Simultaneous tachycardias

Simultaneous

Tachycardias

Agustin Castellanos, Havana, Cuba

Jr.,

M.D.,

Luis

M.D.,

Azan,

and Jose’ M. Calvifio, N.D.

Although the first tracings of simultaneous independent tachycardias were published by Gallavardin,’ in 1920, this arrhythmia did not attract general attention until 19.52, when Bernstein and co-workers8 reported 7 cases which they observed as occurring over a short period of time. These authors were of the opinion that the incidence of this disorder of rhythm was probably higher than that which was normally expected by electrocardiographers. Since we have also observed the presence of this arrhythmia in a proportionally large variety of records,rO it was considered worth while to attempt to clarify the underlying mechanism as well as to describe the different forms.

Our material consists of 15 cases studied from 1952 to 19.58, in the Department of Cardiology at the University Hospital. Five of these cases were published previously.‘0 This incidence is perhaps rather high and may be attributed to the use of additional esophageal leads which have been used as a routine procedure in 90 per cent of the patients observed to have ventricular tachycardias during the period from 1950 to 1955. Initially, the lead in which the P wav-es could best be seen was selected for study. Then, whenever long tracings were available, the differentiation between double tachycardias and the following arrhythmias vvas feasible: (1) \7entricular tachycardia with normal sinus rhythm which was due to the slow atria1 rate and to the independence of the atrial from the v-entricular complexes.” (2) L4berrant ventricular conduction of supraventricular beats, a phenomenon usually appearing when a somewhat premature and bizarre QRS complex followed a long RR interval, with the complexes adopting, generally, the morphology of right bundle branch block. Furthermore, a definite relationship between the atria1 and ventric(3) Ventricular tachycardia with first or second degree retrograde ular activity was found.‘* block. In these cases a logical R-P sequence existed, consistent with the rules of V--4 conduction, so that the irregularities of the P-P intervals when present could not be ascribed to irregular as well as in the aberrant ventricular condischarge of an ectopic center.‘9 In this arrhythmia, duction, carotid pressure could affect the atrial rhythm and the A-V? or V-A conduction time in such a way as to assure a definite relationship between atria1 and ventricular activity. On the other hand, in all cases of simultaneous independent tachycardias the rapid atrial complexes showed no relationship whatsoever to the QRS complexes, and the P waves fell on various parts of the ventricular cycles. It is to be noted that the differentiation of ventricular tachycardia from A-V From the Departments Havana. Cuba. Aided by a grant from Received for publication

of the

Cardiology,

Catedra July 24,

Hospital

de Patologia 1959.

Vniversitario General 358

(University

and

Hospital of Havana

Clinico School

Quirurgico, of Medicine).

Volume Number

59 3

nodal tachycardia with aberration can seldom be made with absolute certainty unless fusion beats are present.8,” In a!! other instances the diagnosis of ventricular tachycardia is not intended to exclude the possibility of nodal tachycardia with aberrant ventricular conduction. Atria! librillation was excluded from this study. The initially present atria! tachycardias, as well as the A-V nodal tachycardia in Figs. 11, 12, and 13, originally had some degree of A-V block. Moreover, their production by digitalis was established after the use of short-acting preparations such as ouabain, strophanthidin, and acetyl strophanthidin on these patients. Following the injection of these drugs, a second pacemaker occurred, a finding which can be considered clearly deleterious and was not observed when the tachycardia was not due to digita!is.3a Likewise, Figs. 8, Y, and 10

constitute examples of drug hypersensitivity, because an ectopic ventricular rhythm was seen without the disappearance of the initial nondigitalis-induced tachycardias. ivhen drug overdosage was suspected, digitalization was performed according to the original method proposed by Lown and Levine,*’ and the amounts of digitalis administered were noted on the corresponding records. Only tracings with r-ertain pecnlinrities will he presented.

SimtLltaneous Afrial and I~entricular l’ackycardias (7 Cases).-The upper record of Fig. 1 shows an atrial tachycardia with a 2:l A-V block produced b>, digitalis overdosage. The atria1 rate varies from 200 to 250 per minute, due either to ventriculophasic arrhythmia or to an irregular discharge of the ectopic center. TIME

LEAD

Y,

ACETYL

STROPHANTHIDIN

0

0

A A-V T-

Fig.

I.-Simultaneous X11 brarings

atria1 and in t.his figure.

vrnLricular and in all

tachycardias. others, are fully

Diagrams disrusserl

are corlvent~ional.“’ in the text.

In the lower record, taken 3 minutes after the administration of 0.15 mg. of acetyl strophanthidin, the sixth I’ xvave can be seen to become apparent 0.33 second after the preceding oue, thus representing the longest P-I’ interval. Therefore, it furnished enough time for the appearance of a11 extrasystole, which would not have been present in the usual P-P sequence. This extrasystole, in turn, initiates a short run of tachycardia, and the resultant picture is one of an A-V dissociation in the presence of a 2:l A-V block. As in all instances of this disorder of rhythm, the ventricular rate of 115 per minute, which is slower than the atria1 rate of 214 to 275 per minute but is faster than twice the P-P interval of 109 to 111, persists until a QRS complex falls at the expected time. The same arrhythmia is present in the upper record of Fig. 2. In addition, multiple complexes of intermediate contour are observed as the result of obviously fusion

Iwats, so that the vetttricular rh~~thni, tlot~l~tlessl~~, is 110t ;LII ‘\-\’ tach~~c~~t-cli;~ \\,ith al)errntiott. After ;I seco~ttl ittjcctiott of ;tc-et\.1 stt-o~~h~tttthitlitt, the total ;~ntottttl 11ow being 0.30 mg., the elec.troc~~rtlio~t-~~l~hic image is that oi simultatteous indepettdettt atria1 a~ttl vetttt-icular t;tch\xxrdias (second atttl third strips). Finally, sinus rh\.thtii is restored b\. the itttravettous atlntittistratiott of potassiunt. This rhythm is- interrupted b!- itttet-mittettt vetttricular extrasystoles which have the s;1me origitt ;~s the prc\.iottsl\ol~scr\~~tl I)iz;tt-t-c vctttt-icttl;tr c~ottll)leses. ACETYLo,S:~~,PnANTHICIN

TIME _- :..,

:.

0.30

IO MIN.

I6 *. i

MIN.

0.30

POTRSSIUM

ma.

_

mq.

_.

73 mEq

Electrocardiograms similar to the Ixcwdittg OIIC’ it1 which the onset of ;I double rhythm catt be observed have 1)ce11 published 1)). Katz and Pick (Fig. 214)” and b\- Dressler attd Iioessler (Fig. 41.~’ III ~vet-~- ittstattc-e it has been clear that the ventricular center wa “x?ive.” that is, \vith its owtt ;~utomatism and evidentI>. not bl- a succession of escapes (passive rh!~thm) as frequentl>. happens when sinus r-h>-thm is the uttderl>Ang atrial mechanism ac-corlll,;tn!,ittR dissociation with interference in 1:l A-V block. Simultaneous Atritrl (znd b’itlivcdiond I.r~nfric-dav l’trchycardius (3 Cases).In the upper strip of Fig. 3 mt atria1 tach~xxrdia lvith ;I rate of 150 per minute with irregular A-\- block can be seen; it is obviousI>- due to digitalis overdosagc. The middle strip, taken after acetyl strophattthitlitt was admittistered, shows the onset of a bidirectiottal ventricular tach>xxrdia lthich succeeds ;L tlormall~. conducted beat labeled Ii S.” Finall>., the bottom stril) showittg esophageal leads, obtained a few mittutes later, reveals the ittdepettdettce of the atria1 from the ventricular complexes, establishing the diagnosis of double tachycat-dias. The atria1 rate has increased to 1X7 per minute, butt the ventricular tachycardia remaitts unchanged.

The effects of intravenous procaine ;wiidc are Ixesented in ITis. 4. ‘l‘hc ventricular tach~xxrdia has clklppeared after the xlmillistration of otll~, 300 mg. of procaine amide (shoxvll iu the upper tracing taken 30 minutes after starting Ihe test 1. The atrial rhythm has clew-reased to 165 per minute but is still a11 atrial STROPHANTHIDI 0

RATE 150

TIME 0

ATRIAL : IS5 VENTRICULAR I66 166

N

0.15mq.

0.15mq.

IO MIN.

TIME

40

RATE

MIN.

‘SINUS

PRONESTYL

RtkYTHM

900

l-69.

tach~~carclia \vitii \.;~r!.illg :\-\’ c.olltlrtc.tiotl. \Iorco\-Ed-, ;IS ;I t~mw(~~~e~~rc of the ;Itllniliistratioli of 600 mg. oi l)rocailie aniitle, as iIitliwtctl ill the mitltlle tracillSg, a further reduction ill the rate to 14.5 per minute c;ul be see11 \vith the establishment of 1 :l LA-\7 conductioli with prolonged -4-I. conduction time (0.20 second).

362

CASTELLANOS,

MAN,

AND

Am. Heart J. March, 1960

GKVIfiO

In the lower tracing, sinus rhythm is again present after the injection of 900 mg. of procaine amide. The third ventricular complex corresponds to a premature atria1 systole, probably arising from the same focus as the tachycardia. An arrhythmia similar to that described in the preceding paragraph is illustrated in Fig. 5. A careful analysis of the upper strip reveals the existence of an atria1 tachycardia with a prolonged P-R interval (0.20 second), corroborated by carotid pressure, a maneuver which produced second degree A-V block (not shown). Five minutes after acetyl strophanthidin was injected, a bidirectional ventricular tachycardia appeared, coexistent with the atria1 tachycardia shown in the middle strip. However, the correct diagnosis was established only after the recording of the esophageal leads. Paradoxically, a decrease in the atria1 rate, as compared with control values, is evident in the latter, combined with an irregular spacing of nearly all P-P intervals. Yet, the P waves are not related to the QRS complexes, the rate of these still being 170 per minute. Hence, the exact electrocardiographic interpretation is double tachycardias, one originating in the atria and t-he other, bidirectional, in the ventricles. Two similar cases h ave been reported b!r I
Pig.

5.--Simultaneous

indrpendent

atria1

and

bidirecl~ional

ventricular

tachycardias.

Simultaneous Atria1 and A- 1,. Xodal Zhchycardia (1 Case). ~-Figs. 6 and 7 are examples of how double tachycardias were produced during digitalization in a 9-year-old girl with rheumatic fever. The top tracing in Fig. 6 shows a sinus tachycardia with a rate of 123 per minute before the administration of oral digoxin, 2 mg. in two doses 8 hours apart. In the other strips, I.eads I alld II, an atria1 tachycardia with first degree A-\’ block is present with a rate of 145 per minute, with all P waves having a different morphology than the slightly slower sinus ones. Occasionally, an interesting form of alternation appears in which a short R-R is preceded by a longer R-R. Because interatrial timing is constant, the mechanism must be considered to he a form of alternation of A-\’

Volume Number

59 3

SIMULTANEOUS

363

Tr\CH1-‘(‘AKDId\S

conduction, a term introduced by Langendorf. 2o Indeed, it can be appreciated that the shorter P-R intervals follow the shorter R-P intervals and, vice versa, the longer P-R intervals follow the longer R-P intervals (all values marked on the bottom tracing are expressed in hundredths of a second). This suggests a supernormal phase of A-1: conduction. Unfortunately, the attending physician administered an additional 0.5 mg. of digoxin because of what he interpreted on the basis of auscultation as onI>- an increase in the sinus rate. The resultant

Fig.

Fig.

G.--Sinus

7.-Atria1

tachycardia (upper strip) ; first degree auriculoventricular A-V conduction time due to the supernormal phase

tachycardia

with auriculoventricular A-V nodal tachycardias

block (loner

(lower

(upper strip) strips).

block with strips).

; simultaneous

alternation

atria1

of

and

picture, which is presented iI1 the strip) I;~bcletl 7-/I~.ii iI1 Fig. 7, is that d ;III atrial tach>~cardia with the irregular AA-\’ bLock ha\illg al)l,rosilil;ltel\, the smut’ rate as before. One da!. later, t;-10-55, in spite of 110illrther digitalizat ioll ;LII ;I-\coexisting with atrial ;lrtach\-cardia appeared with a rate of 133 per minute, rhythmia, the rate of the latter having illcreased to 170 per minute. ‘l’hus, simultaneous dissociated actioli of both p~~cem;tl~e~-s is l)reseiit. I ii tht- lower strip) :I curious phenomeno~i is noted I\-hen ;I vrlltric.ul;ir ~stras!.stole is retrograclel>~ contlucted to the :I-\’ ceiiter, suppressiliy it. Since tlic efTert is revealed 1)). the unexpected failure of the ~m~~~~l~er to alqwa~- whc~r expected, it (XII be ~~onsideretl as a11 w~rn~~le 0i r01~ce;~letl retroqxde cmiit1uc.t ioll ;LS (-oncei\ t)! I.;lngendorf.z” TIME 0

4 MIN.

RATE rps

ACETYL

136

STROFtMMTHIMN 0

O.lSmg.

the ventricles, l!nderstand~Lbl?., the ollcomillg :ltrial iml,ulse, I ‘,, c:~lluot activate but b>. the time P:! reaches the X-V jullr.tioll, transmission coultl have been possible. Because this impulse is also blocked, it has to be accepted that an unusually prolonged state of A-L: refractoriness is the cause for such stoppage. The succeeding I’ wave, I’:!, is conducted to the veIltricks because oi the tlepression of the A-1,’ center at a time when ‘4-i’ c-ontluctioll \V;IS feasible.“” Thereafter, I’, is blocked ant1 1’5 is conducted. ‘The nodal center then “warms up” and the A-\: tach)~cardia starts anew, so that again two completely independent tachycartlias are simultaneously present. ?‘a(-hyc-urdins (3 Cmcs). -~‘I’he SillllLlfU?W OILSA-V L~otInl nmf [~r~~fvicul~~r tracings shoxvn iI1 Fig. 8 w~-e recorded 011 a patient with ellrephalom!-ocarditis A reveals an A4-\’ Tracing 110 digitalis previousI>.. who definitely had received nodal tach~~carclia with a rate of 136 per minute, with retrograde stimulation of the atria which is not due to digitalis. In tracing b’ an initial injection of acet>,I strophanthidiu produced intermittent vcntricul;~r cxtrasystoles with a verlloiig coul)liilK. J’rcc-isely, it is tluc to suc.li ;I loiig corildiilg th;it their rc~trogr;kcl(:

conduction reached the A-V center after it had already discharged toward the atria (all I’-I’ intervals are identical), thus creating an impedance to transmission of the nodal beats toward the ventricles. Finally, iI1 tracing C the same late estrasystoles are seen after each nodal beat and represent a true bigeminl,. The tracing in Fig. 9 was obtained 24 hours later from the same patient as in Fig. 8, after the administration of 0.15 mg. of ;~~tyl strophanthidin. The fourth QRS complex is, beyond doubt, a ventricular cxtrasystole, which, in turn, initiates a run of bidirectional ventricular tachycartlia with all beats having retrograde conduct ion to the atria, as revealed ill the diagram. (‘onsequentl!., because the I\-\’ center was reached and suppressed, a double tach>xa-dia did not exist. Twenty-four hours later the patient under consideration received a11 illjection of 0.10 mg. of ouabaill (1:ig. 10). The basic rh>.thm was no\v an .\-I’ nodal tath~xxrtli;~ w-ith preceding activation of the atria (first and ,last three beats). A++lin an a-topic (second) QRS comples initi;ited a run of bidirectiolial ventricular tach\-cardia. However, OII this ocwsion, plotting the P-1’ intervals revealed 110 change iI1 atria1 activatioll. I;or this reason it must be accepted that the retrograde con~luct ioll of the cstr~~s!.stolc.tlitl not reach the :I-\’ c-enter, so that the rh~~tlimic;il xtivit\. to the ;ltri;l \v;Ls ilniliterru~)tetl >-et causing impctl~mce to the transmission to the velltrklcs. (‘o~~scquentl~ , it is clear th;lt two simultaneous t;lchg-cartlias existed side 1)~. side, one origillatitlg in the ul)per region of the :\-\- julictioii ;~iid the otlic2-, 1)itlircc.t ioilal, iIi the ventricles. 7 MIN:

AFTER

O.IS

mg.

OF STROPHANTHIDIN I

7MlN.

AFTER

O.IOmg.

OF OUABAIN

‘(

366

CASTELLANOS,

MAN,

XND

Am. Heart J. March, 1960

CALVlfiO

Another example of this arrhythmia is presented in Figs. 11, 12, and 13. Initially, the upper record of Fig. 11 shows a sinus rhythm with a rate of 97 per minute, which changes, toward the middle of the tracing, into an apparentI)passive A-V rhythm with a rate of 79 per minute, with first degree A-V block and a P-R interval of 0.12 second. This patient had been receiving 0.25 mg. of digoxin daily for the previous months, without any sign of intolerance. Yet 1 week later when the dose was abruptly increased to 1.5 mg. because of unequivocal signs of congestive heart failure, a nonparoxysmal A-V tachycardia with a rate of 136 per minute appeared, and is seen in the lower strip. Note that the P-R interval was still 0.12 second. Because some observers had serious doubts whether the tachycardia was drug induced or simply a spontaneous arrhythmia appearing during an episocle of congestive failure, ;I test of digitalis tolerance was carried out. In tracing A of Fig. 12 the atria1 rate sholvs ait increase to 167 per minute after 0.20 mg. of strophanthidin, and a velltrirular tachycardia becomes evident. The rate of the latter was originally 140 per minute, but as the pacemaker “warmed up,” it increased to 172 at the entl of the tracing. \‘et, both pacemakers are completely independent, the record showing the ~~~-csenc-e oi simultaneous A-V and ventricular tarhyrardi;i.

Fig.

Fig.

Il.--Sinus

rhythm

12.--A. Simultaneous independent A-V

changing

into

IL-\- nodal lachycardia

independent A-V nodal and ventricular

rhythm (lowc~r

(upper’ sl rip).

nodal and ventricular tachycardias, the

strip)

: nonparosysmal

tachycardias. latter with 2:l

A-V

B. Simultaueous exit block.

nodal

Volume Number

59 3

SIMULTANEOUS

TACHYCAKDIAS

367

In tracing B of Fig. 12 a ventricular rhythm is seen dissociated from the A-V center. All inverted P waves fall in various parts of the R-R cycle, and the fact that the ventricular rate of 86 per minute is exactly half of that of the tachycardia which occurred at the end of B is noteworth>-. Evidently, in this case the assumption of a ventricular tachycardia with a 2 :l exit block is justified and, furthermore, corroborated by the finding of a QRS complex occurring midway from the sixth and eighth ventricular deflections. The similarity of this complex with those in tracing B is to be noted, and its slight widening is probably due to a more sinuous spread of activation through the ventricles when the pacemakers speeded up and can be explained by a transient disappearance of the exit block. The resultant picture is that of simultaneous independent A-V nodal and ventricular tach\.cardias, the latter with a 2:l exit block. The phenomenon presented in Fig. 13 took place in spite of no further digitalization (B, C, and D are continuous). Jn tracing A, recorded 2 minutes after the preceding Fig. 12, the A-\’ nodal tachycardia persists at the usual rate, but no\v an additional, moderateI>rapid ventricular rhythm, independent of the nod;4 t-h>-thm, can be seen. The QRS complexes are wider and have a tlif-

A

Fig. 13.--A, Simultaneous independent A-V nodal and ventricular tachycardias. B, Simultaneous independent A-V nodal and ventricular tachycardias. the latter possibly having varying exit block as well as irregular intraventricular propagation. C. A-V nodal tachycardia with 2:1 exit block. D, Transition to dissociation with interference due to the reappearance of the ventricular tachycardia with ~:1 exit block.

hellt niorpholog>. thali those ot~servett in the lower strip) oi I;ig. 12. C‘o~iseclue~ltt~,, a different origin can be postulated, bul 011~ pacemaker ma>. bc operatilrg on both occasions >‘et with different propagation through the velltrictes. Both types of complexes are alternat ivet>, present in trarillg E, whereas tht 2-L‘ nodal tach!.cardia remains undisturbed so that the ~tectl-oc;trdic)graphic image is that of a bidirectional ventricular tachycardia. Its st)ollt;uleous transient dis;ll)pe:~r;~nce can be observed towartt the cncl of the fr;tciiip. I;ii-st, the tto\vnward direc,tett complexes vailish, Ijut the LIl)\vartl ttirectett ollcs t)ersist uiitit their sut)pressioll b>. ;I ventricular extras>-stole. ‘I‘he possibitit). of t\vo indet)eiident ventricular rh>.thms can also be considered ill this recortt, m;Aillg ;I total of three simutt;tlleous tach>.cardias, although a single ventricular t~~maker \\-ith var).illg exit block ;III~ alternalioll in its prot~agation through the vent rictes is more likeI\-. ‘l‘hesc difficulties ;~t’pl~. to the undet-st;llltliil~ of ;tII theories \vhich tt-1. to explain the galesis of bidirectiol~al tach\.c-artlias (I;ig. 115”). Ho\vever, ill t-his particular case ;I sul,r;‘ventricut~~lorigin (xi1 be rutetl out t)ecause of the tinding of fusion beats (see below). Sest, C, continuous \vith H, shows that after the extras>-stole the nod:tt t:tc-hJ,c-arttia has rcatq)c;lrett, iiou h:i\-ing ;L secolid degree .A-\’ block. I~.iii;itl?~, this t>‘t’c’ oi conduction t)vrsists ulitit the ec.tol)ic cto~~n~~rtt ventricular conit)lexes are agaiii observed ill II, so that both t)aceniakcrs ;lre LIIIqueslionabl~. dissociated. The presence of a fusion be;ll ( F) assures the \.relltricutar origin of Ihe tower rh\.thm. (‘o~lsectue~ltt~~, A-\- nodal tach~.cardi;t with aberration can be discarded, a~~tl at1 upper -i-i’ 11otlat tach~xarttia coexists with ;L ventricular tach?.cardia. Thus, the diagnosis in this last part of D is dissociatioll with interference in a 2 :l .A-\- block.

.S’inzultun(~ou.s /~ztlc,t~ntl~~nt example of this departniclrt .li

:irrh>.thmi:l

A- 1. l‘nrkyrcutlitls (1 GIW). The only was rq)orted in ;I rcc‘elit c-ommunicatioil

published from our

One of the most controversial points concerning double tach),cardias is whether atria1 impulses are stopped at the A-V junction b>. the normal or by an abnormall~~ prolonged refractoriness (true block) provoked in the latter tissues by the tower pacemakers. Whenever the rate of the lower center is rapid enough, it is conceivable that the impulses reach the intermediate tissues in such rapid succession that the!, are kept in a permanent state of normal refractoriness.” However, from the examples presented in this communication it was evident that prior to the appearance of the lower pacemaker an atria1 or a nodnt (Fig. 11 j tachycardia with AA-\’ conduction disturbances existed. ‘The belief that the mechanism was a true block was suggested by the following findings: (1) the disorder of rhythm was digitalis induced, except in Fig. 8, and (2) the atria1 rate bl, itself was occasionatt~. too slow to account for the abnormal X-I’ conduction, l;igs. 3 and 4 (see Reference 11, t;igs. 173 ;IIKI 174). .Ilso,
111 conclusion, enough evidence has been accumulated so that it can IK assumed that, certainI>., in a great number of cases of double tach>.cartlia some degree of impedance to A-V conduction is present but a complete A-\’ block does not exist, however. ‘I‘he incidence of the arrh\.thmia under ronsitieratioll is possibly greater than one is led to believe in view of the few published eiectrocardiograms. Ipor instance, in support of this xgument it can be stated that Hernsteill and his associates” reported 7 cases in a lo-month period. I’erhaps ill one or two of his tracings, coarse atria1 fibrillation could have been the supravelltricuiar rhythm. In our previous studies on double tachyxdias, as a-eil as ill Figs. 3 and 5 of the presetit report, the correct interpretatiol~ would have been impossible except for the use of esophageal leads. IIuring the period 1052 to 1955, \~e emplo\-edi esophageal leads routineI\in about 90 per cclit of olir cases of ventricular tach~xxrdia. ITor this reason our incidence oi double tachyxrdias is probabi>higher thall in a series in which onI>. the collventiollal twelve 1eads are recorded. -4 detailed awaiysis of case histories revealed that the disorder oi rh).thm LVLLSdigitalis induced except in one patient (Figs. 8, 9, and 10). Eve11 in that case it LV;LS cleat-l!. sho\lrll that the drug, although not responsible for the nodal tach>.cardia, indeed produced the bidirectional ventricular tach~xxrdia. 1 II contrast, onl>. 58 per cent of Bernstein’s cases had that origin. Ho\yever, ;I revielv of the literature since the original experiences of Luten in 1915, reveals that digitalis pia~wi ;m important role in over 75 per c‘ellt of the cases 011 which required tlata were included (~rI‘abie 1). ‘I’hroughout Figs. 1 to 12, xve presented the sequence ill which the arrh~~thmi;~ appeared. First, the atria1 tachycardia appeared, followed b!- the nodal or ventricular tach>wrdia, the former in a nonparoxysmal form and the last two in either n proxysmal or in a lloli1);1rox?.sni;ll form. Also, it is to be noted in l;igs. 1 to 10 that the lower rhJ.thm was produced by progressive increments of intravenous digitalis drugs. In spite of acetl-1 strophanthidin being considered extremeI\. toxic, our experience led us to believe that its effects were similar to those OI strophanthidin or ouabain. This is well illustrated ill Figs. 8. 9, and 10, in which a similar arrh!~thmia w;\s produced on three different- occasions 1,)~ three tliffere~~t clrugs. Severtheless, some factors must be kept in mind \vliei~ ilitcrpretiiig the test of digitalis tolerance, for there is reason to believe that a11 increasingly grave electroc;~rdiogr~Iphic picture due to the appearance of velltricuiar ectopic rh?.thms does not net-essaril>. indicate that the pre-existing tach~~cartlia uxs due to digitalis excess. 111 some rare cases, h?.perseiisitivit?ma>- be the cause of these aitkratiolls. ITor instance, Figs. 8, 9, a~lti 10 show how minor amounts of intravenous prepar;tt ions produced a toxic response in a patient whose basic rhythm was ~111 .A-\’ nodal tach\-cardia which was definitely spontaneous. &A thorough study of the case history revealed positively that digitalis had not bee11 :ldministered I)reviousl>,. .~crordin~l~, \ve hatl to accel)t the fact th;lt tosic. effects became evident before the therapeutic effects were achieved (considered as the abolition of the -4-I’ tachycardia).

370

Ci\STELLANOS,

AZAN,

AND

Am. Heart J. March, 1960

CALVIE

Therefore, it has to be admitted that hypersensitivity may lead the observer to believe that large doses of digitalis have been administered previously, when such is not so. Yet, such findings are infrequent and, as a rule, the therapeutic implications will be the same in each instance, namely., that further digitalization is contraindicated. On the other hand, in nearly all instances of atria1 tachycardia with first degree A-6: block due to digitalis poisoning (except in Fig. 5) a second degree block was induced before the beginning of the lower tachycardia. It is to be seen that in Figs. 11, 12, and 13 such a block appeared after the end of the ventricular tachycardia. In these rhythms a toxic effect was definitely the only possibility because no therapeutic results were to be expected. A drug-induced toxic rhythm could not be abolished by the same drug which induced the arrhythmia. This finding is in contrast with what occurs when one is dealing with spontaneous atria1 tachycardias, because in this case the abolition or no modification of the abnormal rhythm is the rule after digitalization.32 Invariably, the prognosis of double tachycardias is poor, not solely on account of the arrhythmia but because it usually exists in patients with a badly damaged myocardium. The great majority of the individuals in this study were elderlq'TABLE

I.SUMMAKY

0~ THIT REPORTED

C4sEs

oF L)~UBLE

CASES

i\trial*

and Ventricular G&rardin*

i\-V

and A-V Nodal Tachycardias: Lute+ HowardI SchotF4 Bernstein, et al.x Calviiio, et al.‘” Katz and Pick” Shmagranoff and Jickl” Calvifio, et al.‘@ Marriott, et aLzg Nodal and Ventricular Tachycardias Miller and Scharett12

Simultaneous A-V Tachycardias: Castellanos, et al.17 Simultaneous Ventricular Tachycardias: No case has been reported *Atrial

flutter

included.

Y,iAK

Tachycardias:

Lutena: McMillan and Bellet” Stern6 Kayden, et al.? Bernstein, et al.8 Dressier and Roessler” Calvifio, et aLlo Katz and Pick” Miller and Scharett’? Anderson and Rubin3’ Atrial*

~

?‘ACHYCARDIAS

: 3

2 1 ii 1 5 1 :

1920 1924 1925 1932 1937 19.51 1952 1952 1955 1956 1957 1958

1

1925 1927 1946 1952 1955 1956 1957 1957 1958

1

1957

I

1958

1 1

1 1 : 1 1

Yes Yes Yes > 3 NO ;ct; (3 cases) ;z > +es Yes Yes > +es Yes Yes Yes i

Yes

(5 cases)

patients with arteriosclerotic heart disease and refractory heart failure. The only exception was a 9-year-old girl with rheumatic fever (Figs. 6 and 7), which to our knowledge is the only published case of this arrhythmia in children. It is true that in many patients, death has been caused by the ectopic rapid rhythm, which can lead to ventricular fibrillation. Yet all deaths should not necessarily be attributed to this cause, because poor myocardial function with refractory heart failure can, in all probability, be responsible. For example, the patients whose tracings are presented in Figs. 6 and 10 died several days after sinus rhythm was re-established by appropriate treatment. When short-acting digitalis preparations produced the arrhythmias, they were treated either with procaine amide or potassium. Both drugs had a similar effect, detected whenever long tracings were obtained. Initially, the ventricular tachycardia disappeared, and then the pre-existing atria1 tachycardia with irregular A-V conduction was again observed. Thereafter, 1 :l A-V conduction accompanied by a progressive decrease in rate and P-R interval was seen until the return of sinus rhythm. The shortening of the P-R interval is a paradoxical finding, for it is known that toxic doses of Pronestyl prolong A-V conduction time.25 Because of this behavior the similarity between atrial tachycardia with block and experimental tachycardias produced by. electrical stimulation was stressed in a previous communication.“6 Furthermore, one case of atria1 tachycardia associated with digitalis administration with a 2:l exit block has been reported, a phenomenon which is a property of automatic rhythms.16 In view of the foregoing arguments, it is possible that atria1 tachycardias produced by digitalis can be due to an automatic center in the atria. Then perhaps it can be more than a coincidence that a case of double tachycardias has been published in which the ventricular rhythm was parasy-stolic (automatic) (Reference 11, Fig. 214). Another interesting finding evident in Figs. 1, 2, and 5 was a marked irregularity of the P-P intervals during atria1 tachycardias. Careful analysis revealed that they were not due solely to ventriculophasic arrhythmia and could be explained on the basis of an irregular discharge of a single pacemaker. This possibility was postulated in clinical cases by Katz and Pick” (page 284) and positively demonstrated in the laboratory by Scherf and associatesz7 Moreover, in the latter experiments it was shown how aconitine-induced atria1 tachycardias could respond dually to vagal stimulation. This maneuver could slow as well as increase the rate of the automatic center. Also, an irregular spacing of the P-P interatrial intervals could be seen in their tracings. A similar dualistic behavior can be noticed in the original experiments of Lewis.“8 These findings have due to digitalis toxicity drug was administered, (Figs. 1 and 2) as well different effect on atria1 digitalis.

a counterpart in some of the cases of atria1 tachycardias presented in this communication. For instance, when this an increase in rate usually ensued (Fig. 3), but no change as a decrease have also been observed (Fig. 5). Such a rate can be explained on the basis of the vagal action of

\‘arious combinations of simultaneous txhg-cardk have been observed :itrkt ;~nd ventricular to occur in the human heart. A s ;I rule, the coexisting forms x-e the most frequent. When esophageal leads \vere used, the incidence of these :lrrh?-thmias WAS found to be greater than that reported by other authors. This greater incidence WLS due to t.he fact that without esot>hageat leads the atria1 rhythm iu rna~l?- cases could 11ot be interpreted correctI\. because the widened &KS comI)teses sometimes obscured the atrint dettect ions. DiKitatis was the cause of these :Lrrh\.thmias in over 75 t)er ce~lt. the cases studied. This NXS welt demonstrated in c;~ses in which the double rhl-thms \\-ere induced bl. the intravenous ;~ttministratioli of short4ct illg ttigitatis txet)xxtions. X~protx-iate treatment with t)otassium and twocaine :miide usuatt~~ :tbotished the tach~xxdias tx-omptt>-. (‘ontrar)~ to the usual belief, the txognosis WLS not necessarit\~ det)endent upon the nature disorder 01‘ the I-h!-thm but chiefi>, upon the -4s ;I rule, these xrh).thmi;w were tx-ecxious conditions of the m)wxdium. most frectuentt\~ see11 ill eltterl\~ p:ltiellts with arteriosclerotic hwrt dkxsc. ;1 sillgte csceptioll was th;lt of siniutt~tneous t;lch)xxrttias occurring ill in %)-ear-old girl with rheumatic who died sevtwl da)-s after sinus rhythm se wns restored. \\‘hencver the rate of the to\\-er ~~c-en~ker wxs rapid e~lou,&, it was conceivable that the atria1 imtmtses could IIOL trwlsverse the !I-\- junction because of the refractoriness provokect in the tatter 1)~ the tohver lxwemaker. However, it was demollstratetl that some degree of abnorm;d refrxtoriness or true block X\:;IS present. J7et, obviousI\-, ;L complete r1-\’ block did not exist. This ni;Lint?- to thtz toxic effects of tti~it:~tis. irtit)edallce to c-onductioll w;w klscribed

oi

oi the

lever

1. 2. .i. 4. 5. 6. 7. 8. 9. 10. 11. 12. 1.3.

11.

Gallaxardin, L.: .L‘achycardie 1 elltriculaire termillale grclfc >ur line tach>Gstolie auriculaire, Arch. mal. coeur 13:210, 1920. Barker. I’. S.: Ventricular ‘I’achycardia 1 )uring an :\ttack of Paroxysmal i\uricular ‘l‘achycar&, Heart 11:67, 1921. Lutell. I-).: Clinical Studies of Digitalis. II. Toxic Rhythms, \\:ith Special Reference to the Similarity Between Such Rhythms in hlan and in the Cat, Arch. Int. Med. 35:71, 1925. Luten, D.: Clinical Studies of L)igitalis. III. .\dvanced Toxic Rhythms, Arch. Int. Med. 35:87. 1925. McMillan, ‘1‘. M., and Bellet, S.: .Auricular Flutter: Some ol Its Clinical Manifestations and Its Treatment, Am. J. M. SC. 184:33, 1932. Stern, N. S. : I’aroqwnal Ventricular Tachycardia: Hcport of ,? Cases;. ,\nn. Int. Sled. 11:jlO. 1937. Kayden, H. J.. Steele, 1-I. hr., &lark, L. C., and 13rodie, R. B.: .l‘he I’se of Procaine .-\mide ill Cardiac Arrhythmias, Circulation 4:13, 1951. Rcrllstein, L. hl., Pascale, L. R., Littman, .\., and Foley., l+:. F.: Simultaneous Independent Paroxysmal Tachycardias, J.A.M.4. 150&6, 195%. I)ressler, WI, and Roes&r, H.: The Occurrence in I’aros\xllal Ventricular Txhvcardia of \‘entrlcular Complexes Transitional in Shape to Sik~auricular Beats, AM. -He.i~r J. 44:485, 1952. Cal\-ifio, J. R/I., .\zan, L., and Castellanos, ,\. Jr.: i.alor de las derivaciones esofagicas ell 1;~ arritmias complejas, Rev. cubana cardiol. 16:293, 1955. Katz, L. N., and Pick, .A.: Clinical Electrocardiography, Part I, The ;\rrhythmias, Philadelphia, 1956, Lea & Febiger. Miller, R., and Scharett, Ii. H.: Interference I dissociation, Circulation 16~303, 1957. I~loward, T. : I~o~hle Tachycardia: Coexisting iluricular and Ventricular ‘Tachycardia dtlc t,, I)igitalis, Am. J. M. SC. 173:165. 1927. Schott, :A.: Paroxysmal Auricular Tachycardia \Vith Auriculoventricular Block; Follow-l Ip, ‘l‘ransirnt I)issociation \IYth Interference, l’roc. Roy. SW. Med. 39:302, 19.U).

15 16. 17. 1x. 19. 10.

11. 12 23

Shmagralloff, G. L., al:tl Jick, S.: Simultaneous :1trial and Nodal ‘l‘achycardias, .\M. IlbxR’r J. 54:417, 1957. Calvifio, J. M., Xzan, L., and Castellanos, A.. Jr.: I’aroxysmal Tachycardia \Vith 2 :l Exit Block, AM. HEART J. 54:&N, 19.57. Castellanos, A., Jr., Azan, L., and Cal\Tifiy, J. M.: 1)issociatiun \Vith Interference Betnwl1 Pacemakers Located b’ithin the A-\ Conducting System, 21~. HKAR.I. J, .56:562, 1058. Lallgendorf, R. : Aberrant \~‘cntricular Conduction, r\M. HURT J. .41:700, 19.5 1. IIahnim, I., and Barrelet, J. A.: ‘I‘achycardie ventriculaire avec conduction rbtrogradt: c’t periodes de Wenckehach in\,er&es, Cardiologia 19:62, 1951. Langendorf, R.: Alternation of A-Y Conduction Ike. .\a~. HEART J. 55:181, 1958. Loaw, I<., and Levine, S. 3.: Current Concepts ill Digitalis ‘Ikrapy, Boston, 1954, Little, Brown 8r Company. Langcndorf, I~., and Pick, .\.: Concealed Condrlrtion. Further Evaluation of a Fundame~ltal Aspect of Propagation of the Cardiac Impulse, Circulation 13:381, 1956. I’ick, .I., Langendorf, R., and Katz, I,. N.: Depression of Cardiac Pacemakers 1)~. I’rcmat ure Impulses. AM. HURT 1. 41:19. 1951.

24. 25.

26 Scherf,

.11 32.

I)., 13lumenfeld, S.. blueller, I’., and Uleinfeld, \\‘. H.: 011 the Response nf E:rtopic :SuricuIar ‘l‘achycardias to Vagus Stimulation, .\M. HuR.1 J. 45:95, 195.1. Lewis, ‘I‘.. Ikury, .\. N., and Ijulper, H. A.: Flutter and Fihrillntion. The ENecte of \‘agaI Stimulation. Heart 8:141, 1921. Rlarriott, II. J. I~.. Schuhart, A. F., antI I