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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