Download The Spatial Characteristics of Atrial Activation in

The Spatial Characteristics of Atrial Activation
in Ventriculo-Atrial Excitation*
M. Mirowski, M.D.,O0 and Bernard Tabatznik, M.D.f
Spatial characteristics of atrial activation were analyzed in arrhythmias displaying a ventrimlo-atrial sequence of excitation: junctional rhythm with preceding ventricular activation, "reciprocal" atrial beating, complete or high-grade
A-V block with ventriculoatrial response and venlricular extnqstoles with
ventriculoatrial response. It was found that the coupled P waves were markedly
dissimilar with regard to their polarity and vectorial characteristics. Vectorial
analysis suggested that the c o w of the anomalous atrial activation is consistent with an A-V nodal origin of impnlses in a minority of cases only, while
in the majority the depolarization process appeared to originate in various
portions of both atria This interpretation is in codiict with the theory postulating retrograde conduction of impulses through or from the A-V node as the
basic mechanism of ventrimlo-atrial excitation, and raises the possibility that
the "retrograde" P waves are frequently due to stimuli origioating h various
automatic atrial centers induced, in some way, by the preceding ventriculat
activity.
T h e diagnostic criteria for atrioventricular
rhythm (A-V rhythm, A-V junctional rhythm,
A-V nodal rhythm) have traditionally been based
on P wave alterations in the extremity leads. However, when such rhythms, characterized by inversion of the P waves in leads 11, 111, and aVF, are
For editorial comment, see page 2
analyzed in the precordial leads, the configuration
of atrial deflections does not follow a uniform pattern. Thus, one may encounter three distinct precordial patterns:'**
( 1) Negative, isoelectric, or isodiphasic P waves
in lead V1 and upright P waves in the left
precordial leads ( Fig 1).
( 2 ) upright P waves in-the right precordial leads
and inverted P waves in the left precordial
leads (Fig 2).
'From the De artment of Medicine, Sinai Hospital of
Baltimore, anBthe Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland.
''Director, Coronary Care Unit, and Assistant Physician-inChief, Sinai Hospital; Assistant Professor of Pediatrics,
Johns Hopkins University School of Medicine.
fchief, Cardiolo Division, Sinai Hospital, and Assistant
Professor of ~ e g c i n eJohns
,
Hopkins University School of
Medicine.
(3) P wave inversion in all the precordial leads
(Fig 3).
Because the mean spatial P vectors in these
groups point in entirely different directions, an origin of the impulses from a common focus was
difficult to conceive. When the mean spatial P vector points posteriorly, superiorly, and to the left as
in pattern (1) the vectorial characteristics of atrial
activation are consistent with an A-V nodal origin
FIGURE
1. A-V junctional rhythm. Inverted P waves in leads
11, 111, aVF, and in V1-V,, upright in the left precordial
leads. The mean atrial vector points posteriorly, superiorly,
and to the left.
Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21487/ on 05/12/2017
MIROWSKI AND TABATZNlK
RGURE2. Inverted P waves in leads II, III, aVF, and in
V,-V,, upright in V1-V8. The mean spatial P vector points
anteriorly, superiorly, and to the right, suggesting a postero-inferior left atrial pacemaker.
of impulses. However, when it points anteriorly,
superiorly, and to the right as in pattern (2) it has
been suggested that the pacemaker is located postero-inferiorly in the left atrium;' and when it points
posteriorly, superiorly, and to the right as in pattern (3), the postulated pacemaker site is anteriorly
and inferiorly in the left atrium.2
The concept that many rhythms which by conventional criteria would be considered as originating in the A-V junction are in fact initiated in the
left atrium deserves critical scrutiny at various levels. While final proof or disproof will have to be
established on the basis of experimental evidence,
valuable additional information may be obtained
through study of clinical tracings.
Since previous observations1-awere made in cases
in which the P waves preceded the QRS complex,
Marriott' suggested a survey of the precordial P
waves in patients with A-V rhythm in which the P
waves follow the QRS, because "there is perhaps
greater assurance of the A-V origin of atrial waves
when they follow the QRS in constant relationship
than when they precede it."
This pertinent suggestion has been followed, and
during the last few years a search has been made
for clinical tracings displaying A-V nodal rhythms
characterized by atrial complexes which follow the
ventricular complexes at a fixed interval, the atrial
cycle length being identical to the ventricular cycle
length.
In addition, other arrhythmias which may display a similar venticulo-atrial sequence of activation and in which it is acce~tedthat the im~ulses
enter the atria from or thmGgh the A-V nod; such
as reciprocal beating of the atria, advanced or complete A-V block, and ventricular extrasystoles have
also been surveyed. The P waves were studied for
their polarity and configuration and analyzed vectorially according to principles defined in detail in a
previous paper.*
The purpose of this communication is to present
the results of such a study and to discuss their pos-
FIGURE
4. A-V junctional rhythm with preceding ventricular
activation. The P wave configuration is similar to that reproduced in Figure 1.
sible implications. To our knowledge, no similar
investigation has as yet been reported in the literature.
A. A-V nodul rhythms with preceding oentricuhr
activation
FIGURE3. Note P wave inversion in all the pmrdial
leads as
as in I19
and aVF* suggesting a posterior,
superior, and rightward orientation of the atrial vector, best
explained by the presence of an inferior and anterior left
atrial focus.
Eight cases were available for analysis. Four different P wave patterns were observed in this group.
The first three were similar to those previously observed in A-V rhythm with preceding atrial activation. The representative examples are reproduced
in Figures 4 to 7.
Figure 4 displays inverted P waves in leads 11,
111, aVF, as well as in the right precordial leads;
they are upright in Vn and 6.
?;he spatial mean
P vector thus points superiorly, posteriorly and to
the left. This P wave pattern closely resembles the
one reproduced in Figure 1.
CHEST, VOL. 57, NO. 1, JANUARY 1970
Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21487/ on 05/12/2017
SPATIAL CHARACTERISTICS OF ATRIAL ACTIVATION
~ U R 5.
E
A-V junctional rhythm with preceding ventricular
activation. The P wave configuration resembles that present in Figure 2.
Figure 5 exhibits typically inverted P waves in
the extremity leads, but the precordial P waves are
upright in V1, Vt, and inverted in Vl-V6. Consequently, the mean P vector points superiorly, anteriorly, and to the right. The characteristics of atrial activation are similar to those present in Figure 2.
The electrocardiogram shown in Figure 6 is characterized by P wave inversion in all the precordial
leads as well as in 11, 111, and aVF. These changes
are similar to those seen in Figure 3. Vectorial
as in leads Vs-Va. The mean P vector is directed
inferiorly, anteriorly, and to the left. These P waves
are quite similar to those observed in sinus beats
or sinus rhythm. It is impossible to say whether this
arrhythmia is sinus rhythm with first degree A-V
block or a junctional rhythm with ventriculo-atrial
activation. However, this tracing is included in the
present study because a similar ventriculo-atrial sequence of activation with upright P waves in leads
11, 111, and aVF has been observed in several arrhythmias where first degree A-V block can safely
be excluded (Fig 8,10,14, and 15). Moreover, cases
with similar features have been published as exam~ I e sof A-V nodal rhvthm with ventricular activaL
tion preceding atrial activati~n.~
B. "Reciprocal" beating of the atria.
This diagnosis requires a brief definition. It is
generally accepted that due to unidirectional conductivity in some fibers of the depressed A-V junction, a sinus or auricular impulse can be reflected
in the A-V node on its way to the ventricles and
FIGDRE 6. A-V junctional rhythm with preceding ventricular activation. Note P wave inversion in all the precordial
leads similar to that in Figure 3.
analysis suggests a superior, posterior, and rightward spread of activation.
The tracing reproduced in Figure 7 differs significantly from the previous recordings in that the
P waves are uprigit in the extremity leads as well
~ C U R E7. The P waves are of sinus origin. For further explanation see text.
FIGURE
8. Atrial *'reciprocalDrhythm. The P-R intend is
0.22. The P waves that follow the QRS complexes are
inverted in lead I and in the left precordial leads and u p
right in 11, 111, aVF, and V1 where typical "dome and dartn
configuration is present. The mean atrial vector of the
"reciprocal" beats points inferiorly, anteriorly, and to the
right, suggesting a supposterior left atxial focus.
re-enter the atria in a retrograde directionP4 Therefore, the diagnosis of reciprocal beating of the atria
is usually considered when a QRS complex is sandwiched between an atrial deflection and a coupled
retrograde P wave. In addition, the diagnosis may
even be considered when the coupled P wave is
upright because, according to Waldo and associates: " . . . evidence of retrograde atrial activation
from the A-V junctional pacemaker is afforded by
CHEST, VOL. 57, NO. 1, JANUARY 1970
Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21487/ on 05/12/2017
MIROWSKI AND TABATZNIK
the right, a direction similar to that observed in
Figures 2 and 5.
In the third example, only lead I1 is available
(Fig 10). This record is, however, of importance
because the "reciprocal" atrial beats are upright in
this lead. Such a polarity suggests an inferior orientation of the atrial electrical forces.
C . Complete or high-grade A-V block with
ventriculo-atrial excitation.
FIGURE9. The P-R interval is 0.17. The "reciprocal" atrial
beats are inverted in leads 111, aVF and V6 and upright in
V,. The mean vector of these beats points anteriorly, superiorly, and to the right as in Figures 2 and 5, suggesting
a postero-inferior origin of atrial activation.
the identity of P-P and R-R intervals over a range
of ventricular cycle lengths and by a constant temporal relationship between the ventricular complex
and the P wave" rather than by the morphology of
the P wave.
Three cases in which the diagnosis of "reciprocal"
atrial beating was considered are presented. The
term "reciprocaln is in quotation marks because in
these cases an alternate mechanism may play a role.
The first case is shown in Figure 8. The lower
strip (lead I ) demonstrates a normal sinus rhythm
at 90 beats per minute with a P-R interval of 0.22
sec. The sinus P waves are indicative of left atrial
hypertrophy. The striking feature of this tracing is
represented by atrial deflections which follow the
QRS complex with an R-P interval of approximately
0.15 sec. These deflections are upright in leads 11,
111, and aVF, inverted in I, aVL, V3-V6. The P
wave in lead V1 displays a "dome and dart" configuration. The mean P vector points inferiorly, anteriorly, and to the right.
The second tracing is shown in Figure 9. In this
case the "reciprocal" atrial beats are inverted in
leads 11, 111, and aVF, as well as in Va through Vg;
they are upright in lead V1. The mean P vector of
these beats is oriented superiorly, anteriorly, and to
Only two cases were available for analysis. In the
first the P waves which are coupled to the QRS
complexes are inverted in leads 11, 111, aVF, as well
as in all the precordial leads. Such P wave polarity
is similar to that present in Figures 3 and 6. The
second case is reproduced in Figure 11. The ventricular complex is followed by sharply inverted P
waves with -an R-P interval of 0.06 sec. Simultaneous leads (Fig 12) disclose that the "retrograde"
P waves are inverted in 11, 111, aVF, V4-V6, and
upright in V1 and VZ. A close examination of lead
V1 suggests that th,e P wave which starts 0.06 sec.
after the beginning of the QRS complex displays a
"dome and dart" configuration. Vectorial analysis
of the anomalous P waves reveals a superior, anterior, and rightward direction of the activation
process similar to that present in Figures 2, 5, and 9.
D. Ventricular extrasystoles with uentriculo-atrial
excitation.
This rhythm disturbance is quite common and 16
such cases were available for analysis. In general,
all the P wave patterns encountered in the other
arrhythmias reported herein were also observed in
this group. Three representative tracings will be
shown.
Figure 13 displays atrial beats originating probably in the left atrium and normally conducted to
the ventricles. These beats are followed by ventricular extrasystoles with coupled atrial deflections of
similar form and polarity as the conducted P waves.
The R-P interval is 0.11 sec. The direction of the
mean P vector is identical in the conducted and in
the "captured" atrial beats and suggests superior,
anterior, and rightward spread of the depolarization
process similar to that observed in Figures 2, 5 and
9.
Figure 14 shows ventricular beats followed by
FIGURE10. Note that the third and fifth QRS complexes are sandwiched between conducted
sinus P waves (P-R = 0.16, 0.17 sec.) and upright P waves of different configuration than the
sinus beats. The differential diagnosis is between atrial reciprocal beating and nonconducted
coupled high atrial extrasystoles. For further discussion see text.
CHEST, VOL. 57, NO. 1, JANUARY 1970
Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21487/ on 05/12/2017
SPATIAL CHARACTERISTICS OF ATRIAL ACTIVATION
FIGURE11. Note complete or high-grade A-V block with ventricular rate of 57 per minute
and sinus rate of 90 per minute. Almost every second QRS complex in the two upper rows
is followed by a sharply inverted P wave with an R-P interval of 0.06. In the lower row these
inverted P waves follow several consecutive QRS complexes.
atrial deflections which are upright in leads I and
aVF, and inverted in all the precordial leads. The
P vector points inferiorly, posteriorly, and to the
right. Similar P wave patterns have previously been
reported.*
Figure 15 exhibits in each lead a normally conducted sinus beat and two ventricular extrasystoles
originating in different foci. While the second extrasystole is followed by atrial deflections which are
inverted in leads 11, 111, V5, Vs,and probably lead
I, the P waves coupled to the first extrasystole are
FIGURE12. Same case as in Figure 11. Leads I, I1 and 111,
a m , aVL and aVF; V1,Vt and V,; and V4, V6 and V6
are recorded simultaneously. The retrograde P waves are
inverted in 11, 111, aVF, V4-V6 and upright in a m , aVL,
Vl and V,. The mean vector of the retrograde P waves
points superiorly, anteriorly, and to the right. Note that the
retrograde P wave in lead V1 is possibly of "dome and dart"
configuration.
upright in these leads, indicating a different origin
of atrial activation.
DISCUSSION
In 1915, on the basis of what might probably be
considered the first attempt to analyze atrial deflections vectorially, Wilsonlo concluded that the P
wave changes in A-V nodal rhythm indicate an
average upward and leftward direction of spread of
the excitatory process, a direction "in harmony with
the location of the atrioventricular node." Wilson's
interpretation, confined to the events reflected by
the plane of the Einthoven triangle, was complemented 30 years later by Ruskin and Decherdl'
who recognized the backward progression of nodal
impulses in space. The appreciation of the tridimensional orientation of atrial forces in nodal arrhythmias has recently resulted in their differentiation
from other atrial rhythms.1.2.12
There were good reasons, therefore, to anticipate in arrhythmias characterized by a ventriculoatrial sequence of excitation and in which the impulses presumably enter the atria from the A-V
node, a superior, leftward, and posterior orientation
of atrial electrical forces and, accordingly, a rather
uniform P wave pattern in the precordial as well as
in the extremity leads. Surprisingly, this was not the
case. As our results demonstrate, the P waves which
follow the QRS complexes in the studied cases are
markedly dissimilar with regard to their polarity
and vectorial characteristics. While their configuration was occasionally consistent with that expected
in impulses originating in the A-V node or its vicinity, in most instances the P waves were similar
to those described in various types of left atrial
rhythms (Fig 5, 6, 8, 9, 12, 13, 14, 15) or to those
observed in sinus rhythm (Fig 7,10 and 15).
There is bound to be much difference of opinion
CHEST, VOL. 57, NO. 1, JANUARY 1970
Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21487/ on 05/12/2017
MIROWSKI AND TABATZNlK
Each lead shows a
normally
conducted
atrial
(probably left atrial) beat and a
ventricular
extrasystole followed by a coupled atrial deflection. The direction of the
mean P vector is identical in
the conducted and in the "captured" atrial beats.
FKNRg 13.
as to how these observations should be interpreted.
It seem&that two alternative interpretations should
be taken into consideration.
The first is based on vectorial analysis of the
anomalous P waves which follow the QRS complexes at fixed intervals. This analysis suggests that
the course of the anomalous atrial activation is consistent with an A-V nodal origin of impulses in a
minority of cases only, while in the majority the
depolarization process seems to originate in various
portions of the left and the right atrium. This,in
turn, invites the hypothesis that the abnormal P
waves might frequently be due to stimuli originating
in various automatic centers in the atria and induced, in some way, by the preceding ventricular
excitation. Such a hypothesis is in contrast with the
prevailing theory postulating in the arrhythmias
under consideration retrograde conduction of impulses through the A-V node, but has the advantage
that it explains both the spatial characteristics of
atrial activation and the ventriculo-atrial sequence
of excitation on the same basis. The concept that the
ventricles are able to stimulate potential atrial pacemakers had already been advanced in the early
days of electrocardiography by those who could not
conceive that retrograde conduction can occur in
complete forward block.laJ4 The working hypothesis as suggested by the present study represents
an extension of this concept to a large group of arrhythmias in which a ventriculoatrial sequence of
excitation is the outstanding feature.
An alternate interpretation of our findings is suggested by Waldo and associates* assertion that
"the apparent polarity and morphology of the P
waves are at best an unreliable indication of the
site of origin of atrial activity in A-V junctional
rhythms." This is in keeping with a more inclusive
statement of Cranefield and Ho&nan16 that "the P
wave does not necessarily indicate the site of origin
of the impulse or the path over which the impulse
spreads." Such a thesis implies a serious limitation
inherent in the electrocardiographic method in general, which makes any attempt to determine clinically the nature of atrial beats and rhythms open to
error. If these conclusions are correct, a valid diagnosis of the site of the atrial pacemaker based on
the form of the P wave is not possible. A clinical
study endorsing this viewpoint has recently been
published."
The crucial difference between these two approaches resides in the divergent assessment of the
value of P wave configuration in the identification
FIGURE14. Ventricular extrasystoles with coupled atrial
deflections which a- upright in leads I and aVF and inverted in the precordial leads.
CHEST, VOL. 57, NO. 1, JANUARY 1970
Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21487/ on 05/12/2017
15
SPATIAL CHARACTERISTICS OF ATRIAL ACTIVATION
FIGURE15. TWOtypes of "rek o ~ a d e "atrial activation in the
same patient. Note Merent
configuration of the P waves
which follow the two ventricular extrasystoles in each lead.
See text.
of the site of origin of impulses. Because of o w conviction that vectorial analysis of the P waves represents the key to the understanding of atrial electrical activity in its natural tridimensional context,
and because the results of such an analysis are
sdliciently accurate to be useful for clinical purposes, only the first interpretation appears acceptable to us. There is enough evidence to support the
view that the same principles of analysis currently
used for evaluation of ventricular depolarization
and repolarization can safely be extrapolated to the
study of atrial activation. For example, the vectorial
approach has proved essential in clarifying the nature of the P wave changes in various types of atrial overl~ading.l~-~"
Vectorial analysis was also instrumental in elucidating the significance of the
"dome and dart" P waves." These distinctive deflections have been interpreted as indicating a posteriorly located left atrial pacemaker and the evidence is now conclusive that a similar P wave
configuration can be reproduced by left atrial stirnulation in dog and in man."'-4 Furthermore, the
remarkable constancy in the orientation of the mean
atrial vector in sinus rhythm is worth emphasizing.
This vector points downward, forward, and to the
a direction in harmony with the location
of the sinus node; when the sinus node is located on
the left as in mirror-image dextrocardia, there is a
corresponding mirror-image shift of the vector to
the right." This point also demonstrates that regardless of whether one conceives the spread of the
atrial impulse as a radial phenomenon or as a
spread through rapid preferential pathways as postulated by Jame~,~"he direction of the mean vector remains consistent with the site of impulse formation. Finally, at the experimental level, a high
degree of correlation has been found between the
direction of the resultant vector and the site of
stimulation both in dogs and in man.24.27
It should be emphasized however, that the direc-
tion of the spatial vector as determined from the
surface electrocardiogram must be regarded as a
crude approximation rather than a perfect image of
the average orientation of atrial electrical forces.
The vectorial approach has limitations sufficiently
important to make any inferences only suggestive
rather than conclusive. These limitations have been
detailed in a previous r e p ~ r t On
. ~ the other hand,
they do not seem to be more serious than those
inherent in other electrocardiographic concepts
used with benefit at the clinical level. The fact remains that vectorial analysis of the P waves is the
only method available by which one may obtain an
approximate idea of the tridimensional character
of atrial electrical activity from body surface leads.
The working hypothesis that has emerged from
the present study finds additional support in a series
of clinical and experimental observations dMcult to
reconcile with the conventional concept that ventriculo-atrial sequence of activation always results
from retrograde propagation of a ventricular or
junctional impulse toward the atria through the A-V
node.
1. Although a viable conduction system is essential
for retrograde transmission of impulses, this is
clearly not present in advanced or in complete
A-V block. In order to explain the mechanism by
which retrograde activation occurs when antegrade conduction is completely disrupted, one
has to assume that antegrade and retrograde
pathways are not necessarily identical and that
impulses ascending from the ventricles may still
progress toward the atria iq spite of the fact
that the antegrade path is blocked. This assumption, however, does not explain some classic experimental observations. For example, Cullis and
DixonZHshowed the persistence of a ventriculoatrial sequence of excitation after complete section of the A-V node in the rabbit. Similarly, in
surgically induced complete A-V block in iso-
CHEST, VOL. 57, NO. 1, JANUARY 1970
Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21487/ on 05/12/2017
MIROWSKI AND TABATZNIK
2.
3.
4.
5.
lated frog hearts, Segers2@
described a ventriculo-atrial interaction, which he attributed to "synchronization."
Many authors have demonstrated that in arrhythmias believed to originate in the A-V node
the left atrium is often activated and contracts
before the right.16.30.31The same phenomenon
has also been reported in a ventricular extrasystole with retrograde atrial activation where
the contraction of the left atrium preceded that
of the right by 60 msec." One may question
why the left atrium should be activated first if
the impulses enter the atria through a right atrial
structure such as the A-V node. In order to explain this along conventional lines, it is necessary
to postulate the existence of rapidly conducting,
preferential pathways connecting the A-V node
with the left atrium.? Such pathways, to our
knowledge, have yet to be demonstrated.
If impulses enter the atria from the A-V node,
initial activation of the lower atrial regions with
later activation of the sinus node area would be
expected. However, in reciprocal atrial beats produced by Wallace and DagetP3 during vagal
stimulation in dogs, two types of activation were
found, one consistent with the above assumption, and a second characterized by initial activation of the S-A node region. Both patterns of
activation were shown to occur in the same animal. Although other explanations are conceivable, these findings are consistent with the idea
that more than one atrial pacemaker was, in fact,
stimulated in these experiments.
The conventional explanation of reciprocal atrial
beating demands a prolonged A-V conduction
time, sufficient to permit recovery of the return
p a t h ~ a y . " ~ However,
'
in several published examples of this arrhythmia the P-R interval is not
pr~longed.:~""Even in the case reported by Moe
and associatess7 as "a striking example of atrial
reciprocal beat," the P-R interval did not increment beyond 0.16 sec and in at least one reciprocal beat was only 0.11 sec. In our three cases the
P-R interval was 0.22 sec (Fig 8), 0.17 sec (Fig
9), and 0.16 sec and 0.17 sec (Fig 10). The
question therefore arises whether our cases are
indeed reciprocal atrial beats or whether an alternate mechanism exists.
Retrograde conduction in the mammalian heart
One would
is slower than antegrade cond~ction.~
anticipate, therefore, in advanced or complete
A-V block with idioventricular rhythm, an R-P
interval longer than the P-R interval when antegrade conduction occurs. However, in several instances of complete A-V block with retrograde
atrial activation from presumably ectopic ventricular centers (idioventricular as opposed to
idionodal rhythm), the R-P interval is surprisingly short, shorter than the antegrade conduction of the sinus impulses in these cases.? Furthermore, at least two published tracings (reference 38, Fig 6, and reference 39, Fig 5)
demonstrate that the P-R interval of the conducted sinus beat in advanced A-V block is
longer than the stimulus-to-P' interval (R-P')
during ventricular pacing.
6. The observation of "dome and dart" P waves in
one of our cases (Fig 8 ) and possibly in a second (Fig 12) is noteworthy. These distinctive P
waves are highly suggestive of a posteriorly located left atrial p a ~ e m a k e r . ~ . ~Their
l - * ~ presence
in instances of ventriculo-atrial excitation is difficult to explain in the light of the conventional
concept.
The above considerations demonstrate several
weaknesses in the conventional concept explaining
the ventriculo-atrial sequence of activation exclusively by retrograde conduction, and indicate a
need for its reappraisal. By viewing these rhythm
disturbances more as an abnormality of impulse
formation rather than of conduction, the alternate
hypothesis postulating stimulation of potential atrial
pacemakers by the ventricles reduces significantly
the number of inconsistencies inherent in the conventional approach. Even if the working hypothesis
suggested by this report should subsequently be
proved unwarranted, the clinical and experimental
observations discussed above might still need an
explanation different from that generally accepted.
The precise way in which ventricular stimuli may
excite atrial automatic centers as postulated above
is obscure. The material presented in this paper and
a perusal of the literature shed little light on this
problem. Those few investigators who had previously advanced a similar hypothesis to explain the
occurrence of retrograde P waves in complete A-V
block, suggested that the stimuli might be of mechanica11"14 or of e l e c t r o t ~ n i cnature.
~~
However,
experimental work in this field is scant and much
remains to be elucidated.
1 Mmowsm, M.: Left atrial rhythm. Diagnostic criteria
and differentiation from nodal arrhythmias, Amer. I .
Cardiol., 17:203, 1966.
2 M m o w s ~ ~M.:
, Ectopic rhythms originating anteriorly
in the left atrium. Analysis of 12 cases with P wave
inversion in all precordial leads, Amer. Heart I., 74:
299, 1967.
3 Mmowsm, M., NEILL, C. A., AND TAUSSIC,H. B.: Left
atrial ectopic rhythm in mirror-image dextrocardia and
CHEST, VOL. 57, NO. 1, JANUARY 1970
Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21487/ on 05/12/2017
SPATIAL CHARACTERISTICS OF ATRIAL ACTIVATION
in normally placed malformed hearts. Report of twelve
cases with "dome and dart" P waves, Circulatwn, 27:
864, 1963.
4 M a m o m , H. J. L.: Nodal mechanisms with dependent
activation of atria and ventricles, in DREINS, L. S..
AND LIKOFF,W., (Eds.): Mechanisms and therapy of
cardiac arrhythmias, 14th Hahnemann Symposium,
Cmne & Stratton, New York, 1966.
H.: Premature beats in
5 DRESSLER,
W., AND ROESSLGR,
atrioventricular rhythm, Amer. Heart I., 51:261, 1956.
6 K a n , L. N., AND PICK,A.: Clinical electrocardiography.
I. The arrhythmias, Lea & Febiger, Philadelphia, 1956.
7 SCHERF,D., AND COHEN,J.: The atrioventricular node
and selected cardiac arrhythmias, G ~ n e& Stratton,
New York, 1964.
8 MOE, G . K., AND MENDEZ,C.: The physiologic basis of
reciprocal rhythm, Progr. Cardiouasc. Dis., 8:461, 1966.
9 WALDO,A. L., V ~ C A I N E K.
N , J., HARRIS,P. D., MALM,
J. R., AND HOFFMAN,B. F.: The mechanism of synchronization in isorhythmic A-V clissociation. Some observatiom on the morphology and polarity of the P
waves during retrograde capture of the atria, Circtrlation, 38:880, 1968.
10 WILSON, F. N., 1915; quoted in WILSON,F. N.: The
distribution of the potential differences produced by the
heart within the body and of its surface, Amer. Heart
I., 5:599, 1930.
11 RUSKIN,
A., AND DECHERD,
G.: Momentary atrial electrical axes. 111. A-V nodal rhythm, Amer. Heart J., 29:
633, 1945.
M., AND ALKAN,W. J.: Left atrial impulse
12 MIROWSKI,
formation in atrial flutter, Brit. Heart I., 29:299, 1967.
13 COHN,A. E. AND FRASER,F. R.: The occurrence of
auricular contractions in a case of incomplete and complete heart block due to stimuli received from the
contracting ventricles, Heart, 5:141, 1914.
14 WILSON,F. N., AND ROBINSON,
G. C.: Heart block I.
Two cases of complete heart block showing linlislial
features, Arch. Int. Med., 21:168, 1918.
15 CRANEFIELD,
P. F., AND HOFFMAN,
B. F.: The electrical
activity of the heart and the electrocardiogram, I.
Electrocardiolog!/, 1:2, 1968.
16 PUECH,P.: L'actioite electriqcie atrric~rlarienormale ('1
pathologiyr~e,Masson & Cie, Paris, 1956.
17 MASSIE,E., A N D WALSHT. J.: Clinical vectorcardiography and electrocardiography, The Year Book Medical
Publishers, Inc., Chicago, 1960.
18 MORRIS,J. J., ESTES,H., JR., WHALEN,R. W., THOXIPSON,H., JR., AND MCINTOSH,
H. D.: P wave analysis in
valv~ilarheart disease, Circulation, 29942, 1964.
19 Mmowsm, M., A ~ J VURE,
J
E.: The occurrence and mechanism of P wave inversion in lead I in right atrial overloading, Amer. Heart I., 72:102, 1966.
20 Z ~ I X I E R X I A
H.N ,A., BERSANO,
E., AND DICOSKY,C.:
The aurictilar ekcrrocardiogram, Charles C Thomas,
Springfield, Illinois, 1988.
M.: Experimental left atrill1
21 ROCEL,S., AND MIROWSKI,
rhythm, Israel J. Med. Sci., 2:352, 1966.
22 hM~ssuh11,R., AND TAWAKKOL,
A. A.: Direct stridy of
left atrial P waves, Amer. 1. Cardiol., 20:331, 1967.
23 Moss, A. J., RIVERS,R. J. JR., CRIFFITH,L. S. C..
CARXIEL,
J. A., AND MILLARD,
E. B. JR.: Transvenolis
left atrial pacing for the control of recurrent ventricular
fibrillation, Neco Eng. I. Med., 278:928, 1968.
S. 111, K R O ~F.,
24 HARRIS,B. C., SHAVER,J. A., GRAY,
W., AND LEOSARD,J. J.: Left atrial rhythm. Experimental production in man, Circuldion, 37:1000, 1968.
25 NEILL, C. A., AND MIROWSKI,M.: Dextrocardia, in
CASSEL,D. E. AND ZIECLER, R. F . (Eds.): Electrocardiography in infants and children, Grune and Stratton, New York, 1966.
26 JAhln, T. N.: The specialized conducting tissue of the
atria, in DREINS, L. S., AND LIKOFF,W., (Eds.): Mechanisms and therapy of cardiac arrhyhmias, 14th Hahnemann Symposium, Grune & Stratton, Inc., New York,
1966.
I., DRAJW, S., NEUSTAD,D., AND CHER27 BERKONSKY,
JOVSKY,R.: Ritmos auricular izquierdo experimental.
Comparacion con otros ritmos, Rev. Arg. Cardiologia,
35:8, 1968.
28 CULLIS,W. C., AND DIXON,W. E.: Excitation and section of the auriculo-ventricular bundle, I. Physiol.,
42:156, 1911.
29 SEGERS,M.: Les phenomenes de synchronisation au
nivea~i du coeur, Arch. Intern. Physiol., 54:87, 1946.
C.J., A ~ X I SCHERF,D.: Zlir kenntnis der
30 ROTHBERGER,
erregungsaus-breitung vom sinusknoten auf den vorhof,
Ztschr. ges exper. Med., 53:792, 1927.
J. V.: The sinoatrial node, the atrioventricular
31 BRUXILIK,
node, and atrial dysrhythmias, in KOSSX~AN,
C. E.
(Ed) Advances in electrocardiography, Gnine & Stratton.
Inc., New York, 1958.
32 KRAUS,Y., Y A ~ MJ., H., AND NNFELD,H. N.: Retrograde activation of the left atrium. Evidence by simultaneous indirect recording of left and right atrial mntractions, Israel J. Med. Sc., 2:350, 1966.
33 WALLACE,
A. G.,AND DACCFIT, W. M.: Re-excitation
of the atrium. "The echo phenomenon," Amer. Heart
I., 68:66l, 1964.
34 LANGENDORF,
R., AND PICK, A,: Approach to the interpretation of complex arrhythmias, Progr. Cardimarc.
Dis., 2:706, 1960.
35 BIX, H. H.: Various mechanisms in reciprocal rhythm
Amer. Heart I., 41:448, 1951.
H. E.:
36 HARRIS,W. E., SELILW,H. J., AND GRISWOLD,
Reversed reciprocating paroxysmal tachycardia controlled by guanethidine in a case of Wolff-ParkinsonWhite syndrome, Amer. Heart I., 67:812, 1964.
37 MOE, G. K., MENDEZ,C. AND HAN,J.: Some features of
, S.. AND
a dual A-V condriction system, in D ~ n m s L.
LIKOFF,W., (Eds.): Mechanisms and therapy of cardiac
arrhythmias, 14th Hahnemann Symposium, Cmne &
Stratton, New York, 1966.
38 LANGENDORF,
R., PICK, A., EDELLST, A., A N D K A ~ ,
L. N.: Experimental demonstration of concealed A-V
conduction in the human heart, Circulation, 32:386,
1965.
o , AND SAXIET,P.: Retrograde conduction in
39 C a s ~ n ~C.,
complete heart block, Brit. Heart J., 29:553, 1967.
40 SCHERF,D.: Retrograde conduction in complete heart
block, Dis. Chest, 35320, 1959.
41 VIDELA,J. G.: El diagnostico del origen del estimulo
por los caracteres de la deflexion auricular. Evalriacion
de 10s signos diagnosticos de los ritmos auricrilares ixquierdos, Rev. Argent. de Cardiol., 35:105, 1968.
Reprint requests: Dr. Mirowski, Sinai Hospital, Baltimore,
Maryland 21215.
CHEST, VOL. 57, NO. 1, JANUARY 1970
Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21487/ on 05/12/2017