three hadundergone pulmonary artery banding in infancy,and therefore at the time of repair of their lesiontheir condition hemodynamically resembled TF.The VSD of six patients was corrected via a rightCirculation, Volume XLIV, December 1971

ventriculotomy and the last patient's lesion (case21) was corrected throuigh a right atriotomy. Allhad membranous or suberistal VSD. Electrocardio-grams (ECG) recorded in the operating roomprior to thoracotomy were comparable in allrespects to those recorded 1 to 3 days prior tosurgery. All patients had a QRS duration of 80msec or less prior to surgery. RBBB was defined1':as (1) QRS duration greater than 100 msec, (2)wide slurred S in leads I anid V;. anid (3) slurredR' iin leads IIl,aVI , atid V]

All studies were performed during the period ofcardiopulmonary bypass. Each patient wasstudied duiring spontaneous atrial rhythm orduring atrial rhythm produced by pacing the atriathirough a bipolar electrode placed in the regioniof the sinoatrial node.14 The atria were paced ata rate slightly in excess of the spontanieous rate.Stimuli were provided by a special digitaltlhreslhold stimulator (Medtronics 1187). All leadsin contact xvith the heart were isolated both fromground an-d from the recording instruments byisoation transiformers. Using a hand-held probecontaining three silver electrodes,'4 bipolar electrograms were recorded from 10 selected sites onthe epicardial surface of the right velntricle (fig.1). Recordings were obtained befole aniy suirgical

Figure 1Anterior aspect of the human heart showing the 10reight ventricular epicardial recording sites. Dashedline indicates vertical ventriculotomy inicision. Aonaorta, PA =pulmonary artery, RA =right atrium, RV

right ventricle, LV = left ventricle.

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Table 1Clinical Data for 22 Patients Studied

Age(yr);

atient Lesion sex

1 TF 9m

2 TF 6m

3 TF 3M

4 TF 13M

TF 6m

6 TF 10m

7 TF 11m

8 TF 8F

9 TF 15

10 TF 9M

11 TF 15

12 TF 9F

13 TF 19m

14 TF 7F

15 VSD 7PA band F

16 VSD 7PA band M

17 VSD 9PA band M

18 VSD 8F

19 VSD 12M

20 VSD 7M

21* VSD 12F

22 PS 17F

Preanestheticmedication (mg)

S 40MS 3

S 40MS 2

S 40MS 2S 100MS 6

S 50MS 3

S 50m S 5-S 100A 0.4S 30

MS 2S 100

MS 8S 50

MS 3S 100A 0.4S 50A 0.3S 150A 0.4S 40

MS 3S 50

MS 5S 50

MS 3S 50

MS 3S 50

MS 3S 60

MS 4S 50A 0.3S 65

MS 5S 100

Anesthesia (mg) TemperatureInduction Maintenance (°C)

C

SDC 15HCNP 125SDC 40CSDC 30cSDC 40SDC 200

SDC 30

SDC 60CSDC 40CSDC 80P 350SDC 25CSDC 100P 250SDC 20CSDC 40CC

C

NHH 32

H 32

H 36

H 32

H 35

H 36

H 36

H 37

H 32

NHH

36

36

H 33

H 30

H

H

37

37

H 37

SDC 30

C

C

SDC 40CP 175SDC 100

H 37

H 37

NHH

36

34

H 36

*No ventriculotomy.Abbreviations for lesions: TF = tetralogy of Fallot; VSD = ventricular septal defect; PA

band = pulmonary artery banding; PS = pulmonic stenosis (valve and infundibular).Abbreviations for drugs: A = atropine; C = cyclopropane; H = halothane; MS = morphine

ulfate; N = N20; P = thiopental (Pentothal); SDC = succinylcholine; S = scopolamine.

manipulation upon the heart was performed andthen after each of the following surgicalprocedures, in order: (1) after the vertical right

ventriculotomy (an incision usually about 4 to 6cm long) which always was made between sites 1to 3 and 4 to 6 (fig. 1), (2) after subpulmonic

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infundibular resection, (3) after repair of theVSD, and (4) after the repair of the ventriculoto-my. Patients with just a VSD of course had nosubpulmonic infundibular resection, and thepatient with infundibular and pulmonary valvestenosis had no repair of a VSD. During fourstudies, the surgical repair required transientcross clamping of the aorta. Recordings afterperiods of aortic cross clamping were made aftera period of reperfusion of the heart such thatthere was no evidence of conduction abnormal-ities related to the recent cross clamping.The electrograms were monitored simultaneous-

ly with ECG leads I, aV]p, and either aVL or aVF on a switched-beam oscilloscope (Electronicsfor Medicine model DR-12) and recorded onphotographic paper moving at a speed of 100mm/sec. ECGs were recorded at a sensitivity of 2cm/mv. During periods of data collection, bodytemperature, measured from the retrocardiacportion of the esophagus or from the rectum,varied from patient to patient as determined bythe requirements of the surgical procedure. Therange was 32 to 37°C for all patients studiedexcept one in whom the temperature was 300Cduring the procedure. For each patient, allrecordings were made at the same temperature.The relative sequence of activation of the rightventricular recording sites was determined bymeasuring the interval from the earliest recordedonset of the QRS complex in the bipolarelectrograms recorded from each site. Measure-ments of all intervals were made from the recordsusing a vernier measuring device having anaccuracy of + 1 msec.To obtain data on the incidence of an RBBB

pattern recorded following open-heart surgery atour institution, in a retrospective 4-year study(January 1967 to December 1970), the preopera-tive and postoperative ECGs of patients with thefollowing defects were analyzed: TF, VSDrepaired through a ventriculotomy, VSD repairedvia an atriotomy, and PS repaired from thepulmonary artery or through a right ventriculoto-my.

Results

Relationship of RBBB Pattern to RightVentriculotomyAn electrocardiographic pattern of RBBB

occurred in all patients in whom right verticalventriculotomy was performed as part of thesurgical repair. ECGs for a representativepatient recorded 2 days before and 9 daysafter surgery are shown in figures 2 and 3.Associated with the appearance of the RBBBpattern in this patient, the QRS complexCirculation, Volume XLIV, December 1971

increased 40 msec in duration. An averageincrease of 39 msec in QRS duration occurredin all patients who had a ventriculotomy. It isof interest to note that the greater postopera-tive increases in QRS duration occurred inpatients with the narrower QRS complexespreoperatively (table 2). In each instance inwhich the RBBB pattern was recorded afterventriculotomy, prolongation of the QRScomplex was associated with the appearanceof a slurred S wave in ECG lead I and an R'deflection in lead aVR. Patient 21, whounderwent repair of her VSD through theright atrium, and hence did not requireventriculotomy, did not develop a postopera-tive ECG pattern of RBBB. A transientincrease in QRS duration of 10 msec didoccur, but the duration returned to thepreoperative value within 3 days.

Epicardial Activation Times in Relationto Ventriculotomy

Activation time measured from onset of theearliest deflection of the QRS complex to eachof the 10 right ventricular epicardial recordingsites during the various stages of repair for arepresentative patient with TF is shown infigure 4. Activation times of all 10 sites duringcontrol recordings (panel A) in this patientvaried from 37 to 43 msec. Immediately afterthe vertical ventriculotomy (panel B), therewas little or no change in the time ofactivation of sites 1, 2, 3, and 10. However,time of activation of all sites lateral to theventriculotomy, i.e., sites 4 to 9, increased by56 to 61 msec. Concomitant with this increasein activation times there was a change in theQRS morphology and duration. The initialQRS duration of 78 msec increased to 118msec. Associated with the changes in activa-tion time following ventriculotomy was anobvious slurring of the S wave (panel B),which produced the increase in the durationof the QRS complex. Panels C and Drepresent activation times of the epicardialsites after resection of the subirnfundibularpulmonic area and repair of the VSD,respectively. Neither a further increase inactivation time of any of the 10 epicardial sitesnor changes in the QRS morphology or

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-.

aR

i

Lq L@--

P~~~~r.paTiw

AVF

J1 mV

.2 secFigure 2

ECG of patient 6 taken 2 days prior to surgery. Right-axis deviation is present. Note that theQRS interval measures 80 msec and there is no evidence of right bundle-branch block onlimb or precordial leads.

duration occurred after these latter twosurgical procedures. Similar increases in acti-vation times of sites 4 to 9 occurred in allpatients who had a right ventriculotomy as

part of their surgery (table 3). Activationtimes prolonged by 34 to 68 msec, whereasactivation time of sites 1, 2, 3, and 10remained essentially unchanged throughoutsurgery. Prolongations of the QRS complexand changes in QRS morphology were re-

corded in all these patients only immediatelyafter the ventriculotomy.An analysis of the activation times in the

one patient who had VSD corrected throughthe right atrium is shown in figure 5. In panelA, control activation times are noted. Activa-tion times to the epicardial sites ranged from

29 to 33 msec. After repair of the VSD (panelB) activation times to the epicardial sites weresimilar to control values. They ranged from 29to 35 msec. Lead-I QRS complexes before andafter repair of the VSD are also shown. Notethat no changes occurred in QRS morphologyor duration.

Epicardial Activation Time in Relationto the QRS ComplexA representative example of the changes in

QRS configuration and duration which occur

after ventriculotomy is shown for patient 9with TF (fig. 6). Panel A is a lead-I QRScomplex recorded prior to ventriculotomy.Lead-I QRS morphology (rS) is typical of a

patient with TF.13 QRS duration is 60 msec.

Activation of epicardial sites 1 to 10 occurredCirculation, Volume XLUV, December 1971

VI

v2,A-!__,?L

V3

V4

V5

V6

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1'II

AVR

AV,

AVF *FSs

v~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

V3

V4 *',

V5

j mv.2 sec

Figure 3ECG of the same patient as in figure 2, taken 9 days after surgery. QRS interval now hasincreased to 120 msec. A prominent slurred S is present in leads I and aVL, and a slurred Rin lead aVR. Precordial lead V1 has the typical broad slurred R', and lead V6 has the slurredS wave observed in RBBB.

between 26 and 39 msec after the beginningof the inscription of the QRS complex. Panel Bshows the lead-I QRS complex immediatelyafter the vertical ventriculotomy. The durationof the QRS complex prolonged to 118 msecand was associated with the appearance of amarkedly slurred S wave. Activation times ofsites 1, 2, 3, and 10 were unchanged fromcontrol. Activation times of sites 4 to 9 nowwere prolonged to 64 to 77 msec whencompared to the control activation times. Notethat sites 4 to 9 are activated during theinscription of the slurred S wave of the QRScomplex.

In contrast, figure 7 demonstrates the timeof activation of the right ventricular epicardialCirculation, Volume XLIV, December 1971

sites superimposed on a lead-I QRS complexbefore and after surgical repair of a VSDwhich was corrected without a ventriculot-omy. QRS morphology was not altered by thesurgical procedure; the duration of the QRScomplex (78 msec) was identical before andafter total correction of the lesion; andepicardial activation times to all sites beforeand after the repair did not significantly differ,i.e., they ranged from 29 to 33 msec beforeand 29 to 35 msec after surgery.

Retrospective Analysis of Preoperativeand Postoperative ECG

Preoperative and postoperative ECGs of allpatients with the anatomic diagnosis of TF,VSD, and PS during the 4-year period

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Table 2Electrocardiographic Data

QRS duration in ECGQRS (msec) Postoperative ECG RBBB

Patient Lesion V axis RVH Preop. Postop. Slurred Si R' aVF pattern

1 TF + +120 ± 80 110 4- + ±2 TF + +120 + 80 110 + + +3 TF + +4110 + 80 120 + + +4 TF + +120 + 80 120 + + +4 TF + + 121)0 + sO 120 + + +6 TF + +150 + 80 120 + + +6 TF + +110 + 70 120 + + +7 TF + +113 + 80 110 + + +8 TF +- +100 + 70 120 + + +-9 TF + +4150 + 75 120 + + +10 TF + +130 + 80 120 + + +11 TF + +110 + 80 110 + + +12 TF + +120 + 70 115 + + +13 TF + +135 + 80 120 + + +14 TF + +120 + 70 115 + + +15 VSD, PA band + +110 + 80 120 + + +16 VSD, PA band + +105 + 70 11.5 + + +17 VSD, PA band + +105 + 80 120 + + +18 VSD + + 60 - 60 100 + + +19 VSD + + 75 60 110 + + +20 VSD + 0 - 60 115 + + +21 VSD - 0 - 70 80 - - -22 PS + +120 + 75 115 + + +

Abbreviations: those for lesions same as in table 1; V = ventriculotomy; + -present;-not present; RBBB - right bundle-branch block; RVH = right ventricular hypertrophy.

Table 3Epicardial Activation Times and QRS Duration (Msec*) in Representative Casesfollowing Surgical Procedures

Activation times* at recording sites QRSLesion 1 2 3 4 5 6 7 8 9 10 duration

TFt C 39 36 37 44 42 42 45 44 44 44 76After V 41 39 36 104 99 96 102 101 99 42 115After I 41 42 39 106 102 102 103 99 101 44 118After VSD repair 39 41 40 103 102 103 99 97 97 40 117

VSD withPA bandt C 40 42 38 39 41 41 43 44 45 44 78After V 38 39 41 90 94 91 93 95 90 42 117After I 42 41 42 95 96 94 94 95 93 4,5 121After VSD repair 42 43 42 94 99 92 93 93 91 45 122

VSDt C 35 35 34 38 37 36 37 37 36 36 68After V 34 34 33 86 89 90 92 92 94 38 105After VSD repair 36 38 38 89 92 91 90 91 93 38 108

VSDt C 31 30 29 33 29 29 31 31 33 31 70After VSD repair 33 30 29 34 31 30 35 34 34 32 78

PSt C 31 29 29 31 31 30 28 30 30 34 76After V 34 31 34 68 72 74 71 74 76 34 110After I 34 32 33 69 73 73 72 74 76 34 113

*Time of activation in milliseconds from onset of first deflection of the QRS complex.fLesion corrected with ventriculotomy.tLesion corrected without ventriculotomy.Abbreviations: those for lesions same as in table 1; C = control; V = ventriculotomy; I

infundibular resection; VSD = ventricular septal defect.

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A

ECGI EG I

100 msec

Figure 4Effect of a vertical ventriculotomy on the activationtimes to the right ventricular epicardial recording sitesin a representative patient (case 11). Each panel showsa schematic drawing of the right ventricle with thetime of activation to each site illustrated. Below theright ventricular drawing is an electrocardiographicWead-I QRS complex recorded during the period ofmeasurement of the activation times. (A) Activationtimes made prior to the ventriculotomy ranged from37 to 43 msec for the 10 epicardial sites. The QRSinterval is 78 msec. (B) Immediately after the ven-triculotomy (dashed line), epicardial activation timesto sites 1, 2, 3, and 10 remained unchanged while ac-

tivation time to sites 4 to 9 significantly increased(range 99 to 103 msec). The QRS complex has pro-

longed to 118 msec, associated with the appearance ofa slurred S wave. (C and D) Activation times afterinfundibular resection and repair of the VSD. Thereare no further changes in epicardial activation time,QRS duration, or morphology after these procedures.Time scale: 100 msec as indicated.

(1/1/67 to 12/30/70) were analyzed todetermine the incidence of a postoperativeCirculation, Volume XLIV, December 1971

ECGI l ECG I

100 msec

Figure 5

Right ventricular epicardial activation times after re-pair of VSD via the right atrium (case 21). Each panelshows a schematic drawing of the right ventricle withthe time of activation to each site illustrated. Belowthe right ventricular drawing is an electrocardiographiclead-i QRS complex recorded during the period ofmeasurement of the activation times. (A) Activationtimes to the 10 epicardial sites prior to VSD repair.These activation times ranged from 29 to 33 msec.The QRS interval measured 78 msec before repair ofthe VSD. (B) Activation times to the 10 epicardialsites are essentially unchanged (29 to 35 msec) afterrepair of the VSD. The morphology and duration (78msec) of the QRS complex are also unchanged. Timescale: 100 msec as indicated.

RBBB pattern (table 4). One hundred thirty-nine patients with TF, 55 with VSD, and 12with infundibular PS had open-heart surgeryin which total correction of their lesionsnecessitated a vertical ventriculotomy. Noneof these patients had an RBBB patternrecorded in the preoperative ECG, but alldeveloped an RBBB pattern following surgery.On the other hand, there were 26 patientswith VSD and 19 with valvular PS who hadsurgical correction either from a right atrialapproach (VSD patients) or via the mainpulmonary artery (PS patients); none of thesepatients developed ECG evidence of a RBBBpattern following surgery. Thus the incidenceof an RBBB pattern following right ventricu-lotomy was 100%, but was 0% when noventriculotomy was performed, despite thefact that patients with similar anatomic lesionsare included in both groups.

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Table 4

Incidence of a Right Bundle-Branch Block Pattern in Postoperative Electrocardiograms:Retrospective and Prospective Study

PatientsNumber

Lesion Present study Retrospective Total V wwith RBBB

TF 14 139 153 153 1(0VSD 6 .. 61 61 100VSJ)* 1 26 27 0 0PS 1 12 13 13 100PSt 0 19 19 0 0

*VSD corrected via atriotony. tValvotomy only.Abbreviations for lesionis same as iil table 1; RBBB = right bundle-branch block pattern; V-

ventriculotomy.

DiscussionThe electrocardiographic pattern of RBBB

which is recorded postoperatively from pa-tients with VSD has been attributed mostoften to surgical damage to the proximal rightbundle branch,4 since the bundle branch lies

B

rn-F-,9 1

o 2040 60 80msec

o10

0 20 40 60 80100 120msec

Figure 6

Temporal relation of the time of activation of the 10epicardial sites plotted on an electrocardiographic lead-1 QRS complex before (A), and immediately after (B),ventriculotomy in patient 9. (A) The QRS duration is60 msec. Note that activation times to the 10 epi-

cardial sites occurred between 26 and 39 msec. (B)After the ventriculotomy a slurred S wave appearedand was associated with an increase of the QJRS dura-tion to 118 msec. Activation times to sites 1, 2, 3, and10 are unchanged. However activation times to sites4 to 9 have prolonged to 64 to 77 msec and occur dur-ing the inscription of the slurred S wave. Time scaleas indicated.

on the posterior-inferior aspect of the VSD.10Anatomic studies of the ventricular conduct-ing system in TF demonstrated that in thislesion the conducting system is also posi-tioned in the posterior-inferior portion of thedefect.9' 1 Hence the RBBB which invariablyfollows surgical correction of TF has beenattributed to injury to the proximal conduct-ing system occurring when the VSD wasrepaired."' 12 On the other hand, Esmond andothers,'6 studying the peripheral ramificationsof the cardiac conducting system in thehuman heart, demonstrated that an operativeincision in the anterior wall of the rightventricle may result in RBBB due to interrup-tion of the Purkinje fiber network distal to themoderator band. Fisher and associates17 de-scribed changes in the postoperative ECG ofpatients who had their VSD corrected and feltthat ventriculotomy was crucial to the de-velopment of an RBBB pattern. Coggin andothers8 supported the pathologic study ofEsmond's group which described for allpatients undergoing VSD repair the onset ofan RBBB pattern at the precise moment ofincision of the right ventricle.

Indirect support for our observations isprovided by experimental studies on caninehearts.18-20 These studies have demonstratedthat right ventricular activation in the dognormally begins in the lower and anteriorapical area adjacent to the anterior interven-tricular groove. Activation then proceedslaterally over the epicardial surface. Genenderand associates'8 have shown that when a


A

ECG I

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ECGI

0 20 40 60 80

Figure 7

Temporal relation of the time of activation of the 10epicardial sites plotted on an electrocardiographic lead-I QRS complex in patient 21 who had a VSD repairedwithout ventriculotomy (i.e., via a right atriotomy).Prior to VSD repair activation times to the 10 epi-cardial sites occurred 29 to 33 msec after the onset ofthe QRS complex (A). After repair of the VSD, activa-tion times are essentially unchanged, 29 to 35 msec(B). Note also that there was no change in QRS dura-tion or morphology. See text for further discussion.Time scale as indicated.

ventriculotomy is made lateral to the free-running Purkinje fibers, there is a consistentalteration in the sequence of activation of theright ventricular epicardium as well as aprolongation in the total time required forright ventricular depolarization. However,there were no changes resembling RBBB inthe ECG. Hill and others,20 studying the timeand sequence of right ventricular epicardialactivation in the dog, demonstrated that inexperimental and spontaneous RBBB there isa later activation of the right ventricularepicardial sites than in normal dogs.

It is clear from our physiologic data that thevertical ventriculotomy alone was responsiblefor the occurrence of the RBBB pattern in the

ECGs in our cases. Furthermore, the retro-spective comparison of the ECGs of patientsundergoing TF repair, correction of VSDswith or without a ventriculotomy, or PS repairwith or without a ventriculotomy at ourinstitution also indicates that the ventriculot-omy was responsible for the RBBB pattern inthese patients as well. If the repair of the VSDper se results in trauma to the right bundlebranch with consequent interruption of theright bundle branch, then one would expectan equal or similar incidence of RBBBfollowing VSD repair regardless of the surgi-cal approach, but clearly this is not true. Anincidence of RBBB of 100% in patients withVSD corrected via a ventriculotomy and anincidence of 0% when no ventriculotomy wasnecessary support our physiologic data andthe earlier studies of Coggin8 and Esmond16and their associates.

It is of paramount importance to emphasizethat all 21 of our patients who requiredventriculotomy developed the characteristicelectrocardiographic pattern of RBBB. QRSduration increased by about 40 msec mainlydue to the appearance of slow terminal rightventricular depolarization (slurred S wave inlead I). This occurred simultaneously withthe termination of the ventriculotomy. Activa-tion time of sites that were lateral to theventriculotomy significantly prolonged (34 to68 msec) while activation time of those sitesthat were medial to the ventriculotomyremained unchanged. Since activation time ofthese latter sites remained unchanged, weassume that no further injury to the rightventricular conduction occurred with furthersurgical procedures. From the studies byDurrer and co-workers2' on the normalsequence of ventricular activation )f thehuman heart, if trauma to the proximal rightbundle branch had occurred at any timeduring surgery, we would have expected aprolongation in activation time of all sites onthe right epicardial surface, not just those siteslateral to the ventriculotomy. The studies ofHill and others20 on the canine heart alsosupport our thesis.


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We have demonstrated that when verticalventriculotomy is employed during cardiacsurgery for TF, VSD, and PS, the ventriculot-omy is the prime factor responsible for theelectrocardiographic pattern of RBBB seenpostoperatively. Careful examination of theother reported examples of damage to the A-Vconduction system is instructive. Rosenbaumand associates12 reported four cases of RBBBand left anterior hemiblock following correc-tion of TF. They suggested that both the rightbundle branch and left anterior branch weretraumatized at surgery at the time of repair ofthe defect in the ventricular septum. In lightof our data, we would suggest a differentinterpretation, namely, that the RBBB patternresulted from the ventriculotomy and the leftanterior hemiblock may have resulted fromtrauma to a portion of the left bundle branch.In fact, it is of interest that in one of thesecases the left anterior hemiblock was transientwhile the RBBB remained. In this case, theright ventriculotomy probably was responsiblefor the RBBB, and edema for the hemiblock.As the edema regressed, the left anteriorhemiblock resolved. If indeed there wassurgical interruption of the right bundle andleft anterior division, then both electrocardio-graphic manifestations should have remained.Our data suggest that it may be necessary to

reconsider the significance of the criteriaemployed in clinical cardiology to diagnoseRBBB. It is apparent from our studies, andfrom the conclusions of Scherlis and Lee5 andScherf,22 that these criteria may not bediagnostic of right bundle-branch block. Wehave shown that a typical electrocardiographicpattern of RBBB can occur without injury orimpairment of conduction over the main rightbundle branch. A vertical ventriculotomy canresult in a significant delay of right ventricularactivation which is capable of producing wideslurred S waves in leads I and V6, an R' inleads III, aVR, and VL, and marked prolonga-tion of the QRS duration.The conclusions from our data are of

important prognostic value because patientswho undergo corrective open-heart surgerywhich includes a ventriculotomy develop a

RBBB pattern which is not due to injury tothe main right bundle. Therefore, if leftbundle-branch block occurs at a future time,these patients will not have complete heartblock since the main right bundle branch isstill intact.

References1. GRFFiTHs SP, MALM JR: Medical problems in

total correction of tetralogy of Fallot. ProgrCardiov Dis 8: 64, 1965

2. ALLiSON DM, GuNNI AJ, HAMILL J, MODYSM: Fallot's tetralogy: A postoperative study.Circulation 28: 525, 1963

3. KHOURY GH, DUSSHANE JW, ONGLEY PA: Thepreoperative and postoperative vectorcardio-gram in tetralogy of Fallot. Circulation 31: 85,1965

4. ZIMMERMAN HA, MARTINS DE OLEIRA J,NOGUEIRA C, MENDELSOHN D, KAY EB: Theelectrocardiogram in open heart surgery:Disturbances in right ventricular conduction. JThorac Cardiovasc Surg 36: 12, 1958

5. SCHERLIS L, LEE YC: Right bundle branch blockfollowing open heart surgery. Amer J Cardiol8: 780, 1961

6. BRIsTow JD, KASSEBAUM DC, STARR A,GRIswoLD HE: Observations on the occur-rence of right bundle branch block followingopen repair of ventricular septal defects.Circulation 22: 896, 1960

7. KITrLE CF, SANTOs EM, DIMOND EG: Persis-tent right bundle branch block due topulmonic valvotomy and infundibulectomy.Amer Surg 22: 80, 1956

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11. KuLBEurus HE, COYNE JJ, HAILLlIE-SMIIuKA: Conduction disturbances before and aftersurgical closure of ventricular septal defect.Amer Heart J 77: 123, 1969

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HOFFMAN BF: Effects of right ventriculotomyupon activation of the epicardial surface of thecanine right ventricle. Circulation 27: 828,1963

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O. BOWMAN, JR., JAMES R. MALM and BRIAN F. HOFFMANHENRY GELBAND, ALBERT L. WALDO, GERARD A. KAISER, FREDERICK

Correction of Tetralogy of FallotEtiology of Right Bundle-Branch Block in Patients Undergoing Total

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