Coexistence of Sick Sinus Rhythmand Atrial Flutter-Fibrillation

JOSEPH ANTHONY C. GOMES, M.D., PRITPAL S. KANG, M.D., MARIANNE MATHESON, R.N.,WILLIAM BRADLEY GOUGH, JR., PH.D., AND NABIL EL-SHERIF, M.D.

SUMMARY A 58-year-old man with hypertensive cardiovascular disease and atrial flutter underwent elec-trophysiologic studies, including multiple intra-atrial recordings and atrial stimulation. Although the surfaceECG suggested the presence of atrial flutter, intra-atrial recordings demonstrated the presence of (1) sinus-likerhythm localized to an area of approximately 5 mm in and around the region of the sinus node, which was pro-tected by entrance block; (2) flutter and/or fibrillation of the remaining parts of the right atrium; (3) fibrilla-tion of the left atrium; and (4) transient degeneration of flutter into fibrillation at right atrial sites, withpredominant flutter activity. Although a major part of the right atrium was in flutter and/or fibrillation, wecould assess sinus node function by overdrive stimulation of the area of sinus node activity. Sinus node functionstudies revealed an underlying sick sinus syndrome.

THE DIAGNOSIS of atrial arrhythmias is essenti-ally based on the analysis of the configuration, timing,and rate of P waves on the surface ECG. However,recent studies in selected patients have demonstrateddissimilar atrial rhythms with direct intra-atrialrecordings otherwise not discernible on the surfaceECG."3 In this paper we report the electrophysio-logic findings in a patient in whom the ECG revealedatrial flutter and intra-atrial recordings demon-strated the presence of sinus-like rhythm in andaround the region of the sinus node, flutter and/orfibrillation of the remaining parts of the right atriumand fibrillation of the left atrium. We also assessedsinus node function, although a major part of the rightand left atria were in flutter and/or fibrillation.Assessment of sinus node function revealed an under-lying sick sinus syndrome.

Case ReportA 58-year-old man with hypertensive cardio-

vascular disease was admitted to the Medical Serviceof the Brooklyn Veteran's Administration MedicalCenter for uncontrolled hypertension, congestiveheart failure and atrial flutter of recent onset. A 12-lead ECG suggested the presence of atrial flutter at arate of 240 beats/min, with a ventricular response of120 beats/min and poor R-wave progression from V1to V3 (fig. 1). Chest x-ray film showed cardiomegalyand pulmonary congestive changes. Echocardiogramrevealed left atrial and left ventricular enlargement.The patient's hypertension and congestive heart-failure responded promptly to medical therapy. Hewas then referred to the cardiology service for electiveelectrical conversion of the atrial flutter after medicalconversion with digitalis and quinidine had failed.

From the Cardiology Department, Brooklyn Veterans Ad-ministration Medical Center, and Downstate Medical School, StateUniversity of New York, Brooklyn, New York.

Address for correspondence: Joseph A.C. Gomes, M.D., Elec-trophysiology Laboratory, Department of Cardiology, BrooklynVeterans Administration Medical Center, Brooklyn, New York11209.Received December 5, 1979; revision accepted May 7, 1980.Circulation 63, No. 1, 1981.

Electrophysiologic Studies

The patient underwent electrophysiologic studies toconvert the atrial flutter by overdrive atrial stimula-tion. The procedure was explained to the patient, whogave signed consent. The electrophysiologic studieswere performed after withholding digitalis andquinidine for 2 days. Serum digoxin level was 0.5ng/ml on the day of the study. Two quadripolar #6FUSCI catheters with 10-mm interelectrode distancewere introduced percutaneously into the femoral veinand positioned in the right atrium. Three standardECG leads and intra-atrial electrograms, filtered atfrequency settings of 40-500 Hz and time linesgenerated at 40, 200 and 1000 msec, were displayed ona multichannel oscilloscope (Electronics for MedicineVR 12) and recorded on a tape recorder (HP#3698A)and on thermal paper at paper speeds of 50, 100 and150 mm/sec. The right and left atria were mapped bysequentially positioning the catheters in the high, mid-dle, low and septal right atrium and the coronarysinus.When one of the two catheters was positioned in the

high right atrium in close proximity to the location ofthe sinus node, a combination of the distal two polesof the catheter recorded a distinct atrial electrogramat a cycle length of 1170-1360 msec (rate 44-51beats/min), whereas the two proximal poles of thesame catheter recorded atrial activity suggestive ofatrial flutter-fibrillation (fig. 2A). The electrogramrecorded with the distal poles had no relationship withthe flutter activity or the QRS complex. The proximaland distal connections of the second catheter, whenpositioned in the low and septal right atrium and thecoronary sinus, recorded, respectively, atrial activitysuggestive of atrial flutter (fig. 2A), atrial activity sug-gestive of atrial flutter-fibrillation (fig. 2B) and atrialfibrillation (fig. 2C). Variations in rates at sites ofmore regular atrial activity and transient degenera-tion to atrial fibrillation were often observed (figs. 2A,B and 3A-C). We believed that the distinct atrial elec-trogram observed in the region of the high atriumusing the distal two poles of the catheter (fig. 2A) wassinus node activity. The area of the latter recordingwas then mapped by advancing the electrode catheter

80

by guest on April 28, 2018

http://circ.ahajournals.org/D

ownloaded from

SICK SINUS SYNDROME AND ATRIAL FLUTTER-FIB/Gomes et al.

"T-T T U .1 1.1.1

I.A 1.

11-7TT-1-FT-1 H [A rt--

h A k

:..; :' :.' ;. ---r t')-..,

t; xj., .'i' :'. .1s .,,. t... t' :':-4... ..,, ... .,,, .,.. ..!. .... :t.zE=:Sxmm-mr .. z z mI z z z w

i~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~1-.j-al.. .. TT: :T :....'' U .t-.-t.,1i8tei.......:U-l ... -.1 :: -.::! :.X ,; n |t .' 1l :}

FIGURE 1. A 12-lead ECG demonstrating atrial activity at a rate of240 beats/min with a 2:1 ventricularresponse of 120 beats/min. Arrows point to the P waves. CSM = carotid sinus massage.

located in the high atrial region both cephalad andcaudally. When the catheter was advanced cephaladby approximately 5 mm, sinus node activity was notedin the proximal poles (fig. 3A); pulling back thecatheter to its original position revealed sinus node ac-tivity in the distal poles (fig. 3B), and pulling thecatheter more caudally by approximately 5 mmrevealed irregular decremented atrial activity sug-gestive of atrial fibrillation (fig. 3C). To assess theeffects of autonomic modulation on the atrial activityin the region of the sinus node, more maneuvers wereperformed. Carotid sinus massage revealed slowing ofthe atrial rate (fig. 4A). Atropine, 1 mg, demonstratedspeeding of the atrial rate (fig. 4B) from an averagerate of 47 beats/min to 54 beats/min. We alsoattempted to supress the atrial activity and assess itsrecovery time by positioning the second catheter inclose proximity to the distal poles of the first catheter(fig. 5). Recovery times were assessed by pacing for 1minute at cycle lengths of 1100, 900, 700 and 600 msecduring control and after atropine. The correctedrecovery time was prolonged during control and de-creased after atropine. The longest corrected recoverytime during control was 850 msec after pacing at a cy-cle length of 900 msec (fig. 6A). The longest correctedrecovery time after atropine was 500 msec after pac-ing at a cycle length of 700 msec (fig. 6B). In addition,secondary pauses greater than 4 seconds were oftenobserved (fig. 6A).

Atrial pacing of the low atrium at rates greater thanthose of atrial flutter resulted in transient capture ofthe respective atrial site, but did not result in captureof the area of the sinus node. The flutter could be

transiently converted to fibrillation by rapid atrialpacing but could not be converted to sinus rhythmdespite repeated attempts at pacing different rightatrial sites.To assess the reproducibility of our findings, the

catheters were left in situ and the next day, the record-ings were reattempted. The recordings were con-sistent with those of the previous study. DC cardio-version was attempted with the catheters in place. Itresulted in transient conversion to an ectopic atrialrhythm, but the patient immediately reverted back toatrial flutter-fibrillation.

DiscussionSince Schrumpf's original publication4 of the first

ECG that he interpreted to represent atrial dissocia-tion in a patient with digitalis toxicity, several clinicalstudies have shown the existence of atrial dissociationand dissimilar atrial rhythms in man.'-9 Despite elec-trocardiographic observations, the existence of dis-similar atrial rhythms was questionable because directintra-atrial recordings were rarely performed. How-ever, recent observations with the use of intra-atrialelectrode catheter recordingsl'3 in selected patientshave revealed (1) atrial fibrillation in one atrium andatrial flutter in the other atrium; (2) no recordableatrial activity in one atrium and a tachyarrhythmiarecorded in the other atrium; (3) atrial flutterdegenerating into atrial fibrillation in a segment of thesame atrium; (4) paroxysmal left atrial tachycardiawith separation of left and right atrial components ofthe P waves by an isoelectric period due to intra-atrial

....

'49

81

., ....

tf *_,

by guest on April 28, 2018

http://circ.ahajournals.org/D

ownloaded from

VOL 63, No 1, JANUARY 1981

L

HRAd 120 1280 1250 A 124012360 1013601340HRAd --0 - -l-t-13*+f4+0 S

LRAd

LRAp kk I 'z'

TL

L2

HRAd. 1250 i 1280 1250 1240 i 20 i 1260 J

SRd oo tw ON o-r - _

SRA m * oA, pm. M *Ah A .s ...4 , ..p~~~~~~~~~~~~~~~~~~I W 1 1-w

T - 1- 1I -- X1 - 11

s-? T t ? 4 CZ f jk

AL A A I A

,CSd_

CspTL

- -vP,-

r,1 i i1h^-r- LL-r- ry -1-1 1Xr

1. ,._ e h I bhg, -1,1 e a -- ' h. '*a M,

IA, LL.1 It l, .lj 1.A 1, .,1 11 I. L.' --d .1'-_

FIGURE 2. Intra-atrial electrograms from different right atrial sites and the coronary sinus. (A) Simulta-neous recordings from the high right atrium (HRA) and low right atrium (LRA). The combination of thedistal poles of the catheter located in the high right atrium (HRAd) reveals a distinct atrial electrogram; a

combination of the proximal poles (HRAp) demonstrates atrial activity suggestive offlutter-fibrillation. Theatrial electrogram on the HRAd has no relationship to the flutter activity or to the QRS complex. Record-ingsfrom the LRA revealflutter activity. Flutter activity transiently degenerates into atrialfibrillation at thesame recording sites (solid arrows). (B) Simultaneous bipolar recordings from the HRA and septal rightatrium (SRA). Note the presence offlutter-fibrillation in the SRA recordings. (C) Simultaneous bipolarrecordings from the HRA and coronary sinus (CS). Whereas the HRAd demonstrates a distinct atrial elec-trogram and the HRAp demonstrates atrial flutter, recordings from the CS show atrial fibrillation. L1, L2and V1 = standard ECG leads; TL = time lines; d = bipolar recordings from the combination of the distalpoles of the catheter; p = bipolar recordings from the combination of the proximal poles of the catheter.

conduction delay; and (5) right atrial standstill and leftatrial activity without contraction.The surface ECG in our patient suggested atrial

flutter; however, intra-atrial recordings from multipleatrial sites revealed distinct atrial activity at a rate of44-51 beats/min in and around the region of the sinusnode, atrial flutter and/or fibrillation in remainingsegments of the right atrium, atrial flutter transientlydegenerating into atrial fibrillation in the same seg-ments of the right atrium, and atrial fibrillation of theleft atrium. While both right and left atria were in

flutter and/or fibrillation, a discrete island of atrialtissue approximately 5 mm around the region of thesinus node was in sinus rhythm. Although it is difficultto establish unequivocally sinus node activity withoutdirect recordings of a sinus node electrogram,10 theatrial activity around the region of the sinus node wasindeed sinus-like, as suggested by (1) slowing of theatrial rate by carotid sinus massage; (2) speeding up ofthe atrial rate after the administration of atropine; (3)presence of secondary pauses after overdrive suppres-sion, and (4) localization of the atrial activity in and

A

B

TL

LlL2V,

cHRAd

HRAO . .4 e ' -nk - -. 10 #V '1.11q 'I R'f ,~0 bt

404

CIRCULATION82

by guest on April 28, 2018

http://circ.ahajournals.org/D

ownloaded from

SICK SINUS SYNDROME AND ATRIAL FLUTTER-FIB/Gomes et al.

Ar~ .O

_~~~~~~~~~~-1

LlL2V,HR A.

A

LRAp i,.+i+ P IJ. L a A- -w.-

LR

r-,7 IM -IFr g

TL

_ - -_ vP

w~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

LlL2V,

A A

LRAd e

LRA +4_ JJ;4

TLI

1 ho-044t--~ V .00 *44~~~ ~ A-A- f W00- p044~0 l 0kwj

1 'j J-v + ¢-

TLFIGURE 3. Mapping of the area of sinus node activity. (A) When the catheter in the high right atrium(HRA) is advanced cephalad by approximately 5 mm, the distinct atrial electrogram originally seen in thedistal combination (fig. I) is seen on the proximal combination (HRAp); the distal connection shows no

atrial activity (HRAd). Recordings from the second catheter in the low right atrium (LRA) revealflutter ac-

tivity with transient degeneration to fibrillation. (B) Pulling back the catheter by approximately 5 mm to its

original position reveals the distinct atrial electrogram on the HRAd and flutter activity on the HRAprecordings. (C) Pulling the catheter caudally by approximately another 5 mm reveals irregular decrementedatrial activity suggestive of atrial fibrillation. Abbreviations: See figure 2.

A

B HRAd -h----

HRAp _

LlL2V,HRAd

HRAp

a _ .

LRA 1---I.4

LRAp ,1*l

1% #-%a

mow~ '-- 9

A $ -A-111, 11

to. 0 --##- --- 10 * 00. -" -*.~ --- -- .1to - 'M -, --- ---

!

dh --- 0. -- -- -~ --- --- -- - 0- .0-

83

A -- jot - -4c - v v -- V'

V-11.

m so.

by guest on April 28, 2018

http://circ.ahajournals.org/D

ownloaded from

VOL 63, No 1, JANUIARY 1981

'-1 v -Y r S,r- SL2

r 1

CSM

TL

BLlL2

A 1100 A 1100 20A

HRApD08

ATROPINE

TL

FIGURE 4. The effect of carotid sinus massage (CSM) and atropine. (A) CSM induced slowing of the atrial rate; the longestpause was 2820 msec. (B) Administration of 1 mg ofatropine intravenously resulted in a decrease in cycle length from a controlvalue of 1260 msec to 1104 msec. The atrioventricular nodal response to both CSM and atropine, as reflected in changes of theaverage ventricular rate, was normal. Abbreviations.. See figure 2.

LlL2

AA AHR2 1240 1230 1230 1260 , 1240H Ad r 1.0h- 1

TL

FIGURE 5. Simultaneous intra-atrial electrograms from the region of the high right atrium (HRA) obtained by positioning

the two catheters in close proximity to each other. That the distal poles ofcatheter 2 (HRA 2d) are in close proximity to those of

catheter 1 (HRA 'd) is evidenced by the fact that the atrial electrogram on HRA 1d and HRA2d are coincident with each other.

The distal poles of the second catheters (HRA2d) were used to stimulate the region of the HRA showing sinus node activityfor

assessment of sinus node function. Abbreviations: See figure 2.

A

iw -v t - wi _rv- -.t- ---ri---lkr-- +_

A,.

84 CIRCULATION

.Lv

-L-1 r v v v

by guest on April 28, 2018

http://circ.ahajournals.org/D

ownloaded from

SICK SINUS SYNDROME AND ATRIAL FLUTTER-FIB/Gomes et al. 8

Aa

F- -, .

HRd-i 0 t 2180 2380 A 2300 4940AS 1~~~~~~~~~~~~~~~~~~~ I

HRA ~ ~ ~ -? 9-

V,HRAd ~ 700 ci0 10 1740 12 7016

HRAd,

M ill 'I I, 'I

FIGURE 6. Sinus node recovery time during control and after atropine. (A) Pacing of the high right atrium(HRA) region at a cycle length of 900 msec (first two beats). The recovery time of the first sinus beat aftercessation ofpacing was 2180 msec. The corrected sinus node recovery time was calculated to be 850 msec.Note the secondary pause of4940 msec after cessation ofpacing. (B) Pacing of the HRA region at a cyclelength of 700 msecs after atropine. The recovery time ofthefirst sinus beat is 1600 msec. The corrected sinusnode recovery time is 500 msec. Abbreviations.: See figure 2.

around the region of the sinus node. Coexistence ofsinus-like activity with flutter-fibrillation of the rightand left atria suggests that a mass of atrial tissue sur-rounding the sinus node was protected by entranceblock. The observation that capture of the low atriumdid not result in capture and suppression of the sinusnode area supports this hypothesis. Although we donot know whether the causative lesion for entranceblock in and around the sinus node is an anatomic orphysiologic barrier, it is probably related to con-siderable fibrosis in the approaches to the sinus nodeand atrial myocardium."' 12

We could assess sinus node function in our patient,although a maj'or part of the right and left atria werein flutter and/or fibrillation. The presence of an under-lying sick sinus syndrome'31 is supported by (1) thepresence of sinus bradycardia; (2) dampened responseto atropine; (3) prolonged corrected sinus noderecovery time, and (4) secondary sinus node pausesafter overdrive suppression.

Segmental right atrial flutter-fibrillation is prob-ably related to the presence of isolated islands of dis-sociated atrial activity. Impulses from the fibrillatingleft atrium or parts of the right atrium could exciteother areas of the right atrium to produce regular ac-tivity, the latter depending on the frequency ofstimulation and refractory period of the right atrium.'Variations in rates at sites of more regular atrial ac-tivity and transient degeneration to atrial fibrillationsupport the latter possibility. However, as indicatedby Wells et al., the atrial activity suggestive of atrialflutter and/or flutter-fibrillation may represent a typeI atrial fibrillation or type IV atrial fibrillation.'7' `

Atrial stimulation is one method for convertingatrial flutter to sinus rhythm."'-"' However, previous

studies have indicated a variable success rate in con-verting flutter by atrial stimulation.1' 20 Our inabilityto convert atrial flutter to sinus rhythm may be relatedto the presence of dissimilar atrial rhythms, as sug-gested by Zipes and DeJoseph,' or to the possibilitythat dissimilar atrial rhythm may be one of the expres-sion of atrial fibrillation.`7

Clinical ImplicationsOur findings and those previously reported'117' SUg-

gest that (I) the ECG may not accurately reflect atrialactivity; (2) sinus rhythm may coexist with atrialflutter and or fibrillation; and (3) it may be possible toassess sinus node function and diagnose the presenceof sick sinus syndrome even in the presence of atrialflutter-fibrillation if the area of the sinus node isprotected by entrance block. An underlying sick sinussyndrome warrants a temporary pacemaker beforeattempted conversion by DC shock.

AcknowledgmentThe authors acknowledge Theresa Luppowitz for preparation of

the manuscript and Mike C.S. Yu for the art work.

References

1. Zipes DP, De Joseph RL: Dissimilar atrial rhythms in man anddog. Am J Cardiol 32: 618, 1973

2. Wu D, Denes P, Amat-y-Leon F, Chhablani RC, Rosen KM:Limitations of the surface electrocardiogram in diagnosis ofatrial arrhythmias. Further observations on dissimilar atrialrhythms. Am J Cardiol 36: 91, 1975

3. Friedman HS, Gomes JA, Tardio A, Levites R, Haft Jl:Appearance of atrial rhythm with absent P wave in longstand-ing atrial fibrillation. Chest 66: 172, 1974

85

---1 L -1 - -- ---1-

TL liffilBL,L!>

by guest on April 28, 2018

http://circ.ahajournals.org/D

ownloaded from

VOL 63, No 1, JANUARY 1981

4. Schrumpf P: De l'interference de deux rhythmes sinesaux.Preuve du dualisme du nodule de keith. Arch Mal Coeur 13:168, 1920

5. Cohen J, Scherf D: Complete interatrial and intraatrial block(atrial dissociation). Am Heart J 70: 23, 1965

6. Marques MG: Atrial dissociation Br Heart J 20: 235, 19587. Chung EK: A reappraisal of atrial dissociation. Am J Cardiol

28: 111, 19718. Waldo AL, Vitikainon KJ, Kaiser GA, Bowman FO, Malm

JR: Atrial standstill secondary to atrial inexcitability (atrialquiescence). Circulation 46: 690, 1972

9. Legato MG, Ferrer MI: Intermittent intra-atrial block: itsdiagnosis, incidence and implications. Chest 65: 243, 1974

10. Kramer M, Harriman RJ, Boxer R, Hoffman BF: Electro-grams from the canine sinoatrial pacemaker recorded in vitroand in situ. Am J Cardiol 42: 939, 1978

11. Kaplan MB, Langendorf R, Lev M, Pick A: Tachycardia-bradycardia syndrome (so-called "sick sinus syndrome").Pathology, mechanism and treatment. Am J Cardiol 31: 497,1973

12. Rasmussen K: Chronic sino-atrial heart block. Am Heart J 81:38, 1971

13. Narula OS: Disorders of sinus node function: electro-physiologic evaluation. In His Bundle Flectrocardiography andClinical Electrophysiology. Philadelphia, FA Davis, 1975, p275

14. Mandel WJ, Hayakawa D, Danzig R, Marcus HS: Evaluation

of sinoatrial node function in man by overdrive suppression.Circulation 44: 59, 1971

15. Talano VJ, Euler D, Randall WC, Eshaghy B, Loeb HS, Gun-nar RM: Sinus node dysfunction. An overview with emphasison anatomic and pharmacologic considerations. Am J Med 64:773, 1978

16. Benditt DG, Strauss HC, Scheinman MM, Behar VS, WallaceAG: Analysis of secondary pauses following termination ofrapid atrial pacing in man. Circulation 54: 436, 1976

17. Wells LJ Jr, Karp RB, Kouchoukos NT, Maclean WAH,James TN, Waldo AL: Characterization of atrial fibrillation inman: studies following open heart surgery. PACE 1: 426, 1978

18. Wells JL Jr, Maclean WAH, James TN, Waldo AL: Charac-terization of atrial flutter. Studies in man after open heart sur-gery using fixed atrial electrodes. Circulation 60: 665. 1979

19. Haft JI, Kosowsky BD, Lau SH, Stein E, Damato AN: Ter-mination of atrial flutter by rapid electrical pacing of theatrium. Am J Cardiol 20: 239, 1967

20. Zipes DP: The contribution of artificial pacemaking to under-standing of pathogenesis of arrhythmias. Am J Cardiol 28: 21 1,1971

21. Vergara GS, Hildner FJ, Schoenfeld CB, Javier RP, Cohen LS,Samet P: Conversion of supraventricular tachycardia withrapid atrial stimulation. Circulation 46: 788, 1972

22. Rosen K, Sinno MZ, Gunnar RM, Rahimtoola SH: Failure ofrapid atrial pacing in the conversion of atrial flutter. Am J Car-diol 29: 524, 1972

86 CIRCULATION

by guest on April 28, 2018

http://circ.ahajournals.org/D

ownloaded from

J A Gomes, P S Kang, M Matheson, W B Gough, Jr and N El-SherifCoexistence of sick sinus rhythm and atrial flutter-fibrillation.

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1981 American Heart Association, Inc. All rights reserved.

is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231Circulation doi: 10.1161/01.CIR.63.1.80

1981;63:80-86Circulation. 

http://circ.ahajournals.org/content/63/1/80the World Wide Web at:

The online version of this article, along with updated information and services, is located on

  http://circ.ahajournals.org//subscriptions/

is online at: Circulation Information about subscribing to Subscriptions: 

http://www.lww.com/reprints Information about reprints can be found online at: Reprints:

  document. Permissions and Rights Question and Answer information about this process is available in the

located, click Request Permissions in the middle column of the Web page under Services. FurtherEditorial Office. Once the online version of the published article for which permission is being requested is

can be obtained via RightsLink, a service of the Copyright Clearance Center, not theCirculationpublished in Requests for permissions to reproduce figures, tables, or portions of articles originallyPermissions:

by guest on April 28, 2018

http://circ.ahajournals.org/D

ownloaded from