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Intraventricular block
The American Journal \‘OLUME
VI
NOVEMBER
of Cardiology
1360
NUMBER
5
EDITORIAL
Intraventricular
I
1909 Eppinger and Rothberger investigated the alterations in the pattern of the electrocardiogram caused by- lesions in the myocardium. Being unable to create such lesions in an acute experiment (the idea of ligating a coronary artery occurred to Smith much later), they injected solutions of silver nitrate into the ventricular wall. To their astonishment tht, injection of large amounts of this substance often causrd only minor changes in the size of QRS complexes. Occasionally, however, a necrotic focus produced by a very small amount of silver nitrate provoked ma,jor changes and, in particular, a remarkable widening of the QRS complex. Ttlis obserlration led the authors to sever the main stem of the bundle branches and to the disco\.ery of the bundle tjranch block pattern in the elcctrocardio,gram.’ The same authors also described this abnormality in man and reported histologic findings which, to their satisfaction, proved the interrupThis report tion in one of the bundle branches. started a fallacy which lasted many years and handicapped the development of the theoretic Ijasis of the electrocardiogram and clinical electrocardiography. It became clear only much later, particularl!. through the investigations of M’ilson and his school, that the bundle I)ranch block was located on the wrong side, and what was considered right bundle branch block actuallv was a left one and vice versa. The “new norncn&ature” was very slowly accepted and as late as 1933 Rothberger rejected it,2 quoting a series of histologic reports by various authors supporting his original conception. This confusion and perserverance with mistaken ideas had several reasons which are of interest and have practical importance. ‘Toj)ogra@y OJ Conduction System: First, the histologic recognition and localization of the A-t’ conduction system is difficult; its topograph) rather than its particular structure perN
Block mits identification in man. Thus the’ \.er! existence and function of the A-\. svstem ha1.e been repeatedly denied even in recent years. Several important aspects of the A-V conduction system are not clear and await elucidation. M:e know little about the relation between the A-\’ node and coronary sinus node (Zahn’s node). It is established that the area at the orifice of the coronary sinus vein is endowed with a high degree of automaticity. Is this area an extension of the atria1 portion of the A-V node or is it a separate unit in loose contact with the A-\node? Is it an equivalent of the sinus node? Takahashi” speaks of it as a lower sinus node and Doer+ points out that the orifice of the coronar) sinus vein is situated in the former xinoatrial area and the coronary sinus node ma)’ t)e the equivalent of the node of Keith and Flack. Little is also known about the connections between the A-V node and the atria. In almost all textbooks on electrocardiograph)and physiology the A-V node is depicted as bein? situated in the right atrium and in contact only with its muscular Ilands and the right side of the atria1 septum. This is certainly not correct since during A-\’ rhythm the left atrium of the do,q conIjcfore the right one.” C:onnections tracts must therefore exist between the A-\’ node and the left sicle of the septum. Bilateral Bundle Branch Iwohement: A second cause for the initial confusion in the localization of the bundle branch block in man is the finding emphasized by MahaimGa and Yater,’ namely, that in man)- instances both bundle tjranchcs arc invollred, only one more than the other. Thcrcfore. one ma)- assume that during the difficult and time-consuming histologic examination of the bundle branches many examiners stopped looking as soon as they found a lesion in OIIC bundle branch. The difficulty of such in\.cstigations, on the other hand, has recertly been illustrated again I))- the fact that the frequent
Editorial occurrence of bilateral lesions has been denied.” Auxomerous Conduction: A third reason for the confusion is the experience that definite damage of the bundle branches was found histologically without the presence of a bundle branch block on This is explained by the the electrocardiogram. fact that conduction in the heart is “auxomerous,“g that is, it is not dependent on a certain width of the path. Cullis and DixonlO found that in the heart of the rabbit the smallest portion of the bundle, if undivided, “can carry Therefore, lesions in the all the conduction.” common bundle and bundle branches which do not involve the whole cross section of the pathThe lower way may not impair conduction. limits of this law, the smallest numt)er of fibers necessary for conduction with normal speed, are not known. Complete Bundle Branch Block: Arljitrarily and empirically complete bundle branch block is diagnosed by many when the width of the QRS complexes is 0.12 second or more. Mahaim6” an instance of bundle described, however, branch block in which the width of the QRS complex was only 0.09 second and QRS complexes of 0.11 second are not rare in right bundle On the other hand, left ventricubranch block. lar hypertrophy may cause QRS complexes with a width of 0.11 second, and it seems that in such cases an additional intraventricular conduction disturbance without involvement of the bundle branches may cause sufficient widening to imitate left bundle branch block. The term “complete bundle branch block” is often a misnomer t)ecause a complete interruption of conduction is not present even if the electrocardiographic pattern is typical. A delay of conduction in one bundle branch by more than 0.03 to 0.04 second causes the same picture as complete blockade since the impulse reaches the corresponding In many inventricle over the other bundle. stances of transient or intermittent bundle branch block, a delay of conduction in only one bundle existed and not “complete block.” Incomplete Bundle Branch Block: Because of the law of auxomerous conduction, incomplete bundle branch block does not seem to be caused by a lesion of only a part of the cross section of the bundle. Incomplete bundle branch block is rather a lesion in which the conduction in one branch is delayed by less than 0.04 second. With increasing delay of conduction in one bundle the QRS complexes show progressive changes since an increasing portion of the corresponding ventricle is excited via the other
ventricle. Here \-cr) slight delays lead to marked changes of the QRS complexes which show features midway- between the normal ones for this particular patient and bundle branch block. Such tracings are readily obtained expcrimentally when one impairs conduction by exerting slight pressure on a bundle branch with the It is back of a knife and registers the recovery. striking in such experiments”-lJ how quickly: often within a few beats, recovery takes place and the QRS complexes regain their normal appearance. This is due to the fact that the pattern of the electrocardiogram remains the same in complete block (immediately after the damage of the bundle) and during the entire rccovery phase until the delay at the damaged area is less than 0.04 second. We doubt, holeever, that this form of incomplete bundle branch block is as common in man as is often stated and that it can be as readily diagnosed as some textOne reason books and articles seem to assume. is that the pattern interpreted as incomplete bundle branch block is often observed without It is knolvn any change for months and longer. that a higher sympathetic tonus improves conduction in the ventricles and that improvement of even a few milliseconds would change the scquence of activation of the involved ventricle and therefore the form of the QRS complexe5. However, in a study of patients with the accepted pattern of incomplete right or left bundle branch block we were not able to change the form of the QRS complexes by exercise or the inhalation of amyl nitrite, factors which alter a delayed A-\conduction markedly. Neither does carotid sinus pressure leading to a marked prolongation of ventricular diastole change such QRS complexes. Most instances of partial X-V block lessen or disappear when the electrocardiogram is taken with the patient in the erect posture ancl usually a very prolonged P-R interval becomes instantly normal when the patient stands. No changes in the form of the QRS complexes appear when this procedure is followed in patients with so-called incomplete bundle branch block. Diagnosis of Incom$etr Bundle Branch Block: The assuredness with which incomplete bundle branch block is diagnosed in man is in sharp contrast with the difficulty of this diagnosis. Slight widening of the QRS complex alone dots not prove the existence of this lesion; on the other hand, incomplete bundle branch block even with a QRS duration of 0.13 second has been described. M A broader S wave in lead I ‘THE
AMERICAS
IOlJRSAL
OF
CARD101
OC1’
Editorial and a secondary R wa\re in lead L7t can occur in normal persons and do not pro1.e the presence of an incomplete ri+t t)unclle branch Mock. \\.ht.n these waves arc found in normal subject,, it is perhaps not ,justified to say that incomplete it is I ~~titlle block occurs in normal persons: safer to state that the acti\ration of certain parts of the right \.t‘ntricle in comparison with the left aitlc of the ventricular septulii differs from the i mown normal pattern. The differentiation of ~01tt(’ of the dcscril~ed tracings of incomplete I~~ntllc l)ranch I~lock frotn patterns seen in h\,pl\rtrophy of tltc ventricles is difficult; and un;il OII~ kttowlcdyc on this question improves, it WWIS safer to diagnose intra\.entricular conduction disturl~ancc \vithout an attetnpt at further tlifft~rcntialiori. T‘ctnporarity, for on? or a few I)f.ats, an incomplete trundle branch Mock can it pp~ar ancl t)c rlia~noscd with greater certaitirv.‘” Since in incomplete trundle branch block the sequence of activation of some portions of the in\,olved ventricle dift‘ers from the normal, one must consider the possihititv that similar atmortttatities could appear on the electrocardiogram \\hen branches of the tnain stetn of the bundle The modifiI,tanches are damaged by disease. cations of the electrocardiographic pattern I,)WZ~ lesions were investigated by two research ~~wII~“?~‘~ ‘ and the results were identical; the\. ;IIT rrtnarkal)le and too often neglected. The c~spcriments, pcrformcd on dogs, revealed that interruption of the whole anterior or posteriot di\Giotn of the left Ilundle branch soon after the t,ifurcation of the main bundle, or interruption of‘ concluction in those fibers which spread to\vard the apex often did not change the width of It remained 0.04 or the QRS comples at all. 0.05 second despite marked changes in the form If widening occurred in some esof the waves. ptariments, it did not surpass 0.01 second. One tnust therefore conclude that activation of a ttt;t,jor portion of the left ventricle via other pattt~tys ttccd not cause a widening of the QRS comThis result should tnake us cautious of a plcres. diagnosis of “incotttplete bundle branch block” if QKS complcscs arc lvidened to 0.11 second ot tttorc. The possit)ilil!has been considered, as menpreviously. bundle tionc*d that incomplete I)ranch hluck originates in the main hundle I,rattches when only a portion of the cross secThe law of auxotnerous contion is damaged. duction would preclude this possibilitv unless it could l)e demonstrated that a fun&onal dif\,)Vb.Yt3I:R
1060
ferentiation exists in the tnain stcttt of the hundIes and that certain portions of them conduct itttpulses to particular portions of the \.cntricles. llbnckrhach
Phnomrnon
in th
Nwdt~
Hrcuwttt .r:
conduction ciisturl)ancc cotnparat)lc IO tltt* Lt’ettckel)actt phenomenon i< another form of inIt is surprising that rltis form i, cotnplete ljlock. cxceedirtql)rare in man. \Vhrn OIl(’ Illltltll~ branch is completely xe\.erecl in tlrc%~10~ ttc’art 01 sifrr and pressure is exerted on tltc othrr t)ranclt with the Ijack of the knift,, complete :\-\. I)lock appears at tirst: soon rrco\.ct-y takes place and during the rccovcry proccqs all t! pus of partial A-V I)lock arc rcadil!. ol)~cr\~cd.‘” (btnparc~cl with this csprriencr the rarity. of partial I)undtc Of course*. 3: 1 branch I)lock in man iq striking. and 4: 3 I)undlc t)ranch I~lock arc ol)s~r\~ccl and usuallv called intermittent t)undlc I>ranclt t~tock. Ho\ve;.tlr, a qraduat widening of the QliS co~ttplcscs frotn t>Fat to tIeat endin? with it typical bundle I)ranch t)lock pattern and this in turn followed I+. ;I normal QRS cotnplcs rcprc,scntinL: a LVcnckcl)ach phenomenon in a I~ttndl~ has not been described in man or in the cxpcritttcnt with normal rhythm and rate. One case which coulcl be interpreted in this way has I)ecn dvsct-il)cd I)\ Holztnann’7 Ijut in this patient a mark~cl \‘cnThe LVenckrt)aclt tricular arrhvthmia existed. phenomenon in one bundle was clearly ol~~\~ccl in the do?‘” but only when tttc rate was rapid beit is known that under cause of atria1 flutter; conditions conduction follo~vs special these rules. One reason for the rarity of the \\~cnckcl)aclt phenomenon in the bundle tjranch as compared with its frequency in A-V Mock is the fact that in A-V Mock after complete I)locking of one heat the conduction systetn sotnehow recovrrs and the following itnpulse is conducted well. How this recovery takes place is still not understood since it i$ not known why the damaged tissue which ,just failed to conduct an impulse does it well when the next one arrives. Recovery is made more difficult in I,undlc branch l)lock; I)ccaust when the Ijundle branch dots not conduct att impulse to the ventricle, the impulse arrive, there via the other ventricle ancl ih conducted in the invol\~ecl I)undlc I)ranclt retrograde Another reason why such electrocardiographic patterns have not been seen in tnan is the experience that when conduction improves after the Mocked impulse in a Wenckebach phenomenon it still often retnains prolongedlY and, as pointed out previously, any delay of conduction t))- mart than 0.04 second will cause the satnc pattern on A
Editorial the electrocardiogram as in complete bundle branch block. Focal and Par&al Block: Whether widening of the QRS complexes occurs because of abnormal conduction from fiber to fiber in the common myocardium (fiber block, focal block, parietal block) as opposed to a lesion of the conduction Widening of the systemzO is not yet certain. QRS complexes after injection of procaine” or quinidineZ2 into branches of the coronary arteries need not indicate such a block since damage to peripheral branches of the conduction system cannot be ruled out. The widening of the QRS complexes seen after administration of quinidine may also involve the specialized tissue and need not indicate damage to working muscle alone. Certainly further studies of this question are required. It seems doubtful whether widening of the QRS complexes appears as a consequence of myocardial infarction “peri-infarction” block23 without participation of the bundle branches only because the impulse is prevented from activating the ventricular myocardium from inside out. The experiments with silver nitrate cited The earlier speak against this assumption. presence of bundle branch block and infarction would explain most of these tracings. Arboritation Block: The “arborization block,” usually mentioned in quotation marks, is rare The very wide and its mechanism controversial. and very low QRS complexes are often said to be due to a lesion “below the main stem of the bundle.” This seems certain but does not exIt is argued that the term should plain much. not be used since it implies a lesion of the Purkinje network; however, this explanation has not Destruction of large been seriously considered. areas of the subendocardial muscular layers with the smaller branches of the specialized A-V system by scraping with a small knife did not cause widening of the QRS complexes in our exIn recent years arborization block perience. has been attributed to focal damage of the myocardium; this is improbable in view of the experiments quoted previously. Neither could block in some ramifications of one bundle branch cause such a pattern on the electrocardiogram. We believe that complete block in one bundle branch and almost complete block in the other could cause the electrocardiographic pattern of arborization block. Thus, a complete block of the right bundle branch and a block in the left main stem below the origin of the small branch which activates the upper left septum24
could produce this pattern ; it would force the impulse to utilize mainly the common myocardium for its spread over the ventricles and the impulse would spread from a central point in all directions.6” DAVID
SCHERF, M.D., F.A.C.C.
Department of Medicine .Vew Ihrk Medical College .Yew York, ;\:ew York REFERENCES 1. EPPINGER, H. and ROTHBERGER, C. J. Ueber die Folgen der Durchschneidung der Tawaraschen Schenkel des Reizleitungssystems. Ztschr. klin. Med.. 70: 1, 1910. 2. ROTHBERGER, C. J. Zur Diagnose des Schenkelblocks. Ztschr. klin. Mud., 123: 460, 1933. 3. TAKAHASHI, H. Ueber das spezifische Muskelsystem des Vorhof des menschlichen Herzens. II. Beziehungen zwischen “unterem Sinusknoten” und intrakardiales Nervensystem. TY. J@. Path. Sac., 22: 570, 1932. 4. DOERR, W. Die Morphologie des Reizleitungsund Pathologie. In: systems, ihre Orthologie Spang, K. Rhythmusstoertlngen des Herzens. Stuttgart, 1957. Thieme. 5. ROTHBERGER, C. J. and SCHERF, D. Zur Kenntnis der Erregungsausbreitung vom Sinusknoten auf Ztschr. ges. rxper. Med., 53: 792, 1927. den Vorhof. 6. (a) MAHAIM, I. Les maladies organiques du faisceau de His-Tawara. Paris, 1931. Masson et Cie. (6) MAHAIM, I. Nouvelle forme anatomiques de bloc de coeur, a substituer au bloc dit d’arborisations (bloc bilateral manqut). Compt. rend. Sot. de biol., 109: 183, 1932. 7. YATER, W. M. Pathogenesis of bundle branch block. Arch. Znt. Med.. 62: 1, 1938. 8. LEN~GRE, J. Contribution a I’etude des blocs de branche, comportant notamment lrs confrontaParis, 1958. tions klectriques et histologiques. J. B. BailliZre et Fils. 9. KRIES, J. V. Ueber die Bedeutung der Bahnbreite fuer die Reizleitung im Herzen. Skandinau. arch. physiol., 29: 84, 1913. 10. CULLIS, W. C. and DIXON, W. E. Excitation and section of the auriculo-ventricular bundle. J. Physiol., 42: 156, 1911. 11. RODRIQUEZ. M. I. and SODI-PALLARES, D. The mechanism of complete and incomplete bundle branch block. Am. Heart J., 44: 715, 1952. 12. ROTIIBERGER, C. J. and WINTERBERG, H. Experimentelle Beitraegc zur Kenntnis der Reizleitungsstoerungen in den Kammern des Saugetierherzens. Ztschr. ges. exper. Med., 5 : 264, 1917. 13. SCHERF, D. and SHOOKHOFF, C. Reizleitungsstoerungen im Buendel. IL Win Arch. f. inn. Mrd., 11: 425, 1925. An experi14. WILSON, F. N. and HERRMANN, G. mental study of incomplete bundle branch block and of the refractory period of the heart of the do:. Heart. 8: 229, 1921. 15. BRYANT, J. M. Intraventricular conduction. In: Kossman, C. Advances in Electrocardiography. New York, 1958. Grune and Stratton. ‘THE AMERICANJOURNAL OF CARDIOLOGY
Editorial 16. SCHERF. D. and BOYD, L. J. Clinical Electrocardiography, 4th ed., fig. 40. New York, 1953. Grune and Stratton. 17. HOLZMANN. M. Klinische Elektrokardiographic, 3rd ed., fig. 31. Stuttgart, 1955. Thieme. 18. SCIIERF, D. Experimentellc und klinische Untcrsuchungen uebrr intraventrikulaere Leitunqstocrungen. Wm. Arch. f. inn. Mrd.. 14: 443, 1927. 19. ROSENRAUM, M. B. and LEPESCHKIN, E. Bilateral bundle branch block. Am. Heart J., 50: 39, 1955. 20. Sticms. M. The different types of intra\entricular block. Am. Heart J., 37: 92, 1949.
NOVEMBER 1960
857
21. .\LZAMOR.A-CASTRO,v., ;\BUGAT.T.AS.B., RUBlO, C., BOURONCLE, J., ZAPATA, C., SANTA-MARIA, 1:., BATTILANA, G., BINDER, T.. SURIKIA. R. and PARWES, D. Parietal focal block: an expcrimrntal and elmztrocardiographic stud\,. C’irrulntin,,, 7: 108, 1953. 22. FRAU. G. La pathogenie des troubles dr la conduc. tion vrntriculairc. Cordioluqia. 19 : 2. 1951. 23. FrRsT. S. R.. BAYLE\I., R. H. and BEI)PORI), D. R. Prri-infarction block. Circzrlntzon, 2 : 31 1 1950. 24. SCHERF. D. Zur Entstrhungswrisr drr 6xtrasystolrn and dw extrasystolischcn :Illorhythmicn. Ztschr. ~PJ. rrhvr. .+ftvl.. 51 : 816, 1926.
VI
NOVEMBER
of Cardiology
1360
NUMBER
5
EDITORIAL
Intraventricular
I
1909 Eppinger and Rothberger investigated the alterations in the pattern of the electrocardiogram caused by- lesions in the myocardium. Being unable to create such lesions in an acute experiment (the idea of ligating a coronary artery occurred to Smith much later), they injected solutions of silver nitrate into the ventricular wall. To their astonishment tht, injection of large amounts of this substance often causrd only minor changes in the size of QRS complexes. Occasionally, however, a necrotic focus produced by a very small amount of silver nitrate provoked ma,jor changes and, in particular, a remarkable widening of the QRS complex. Ttlis obserlration led the authors to sever the main stem of the bundle branches and to the disco\.ery of the bundle tjranch block pattern in the elcctrocardio,gram.’ The same authors also described this abnormality in man and reported histologic findings which, to their satisfaction, proved the interrupThis report tion in one of the bundle branches. started a fallacy which lasted many years and handicapped the development of the theoretic Ijasis of the electrocardiogram and clinical electrocardiography. It became clear only much later, particularl!. through the investigations of M’ilson and his school, that the bundle I)ranch block was located on the wrong side, and what was considered right bundle branch block actuallv was a left one and vice versa. The “new norncn&ature” was very slowly accepted and as late as 1933 Rothberger rejected it,2 quoting a series of histologic reports by various authors supporting his original conception. This confusion and perserverance with mistaken ideas had several reasons which are of interest and have practical importance. ‘Toj)ogra@y OJ Conduction System: First, the histologic recognition and localization of the A-t’ conduction system is difficult; its topograph) rather than its particular structure perN
Block mits identification in man. Thus the’ \.er! existence and function of the A-\. svstem ha1.e been repeatedly denied even in recent years. Several important aspects of the A-V conduction system are not clear and await elucidation. M:e know little about the relation between the A-\’ node and coronary sinus node (Zahn’s node). It is established that the area at the orifice of the coronary sinus vein is endowed with a high degree of automaticity. Is this area an extension of the atria1 portion of the A-V node or is it a separate unit in loose contact with the A-\node? Is it an equivalent of the sinus node? Takahashi” speaks of it as a lower sinus node and Doer+ points out that the orifice of the coronar) sinus vein is situated in the former xinoatrial area and the coronary sinus node ma)’ t)e the equivalent of the node of Keith and Flack. Little is also known about the connections between the A-V node and the atria. In almost all textbooks on electrocardiograph)and physiology the A-V node is depicted as bein? situated in the right atrium and in contact only with its muscular Ilands and the right side of the atria1 septum. This is certainly not correct since during A-\’ rhythm the left atrium of the do,q conIjcfore the right one.” C:onnections tracts must therefore exist between the A-\’ node and the left sicle of the septum. Bilateral Bundle Branch Iwohement: A second cause for the initial confusion in the localization of the bundle branch block in man is the finding emphasized by MahaimGa and Yater,’ namely, that in man)- instances both bundle tjranchcs arc invollred, only one more than the other. Thcrcfore. one ma)- assume that during the difficult and time-consuming histologic examination of the bundle branches many examiners stopped looking as soon as they found a lesion in OIIC bundle branch. The difficulty of such in\.cstigations, on the other hand, has recertly been illustrated again I))- the fact that the frequent
Editorial occurrence of bilateral lesions has been denied.” Auxomerous Conduction: A third reason for the confusion is the experience that definite damage of the bundle branches was found histologically without the presence of a bundle branch block on This is explained by the the electrocardiogram. fact that conduction in the heart is “auxomerous,“g that is, it is not dependent on a certain width of the path. Cullis and DixonlO found that in the heart of the rabbit the smallest portion of the bundle, if undivided, “can carry Therefore, lesions in the all the conduction.” common bundle and bundle branches which do not involve the whole cross section of the pathThe lower way may not impair conduction. limits of this law, the smallest numt)er of fibers necessary for conduction with normal speed, are not known. Complete Bundle Branch Block: Arljitrarily and empirically complete bundle branch block is diagnosed by many when the width of the QRS complexes is 0.12 second or more. Mahaim6” an instance of bundle described, however, branch block in which the width of the QRS complex was only 0.09 second and QRS complexes of 0.11 second are not rare in right bundle On the other hand, left ventricubranch block. lar hypertrophy may cause QRS complexes with a width of 0.11 second, and it seems that in such cases an additional intraventricular conduction disturbance without involvement of the bundle branches may cause sufficient widening to imitate left bundle branch block. The term “complete bundle branch block” is often a misnomer t)ecause a complete interruption of conduction is not present even if the electrocardiographic pattern is typical. A delay of conduction in one bundle branch by more than 0.03 to 0.04 second causes the same picture as complete blockade since the impulse reaches the corresponding In many inventricle over the other bundle. stances of transient or intermittent bundle branch block, a delay of conduction in only one bundle existed and not “complete block.” Incomplete Bundle Branch Block: Because of the law of auxomerous conduction, incomplete bundle branch block does not seem to be caused by a lesion of only a part of the cross section of the bundle. Incomplete bundle branch block is rather a lesion in which the conduction in one branch is delayed by less than 0.04 second. With increasing delay of conduction in one bundle the QRS complexes show progressive changes since an increasing portion of the corresponding ventricle is excited via the other
ventricle. Here \-cr) slight delays lead to marked changes of the QRS complexes which show features midway- between the normal ones for this particular patient and bundle branch block. Such tracings are readily obtained expcrimentally when one impairs conduction by exerting slight pressure on a bundle branch with the It is back of a knife and registers the recovery. striking in such experiments”-lJ how quickly: often within a few beats, recovery takes place and the QRS complexes regain their normal appearance. This is due to the fact that the pattern of the electrocardiogram remains the same in complete block (immediately after the damage of the bundle) and during the entire rccovery phase until the delay at the damaged area is less than 0.04 second. We doubt, holeever, that this form of incomplete bundle branch block is as common in man as is often stated and that it can be as readily diagnosed as some textOne reason books and articles seem to assume. is that the pattern interpreted as incomplete bundle branch block is often observed without It is knolvn any change for months and longer. that a higher sympathetic tonus improves conduction in the ventricles and that improvement of even a few milliseconds would change the scquence of activation of the involved ventricle and therefore the form of the QRS complexe5. However, in a study of patients with the accepted pattern of incomplete right or left bundle branch block we were not able to change the form of the QRS complexes by exercise or the inhalation of amyl nitrite, factors which alter a delayed A-\conduction markedly. Neither does carotid sinus pressure leading to a marked prolongation of ventricular diastole change such QRS complexes. Most instances of partial X-V block lessen or disappear when the electrocardiogram is taken with the patient in the erect posture ancl usually a very prolonged P-R interval becomes instantly normal when the patient stands. No changes in the form of the QRS complexes appear when this procedure is followed in patients with so-called incomplete bundle branch block. Diagnosis of Incom$etr Bundle Branch Block: The assuredness with which incomplete bundle branch block is diagnosed in man is in sharp contrast with the difficulty of this diagnosis. Slight widening of the QRS complex alone dots not prove the existence of this lesion; on the other hand, incomplete bundle branch block even with a QRS duration of 0.13 second has been described. M A broader S wave in lead I ‘THE
AMERICAS
IOlJRSAL
OF
CARD101
OC1’
Editorial and a secondary R wa\re in lead L7t can occur in normal persons and do not pro1.e the presence of an incomplete ri+t t)unclle branch Mock. \\.ht.n these waves arc found in normal subject,, it is perhaps not ,justified to say that incomplete it is I ~~titlle block occurs in normal persons: safer to state that the acti\ration of certain parts of the right \.t‘ntricle in comparison with the left aitlc of the ventricular septulii differs from the i mown normal pattern. The differentiation of ~01tt(’ of the dcscril~ed tracings of incomplete I~~ntllc l)ranch I~lock frotn patterns seen in h\,pl\rtrophy of tltc ventricles is difficult; and un;il OII~ kttowlcdyc on this question improves, it WWIS safer to diagnose intra\.entricular conduction disturl~ancc \vithout an attetnpt at further tlifft~rcntialiori. T‘ctnporarity, for on? or a few I)f.ats, an incomplete trundle branch Mock can it pp~ar ancl t)c rlia~noscd with greater certaitirv.‘” Since in incomplete trundle branch block the sequence of activation of some portions of the in\,olved ventricle dift‘ers from the normal, one must consider the possihititv that similar atmortttatities could appear on the electrocardiogram \\hen branches of the tnain stetn of the bundle The modifiI,tanches are damaged by disease. cations of the electrocardiographic pattern I,)WZ~ lesions were investigated by two research ~~wII~“?~‘~ ‘ and the results were identical; the\. ;IIT rrtnarkal)le and too often neglected. The c~spcriments, pcrformcd on dogs, revealed that interruption of the whole anterior or posteriot di\Giotn of the left Ilundle branch soon after the t,ifurcation of the main bundle, or interruption of‘ concluction in those fibers which spread to\vard the apex often did not change the width of It remained 0.04 or the QRS comples at all. 0.05 second despite marked changes in the form If widening occurred in some esof the waves. ptariments, it did not surpass 0.01 second. One tnust therefore conclude that activation of a ttt;t,jor portion of the left ventricle via other pattt~tys ttccd not cause a widening of the QRS comThis result should tnake us cautious of a plcres. diagnosis of “incotttplete bundle branch block” if QKS complcscs arc lvidened to 0.11 second ot tttorc. The possit)ilil!has been considered, as menpreviously. bundle tionc*d that incomplete I)ranch hluck originates in the main hundle I,rattches when only a portion of the cross secThe law of auxotnerous contion is damaged. duction would preclude this possibilitv unless it could l)e demonstrated that a fun&onal dif\,)Vb.Yt3I:R
1060
ferentiation exists in the tnain stcttt of the hundIes and that certain portions of them conduct itttpulses to particular portions of the \.cntricles. llbnckrhach
Phnomrnon
in th
Nwdt~
Hrcuwttt .r:
conduction ciisturl)ancc cotnparat)lc IO tltt* Lt’ettckel)actt phenomenon i< another form of inIt is surprising that rltis form i, cotnplete ljlock. cxceedirtql)rare in man. \Vhrn OIl(’ Illltltll~ branch is completely xe\.erecl in tlrc%~10~ ttc’art 01 sifrr and pressure is exerted on tltc othrr t)ranclt with the Ijack of the knift,, complete :\-\. I)lock appears at tirst: soon rrco\.ct-y takes place and during the rccovcry proccqs all t! pus of partial A-V I)lock arc rcadil!. ol)~cr\~cd.‘” (btnparc~cl with this csprriencr the rarity. of partial I)undtc Of course*. 3: 1 branch I)lock in man iq striking. and 4: 3 I)undlc t)ranch I~lock arc ol)s~r\~ccl and usuallv called intermittent t)undlc I>ranclt t~tock. Ho\ve;.tlr, a qraduat widening of the QliS co~ttplcscs frotn t>Fat to tIeat endin? with it typical bundle I)ranch t)lock pattern and this in turn followed I+. ;I normal QRS cotnplcs rcprc,scntinL: a LVcnckcl)ach phenomenon in a I~ttndl~ has not been described in man or in the cxpcritttcnt with normal rhythm and rate. One case which coulcl be interpreted in this way has I)ecn dvsct-il)cd I)\ Holztnann’7 Ijut in this patient a mark~cl \‘cnThe LVenckrt)aclt tricular arrhvthmia existed. phenomenon in one bundle was clearly ol~~\~ccl in the do?‘” but only when tttc rate was rapid beit is known that under cause of atria1 flutter; conditions conduction follo~vs special these rules. One reason for the rarity of the \\~cnckcl)aclt phenomenon in the bundle tjranch as compared with its frequency in A-V Mock is the fact that in A-V Mock after complete I)locking of one heat the conduction systetn sotnehow recovrrs and the following itnpulse is conducted well. How this recovery takes place is still not understood since it i$ not known why the damaged tissue which ,just failed to conduct an impulse does it well when the next one arrives. Recovery is made more difficult in I,undlc branch l)lock; I)ccaust when the Ijundle branch dots not conduct att impulse to the ventricle, the impulse arrive, there via the other ventricle ancl ih conducted in the invol\~ecl I)undlc I)ranclt retrograde Another reason why such electrocardiographic patterns have not been seen in tnan is the experience that when conduction improves after the Mocked impulse in a Wenckebach phenomenon it still often retnains prolongedlY and, as pointed out previously, any delay of conduction t))- mart than 0.04 second will cause the satnc pattern on A
Editorial the electrocardiogram as in complete bundle branch block. Focal and Par&al Block: Whether widening of the QRS complexes occurs because of abnormal conduction from fiber to fiber in the common myocardium (fiber block, focal block, parietal block) as opposed to a lesion of the conduction Widening of the systemzO is not yet certain. QRS complexes after injection of procaine” or quinidineZ2 into branches of the coronary arteries need not indicate such a block since damage to peripheral branches of the conduction system cannot be ruled out. The widening of the QRS complexes seen after administration of quinidine may also involve the specialized tissue and need not indicate damage to working muscle alone. Certainly further studies of this question are required. It seems doubtful whether widening of the QRS complexes appears as a consequence of myocardial infarction “peri-infarction” block23 without participation of the bundle branches only because the impulse is prevented from activating the ventricular myocardium from inside out. The experiments with silver nitrate cited The earlier speak against this assumption. presence of bundle branch block and infarction would explain most of these tracings. Arboritation Block: The “arborization block,” usually mentioned in quotation marks, is rare The very wide and its mechanism controversial. and very low QRS complexes are often said to be due to a lesion “below the main stem of the bundle.” This seems certain but does not exIt is argued that the term should plain much. not be used since it implies a lesion of the Purkinje network; however, this explanation has not Destruction of large been seriously considered. areas of the subendocardial muscular layers with the smaller branches of the specialized A-V system by scraping with a small knife did not cause widening of the QRS complexes in our exIn recent years arborization block perience. has been attributed to focal damage of the myocardium; this is improbable in view of the experiments quoted previously. Neither could block in some ramifications of one bundle branch cause such a pattern on the electrocardiogram. We believe that complete block in one bundle branch and almost complete block in the other could cause the electrocardiographic pattern of arborization block. Thus, a complete block of the right bundle branch and a block in the left main stem below the origin of the small branch which activates the upper left septum24
could produce this pattern ; it would force the impulse to utilize mainly the common myocardium for its spread over the ventricles and the impulse would spread from a central point in all directions.6” DAVID
SCHERF, M.D., F.A.C.C.
Department of Medicine .Vew Ihrk Medical College .Yew York, ;\:ew York REFERENCES 1. EPPINGER, H. and ROTHBERGER, C. J. Ueber die Folgen der Durchschneidung der Tawaraschen Schenkel des Reizleitungssystems. Ztschr. klin. Med.. 70: 1, 1910. 2. ROTHBERGER, C. J. Zur Diagnose des Schenkelblocks. Ztschr. klin. Mud., 123: 460, 1933. 3. TAKAHASHI, H. Ueber das spezifische Muskelsystem des Vorhof des menschlichen Herzens. II. Beziehungen zwischen “unterem Sinusknoten” und intrakardiales Nervensystem. TY. J@. Path. Sac., 22: 570, 1932. 4. DOERR, W. Die Morphologie des Reizleitungsund Pathologie. In: systems, ihre Orthologie Spang, K. Rhythmusstoertlngen des Herzens. Stuttgart, 1957. Thieme. 5. ROTHBERGER, C. J. and SCHERF, D. Zur Kenntnis der Erregungsausbreitung vom Sinusknoten auf Ztschr. ges. rxper. Med., 53: 792, 1927. den Vorhof. 6. (a) MAHAIM, I. Les maladies organiques du faisceau de His-Tawara. Paris, 1931. Masson et Cie. (6) MAHAIM, I. Nouvelle forme anatomiques de bloc de coeur, a substituer au bloc dit d’arborisations (bloc bilateral manqut). Compt. rend. Sot. de biol., 109: 183, 1932. 7. YATER, W. M. Pathogenesis of bundle branch block. Arch. Znt. Med.. 62: 1, 1938. 8. LEN~GRE, J. Contribution a I’etude des blocs de branche, comportant notamment lrs confrontaParis, 1958. tions klectriques et histologiques. J. B. BailliZre et Fils. 9. KRIES, J. V. Ueber die Bedeutung der Bahnbreite fuer die Reizleitung im Herzen. Skandinau. arch. physiol., 29: 84, 1913. 10. CULLIS, W. C. and DIXON, W. E. Excitation and section of the auriculo-ventricular bundle. J. Physiol., 42: 156, 1911. 11. RODRIQUEZ. M. I. and SODI-PALLARES, D. The mechanism of complete and incomplete bundle branch block. Am. Heart J., 44: 715, 1952. 12. ROTIIBERGER, C. J. and WINTERBERG, H. Experimentelle Beitraegc zur Kenntnis der Reizleitungsstoerungen in den Kammern des Saugetierherzens. Ztschr. ges. exper. Med., 5 : 264, 1917. 13. SCHERF, D. and SHOOKHOFF, C. Reizleitungsstoerungen im Buendel. IL Win Arch. f. inn. Mrd., 11: 425, 1925. An experi14. WILSON, F. N. and HERRMANN, G. mental study of incomplete bundle branch block and of the refractory period of the heart of the do:. Heart. 8: 229, 1921. 15. BRYANT, J. M. Intraventricular conduction. In: Kossman, C. Advances in Electrocardiography. New York, 1958. Grune and Stratton. ‘THE AMERICANJOURNAL OF CARDIOLOGY
Editorial 16. SCHERF. D. and BOYD, L. J. Clinical Electrocardiography, 4th ed., fig. 40. New York, 1953. Grune and Stratton. 17. HOLZMANN. M. Klinische Elektrokardiographic, 3rd ed., fig. 31. Stuttgart, 1955. Thieme. 18. SCIIERF, D. Experimentellc und klinische Untcrsuchungen uebrr intraventrikulaere Leitunqstocrungen. Wm. Arch. f. inn. Mrd.. 14: 443, 1927. 19. ROSENRAUM, M. B. and LEPESCHKIN, E. Bilateral bundle branch block. Am. Heart J., 50: 39, 1955. 20. Sticms. M. The different types of intra\entricular block. Am. Heart J., 37: 92, 1949.
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21. .\LZAMOR.A-CASTRO,v., ;\BUGAT.T.AS.B., RUBlO, C., BOURONCLE, J., ZAPATA, C., SANTA-MARIA, 1:., BATTILANA, G., BINDER, T.. SURIKIA. R. and PARWES, D. Parietal focal block: an expcrimrntal and elmztrocardiographic stud\,. C’irrulntin,,, 7: 108, 1953. 22. FRAU. G. La pathogenie des troubles dr la conduc. tion vrntriculairc. Cordioluqia. 19 : 2. 1951. 23. FrRsT. S. R.. BAYLE\I., R. H. and BEI)PORI), D. R. Prri-infarction block. Circzrlntzon, 2 : 31 1 1950. 24. SCHERF. D. Zur Entstrhungswrisr drr 6xtrasystolrn and dw extrasystolischcn :Illorhythmicn. Ztschr. ~PJ. rrhvr. .+ftvl.. 51 : 816, 1926.