Incomplete Right Bundle-Branch Block

An Electrocardiographic Enigma and Possible Misnomer

By E. NEIL MooRE, D.V.M., PH.D., JoHN P. BOINEAU, M.D.,
AND DONALD F. PATTWSON, D.V.M., D.Sc.
With James Alexander, M.D., and A. J. Kennel, M.D.

SUMMARY
Incomplete right bundle-branch block (IRBBB) usually is thought to be associated
with abnormalities of the peripheral Purkinje system. This paper discusses the results
of a study of six dogs from the same family and three nonrelated dogs with congenital
IRBBB. Cardiac catheterization data were normal, and no evidence or history of car-
diac disease was found before or after death. The depolarization sequence of ven-
tricular epicardial activation was determined, and delays in right ventricular (RV)
epicardial activation times were observed. Multipoint intramural electrodes were used
to study intramural activation of the ventricular septum and free walls. The "electrical
thickness" near the base of the RV mass was more than double that of the normal RV
mass (9 vs 4 mm). Conduction along the right bundle branch (RBB) was analyzed
during cardiopulmonary bypass, and electrograms recorded simultaneously from six
sites along the RBB demonstrated that conduction velocity down the bundle was nor-
mal. The normal time of activation of the endocardial RV Purkinje fibers demonstrated
that conduction in the right peripheral Purkinje system also was normal. Therefore,
IRBBB in these dogs did not result from conduction abnormalities within the RV
specialized conduction system. Interestingly, six of these dogs were members of the F1
generation from a mating of a female beagle with pulmonary stenosis and a male
beagle with ventricular septal defect. Both defects as well as IRBBB were observed
in the F2 generation. The present findings suggest that IRBBB may be a developmental
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variation in thickness of the RV free wall rather than an abnormality of the RV con-
duction system in cases without apparent heart disease. The developmental variant
appears to have a genetic basis.

Additional Indexing Words:

Cardiac developmental variant Conduction delay Focal hypertrophy
Parietal block Right ventricular hypertrophy

INCOMPLETE RIGHT bundle-branch clinical and experimental conditions raises a

block or "parietal block" describes the
electrocardiographic abnormality associated
with a wide variety of heart diseases in which
it is presumed that an abnormality exists in
the peripheral Purkinje conduction system.
However, the fact that the same electrocardio-
gram is recorded in a variety of dissimilar
From the Comparative Cardiovascular Studies Unit,
School of Veterinary Medicine, University of Pennsyl-
vania, Philadelphia, Pennsylvania, and the Depart-
ments of Pediatrics, Medicine, and Surgery, Duke
University Medical Center, Durham, North Carolina.
Supported in part by grants from the American
Heart Association and U. S. Public Health Service
678
question about the specific etiology underly-
ing incompflete right bundle-branch block
(IRBBB). -.-10 There also have been a number
of papers pi ublished in which individuals with
electrocardii ographic evidence of IRBBB have
been found to have no underlying cardiac
grants HE-4885, HE-10995, HE-11307, HE-5372, and
HE-11309.
Address for reprints: Dr. E. Neil Moore, Compara-
tive Cardiovascular Studies Unit, School of Veterinary
Medicine, University of Pennsylvania, Philadelphia,
Pennsylvania 19104.
Received April 5, 1971; revision accepted for
publication July 1, 1971.
Circulation, Volume XLIV, October 1971
 INCOMPLETE RIGHT BUNDLE-BRANCH BLOCK
disease as demonstrated by clinical studies
and by postmortem histologic studies.1-' 5
The present paper concerns electrophysio-
logic investigations on a family of dogs with
definite electrocardiographic evidence of
IRBBB in which no evidence of cardiac
disease could be demonstrated, either ante-
mortem or postmortem. Evidence is presented
that the pattern of IRBBB resulted not from
conduction abnormalities within the atrioven-
tricular specialized conduction system, but
rather was due to focal hypertrophy of the
right ventricle which was a congenital de-
velopmental variant.
Materials and Methods
Genetic Studies
In the course of genetic studies of cardiovasc-
ular malformations in the dog, a female beagle
with hereditary valvular pulmonic stenosis16 was
mated to a male beagle with a small subaortic
ventricular septal defect. These dogs probably
were not closely related as they were obtained
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679
from sources that were geographically distant
from each other. No pedigree information was
available however. The female had an electrocar-
diogram consistent with a mild degree of right
ventricular hypertrophy (right ventricular pres-
sure 72/0, main pulmonary artery pressure
26/18). The electrocardiogram of the male was
within normal limits.
This mating produced seven pups (fig. 1),
none of which had evidence of structural
malformation of the cardiovascular system by
physical examination, thoracic radiography, car-
diac catheterization, or angiocardiography. Six of
the seven dogs were submitted to necropsy
examination and were found to have no gross
evidence of cardiovascular disease. Despite the
absence of gross structural abnormalities, all
members of the litter had electrocardiographic
patterns of the incomplete right bundle-branch
block (IRBBB) type. In three dogs, the pattern
was well developed, and the QRS interval was
near the upper limit of normal for the dog (0.07
sec). In four others, the pattern was less
developed but the spatial orientation of the QRS
forces was similar to that of dogs with fully
developed IRBBB. Terminal QRS forces were

+ + + + + * *

El Normal Male + Neonatal Deoth NO ECG

0 Normal Femole
* Sacrificed f or Study

em IRBBB (well - developed)

VSD
PS
=

=
Ventricular Septal Defect
Valvulor Pulmonic Stenosis
IROBB (lesser- degree)
Figure 1
Female beagle with pulmonic stenosis and a male beagle with a ventricular septal defect pro-
duced seven pups with varying degrees of incomplete right bundle-branch block (IRBBB)
but no gross cardiovascular malformations. Both pulmonic stenosis and ventricular septal
defect as well as IRBBB were observed in the F2 generation. See text for full description.
Circulation, Volume XLlV, October 1971
 680
directed ventrally, cranially, and to the right,
producing R' waves in AVR and V1 and terminal
S waves in leads V3, V6, and Vl0.
Members of the litter were mated inter se to
produce an F2 generation consisting of 17 pups
(fig. 1). Electrocardiograms were recorded in
only eight of the 17 members of the F2
generation, since the remaining nine died in the
early neonatal period. Of the eight studied
electrocardiographically, five had normal electro-
cardiograms, one dog with pulmonic stenosis and
a ventricular septal defect had electrocardiogra-
phic signs of right ventricular hypertrophy, and
two otherwise-normal dogs had an incomplete
right bundle-branch block pattern.
This report deals with findings in six offspring
of the F, generation which were studied by
electrophysiologic methods.
Electrophysiologic Studies
The sequence of epicardial and intramural
activation of the ventricles was determined using
a bipolar electrode to scan 40 points on the right
and left ventricular epicardium, and multipoint,
plunge electrodes to define intramural activation.
These techniques have been previously described
in detail.'0 During the intramural activation
studies using plunge electrodes, special emphasis
was made to record from various right and left
Purkinje fibers both within the free ventricular
walls and septum. The onset of activation of the
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Purkinje fibers was correlated with the onset of
the QRS complex. In addition, new techniques
were developed to determine the sequence of
excitation along the right bundle branch and His-
Purkinje system.17 These investigations were
performed after completing the epicardial-intra-
mural activation studies. Both normal dogs and
dogs with IRBBB were placed on cardiopulmo-
nary bypass, and a right ventriculotomy was made.
Then a 1.0- by 1.5-cm electrode plaque contain-
ing 30 separate monopolar electrode sites located
about every 2 mm was gently sutured over the
right bundle branch (RBB) (as indicated in
figure 5 below). This electrode path enabled
multiple RBB electrograms to be recorded
simultaneously in either a bipolar or a unipolar
mode. It was then possible to determine the
conduction velocity along the RBB since the
geometry of the recording sites on the electrode
patch and the time of activation at these same
electrodes was known. In 10 normal dogs, the
conduction velocity along the RBB using this
technique was 1-3 m/sec.17
Histologic Studies
Three dogs with electrophysiologically docu-
mented alterations of activation of the right
ventricle (RV) had detailed histologic examina-
MOORE ET AL.
tions of the conduction system. Serial sections of
6-8 g in thickness were made by the method of
Pickett and Sommer.'8 Three dogs with normal
electrocardiographic findings were studied in a
like manner. After fixation, multiple measure-
ments were made of the thickness of the free
walls of the right ventricle, of the free walls of the
left ventricle, and of the septum. The weight of
the free wall of the right ventricle was determined
as a percentage of the total ventricular weight
and compared with normal values obtained by
Knight.'9
The following portions of the atrioventricular
conduction system were examined in each case:
portions of the interatrial septum including the
approaches to the atrioventricular (A-V) node,
the A-V node, the penetrating and bifurcating
portions of the common A-V bundle (His
bundle), the proximal 1 cm of the left bundle
branch, the entire right bundle branch from its
origin at the bifurcation to its termination at the
base of the septal papillary muscle, the free-
running false tendons arising at the base of the
papillary muscle through their attachment to the
free wall of the right ventricle, that portion of the
right ventricular free wall to which the free-
running false tendons attached, and, finally,
adjacent atrial as well as ventricular and valvular
structures.
Results
The X, Y, and Z scaler electrocardiograms
and frontal and left sagittal vectorcardiograms
inscribed using the McFee lead system are
shown in figure 2 from one of the dogs
with incomplete right bundle-branch block
(IRBBB). The P-R interval is normal and the
QRS duration is increased by about 10-15 (35
vs 45) msec. The initial forces are normal. The
terminal forces, however, are directed cranial-
ly, dorsally, and toward the right. Note also
that these later terminal forces are markedly
slowed in their inscription. This is a character-
istic feature of IRBBB in man.
Figure 3 illustrates the epicardial sequence
map of ventricular excitation correlated with
the inscribed QRS complex in a normal dog.
The heart is viewed frontally (Ant.) on the
left in the same position as the heart would be
observed upon a midsternotomy, and on the
right it is positioned as observed in a left
lateral thoracotomy (Lat.). The interventric-
ular sulcus is indicated by the coronary
arteries. Below the anterior and lateral views
Circulation, Volume XLIV, October 1971
 INCOMPLETE RIGHT BUNDLE-BRANCH BLOCK 681

F
X

LS
z
'Z
orA
2mv
100 msec.
Figure 2
X, Y, and Z scalar electrocardiograms and frontal (F) and left sagittal (LS) vectorcardiograms
from a dog with IRBBB were recorded using the McFee lead system (dog 37). See text for
discussion.
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II
vs

Ant. Lot. V,

21
0 5 10 15 20
E?igure 3
Epicardial ventriciular depolarization in a normal dog. A frontal (left activation map) and
left sagittal (right activation map) view of the pattern of epicardial excitation (breakthrough)
are shown along with the lead II and pericardial lead V1 electrocardiograms. See text for
discussion.

of the heart is a time key with different
stippling representing the period of time
within the QRS complex in which the
respective epicardial regions were activated.
Lead II and precordial lead V1 QRS complex-
es are shown on the right with time lines
indicated every 10 msec. The time of earliest
Circulation, Volume XLIV, October 1971
epicardial activity in this animal was noted at
10 msec after the onset of the reference ECG.
The pattern of epicardial spread was basically
similar in all normal dogs studied.-10 The
earliest site of epicardial activity was located
in the midright ventricle near the interventric-
ular sulcus. Activity then spread centrifugally
 682
toward the atrioventricular groove, the inflow
and outflow (conus) regions of the right
ventricle (RV), and leftward across the
interventricular sulcus. The left ventricular
(LV) epicardium was also activated in a
centrifugal fashion with earliest activity being
observed in the midregions and late activity
occurring at both the base and a small region
near the anterior interventricular sulcus an-
teriorly. The late activity in the RV conus,
which occurred during the same period of the
QRS complex as did late activity in the LV
base and anterior apex, resulted in considera-
ble cancellation and a normal QRS complex
being inscribed.
The epicardial activation sequence maps
and lead II and V, QRS complexes in figure 4
were recorded in a dog with IRBBB. The time
key below the activation maps contains
stippling corresponding to the time of activa-
tion of the respective regions of the epicar-
dium. The rSR' QRS complex in the precordial
lead V1 is characteristic of IRBBB. The frontal
view of the dog's heart is shown on the left,
and the left lateral view of the heart is
presented on the right. In contrast to the
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normal dog (fig. 3) early activity was
observed on the right epicardium near the
interventricular sulcus and simultaneously at
the apex of the LV indicating relatively later
than normal RV breakthrough. Activity during
the initial inscription of the R' wave in the
1'
Ant.
ZwEEE
0 5 10 15
Epicardial ventricular depolarization in incomplete right bundle-branch block (IRBBB).
Frontal (Ant.) and left sagittal (Lat.) activation maps are presented along with the lead II
and precordial lead V1 electrocardiogram (dog 37). See text for discussion.
MOORE ET AL.
precordial lead V1 (10-15 msec) occurred at
the right and left ventricular bases. However,
unlike the activation sequence in normal dogs,
there was a late 10-msec period of time at
20-30 msec in which activation occurred only
in the outflow tract of the RV (conus) without
any activity being recorded on the LV
epicardium. The peak of the R' wave
coincided in time with this unopposed surface
of activation in the RV. There are several
possible causes of delayed activation of the
RV conus region including alterations in
conduction velocity of the right His-Purkinje
system as well as possible variation in wall
thickness of the RV free wall. Even with
normal radial conduction velocity, the in-
creased thickness of the RV free wall could
result in delayed activation of the thick region
due to increased time for epicardial break-
through. To investigate the mechanism of
delayed epicardial activation, intramural acti-
vation was analyzed using plunge electrodes.
Figure 5 contains simultaneously recorded
intramural RV electrograms obtained from a
normal dog (A), and from a dog with an
electrocardiogram characteristic of IRBBB
(B). Using a constant reference electrogram,
the lead II electrocardiogram was time
normalized with the simultaneously recorded
intramural ventricular activation data as des-
cribed previously. The intramural plunge
electrodes had 15 monopolar electrode sites
II
VI I
20 25 30
6 ,,'
_1
Figure 4
Circulation, Volume XLIV, October 1971
 INCOMPLETE RIGHT BUNDLE-BRANCH BLOCK 683

A B

Lead II V ' Lead II

1-2
Pj 1-2
2-3
2-3
3-4
3-4 -
4-5
4-5 -- 5-6

6-7
100 msec. 7-8
8-9

Figure 5
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A and B contain simultaneously recorded ventricular intramural electrograms recorded using

plunge-type electrodes. The lead II ECG was time normalized with the simultaneously re-
corded ventricular electrograms. A was recorded from the base of the right ventricle in a
normal dog. B was recorded in a dog with incomplete right bundle-branch block (IRBBB)
(dog 37). See text for discussion.

located at 1-mm intervals along the electrode
shaft. In A, recorded from a normal dog, it
can be observed that four bipolar electro-
grams were recorded between five monopolar
electrodes sites, and the "electrical thickness"
of the RV free wall at this conus region
therefore was 4 mm. Note also that the
Purkinje depolarization spike denoted by Pj in
figure 5 recorded on the endocardial surface of
the RV free wall occurred at the onset of the
inscription of the R wave in the lead II ECG.
The activation sequence was also from endo-
cardium to epicardium as indicated by the
progressive delay in onset of activation of
bipolar site 1-2 to bipolar site 4-5.
In figure 5B, the endocardial bipolar
electrode site 1-2 was activated earliest. A
small Purkinje spike was recorded in this
electrogram (Pj) and the onset of depolariza-
Circulation, Volume XLIV, October 1971
tion of the Purkinje fiber was again at the
initiation of the R wave as normally observed.
The "electrical thickness" of the RV free wall
in this dog with IRBBB varied between 8 and
9 mm in the basilar regions and pulmonary
conus region. This is nearly double the normal
"electrical thickness" in this region as deter-
mined in over 30 normal dogs. The spread of
activation radially through the free wall
occurred at a normal conduction velocity.
Note that the endocardial site (site 1-2) was
activated during the R wave in the lead II
ECG while the outermost epicardial site (site
8-9) was activated during the S wave. Similar
increased thickness of the RV free wall in the
conus region was observed in eight other dogs
with electrocardiographic manifestation of
IRBBB.
 684 MOORE ET AL.

EKG

TV,3
~4

~~~~~~5

20 msec.
Figure 6
A schematic diagram of the right ventricular septal surface is shown with the tricuspid valve
(TV) and pulmonary artery (PA) labeled. The arrows numbered 1 through 5 indicate regionls
along the right bundle branch (dark structure on the septal surface) at which simultaneous
electrograms 1 through 5 were recorded using a multielectrode plaque. The five simulta-
neously recorded right bundle-branch electrograms are shown on the right of the figure along
with the lead II ECG (dog 37). See text for discussion.

The intramural activation data demon- 2.5 m/sec. Therefore, since conduction velo-
strated a delay in RV activation which was city in normal hearts using these techniques
due to focal right ventricular hypertrophy. To was between 1 and 3 m/sec, there was no
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investigate whether conduction delays within
the RV specialized conduction system might
also be involved in producing the electrocar-
diographic picture of IRBBB in those dogs, a
technique was developed in which an elec-
trode patch was sutured over the right bundle
branch (RBB) during cardiopulmonary by-
pass, and multiple electrograms were recorded
simultaneously from the specialized conduc-
tion tissue. In this way it was possible to
determine the conduction velocity along the
His-Purkinje system. Using this method it was
found that conduction velocity was 1-3 m/sec
along the RBB in 10 normal dogs.'7
In figure 6, a schematic diagram of the right
septal surface of the heart of one of the dogs
with IRBBB (number 37) is illustrated along
with the sites from which the proximal and
distal RBB electrograms on the right of figure
6 were recorded. Note that activation pro-
gressed from the first site to the fifth site in a
uniform sequence. The propagation velocity in
this heart with electrocardiographic evidence
of incomplete right bundle-branch block was
conduction delay in the main septal RBB in
this heart with IRBBB. In three other dogs
with electrocardiographic evidence of IRBBB,
the same results were obtained with complete-
ly normal conduction velocity along the RBB.
Interestingly, the RV septum was depolarized
in the opposite direction (large depolarization
complexes occurring after the rapid bundle-
branch spikes) from apex to base. Also,
additional evidence that there is not a
conduction delay within the RBB system is
that all of the RBB electrograms occur at the
beginning of depolarization of the ventricles
as displayed in the ECG (top trace).
Figure 7 is a time-aligned illustration of
depolarization along the RV specialized con-
duction system. The lead II ECG is shown
(top trace) along with electrograms recorded
from the proximal right bundle branch (RB
Pj), right ventricular endocardial Purkinje
fiber (RV EnPj), and a right ventricular
epicardial electrogram recorded from the right
ventricular conus region. The lead II ECG
exhibits a prominent S wave, which is
Circulation, Volume XLIV, October 1971
 INCOMPLETE RIGHT BUNDLE-BRANCH BLOCK
Lead ]I
RB Pj
RV EnPj
RV Ep P
50 msec.
Figure 7
Time-normalized illustration of the sequence and ac-
tivation times of the proximal right bundle branch
(RB Pj), endocardial right Purkinje system (RV EnPj),
and the right ventricular epicardial conus region
(RV EpP) during inscription of the electrocardiogram
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(lead II) in a dog with IRBBB (dog 37). See text for
discussion.
characteristic of IRBBB. Note that the proxi-
mal right bundle branch was depolarized
normally prior to inscription of the QRS
complex during the P-R interval. The right
ventricular endocardial Purkinje fiber (Rv
EnPj) was likewise depolarized at a normal
time just after the start of the R wave. The
right ventricular epicardial point (RV EpP),
on the other hand, was activated much later
than normal during the S wave of the lead II
electrocardiogram. Therefore, despite the fact
that there is delayed activation of the conus
region, there does not appear to be any
electrophysiologic evidence of conduction de-
lays along the right ventricular specialized
conduction system.
Although no electrophysiologic evidence of
conduction abnormalities could be found in
the RV specialized conduction system in the
dogs with IRBBB, nevertheless it was consid-
ered important to examine, by serial histolog-
Circulation, Volume XLIV, October 1971
68-05
ic sectioning, the right atrioventricular spe-
cialized conduction tissues. It is not possible,
of course, even with serial sectioning to permit
quantitative conclusions to be made regarding
all of the peripheral arborizations of the RBB
fibers and peripheral Purkinje network which
for obvious reasons could not be studied in
their entirety. The area included in our
histologic examination was that in which
activation abnormalities have been previously
demonstrated to result in electrocardiographic
evidence for incomplete and complete right
bundle-branch block and included the entire
right bundle and Purkinje fibers in the free-
running false tendons.
The atrioventricular node and common
bundle of His were completely normal.
Histologic serial sections showed that the RBB
was intact throughout its entire length. The
free-running false tendons and the arboriza-
tion of Purkinje fibers in the free wall of the
right ventricle likewise appeared normal in all
specimens. No quantitative or qualitative
differences were apparent between cases hav-
ing electrocardiographic evidence of IRBBB
and those designated normal. Areas of fresh
hemorrhage were found in scattered portions
of the specialized tissues of the dogs with
IRBBB in which electrophysiologic studies
were also carried out. These resulted from
intramural electrode penetrations, and in no
case did hemorrhage appear to interrupt
the pathway of the specialized tissue. Ventric-
ular muscle fibers were studied throughout the
heart, and no abnormalities were encountered.
Discussion
The term incomplete right bundle-branch
block (IRBBB) is defined in most electrocar-
diographic textbooks as a QRS configuration
consisting of an rSr' or rsR' in V1 with or
without associated s or S waves in the
standard leads I), II III, and aVF. The QRS
duration is usually prolonged in adults to
0.09-0.11; correspondingly less prolongation
occurs in children. IRBBB is a somewhat
ambiguous term due to the wide variation
observed in QRS configuration and duration
as well as the numerous clinical conditions in
which ECG's with this abnormality are
 686
encountered. The term IRBBB implies that
there is block in the peripheral right Purkinje
system, and cases of IRBBB associated with
acquired, congenital, or experimental lesions
within the right ventricular Purkinje network
have been clearly demonstrated. However,
other instances of IRBBB without demonstra-
ble cardiovascular lesions have also been
reported. Thus, there is clearly a need to
examine the right bundle branch-Purkinje
system using direct electrophysiologic tech-
niques to determine the sequence of right
ventricular myocardial activation, as well as
activation studies on the right ventricular
specialized conduction system in cases of
IRBBB. These types of investigations are
difficult and, in many instances, impossible to
perform in patients. The present investigations
afforded an unusual opportunity to examine
the basis of spontaneous IRBBB in a group of
beagle dogs which were siblings of an F1
breeding of two dogs with congenital heart
disease (fig. 1).
In the present study, six canine siblings
were found to have an electrocardiographic
pattern of IRBBB, but no cardiovascular
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abnormalities could be found on clinical
examination or upon histologic examination of
the heart. The etiology of the IRBBB pattern
was a focal hypertrophy of regions of the right
ventricular free wall near the atrioventricular
margin and pulmonary conus. Myocardial
conduction velocity through these thickened
regions of right ventricular myocardium was
found to be normal; however, the longer
distance that the wavefront had to travel from
the endocardium to epicardium resulted in
delay in the onset of activation of the right
ventricular epicardium at these hypertrophied
regions. Therefore, IRBBB resulted from a
prolonged phase of activation in certain
regions of the right ventricular free wall
caused by focal hypertrophy, rather than from
delay caused by conduction abnormalities
within the peripheral right ventricular
Purkinje system.
Of course, the explanation for the surface
ECG pattern of IRBBB in these animals
cannot be generalized to explain all cases of
MOORE ET AL.
IRBBB in man. However, they do indicate at
least one basis for this electrocardiographic
pattern other than the classically accepted
theory of parietal block of the right Purkinje
network. Strong additional support for focal
regions of right ventricular hypertrophy giving
rise to an ECG pattern of IRBBB is the fact
that two other unrelated dogs of different
breeds (keeshond and a mongrel) also had a
focal right ventricular hypertrophy associated
with an electrocardiographic pattern of
IRBBB. It should be mentioned that when the
ratio of the total weight of the right
ventricular free wall was compared to total
heart weight in these dogs, the ratio was at the
upper limits of normal found by Knight in a
series of 38 normal dogsl9 (24% of total heart
weight in IRBBB dogs vs an average of 22% in
normal dogs). The fact that there was not a
significant increase in right ventricular wall
weight as determined by this method points
out that activation delays in only a small
region of the right ventricle can result in
changes in phase relationships of a sufficient
degree to alter the usual balance of forces,
thereby permitting delayed right ventricular
activation to be expressed as IRBBB. The
thickened right ventricular wall not only
results in phasic changes in right and left
ventricular activation, but also permits the
activation wavefront to occupy a greater area
of the right ventricular wall, thereby causing
the amplitude of the late right ventricular
forces to be increased in the electrocardio-
gram.20
Perhaps of greater significance is the finding
that mild localized right ventricular hyper-
trophy was present in the family of beagles in
the absence of any obvious hemodynamic
stimulus. This suggests that the distribution of
right ventricular mass is determined not only
by the hemodynamic state, but also by genetic
factors which govern the morphogenesis of the
ventricular walls. Such intrinsic mechanisms
may determine to some extent the capacity of
the individual to react to hemodynamic loads
and may account for the variation in right
ventricular hypertrophy encountered in pa-
tients with similar degrees of hemodynamic
Circulation, Volume XLIV, October 1971
 INCOMPLETE RIGHT BUNDLE-BRANCH BLOCK
overload. Also, the present findings suggest
that the frequent occurrence of late anterior-
rightward QRS forces (rSr' and S1S2S3) in
apparently healthy people may in part repre-
sent normal variation in thickness and distri-
bution of the RV mass.
Acknowledgments
The authors wish to thank Ralph Iannuzzi, William
Schnarr, J. H. Kasell, and C. B. Clark for invaluable
technical assistance.
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