Journal, Electrical conversion of atrial flutter to atrial …British HeartJournal, 1972, 34, 12I5-I224. Electrical conversion ofatrial flutter to atrial fibrillation Flutter mechanism

British Heart Journal, 1972, 34, 12I5-I224.

Electrical conversion of atrial flutter to atrialfibrillationFlutter mechanism in man

,Timothy E. Guiney,2 and Bernard LownFrom the Cardiovascular Research Laboratories, Department of Nutrition, Harvard Schoolof Public Health; and the Levine Cardiac Unit, Cardiovascular Division, Department ofMedicine, Peter Bent Brigham Hospital, Boston, Mass., U.S.A.

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If human atrial flutter is due to re-entrant excitation, depolarization as well as repolarizationmust continue throughout the entire atrial cycle. It follows that the atrial vulnerable period forinducing atrial fibrillation is also continuous rather than discrete. This hypothesis was examinedduring cardioversion of I33 patients with atrial flutter who received 280 low-energy shocks. Acomposite analysis of these patients demonstrated that all intervals of the flutter cycle wereequally susceptible to shock-induced atrial fibrillation. The optimal energy was found to be ioWsec. The development of atrialfibrillation was independent of the state of digitalization and wasnot prevented by pretreatment with atropine or propranolol. These findings are consistent withre-entry as the basic mechanism of human atrial flutter.

Attempts to clarify the mechanism of atrialflutter have engaged the energies of numerousphysiologists and clinical investigators overmore than half a century. Polemics have ragedas to whether the arrhythmia is sustained by a

e single discharging focus or by a circulatingwave front of depolarization. In the experi-mental animal there is persuasive evidencethat a flutter-like arrhythmia can result fromeither of these mechanisms. When protoplas-mic irritants such as aconitine (Hayden, Hur-ley, and Rytand, I967; Ishikawa, I967;Prinzmetal et al., I952; Scherf, I947; Scherfand Terranova, 1949; Scherf, Romano, and

i Terranova, I948) or delphinine (Scherf et al.,I960; Scherf, Blumenfeld, and Yildiz, I963)are applied to the atria, the ensuing flutter-like disorder emanates from the site of drug%pplication. The extensive investigation ofThomas Lewis (1925) adduced evidence thatAutter might also result from a circus move-,.ment. Decisive corroboration was providedby the experiments of Rosenblueth and GarciaRamos (i947). They were able to initiate and

Oteceived 24 April 1972.1 Supported in part by grants from the National Insti-tutes of Health, U.S. Public Health Service; and theFund for Research and Teaching, Harvard School of.iublic Health, Department of Nutrition.2 Present address: Cardiac Catheterization Laboratory,Massachusetts General Hospital, Boston, Mass. U.S.A.

maintain a circulating wave front around anobstacle in the right atrium produced by acrush between the vena cavae. The relevanceof these animal models to the disorder en-countered in man remains uncertain.The hypothesis in current favour is that

clinical flutter is due to a re-entrant mechan-ism. As classically formulated by Lewis(I925), an advancing front of depolarization isseparated from its tail of refractoriness byfully recovered tissue, the so-called excitablegap. Some portions of the atria are, therefore,undergoing depolarization at all times, whileother portions are either in a state of refrac-toriness or completely repolarized. It wouldbe inferred that if flutter is the result of re-entry, vulnerability to fibrillation should alsobe present throughout the cardiac cycle. Bycontrast, in the presence of sinus or singlefocus ectopic tachycardia, the vulnerableperiod is located in a discrete part of the car-diac cycle and is of brief duration (Lown,Kleiger, and Williams, I965).The opportunity to test the extent of the

vulnerable period in patients with atrial flutterpresents itself during cardioversion of thisdisorder to sinus rhythm. Low energy elec-trical discharges may convert flutter to atrialfibrillation (Lown, I967). The vulnerableperiod is generaly activated by a narrowrange of low discharge energies. If the trans-

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TABLE I Underlying heart disease in 144patients with atrial flutter subjected tocardioversion

Disease No. ofpatients

Rheumatic heart disease 53Coronary artery disease 32Lone flutter 23Pulmonary disease I2Congenital heart disease 9Hypertensive heart disease 4Pericarditis 4Other 7

formation in atrial rhythm from flutter tofibrillation is dependent upon the stimulusexciting the atria during their vulnerableperiod, only a limited range of energies shouldbe shown to be effective. If the mechanism ofatrial flutter is due to re-entry, it should bepossible to produce atrial fibrillation by asingle electric shock from any part of thecardiac cycle. The present clinical study pro-vides information relating to each of thesequestions.

MethodsThis study involved cardioversion of i44 con-secutive patients with atrial flutter admitted to thePeter Bent Brigham Hospital between AugustI962 and July I970. There were 96 men and 48women. The patients ranged in age from I9 to 89years. Table I lists the cardiovascular diseasesencountered.The technique for cardioversion has been

described previously (Lown, Amarasingham, andNeuman, i962a; Lown, Kleiger, and Wolff, I964).A DC cardioverter was employed, and the elec-trode paddles were positioned anteroposteriorly.All patients were pretreated with IOO mg pento-barbitone sodium given orally one to two hours

TABLE 2 Energy content of initialtransthoracic cardioversion shock administeredto 133 atrial flutter patients

Energy (Wsec) Shocks (No.) Per cent

I 45 24.85 35 I9.3

I0 20 II225 28 I5.550 44 24-3iooand > 9 4-9

Total I8I* 100

* Some patients were subjected to cardioversion morethan once, thus accounting for the additional 48 initialshocks.

before the procedure. Anaesthetics included thio-pentone sodium, methohexitone sodium, com-binations of pethidine hydrochloride and pento-barbitone sodium or pethidine hydrochloride andpromethazine hydrochloride. Over the past fouryears diazepam was used almost exclusively. In6I patients, the doses ranged from 2-5 mg to 40mg, with a mean dose of I3-5 mg. An initial doseof 2-5 mg to 50o mg intravenously was followedby 2-5 mg increments every two minutes untillight sleep was induced. Blood pressure waschecked between successive doses.A complete i2-lead electrocardiographic tracing

was recorded before the cardioversion procedure.The standard limb lead with the most distinctflutter waves was selected for monitoring through-out the procedure. In the majority of cases, leadII was employed. A special damping circuit pro-tected the electrocardiographic recorder and re-sulted in an isoelectric artefact lasting an averageof i-8 seconds. After each shock, the cardiacmechanism was identified in lead II; the rhythmwas then confirmed in lead Vi. This was gener-ally accomplished within 5 to IO seconds afterthe emergence of the first post-shock complex.One of four types of response was identified:(i) persisting atrial flutter, (2) atrial fibrillation,(3) normal sinus rhythm, (4) junctional or othermechanisms. Of the 299 cardioversion shocksemployed, I9 shocks in ii patients were excludedfrom analysis because of the presence of electricalartefacts or uncertainty as to the underlyingrhythm. Thus, the analysis to be described wascarried out on the response to 280 shocks in 133patients.At the beginning of this study all cardioversions

were carried out with an initial setting of IOOWsec. As it became evident that atrial fluttercould be reverted with lesser energies, the initialdischarge energy was progressively reduced. Dis-tribution of energies of the first shock adminis-tered to the I33 patients in this study is shown inTable 2. In 55.3 per cent, the initial shock was IOWsec or less. If sinus rhythm did not result, theenergy content of successive shocks was in-creased. The following sequence was usually em-ployed: i Wsec, 5 Wsec, IO Wsec, 25 Wsec, 50Wsec, 200 Wsec, 300 Wsec, 400 Wsec. If noreversion to sinus rhythm occurred with a 400Wsec discharge, the procedure was stopped. In 5patients, the clinical objective of cardioversionwas to change the rhythm to atrial fibrillation:this was accomplished with low energy shock.The location of the cardioversion discharge in

the flutter cycle varied in different patients. Twofactors determined where the shock fell in relationto the flutter wave, namely the degree ofAV blockand the voltage rise time of ventricular depolariza-tion which triggered release of the electric dis-charge. Analysis of the location of the electricaldischarge in relation to the flutter wave was car-ried out on records of I59 shocks delivered to 79patients. These were selected because the flutterwave, designated as P', could be precisely defined.The interval between the nadirs of successiveflutter waves in lead II (P'P') was measured in



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milliseconds. The point of interception of thisinterval by the shock, designated as S, providedthe P'S interval. The ratio of these two intervals,P'S/P'P', defined the position of the electricaldischarge in the flutter cycle. P'S/P'P' ratios weredivided into quartiles. Thus, if the shock felli6o milliseconds after the nadir of the P' waveand the P'P' interval was 200 msec, the resultingratio was I60/200, or o8o. This was grouped withall ratios occurring in the quartile of 0-75 too099 (Fig. i).To determine whether the emergence of atrial

fibrillation was related to shock-induced releaseof neurohumoral agents (Amory and West, I962;Blinks, I966; Cobb, Wallace, and Wagner, I968;Nelemans, I95I; Ten Eick et al., I967; Vincenziand West, I963; Whalen, Fishman, and Erickson,1958), selected patients were pretreated witheither atropine or propranolol. Twelve patientsreceived atropine intravenously, in doses of o-6tO 2-2 mg, five minutes before administering thecardioversion discharge. Ten patients were givenoral propranolol, in doses ranging from 30 mg to200 mg daily, for two days preceding cardiover-sion, as well as on the day of the reversion. Onepatient, subjected to cardioversion on two differentoccasions, received both atropine and propranolol.Necessarily, these patients were receiving otherdrugs that may have influenced the result ofcardioversion. Of the 133 patients, ii6 were onmaintenance digitalis therapy, ii had not receivedcardiac glycoside at any time, and in 6, digitalishad been discontinued five or more days beforecardioversion. Seventy-eight patients were pre-treated with quinidine, in a dose of o-8 to I-2 g,for the 24- to 48-hour period preceding thereversion procedure.

Results

The 133 patients with atrial flutter received280 transthoracic shocks. Of this number, 82resulted in atrial fibrillation and 96 wererestored to sinus rhythm; the flutter mechan-ism persisted after 87 shocks and in I5 thereensued a junctional or an unidentifiablerhythm. An example of induction of atrialfibrillation is illustrated in Fig. 2. The medianshock energy which resulted in atrial fibrilla-tion was io Wsec (Table 3). A high incidenceof atrial fibrillation was also observed afterdischarges of 5 Wsec. When results of shocksat these two energies are combined, out of Ioidischarges 49, or 48 5 per cent, resulted inatrial fibrillation. Provocation of atrial fibrilla-tion diminished as the energy content of theshock was increased.

After many of the shocks sinus rhythm,junctional rhythm, or some other mechanismdeveloped precluding the emergence of atrialfibrillation. The data were therefore analysedto exclude those who had these rhythmalterations. Only those shocks that were fol-

P'-S/P'-P' RATIO

P'-s 160

~0.80

CardioversionShock (S)

l.

P 160 msec

i200msec

i200msec i 200msec i 200msec i

FIG. i The P'S/P'P' ratio was calculated asindicated in this figure.

lowed by either atrial fibrillation or persistingatrial flutter were included. The energy mosteffective for inducing atrial fibrillation wasIO Wsec, with 66-7 per cent of subjects whoreceived this energy developing atrial fibrilla-tion. There was a stepwise reduction in occur-rence of atrial fibrillation at lower and highershock energies (Fig. 3). There was an increasein incidence of atrial fibrillation at energies ofIOO Wsec or greater; however, only IO shockswere available for the analysis. The existenceof a specific effective energy was shown strik-ingly in one patient. After i and 5 Wsec dis-charges, the atrial flutter remained unaltered.After IO Wsec the mechanism persisted, how-

FIG. 2 Patient with chronic atrialflutter ata rate of 300 a minute. After a 5 Wsecshock synchronized to discharge in the QRS,atrial fibrillation ensued and is clearly seen inlead Vi. (In this and subsequent figuresnotation for watt seconds is WS.)

A. Flutter5WS Shock

I Atriial Fibrillation444W K44.:. .-4-X :1--J4 &--2~2I.;4-l :I|- -LJJ; I -LII-

Atriol Rate 300d .

!tz!f b±L-FH:!-IT- LU

V-1.-Li-.--T



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ever, the wave form was changed and theatrial rate increased slightly. When the energyof the next shock was reduced to 2-5 Wsec,atrial fibrillation resulted (Fig. 4). The factthat atrial fibrillation was produced at aspecific low energy suggested that this phe-nomenon was related to the atrial vulnerableperiod.The next question examined was whether

the vulnerable period was discrete or con-tinuous. The point at which the electricaldischarge intercepted the flutter cycle(P'-S/P'-P' ratio) was examined after I09shocks which either resulted in atrial fibrilla-tion or continued as atrial flutter (Table 4).When the cycle was divided into quartiles,it became evident that no part of the fluttercycle was impervious to the development ofatrial fibrillation. In fact there was no statistic-ally significant difference between quartiles(X2 analysis, P = os5). Similar results were ob-tained for shocks of I0 Wsec or less. Thesefindings indicated that there was no distinctpart of the flutter cycle that was exclusivelysusceptible to the provocation of atrial fibrilla-tion by electrical discharge.

It is possible that the occurrence of atrialfibrillation was related to release of neuro-transmitter by the cardioversion discharge.This question was, therefore, examined in asmall group of patients.

Atropine Twelve patients were given atro-pine in doses of o6 to 2-2 mg intravenouslywithin five minutes before cardioversion. Atotal of 25 shocks was delivered. Of these, iishocks resulted in atrial fibrillation, 5 in sinusrhythm, and 9 remained in atrial flutter. Thus,in 55 per cent of patients given atropine atrialfibrillation followed a transthoracic discharge.The median effective energy in this group wasalso io Wsec (Fig. 5).

Propranolol Ten patients received a totalof 20 shocks at a time when they were receiv-ing propranolol hydrochloride in doses rang-ing from 30 mg to 200mg daily. Atrial fibrilla-tion followed atter five shocks, sinus rhythmafter seven, and the rhythm remained un-altered after eight. One patient was twice sub-jected to cardioversion while pretreated withboth atropine and propranolol. On each occa-sion i Wsec was without effect; 5 Wsec duringthe first cardioversion and I0 Wsec duringthe second resulted in atrial fibrillation(Fig. 6).

Since it has been shown that cardioversionenhances the arrhythmogenic action of digi-talis (Lown et al., I965; Kleiger and Lown,i966), the possible role of digitalis glycosides

TABLE 3 Result of 280 shocks delivered to133 patients with atrial flutter as function ofenergy of electrical discharge

Energy of Number of Responseshock (Wsec) shocks at

each energy Atrial Sinus Persisting Otherfibrillation rhythm flutter rhythms

I 48 I3 3 32 05 56 27 5 24 0I0 45 22 9 I I 325 50 13 25 8 450 59 3 43 6 7iooand > ioo 22 4 II 6 I

Total 280 82 96 87 15

in the emergence of electrically induced atrialfibrillation was examined. Only patients onmaintenance digitalis therapy but not receiv-ing quinidine were examined. This groupincluded 55 patients who were subjected to 83cardioversion shocks. In 28, or 34 per cent,atrial fibrillation resulted. A nearly identicalresult was observed in I0 patients whoreceived neither digitalis nor quinidine; atrialfibrillation followed 37 per cent of the shocks.

DiscussionThe mechanism of human atrial flutter re-mains undefined. Two major and opposingtheories have long held sway, namely, thatthe underlying basis is a rapid firing of anectopic focus or, that it results from circusmovement or re-entry of an entrapped wave.The arguments in favour of each of thesehypotheses have been extensively reviewed(Hecht et al., I953; Katz and Pick, I960;Rytand, I966; Scherf, Schaffer, and Blumen-feld, I953).

TABLE 4 Distribution of cardioversion shocksin quartiles offlutter cycle expressed as ratioin P'S/P'P'

Quartiles of P'P' cycle

0 00-0 24 0o25-049 0o50-074 0 75-0 99

A. Total no. of shocks i8 I7 39 35No. with atrial fibrillation 7 I0 22 I7% Atrial fibrillation 39 59 57 49

B. Total no. of shocks I3 I3 27 25No. with atrial fibrillation 4 8 12 II% Atrial fibrillation 3I 62 44-5 44

Data based upon an analysis of I09 shocks in 79 patients, of which 56 resulted inatrial fibrillation. (A) represents all energies employed, while (B) only energies ofI0 Wsec or less. (The differences are not statistically significant.)



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At the turn of this century, the Americanmarine biologist, A. G. Mayer, induced a con-tinuous recirculating wave of excitation in aring of tissue cut from the bell of the largemedusa, Cassiopea (Mayer, I906). In onespecimen the pulsation persisted for ii days'Mayer, I9I6). Some years later, Mines (I9I3)Lnduced a similar circulating wave of contrac-tion in the tortoise heart from which the sinusvenosus had been excised. He noted that, 'the:ontractions are easily upset by the occurrenceDf an extrasystole'. The term 'circus contrac-tion' was introduced by Garrey (I914), whoroted that a critical mass of heart muscle wasrequired and who also recognized the import-mnce of a localized depression in conductionas a condition favouring such arrhythmia.

It was Thomas Lewis (1925) who providedthe essential theoretical frame of modem:hinking on re-entrant rhythms. He amassedi wealth of data derived from galvanic stimu-[ation of dog atria and from analysis of-lectrocardiographic records of patients withriutter. In animals having atrial flutter, as thebrief after-effect of rapid electrical stimula-tion, Lewis, Feil, and Stroud (1920) exploredthe arrival of the depolarization wave at vari-)us atrial sites. They concluded that some newpart of atrial muscle was activated throughoutthe entire atrial cycle and that the propagatedexcitation traversed a fixed pathway aroundthe orifices of the vena cavae. A limitation ofthese studies was the failure to define themntire pathway of excitation in the left atrium.Modern techniques have permitted Kimura?t al. (I954) to remedy this deficiency inmethod and confirm Lewis's conclusions.

Investigation of the arrhythmia in man wasmore indirect and consisted of mapping thetime course of the flutter wave by determiningthe change in atrial electrical axis during the-ardiac cycle (Lewis, Drury, and Iliescu,[92I). As studied by vectorial analysis, themanifest atrial potential appeared to rotate3600. This circulation was believed to accountFor the continuous undulation of the electro--ardiographic baseline seen in cases of purelutter (Lewis et al., 1920). Prinzmetal et al.:195i) later challenged this interpretation.rhey ascribed baseline motion not to circusnovement, but to the sequence of depolariza-ion and repolarization which altered direction)f the atrial vector.Attempts to define the flutter mechanism

n man have since been largely directed tonapping the time course of arrival of the-xcitation wave described by Lewis to travel.pward in the left atrial wall and downwardn the taenia terminalis of the right atrium*Lewis, I925). Since vectorial analyses have

Trotal Shocks8 L.A.J

8R *Effective Shocks

6060

40is. k 111 I t1 [email protected] 5 10 25 50

ENERGY OF DISCHARGE (w/S

FIG. 3 Incidence of atrialfibrillation afterdifferent energy shocks tabulated both aspercentages of total shock and of effectiveshocks, i.e. those shocks that were followed byeither persistent atrial flutter or developmentof atrial fibrillation (see also Table 3).

yielded conflicting results (Cabrera and SodiPallares, 1947; Duchosal and Sulzer, 1949),many studies aimed to achieve greater prox-imity by means of oesophageal and right intra-atrial electrodes (Duchosal and Sulzer, I949;Enselberg, I95I; Giraud, Latour, and Puech,1955; Grishman et al., 1950; Groedel andMiller, I950; Kato et al., I956, I957; Koss-mann and Berger, I941; Prinzmetal et al.,1953; Rosenblueth, I953; Rytand, I966;Wenger and Hofmann-Credner, I952). Oeso-phageal electrocardiography confirmed, in

FIG. 4 Shocks of Io Wsec (5 Wsec and IWsec not shown) failed to induce atrial fibrilla-tion though there occurred a slight accelerationin atrial rate and change in atrial morphology.After 2-5 Wsec atrial fibrillation resulted.

Atnral Rate236

lOws Atrial Rate244

i I I Iil1. /--J ..Q ..AV.. V4: 1, . I-J.-vlol-.

230 2.5ws atrial fibrillation

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most cases, a caudocephalic direction of thedepolarization wave in the left atrial wall,though the opposite direction was occasionallynoted (Cabrera and Sodi Pallares, I947; Du-chosal and Sulzer, I949; Enselberg, I95I;Grishman et al., I950; Kossmann and Berger,I94I; Prinzmetal et al., I952). Direct mappingof the path of the excitation wave was onlyrarely attempted and the results have beeninconclusive (Groedel and Miller, I9so;Prinzmetal et al., 1953).

Recently Kishon and Smith (I969) haveaddressed themselves to this question. In I0patients with flutter, they timed arrival of theintrinsic deflection by recording simultane-ously from oesophageal and right atrial elec-trodes at different levels. In 4 patients, atrialactivation progressed cephalad in the leftatrium and caudad in the right atrium.Though exploration of the excitatory pathwaywas incomplete, almost two-thirds of the atrialcycle could be defined. They judged thesefindings to be consistent with a circus move-ment. In the 6 other patients no such sequencewas recorded, the excitation wave occupiedonly one-third of the atrial cycle and spreadcephalad simultaneously in both atria. Theyconcluded that two mechanisms operated inhuman flutter. Kishon and Smith (I969)acknowledged that if the circus pathway waslocated low in the atrium, it would not havebeen detected by the techniques employed intheir investigation.The present study of the flutter mechanism

is also indirect but is based upon an entirelydifferent approach. The ability to convertflutter to fibrillation at a discrete low energysuggests excitation of an atrial vulnerableperiod. The observation that vulnerabilityis present throughout the entire atrial cyclesuggests that this is also true for the atrialdepolarization-repolarization sequence. An-drus, Carter, and Wheeler (1930) first showedthat the dog's atrium possessed a sharply de-marcated vulnerable period. Single electrical

E£ er gy5ws

lmg Atropine L.V.

FIG. 5 After i mg atropine intravenously 5Wsec shock did not alter flutter mechanism;however, a IO Wsec discharge induced atrialfibrillation.

pulses when discharged during this time inter-val of the cardiac cycle produce atrial fibrilla-tion. Electrophysiologists (Brooks et al., I95I)have confirmed the existence of such a discretezone in the atrium, which coincides with thedip in the atrial excitability curve. Lown (un-published data) looked for the atrial vulner-able period in the intact dog with transthor-acic shocks and found it to have a duration ofI0 to 20 msec, with i Wsec being the optimalenergy. The vulnerable period was locatedconsistently during inscription of the terminalportion of the QRS complex.There has been no systematic exploration

for an atrial vulnerable period in man. Atrialfibrillation at times has been noted to occurduring right atrial pacing (Ross, Linhart, andBraunwald, I965). In a retrospective analysis,Haft and coworkers (I968) found 26 episodesof atrial fibrillation or flutter-fibrillation in 3normal subjects during single or paired pacingof the right atrium. The interstimulus intervalor the P-stimulus interval for initiatingarrhythmia was the same and ranged fromi8o to 280 msec. In over 2oo other patients,atrial fibrillation was never seen during right

FIG. 6 In a patient pretreated with both atropine and propranolol, atrial fibrillation was notprevented after a 5 Wsec cardioversion discharge.

5WS

L I

Lead ]3:



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atrial pacing outside this time period. Addi-tional support for an atrial vulnerable periodderives from the findings of Killip and Gault(I965) that atrial premature beats which occurearly in the cycle are associated with a highincidence of atrial fibrillation.

Is a vulnerable period present when sinusrhythm is replaced by an ectopic tachycardia ?No data are available for atrial tachyarrhyth-mias. However, the vulnerable period appearsunaltered when the mechanism is ventriculartachycardia. Lown et al. (I965) explored thecardiac cycle with low energy cardioversionpulses during ventricular tachycardia inducedby digitalis overdose. They found a singlesharply demarcated vulnerable period for pro-ducing ventricular fibrillation which was ofthe same duration and energy threshold asdetermined during sinus rhythm. It thereforeappears that when a tachycardia emanatesfrom a single ectopic site, it is associated witha discrete rather than a continuous vulnerableperiod. If repetitive discharge from a singleectopic focus accounted for atrial flutter inman, a similarly circumscribed period of atrialvulnerability should have been observed. Thecontrary findings of the present investigation,that fibrillation could be induced equally wellthroughout the atrial cycle, is thus consistentwith the circus movement hypothesis.A limitation of the present study needs to

be emphasized. The presence of a continuousvulnerable period in atrial flutter was deducedfrom a composite view derived from manydiscrete observations, where each patient pro-vided but a single point of datum. It was notbased on a systematic exploration of the entireflutter cycle in a single individual. Even ifthis were ethically permissible, it would havebeen difficult to accomplish. Since there wasfrequently but one chance to test for vulner-ability, once atrial fibrillation was induced, themechanism usually persisted or reverted tosinus rhythm. There is, however, additionalevidence to support the concept that thechange from flutter to fibrillation was due tostimulation of an atrial vulnerable period. Ifthis rhythm alteration was simply a shock-induced disorganization in heart rhythm, itwould have varied directly with the energyof discharge. This is the case when long ACpulses are administered transthoracically(Lown et al., i962b). While at 75 volts theincidence of atrial fibrillation is 40 per cent, itprogressively increases reaching ioo per centwith a shock level of 450 volts. On the otherhand, when single short DC pulses are de-livered to the heart during the atrial or ven-tricular vulnerable period a narrow range oflow energies exists which is optimal for induc-

2

Atrial rate236

-tF4-- - ia, *: -*~~~~~~~~~~~~~~~~~~~~~~~~~ ' I - +s..-.jM'-:=::-':11=.n'-Ls;;_.

240

FIG. 7 Low energy cardioversion dischargechanged direction offlutter wave withoutsignificantly altering atrial rate.

ing fibrillation. In the present study, the peakincidence of atrial fibrillation occurred at IOWsec, with less effectiveness resulting fromeither lower or higher energies.A phenomenon encountered in 5 of the

patients lends additional support to the circusmovement hypothesis. After a low energyshock the flutter mechanism persisted, butcloser inspection of the electrocardiographicrecord revealed a change in morphology of theatrial complex. In fact the flutter waves werea mirror image oftheir former contour (Fig. 7).An additional shock at a higher energyresulted in atrial fibrillation. It is difficult toexplain this occurrence if the arrhythmia re-sulted from discharge of an ectopic pace-maker. One would have to entertain a numberof assumptions, namely, the existence of twoectopic sites, one held in abeyance by theother and both discharging at nearly identicalrates, furthermore, that they were situated atopposite atrial poles to permit a precise mirrorimaging in wave form. If one holds to thecircus movement hypothesis, such compound-ing ofimprobable assumptions is unnecessary.A reversal of direction of the entrapped wavefrom counterclockwise to clockwise, whenviewed sagittally from the left, would accountfor the observation.A significant question is the frequency with

which a circus movement operates as themechanism of atrial flutter in man. The pre-sent study provides some information. At themost effective energy of IO Wsec, 22 out of33 episodes, or 66f7 per cent resulted in atrialfibrillation. It is possible that IO Wsec wasnot the optimal energy in the ii patients inwhom failure was encountered at this energysetting. Indeed, in 6 of the iI, atrial fibrilla-tion was produced at either higher or lower

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energy settings, while in the remaining 5sinus rhythm occurred in a succeeding shock.Thus, 28 of 33, or 85 per cent of the group,developed atrial fibrillation after a single lowenergy shock. It is not unreasonable to sur-mise that if the initial choice of energies werecorrect, the 5 who reverted to sinus rhythmwould also have developed atrial fibrillation.Thus, it may be that, in I00 per cent of pa-tients with flutter, it is possible to transformthe rhythm to fibrillation by stimulating thevulnerable period randomly in the atrial cycle.The data suggest that human flutter is theresult of but a single mechanism, namely, thecirculation of an entrapped wave, as conceivedby Lewis.An alternative explanation for our data

should be considered. It has been shown thatelectrical discharge releases acetylcholine andnorepinephrine from nerve endings in theheart (Amory and West, I962; Blinks, I966;Cobb et al., I968; Nelemans, i95i; Ten Eicket al., I967; Vincenzi and West, I963; Whalenet al., I958). It is conceivable that the changein rhythm resulted from neurotransmitterliberation. In the experimental animal it hasbeen shown that cholinergic stimuli favourthe emergence, as well as sustenance, of atrialfibrillation (Scherf and Schott, 1953). In man,carotid sinus pressure, which causes reflexvagus stimulation of the heart and acetyl-choline release, may convert atrial flutter toatrial fibrillation (Anbe, Rubenfire, and Drake,I969;Bussan, Reid,and Scherf, I957;LownandLevine, I96I; Rytand, I967; Scherf, Cohen,and Rafailzadeh, I966). Cobb et al. (1968)found that, in dogs, direct current trans-thoracic shock, even at a low setting of IWsec, provoked vagal-like effects manifestedby sinus slowing or sinus arrest. These couldbe prevented by administering atropine. Itis unlikely that shock-induced acetylcholinerelease was responsible for the change fromatrial flutter to fibrillation in man. If neuro-transmitter liberation were the basis, onewould anticipate the following: (I) A greaterincidence of atrial fibrillation both at higherenergy discharge as well as in patients ondigitalis who are more sensitized to cholinergicstimuli; and (2) prevention of emergence ofatrial fibrillation by atropine. None of thesewas observed. The fact that pretreatment withpropranolol did not prevent induction of atrialfibrillation argues also against a role for cate-cholamine release.

Several recent reports (Haft et al., I967;Zeft et al., I969) indicate that atrial fluttermay be reverted to sinus rhythm by rapidright atrial electrical pacing. The pacing ratesemployed have ranged from I80 to 600 a

minute. Atrial fibrillation was an intermediaterhythm in I2 of I3 patients. A similar methodhas been used to convert a disabling and fre-quently recurring atrial tachycardia, for abrief period, to atrial fibrillation (Wiener andDwyer, I968). Haft and coworkers (I967)postulated that frequent atrial stimulationallowed an impulse to fall within the atrialvulnerable period, thereby initiating unstableatrial fibrillation. They also suggested over-drive capture of an ectopic focus as the pos-sible mechanism of conversion in one of theirpatients. Of interest is the observation ofZeft et al. (I969) that it was possible to restoresinus rhythm in one patient without inter-vening atrial fibrillation. This was accom-plished by pacing at a rate of i8o a minutesignificantly slower than the atrial flutter rateof 330 a minute. It was suggested that anappropriately timed atrial stimulus inter-rupted a re-entry pathway of excitation,extinguishing the arrhythmia and permittingthe sinus node to establish pacing hegemony.The ability to terminate a number of

arrhythmias with serial right atrial pacing(Massumi, Kistin, and Tawakkol, I967; Dur-rer et al., I967), single pulses carefully timedin the excitation cycle of the tachycardia(Bigger and Goldreyer, I970; Hunt et al.,I968), low energy cardioversion shocks, andthump version (Lown and Taylor, 1970;Pennington, Taylor, and Lown, I970) allpoint to the prevalence of re-entry as thefundamental mechanism in many diversehuman rhythm disorders.

The authors acknowledge the critical and helpfulcomments of Dr. John Temte.

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Requests for reprints to Dr. Bernard Lown, De-partment of Nutrition, Harvard University Schoolof Public Health, 665 Huntington Avenue, Boston,Massachusetts 02II5, U.S.A.



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Journal, Electrical conversion of atrial flutter to atrial …British HeartJournal, 1972, 34, 12I5-I224. Electrical conversion ofatrial flutter to atrial fibrillation Flutter mechanism