- Email: [email protected]
The genesis of bidirectional tachycardias
The genesis
of bidirectional
Agustin Castellanos, Miami, Fla.
Jr.,
M.D.
S
everal mechanisms for the production of bidirectional tachycardias have been proposed. l-l1 This is not surprising in view of the uncertain origin of arrhythmias which have a rapid rate with prolonged and bizarre QRS complexes.12 As in all cases of complex disorders of rhythm a complete knowledge of cardiac physiology is required. But, in addition, the technician should be taught to obtain long strips of the electrocardiogram, mainly in one lead, so that the greatest number of pathologic mechanisms can be recorded, as can be seen in Figs. 1-7 of this communication. Table
1.
2. 4: 3 5. 6. 7. 8. 9. 10. 11. 12. 13. 11. AHD:
Because of the complexities seen in short (conventional) tracings, certain authors have advanced the theory that bidirectional tachycardia probably represents a heterogeneous group of cases which have similar electrocardiographic configuration.1 For example, some workers have postulated the existence of two pacemakers: either one supraventricular and one ventricular2s3or two ventricular ones.7,821Moreover, others believe that the paroxysm originates in one single focus before’,4,5,6,9-1’,‘3 or after the bifurcation.14J2 Precisely, this communication establishes that not one,
I
I Case
tachycardias
Ate (yr.1
63 68 70 65 88 71 75 69 71 63 65 84 9 9
Arteriosclerotic fibrillation. S.R.: From
Received
733
’ Etiology
AHD AHD AHD AHD AHD AHD ,4HD AHD EM AHD AHD AHD DM NH
~ Heart ~aflure
Digitalis
Yes Yes Yes Yes Yes Yes Yes Yes No Yes Yes Yes No No
++++ ++++ ++++ ++++ ++++ ++++ ++++ ++++
for publication
NO NO
of Medicine.
Sept.
A. F. A. F. A. F. s. R. s. R. A. T. A. T. A. T. .4-V. T. -4-v. T. A. F. A. F. ? A. T.
l+ ++i-+ ++++
heart disease. EM: Encephalamyocarditis. Sinus rhythm. A.T.: Atria1 tachycardia. the Department
Atria1 rhythm during paroxysm
Section
12. 1060.
DM: Riphtheritic A-V.T.: Atrioventricular of Cardiology,
University
AlternaEsophageal
leads Yes Yes Yes Yes Yes Yes Yes Yes No Yes NO
Yes No Yes myocarditis. NH: nodal tachycardia. of Miami
School
tion in direction in Lead VI
Ventvicz~lar
No No No No No
157 1.58 150 167 150-172 115 168 176-188 167-180 170 166 166 130 188-275
rate
NO
No No No No Yes No No No Normal
of Medicine,
heart.
Miami,
A.F.:
Fla.
Atrial
tive fnilurc. ‘The detzilecl clillic.;ll tl. the rate, as well as the interval between the 111;~~ complexes of different morphologies, vary more than 0.04 seco1~1. Results
Fig. 1. Bidirectional tat-hvrardk of atria1 IKI~~II. ‘l‘hcse tracings were obtained from a 9-yex-ol~l asthmatic girl with bouts of “repetitiw parox~ sn~l tachycardia,” but no heart discax!. 12 supravcntricular tuchycardia (rate: 188 per min.) with aberration showing diffcrcnt degrees of right-sided into-a\ ~IItricular cwlduction defect a11 he seen in A1. ‘1%~ esoph;tgea! lend (I3) clearly cstablishcc: the nt trial origin of the paroxysm. In C, diffcrcnt degree> of aberration we seen again. Finally, ilk I?, when t hc rate speeded up to 27.5 per min., a c-lnious fol-m of alternation is prescnl : an rsK’ comples of lcswr dur;ttion and smaller height altwnates with one of greater duration and height. This record is intcrpreted as an example of atrial tachycardia H.ith bidirectional complexes due to nlternating aberrant ventricular conduction. The warming up of the cc,topic center is attributed to a mechanism similar I o the “rhythm of development .“)O
but several mechanisms are involved in the genesis of what has been called bidirectional tachycardia from a simple morphologic configuration. Prognosis and treatment will not be considered here. Material
and methods
0ur material consists of 14 records showing bidirectional tachycardias (other tracings from these patients have been included in previous reports13*‘4). ,411 subjects except 3 (Table J) had arteriosclerotic heart varying degrees of congescl isease and
Of the 14 cases studied there were 5 in which the corresponding records showed certain characteristics which could be of help in clarifying the genesis of bidirectional tnchycardias. These cases are presented in l’igs. 1-7, and the corresponding electrocardiagrams are fully described in the respective legends. Table I shows the basic features. Comment Many theories have been proposed to explain the genesis of bidirectional tach>-cardias.l-lA Some have received widespread ~tttentioii1,‘,6,g,11,1~; others, such as the double circus movement of White and Palmer,Ij have been practically forgotten. One of the earliest assumptions favored the ventricular origin of the paroxysm.7,s This \\ras due to the observation that many cases showed frequent ventricular extrasystotes prior to or after the tachycardia. Thus, it was considered that the two morphologies corresponded to two foci of impulse formation, that is, one in each ventricle. Such a theory has been challenged in later years since the work of Zimdahl and Kramer,” who showed that one of the two complexes in their case could be abolished by carotid sinus pressure, and thus postulated that two active centers were present-one ventricular and one supraventriculnr. Similarly, other authors
Genesis of bidircctio~lal
have since reported instances of disappearnnce of the arrhythmia by this or allied vagomimetic procedures.2-5a13a16 However, the unquestionable ventricular origin of bidirectional tachycardia was established in Figs. 4 and 5 by the presence of fusion beats; the alternating complexes were explained on the basis of irregular intraventricular propagation. Furthermore, this case is a clear example of the abolishment of a ventricular tachycardia by carotid sinus pressure, so that the effectiveness of cannot be related necessaril> this procedure to the existence of a supraventricular tachycardia.’ It should be emphasized that
tachycardias
735
Scherf17J8 has reported the slowing of ventricular parasystole by carotid pressure, indicating the response of ventricular rhythms to vagus stimulation. Similarly, the transition of bidirectional to unidirectional complexes without changes in rate also rules out the diagnosis of double ventricular paroxysmal tachycardia. Evidently, this possibility is to be considered extremely rare because no instance of this arrhythmia was found in a recent review of 15 cases of simultaneous tachycardkh’ Occasionally, it has been considered that the disappearance of one type of beat, with halving of the ventricular rate after
Fig. 2. Bidirectional tachycardia originating in one supravcntricular center, probably in the A-V node. The tracings start with a regular tachycardia (rate: 167 per min.) and QRS duration of 0.06 sec. Note that it is dissociated from an independent sinus rhythm (rate: 103 per min.), and that the I’ waves have a predominant negative deflection in the esophageal lead (E. 30). .Xlternation in the height of ventricular complexes appears toward the middle of the tracing and is best seen in Lead II. The records continue uninterruptedly with that of Fig. 3.
Fig. 3. Bidirectional tachycardia originating in one supraventricular center, probably in the A-\: node. This tracing is continuous with that of Fig. 2, and shows besides an alternation in the height of ventricular complexes a progressive alternation in direction of QRS and T, until the classic-image bidirectional tachycardia appears toward the end of the record. In Figs. 2 and 3 the strictly regular and constant rate, and the gradual evolution from unidirectional to bidirectional alternation, in association with only moderate changes in ventricular duration (which is within normal limits: 0.08 sec.) and rate, lend support to the assumption of a single supraventricular center with Tar\-ing deviation of intraventricular propagation of rapid impulses in alternate cycles. The presence df an independent sinus rhythm is against the existence of a rapid atrial arrhythmia, and favors the diagnosis of A-V nodal tachycardia with varyingintraventricular conduction. Similar QRS Momplexes of lesser duration (0.06 sec.) were seen m this patient after the return of normal basic rhythm.
Genesis of bidirectional
fachycardias
Fig. 6. Bidirectional tachycardia originating in one cerrter, probably ventricular (Lead II). A shows atria1 fibrillation and normal ventricular rate interrupted by a short run of bidirectional tachyrardia (last four beats), its rate ranging between 150 and 156 per sec. B starts with the same tachycardia, but now after the first three complexes it can be appreciatedhow, paradoxically, the smaller complexes vanish and the larger QRS complexes persist at a rate of 75 per min., which is exactly half of the tachycardia previously present. This phenomenon can well be explained by the presence of an intermittent 2:i exit block from the ectopic center and is corroborated by the finding of another complex occurring midway between the seventh and eighth QRS complexes. The classic picture of bidirectional tachycardia can be observed throughout C and the beginning of D. Toward the middle of the latter tracing another puzzling alteration is observed: the alternating beats abruptly change in shape, so that other beats of a third morphology appear, the rate being exactly the same as that of the bidirectional tachycardia (150 per min.). This unusual arrhythmia as a whole can be interpreted as a ventricular tachycardia arising in one center, probably ventricular. The various morphologies of the QRS complexes are due to v.arying and irregular intraventricular propagation. .A similar arrhythmia was previously reported.”
Fig. 5. Electrocardiograms obtained from the same patient as was Fig. 4, and demonstrating the ventricular origin of the tachycardia (Lead VI). A and B, recorded a few minutes after the preceding Fig. 4, show the same tachycardia, but now it is interrupted by ventricular captures (C) and fusion beats (F), which show that the ventricles are activated partly by the oncoming atrial stimulus and partly by the stimulus originating in the ectopic center. Such phenomenon convincingly proves the ventricular origin of the paroxysm. Finally, C records the end of the tachycardia after carotid pressure was applied. Posterior to such a vagal stimulation a fusion beat appears, followed by two idioventricular beats resembling those seen previously. This strip emphasizes that ventricular tachycardia can be stopped by carotid sinus pressure. Thus, the disappearance of an ectopic rapid rhythm by carotid sinus pressure does not necessarily indicate the ventricular origin of the arrhythmia as has been previously assumed. A similar effect on the rate of ventricular parasystole was reported by Scherf.rO,r’
737
vagal stimulation, proves the double origilt of the parosysm.t” J-et, Fig. 6, ;~s \vell it:, Fig. 13 of the article b>- C’astellanos ;111(1 associates,‘” show that 2 :l exit block frottt . postulated originall!, b>- Scherf and Kisch,” and convincingly proved by these authors in cases of atria1 tnchq~ardi;ts,“,“’ and t)> Pick and Langeudorf in instances of A\‘ nodal tachyrardias.” Fig. 1 is ati example of atria1 tactt!.cardia with aberrant ventricular conduc-tion. In some instances this functiott:tl intraventricular, right-sided, block shows persistent alternation, so that the t)-I)ical image of bidirectional tachycardia is see11 in Lead \‘I. In Figs 2 and 3 the slow change from unidirectional to bidirectional alternation, associated with only slight changes in QRS complexes of normal duration (0.08 secotld), supports the assumptiotl of ;I supraveutricular arrhythmia, showing intermittent intraventricular aberration.tl Obviously, it could not arise in the atria, for these ;tttatomic structures are activated by the sitttts ~~otlc. as seen in the esophageal leaci.
Such findings, coupled with the fact that after the disappearance of the tachycardia the morphology of the QRS complex was similar to those in Fig. 2, lend support to the hypothesis which interprets the paroq~stii as A-V ttotl;tl in origitt. One tttaitt characteristic of bidirectional tachycxdias was the finding of alternatiott in tttorpholog>., but not in direction, in Lead \‘, (Table I j. The opposite finding was usuall\-, but not. alwa)-s, seen in 1,ead I I attd at several esophageal levels. Kevert hetess, (‘ase 11 (Table I), and Fig. 0 of l’ic-k and 1,3ngendorf’s paper,” show alternation itt both paratneters in Leads i’t and \,ra~. Yet, positive complexes in Lead L 1, when present, woulcl disprove the idea of a septal center equidistant to the two buttdle branches, with ;dternatitlg itnpairtmtlt of impulse propagatiotx to the two bundle brattches.12 On the other hand, alternating cornpleses it1 right precordial leads are explained 011 the basis of futlctional right bundle branch block in instances of Supraventricul~Ir tachycardiasL”~‘Y (either atrial or A-V nodal) and on the basis of alternating irregular intraventriculx propagation, if the arrhythmia is ventricular.‘” Paroxysmal t achycardia of t tie bidirectional type as considerrcl itt this report
Genesis of bidirectional
is usually, but not invariably, produced by digitalis intoxication. Table I presents evidence of 3 casesin which the main etiological factor was considered to be, respectively, encephalomyocarditis (Case 9), diphtheritic myocarditis (Case 13), and repetitive paroxysmal tachycardia with a normal heart CCase 14). It should be emphasized that excessive digitalization was uot the cause in 2 patients. In one the tachycardia appeared after small and proportional amounts of acetylstrophanthidin, strophanthidin, ouabain, and digoxin (Case 9), previously reported in Figs. 8, 9, and 10 of the paper of C’astellanos and associates.14
7. 8. 9.
10.
11.
12.
13.
Summary
Bidirectional tackycardia is a clescriptive term indicating a tachycardia with alternation in morphology and (or) directiou of QRS complexes. A review of 5 caseswas made, from which it could be concluded that the paroxysm originates iu a single pacemaker, either in the atria, in the A-V node, or in the ventricles. \Ve are indebted to Dr. Louis Lemberg, Dr. Luis Azan, and Dr. Jose Calvin0 for their help in the preparation of this paper. REFERENCES 1. \Veinstein, W. J., and Jick, S.: Bidirectional tachycardia, .%n. J. Cardiol. 3:343, 1959. W. T., and Kramer, L. I.: On the 2. Zimdahl, mechanism of paroxysmal tachycardia with rhythmic alternation in the direction of ventricular complexes, AM. HEART J. 33:218, 1917. 3. Zimdahl, W. T., and Townsend, C. T.: Bidirectional ventricular tachycardia due to digitalis poisoning, AM. HEART J. 47:304, 1954. 4. Hellman. E.. and Lind. A.: Bidirectional tachvcardia, AM. ‘HEART J. $1:140, 1956. J., and Kilser, G. A.: Alternating 5. L’elazquez, bidirectional tachycardia, AM. HEART J. 54:440, 19.57. D.: Clinical studies of digitalis. III. 6. Luten Advanced toxic rhythms, Arch. Int. Med. 35:87. 1925.
14.
15.
16. 17.
18.
19.
20.
21.
22.
fachycardias
739
Felberbaum, D.: Paroxysmal ventricular tachycardia. Report of a case of unusual type, Am. J. RI. SC. 166:211, 1923. Schwensen, C. : Ventricular tachycardia as the result of the administration of digitalis, Heart 9:199, 1922. Scherf, I>., and Kisch, B.: L’entricular tachycardias with variform ventricular complexes, Bull. New York. M. Coil. 2:73, 1939. Scherf, D., and Schott, A.: Extrasystoles and allied arrhythmias, New York, 1953, Grune & Stratton, Inc. Pick, A., and Langendorf, R.: Differentiation of supraventricular and ventricular tachycardias, Prog. Cardiovas. Dis. 2:391, 1960. Katz, L. N., and Pick, A.: Clinical electrocardiography. Part I. The arrhythmias, PhiladeIphia, 1953, Lea & Febiger, Fig. 215. Calvifio, J. M., Azan, L., and Castellanos, A., Ir.: Valor de las derivaciones esofagicas en las arritmiascomplejas, Rev. cubana cardiol. 16:293, 1955. Castellanos, A., Jr., .Azan, L., and Calvifio, 1. M.: Simultaneous tachvcardias. .XM. HEART j. 59:358, 1960. ’ Palmer, R., and White, P. D.: Paroxysmal ventricular tachycardia with rhythmic alternation in the direction of the ventricular complexes of the electrocardiogram, AM. HEART J. 3:454, 1928. Bellet, S.: Clinical disorders of the heart beat, Philadelphia, 19.53, Lea & Febiger. Goblev. iV1.. Ladooulos. C. P.. Roth. F. H.. and SGherf, D.: Chinges of ventricular’impulse formation during carotid pressure in man, Circulation 10:735, 1954. Scherf. D.. Schott. A.. Reid. E. C.. and Chamsai. D. G.‘: Intermittent parasystolk, Cardiologia 30:217, 19.57. Castellanos. A., Calviiio, J. M., Azan, L., and Castellanos. A., Jr.: Supraventricular tachycardia imitating ventricular paroxysmal tachycardia in infancy, J. Pediat. 54:330, 1959. Gaskell, W. H.: On the innervation of the heart, with special reference to the heart of the tortoise, J. Physiol. 4:43, 1833. Lewis, T., and Levy, R.: Heart irregularities, resulting from the inhalation of low percentages of chloroform vapour and their relation to ventricular fibrillation, Heart 3:99, 1911-12. Reid, W. D. : Ventricular ectopic tachycardia complicating digitalis therapy, Arch. Int. bled. 33:23, 1924.
of bidirectional
Agustin Castellanos, Miami, Fla.
Jr.,
M.D.
S
everal mechanisms for the production of bidirectional tachycardias have been proposed. l-l1 This is not surprising in view of the uncertain origin of arrhythmias which have a rapid rate with prolonged and bizarre QRS complexes.12 As in all cases of complex disorders of rhythm a complete knowledge of cardiac physiology is required. But, in addition, the technician should be taught to obtain long strips of the electrocardiogram, mainly in one lead, so that the greatest number of pathologic mechanisms can be recorded, as can be seen in Figs. 1-7 of this communication. Table
1.
2. 4: 3 5. 6. 7. 8. 9. 10. 11. 12. 13. 11. AHD:
Because of the complexities seen in short (conventional) tracings, certain authors have advanced the theory that bidirectional tachycardia probably represents a heterogeneous group of cases which have similar electrocardiographic configuration.1 For example, some workers have postulated the existence of two pacemakers: either one supraventricular and one ventricular2s3or two ventricular ones.7,821Moreover, others believe that the paroxysm originates in one single focus before’,4,5,6,9-1’,‘3 or after the bifurcation.14J2 Precisely, this communication establishes that not one,
I
I Case
tachycardias
Ate (yr.1
63 68 70 65 88 71 75 69 71 63 65 84 9 9
Arteriosclerotic fibrillation. S.R.: From
Received
733
’ Etiology
AHD AHD AHD AHD AHD AHD ,4HD AHD EM AHD AHD AHD DM NH
~ Heart ~aflure
Digitalis
Yes Yes Yes Yes Yes Yes Yes Yes No Yes Yes Yes No No
++++ ++++ ++++ ++++ ++++ ++++ ++++ ++++
for publication
NO NO
of Medicine.
Sept.
A. F. A. F. A. F. s. R. s. R. A. T. A. T. A. T. .4-V. T. -4-v. T. A. F. A. F. ? A. T.
l+ ++i-+ ++++
heart disease. EM: Encephalamyocarditis. Sinus rhythm. A.T.: Atria1 tachycardia. the Department
Atria1 rhythm during paroxysm
Section
12. 1060.
DM: Riphtheritic A-V.T.: Atrioventricular of Cardiology,
University
AlternaEsophageal
leads Yes Yes Yes Yes Yes Yes Yes Yes No Yes NO
Yes No Yes myocarditis. NH: nodal tachycardia. of Miami
School
tion in direction in Lead VI
Ventvicz~lar
No No No No No
157 1.58 150 167 150-172 115 168 176-188 167-180 170 166 166 130 188-275
rate
NO
No No No No Yes No No No Normal
of Medicine,
heart.
Miami,
A.F.:
Fla.
Atrial
tive fnilurc. ‘The detzilecl clillic.;ll tl
Fig. 1. Bidirectional tat-hvrardk of atria1 IKI~~II. ‘l‘hcse tracings were obtained from a 9-yex-ol~l asthmatic girl with bouts of “repetitiw parox~ sn~l tachycardia,” but no heart discax!. 12 supravcntricular tuchycardia (rate: 188 per min.) with aberration showing diffcrcnt degrees of right-sided into-a\ ~IItricular cwlduction defect a11 he seen in A1. ‘1%~ esoph;tgea! lend (I3) clearly cstablishcc: the nt trial origin of the paroxysm. In C, diffcrcnt degree> of aberration we seen again. Finally, ilk I?, when t hc rate speeded up to 27.5 per min., a c-lnious fol-m of alternation is prescnl : an rsK’ comples of lcswr dur;ttion and smaller height altwnates with one of greater duration and height. This record is intcrpreted as an example of atrial tachycardia H.ith bidirectional complexes due to nlternating aberrant ventricular conduction. The warming up of the cc,topic center is attributed to a mechanism similar I o the “rhythm of development .“)O
but several mechanisms are involved in the genesis of what has been called bidirectional tachycardia from a simple morphologic configuration. Prognosis and treatment will not be considered here. Material
and methods
0ur material consists of 14 records showing bidirectional tachycardias (other tracings from these patients have been included in previous reports13*‘4). ,411 subjects except 3 (Table J) had arteriosclerotic heart varying degrees of congescl isease and
Of the 14 cases studied there were 5 in which the corresponding records showed certain characteristics which could be of help in clarifying the genesis of bidirectional tnchycardias. These cases are presented in l’igs. 1-7, and the corresponding electrocardiagrams are fully described in the respective legends. Table I shows the basic features. Comment Many theories have been proposed to explain the genesis of bidirectional tach>-cardias.l-lA Some have received widespread ~tttentioii1,‘,6,g,11,1~; others, such as the double circus movement of White and Palmer,Ij have been practically forgotten. One of the earliest assumptions favored the ventricular origin of the paroxysm.7,s This \\ras due to the observation that many cases showed frequent ventricular extrasystotes prior to or after the tachycardia. Thus, it was considered that the two morphologies corresponded to two foci of impulse formation, that is, one in each ventricle. Such a theory has been challenged in later years since the work of Zimdahl and Kramer,” who showed that one of the two complexes in their case could be abolished by carotid sinus pressure, and thus postulated that two active centers were present-one ventricular and one supraventriculnr. Similarly, other authors
Genesis of bidircctio~lal
have since reported instances of disappearnnce of the arrhythmia by this or allied vagomimetic procedures.2-5a13a16 However, the unquestionable ventricular origin of bidirectional tachycardia was established in Figs. 4 and 5 by the presence of fusion beats; the alternating complexes were explained on the basis of irregular intraventricular propagation. Furthermore, this case is a clear example of the abolishment of a ventricular tachycardia by carotid sinus pressure, so that the effectiveness of cannot be related necessaril> this procedure to the existence of a supraventricular tachycardia.’ It should be emphasized that
tachycardias
735
Scherf17J8 has reported the slowing of ventricular parasystole by carotid pressure, indicating the response of ventricular rhythms to vagus stimulation. Similarly, the transition of bidirectional to unidirectional complexes without changes in rate also rules out the diagnosis of double ventricular paroxysmal tachycardia. Evidently, this possibility is to be considered extremely rare because no instance of this arrhythmia was found in a recent review of 15 cases of simultaneous tachycardkh’ Occasionally, it has been considered that the disappearance of one type of beat, with halving of the ventricular rate after
Fig. 2. Bidirectional tachycardia originating in one supravcntricular center, probably in the A-V node. The tracings start with a regular tachycardia (rate: 167 per min.) and QRS duration of 0.06 sec. Note that it is dissociated from an independent sinus rhythm (rate: 103 per min.), and that the I’ waves have a predominant negative deflection in the esophageal lead (E. 30). .Xlternation in the height of ventricular complexes appears toward the middle of the tracing and is best seen in Lead II. The records continue uninterruptedly with that of Fig. 3.
Fig. 3. Bidirectional tachycardia originating in one supraventricular center, probably in the A-\: node. This tracing is continuous with that of Fig. 2, and shows besides an alternation in the height of ventricular complexes a progressive alternation in direction of QRS and T, until the classic-image bidirectional tachycardia appears toward the end of the record. In Figs. 2 and 3 the strictly regular and constant rate, and the gradual evolution from unidirectional to bidirectional alternation, in association with only moderate changes in ventricular duration (which is within normal limits: 0.08 sec.) and rate, lend support to the assumption of a single supraventricular center with Tar\-ing deviation of intraventricular propagation of rapid impulses in alternate cycles. The presence df an independent sinus rhythm is against the existence of a rapid atrial arrhythmia, and favors the diagnosis of A-V nodal tachycardia with varyingintraventricular conduction. Similar QRS Momplexes of lesser duration (0.06 sec.) were seen m this patient after the return of normal basic rhythm.
Genesis of bidirectional
fachycardias
Fig. 6. Bidirectional tachycardia originating in one cerrter, probably ventricular (Lead II). A shows atria1 fibrillation and normal ventricular rate interrupted by a short run of bidirectional tachyrardia (last four beats), its rate ranging between 150 and 156 per sec. B starts with the same tachycardia, but now after the first three complexes it can be appreciatedhow, paradoxically, the smaller complexes vanish and the larger QRS complexes persist at a rate of 75 per min., which is exactly half of the tachycardia previously present. This phenomenon can well be explained by the presence of an intermittent 2:i exit block from the ectopic center and is corroborated by the finding of another complex occurring midway between the seventh and eighth QRS complexes. The classic picture of bidirectional tachycardia can be observed throughout C and the beginning of D. Toward the middle of the latter tracing another puzzling alteration is observed: the alternating beats abruptly change in shape, so that other beats of a third morphology appear, the rate being exactly the same as that of the bidirectional tachycardia (150 per min.). This unusual arrhythmia as a whole can be interpreted as a ventricular tachycardia arising in one center, probably ventricular. The various morphologies of the QRS complexes are due to v.arying and irregular intraventricular propagation. .A similar arrhythmia was previously reported.”
Fig. 5. Electrocardiograms obtained from the same patient as was Fig. 4, and demonstrating the ventricular origin of the tachycardia (Lead VI). A and B, recorded a few minutes after the preceding Fig. 4, show the same tachycardia, but now it is interrupted by ventricular captures (C) and fusion beats (F), which show that the ventricles are activated partly by the oncoming atrial stimulus and partly by the stimulus originating in the ectopic center. Such phenomenon convincingly proves the ventricular origin of the paroxysm. Finally, C records the end of the tachycardia after carotid pressure was applied. Posterior to such a vagal stimulation a fusion beat appears, followed by two idioventricular beats resembling those seen previously. This strip emphasizes that ventricular tachycardia can be stopped by carotid sinus pressure. Thus, the disappearance of an ectopic rapid rhythm by carotid sinus pressure does not necessarily indicate the ventricular origin of the arrhythmia as has been previously assumed. A similar effect on the rate of ventricular parasystole was reported by Scherf.rO,r’
737
vagal stimulation, proves the double origilt of the parosysm.t” J-et, Fig. 6, ;~s \vell it:, Fig. 13 of the article b>- C’astellanos ;111(1 associates,‘” show that 2 :l exit block frottt . postulated originall!, b>- Scherf and Kisch,” and convincingly proved by these authors in cases of atria1 tnchq~ardi;ts,“,“’ and t)> Pick and Langeudorf in instances of A\‘ nodal tachyrardias.” Fig. 1 is ati example of atria1 tactt!.cardia with aberrant ventricular conduc-tion. In some instances this functiott:tl intraventricular, right-sided, block shows persistent alternation, so that the t)-I)ical image of bidirectional tachycardia is see11 in Lead \‘I. In Figs 2 and 3 the slow change from unidirectional to bidirectional alternation, associated with only slight changes in QRS complexes of normal duration (0.08 secotld), supports the assumptiotl of ;I supraveutricular arrhythmia, showing intermittent intraventricular aberration.tl Obviously, it could not arise in the atria, for these ;tttatomic structures are activated by the sitttts ~~otlc. as seen in the esophageal leaci.
Such findings, coupled with the fact that after the disappearance of the tachycardia the morphology of the QRS complex was similar to those in Fig. 2, lend support to the hypothesis which interprets the paroq~stii as A-V ttotl;tl in origitt. One tttaitt characteristic of bidirectional tachycxdias was the finding of alternatiott in tttorpholog>., but not in direction, in Lead \‘, (Table I j. The opposite finding was usuall\-, but not. alwa)-s, seen in 1,ead I I attd at several esophageal levels. Kevert hetess, (‘ase 11 (Table I), and Fig. 0 of l’ic-k and 1,3ngendorf’s paper,” show alternation itt both paratneters in Leads i’t and \,ra~. Yet, positive complexes in Lead L 1, when present, woulcl disprove the idea of a septal center equidistant to the two buttdle branches, with ;dternatitlg itnpairtmtlt of impulse propagatiotx to the two bundle brattches.12 On the other hand, alternating cornpleses it1 right precordial leads are explained 011 the basis of futlctional right bundle branch block in instances of Supraventricul~Ir tachycardiasL”~‘Y (either atrial or A-V nodal) and on the basis of alternating irregular intraventriculx propagation, if the arrhythmia is ventricular.‘” Paroxysmal t achycardia of t tie bidirectional type as considerrcl itt this report
Genesis of bidirectional
is usually, but not invariably, produced by digitalis intoxication. Table I presents evidence of 3 casesin which the main etiological factor was considered to be, respectively, encephalomyocarditis (Case 9), diphtheritic myocarditis (Case 13), and repetitive paroxysmal tachycardia with a normal heart CCase 14). It should be emphasized that excessive digitalization was uot the cause in 2 patients. In one the tachycardia appeared after small and proportional amounts of acetylstrophanthidin, strophanthidin, ouabain, and digoxin (Case 9), previously reported in Figs. 8, 9, and 10 of the paper of C’astellanos and associates.14
7. 8. 9.
10.
11.
12.
13.
Summary
Bidirectional tackycardia is a clescriptive term indicating a tachycardia with alternation in morphology and (or) directiou of QRS complexes. A review of 5 caseswas made, from which it could be concluded that the paroxysm originates iu a single pacemaker, either in the atria, in the A-V node, or in the ventricles. \Ve are indebted to Dr. Louis Lemberg, Dr. Luis Azan, and Dr. Jose Calvin0 for their help in the preparation of this paper. REFERENCES 1. \Veinstein, W. J., and Jick, S.: Bidirectional tachycardia, .%n. J. Cardiol. 3:343, 1959. W. T., and Kramer, L. I.: On the 2. Zimdahl, mechanism of paroxysmal tachycardia with rhythmic alternation in the direction of ventricular complexes, AM. HEART J. 33:218, 1917. 3. Zimdahl, W. T., and Townsend, C. T.: Bidirectional ventricular tachycardia due to digitalis poisoning, AM. HEART J. 47:304, 1954. 4. Hellman. E.. and Lind. A.: Bidirectional tachvcardia, AM. ‘HEART J. $1:140, 1956. J., and Kilser, G. A.: Alternating 5. L’elazquez, bidirectional tachycardia, AM. HEART J. 54:440, 19.57. D.: Clinical studies of digitalis. III. 6. Luten Advanced toxic rhythms, Arch. Int. Med. 35:87. 1925.
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fachycardias
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Felberbaum, D.: Paroxysmal ventricular tachycardia. Report of a case of unusual type, Am. J. RI. SC. 166:211, 1923. Schwensen, C. : Ventricular tachycardia as the result of the administration of digitalis, Heart 9:199, 1922. Scherf, I>., and Kisch, B.: L’entricular tachycardias with variform ventricular complexes, Bull. New York. M. Coil. 2:73, 1939. Scherf, D., and Schott, A.: Extrasystoles and allied arrhythmias, New York, 1953, Grune & Stratton, Inc. Pick, A., and Langendorf, R.: Differentiation of supraventricular and ventricular tachycardias, Prog. Cardiovas. Dis. 2:391, 1960. Katz, L. N., and Pick, A.: Clinical electrocardiography. Part I. The arrhythmias, PhiladeIphia, 1953, Lea & Febiger, Fig. 215. Calvifio, J. M., Azan, L., and Castellanos, A., Ir.: Valor de las derivaciones esofagicas en las arritmiascomplejas, Rev. cubana cardiol. 16:293, 1955. Castellanos, A., Jr., .Azan, L., and Calvifio, 1. M.: Simultaneous tachvcardias. .XM. HEART j. 59:358, 1960. ’ Palmer, R., and White, P. D.: Paroxysmal ventricular tachycardia with rhythmic alternation in the direction of the ventricular complexes of the electrocardiogram, AM. HEART J. 3:454, 1928. Bellet, S.: Clinical disorders of the heart beat, Philadelphia, 19.53, Lea & Febiger. Goblev. iV1.. Ladooulos. C. P.. Roth. F. H.. and SGherf, D.: Chinges of ventricular’impulse formation during carotid pressure in man, Circulation 10:735, 1954. Scherf. D.. Schott. A.. Reid. E. C.. and Chamsai. D. G.‘: Intermittent parasystolk, Cardiologia 30:217, 19.57. Castellanos. A., Calviiio, J. M., Azan, L., and Castellanos. A., Jr.: Supraventricular tachycardia imitating ventricular paroxysmal tachycardia in infancy, J. Pediat. 54:330, 1959. Gaskell, W. H.: On the innervation of the heart, with special reference to the heart of the tortoise, J. Physiol. 4:43, 1833. Lewis, T., and Levy, R.: Heart irregularities, resulting from the inhalation of low percentages of chloroform vapour and their relation to ventricular fibrillation, Heart 3:99, 1911-12. Reid, W. D. : Ventricular ectopic tachycardia complicating digitalis therapy, Arch. Int. bled. 33:23, 1924.