Download Coexistence of Sick Sinus Rhythm and Atrial Flutter

Coexistence of Sick Sinus Rhythm
and 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 electrophysiologic studies, including multiple intra-atrial recordings and atrial stimulation. Although the surface
ECG suggested the presence of atrial flutter, intra-atrial recordings demonstrated the presence of (1) sinus-like
rhythm localized to an area of approximately 5 mm in and around the region of the sinus node, which was protected by entrance block; (2) flutter and/or fibrillation of the remaining parts of the right atrium; (3) fibrillation of the left atrium; and (4) transient degeneration of flutter into fibrillation at right atrial sites, with
predominant flutter activity. Although a major part of the right atrium was in flutter and/or fibrillation, we
could assess sinus node function by overdrive stimulation of the area of sinus node activity. Sinus node function
studies revealed an underlying sick sinus syndrome.
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THE DIAGNOSIS of atrial arrhythmias is essentially based on the analysis of the configuration, timing,
and rate of P waves on the surface ECG. However,
recent studies in selected patients have demonstrated
dissimilar atrial rhythms with direct intra-atrial
recordings otherwise not discernible on the surface
ECG."3 In this paper we report the electrophysiologic findings in a patient in whom the ECG revealed
atrial flutter and intra-atrial recordings demonstrated the presence of sinus-like rhythm in and
around the region of the sinus node, flutter and/or
fibrillation of the remaining parts of the right atrium
and fibrillation of the left atrium. We also assessed
sinus node function, although a major part of the right
and left atria were in flutter and/or fibrillation.
Assessment of sinus node function revealed an underlying sick sinus syndrome.
Electrophysiologic Studies
The patient underwent electrophysiologic studies to
convert the atrial flutter by overdrive atrial stimulation. The procedure was explained to the patient, who
gave signed consent. The electrophysiologic studies
were performed after withholding digitalis and
quinidine for 2 days. Serum digoxin level was 0.5
ng/ml on the day of the study. Two quadripolar #6F
USCI catheters with 10-mm interelectrode distance
were introduced percutaneously into the femoral vein
and positioned in the right atrium. Three standard
ECG leads and intra-atrial electrograms, filtered at
frequency settings of 40-500 Hz and time lines
generated at 40, 200 and 1000 msec, were displayed on
a multichannel oscilloscope (Electronics for Medicine
VR 12) and recorded on a tape recorder (HP#3698A)
and on thermal paper at paper speeds of 50, 100 and
150 mm/sec. The right and left atria were mapped by
sequentially positioning the catheters in the high, middle, low and septal right atrium and the coronary
sinus.
When one of the two catheters was positioned in the
high right atrium in close proximity to the location of
the sinus node, a combination of the distal two poles
of the catheter recorded a distinct atrial electrogram
at a cycle length of 1170-1360 msec (rate 44-51
beats/min), whereas the two proximal poles of the
same catheter recorded atrial activity suggestive of
atrial flutter-fibrillation (fig. 2A). The electrogram
recorded with the distal poles had no relationship with
the flutter activity or the QRS complex. The proximal
and distal connections of the second catheter, when
positioned in the low and septal right atrium and the
coronary sinus, recorded, respectively, atrial activity
suggestive of atrial flutter (fig. 2A), atrial activity suggestive of atrial flutter-fibrillation (fig. 2B) and atrial
fibrillation (fig. 2C). Variations in rates at sites of
more regular atrial activity and transient degeneration to atrial fibrillation were often observed (figs. 2A,
B and 3A-C). We believed that the distinct atrial electrogram observed in the region of the high atrium
using the distal two poles of the catheter (fig. 2A) was
sinus node activity. The area of the latter recording
was then mapped by advancing the electrode catheter
Case Report
A 58-year-old man with hypertensive cardiovascular disease was admitted to the Medical Service
of the Brooklyn Veteran's Administration Medical
Center for uncontrolled hypertension, congestive
heart failure and atrial flutter of recent onset. A 12lead ECG suggested the presence of atrial flutter at a
rate of 240 beats/min, with a ventricular response of
120 beats/min and poor R-wave progression from V1
to V3 (fig. 1). Chest x-ray film showed cardiomegaly
and pulmonary congestive changes. Echocardiogram
revealed left atrial and left ventricular enlargement.
The patient's hypertension and congestive heartfailure responded promptly to medical therapy. He
was then referred to the cardiology service for elective
electrical conversion of the atrial flutter after medical
conversion with digitalis and quinidine had failed.
From the Cardiology Department, Brooklyn Veterans Administration Medical Center, and Downstate Medical School, State
University of New York, Brooklyn, New York.
Address for correspondence: Joseph A.C. Gomes, M.D., Electrophysiology Laboratory, Department of Cardiology, Brooklyn
Veterans Administration Medical Center, Brooklyn, New York
11209.
Received December 5, 1979; revision accepted May 7, 1980.
Circulation 63, No. 1, 1981.
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FIGURE 1. A 12-lead ECG demonstrating atrial activity at a rate of 240 beats/min with a 2:1 ventricular
response of 120 beats/min. Arrows point to the P waves. CSM = carotid sinus massage.
located in the high atrial region both cephalad and
caudally. When the catheter was advanced cephalad
by approximately 5 mm, sinus node activity was noted
in the proximal poles (fig. 3A); pulling back the
catheter to its original position revealed sinus node activity in the distal poles (fig. 3B), and pulling the
catheter more caudally by approximately 5 mm
revealed irregular decremented atrial activity suggestive of atrial fibrillation (fig. 3C). To assess the
effects of autonomic modulation on the atrial activity
in the region of the sinus node, more maneuvers were
performed. Carotid sinus massage revealed slowing of
the atrial rate (fig. 4A). Atropine, 1 mg, demonstrated
speeding of the atrial rate (fig. 4B) from an average
rate of 47 beats/min to 54 beats/min. We also
attempted to supress the atrial activity and assess its
recovery time by positioning the second catheter in
close proximity to the distal poles of the first catheter
(fig. 5). Recovery times were assessed by pacing for 1
minute at cycle lengths of 1100, 900, 700 and 600 msec
during control and after atropine. The corrected
recovery time was prolonged during control and decreased after atropine. The longest corrected recovery
time during control was 850 msec after pacing at a cycle length of 900 msec (fig. 6A). The longest corrected
recovery time after atropine was 500 msec after pacing at a cycle length of 700 msec (fig. 6B). In addition,
secondary pauses greater than 4 seconds were often
observed (fig. 6A).
Atrial pacing of the low atrium at rates greater than
those of atrial flutter resulted in transient capture of
the respective atrial site, but did not result in capture
of the area of the sinus node. The flutter could be
transiently converted to fibrillation by rapid atrial
pacing but could not be converted to sinus rhythm
despite repeated attempts at pacing different right
atrial sites.
To assess the reproducibility of our findings, the
catheters were left in situ and the next day, the recordings were reattempted. The recordings were consistent with those of the previous study. DC cardioversion was attempted with the catheters in place. It
resulted in transient conversion to an ectopic atrial
rhythm, but the patient immediately reverted back to
atrial flutter-fibrillation.
Discussion
Since Schrumpf's original publication4 of the first
ECG that he interpreted to represent atrial dissociation in a patient with digitalis toxicity, several clinical
studies have shown the existence of atrial dissociation
and dissimilar atrial rhythms in man.'-9 Despite electrocardiographic observations, the existence of dissimilar atrial rhythms was questionable because direct
intra-atrial recordings were rarely performed. However, recent observations with the use of intra-atrial
electrode catheter recordingsl'3 in selected patients
have revealed (1) atrial fibrillation in one atrium and
atrial flutter in the other atrium; (2) no recordable
atrial activity in one atrium and a tachyarrhythmia
recorded in the other atrium; (3) atrial flutter
degenerating into atrial fibrillation in a segment of the
same atrium; (4) paroxysmal left atrial tachycardia
with separation of left and right atrial components of
the P waves by an isoelectric period due to intra-atrial
VOL 63, No 1, JANUARY 1981
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distal 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. The
atrial electrogram on the HRAd has no relationship to the flutter activity or to the QRS complex. Recordings from the LRA revealflutter activity. Flutter activity transiently degenerates into atrialfibrillation at the
same recording sites (solid arrows). (B) Simultaneous bipolar recordings from the HRA and septal right
atrium (SRA). Note the presence of flutter-fibrillation in the SRA recordings. (C) Simultaneous bipolar
recordings from the HRA and coronary sinus (CS). Whereas the HRAd demonstrates a distinct atrial electrogram and the HRAp demonstrates atrial flutter, recordings from the CS show atrial fibrillation. L1, L2
and V1 = standard ECG leads; TL = time lines; d = bipolar recordings from the combination of the distal
poles of the catheter; p = bipolar recordings from the combination of the proximal poles of the catheter.
neous
conduction delay; and (5) right atrial standstill and left
atrial activity without contraction.
The surface ECG in our patient suggested atrial
flutter; however, intra-atrial recordings from multiple
atrial sites revealed distinct atrial activity at a rate of
44-51 beats/min in and around the region of the sinus
node, atrial flutter and/or fibrillation in remaining
segments of the right atrium, atrial flutter transiently
degenerating into atrial fibrillation in the same segments of the right atrium, and atrial fibrillation of the
left atrium. While both right and left atria were in
flutter and/or fibrillation, a discrete island of atrial
tissue approximately 5 mm around the region of the
sinus node was in sinus rhythm. Although it is difficult
to establish unequivocally sinus node activity without
direct recordings of a sinus node electrogram,10 the
atrial activity around the region of the sinus node was
indeed sinus-like, as suggested by (1) slowing of the
atrial rate by carotid sinus massage; (2) speeding up of
the atrial rate after the administration of atropine; (3)
presence of secondary pauses after overdrive suppression, and (4) localization of the atrial activity in and
SICK SINUS SYNDROME AND ATRIAL FLUTTER-FIB/Gomes
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(HRA) is advanced cephalad by approximately 5 mm, the distinct atrial electrogram originally seen in the
distal 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 activity 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 HRAp
recordings. (C) Pulling the catheter caudally by approximately another 5 mm reveals irregular decremented
atrial activity suggestive of atrial fibrillation. Abbreviations: See figure 2.
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VOL 63, No 1, JANUIARY 1981
CIRCULATION
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value of 1260 msec to 1104 msec. The atrioventricular nodal response to both CSM and atropine, as reflected in changes of the
average ventricular rate, was normal. Abbreviations.. See figure 2.
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the two catheters in close proximity to each other. That the distal poles of catheter 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 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 activity for
assessment of sinus node function. Abbreviations: See figure 2.
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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 after
cessation of pacing was 2180 msec. The corrected sinus node recovery time was calculated to be 850 msec.
Note the secondary pause of 4940 msec after cessation of pacing. (B) Pacing of the HRA region at a cycle
length of 700 msecs after atropine. The recovery time of thefirst sinus beat is 1600 msec. The corrected sinus
node recovery time is 500 msec. Abbreviations.: See figure 2.
around the region of the sinus node. Coexistence of
sinus-like activity with flutter-fibrillation of the right
and left atria suggests that a mass of atrial tissue surrounding the sinus node was protected by entrance
block. The observation that capture of the low atrium
did not result in capture and suppression of the sinus
node area supports this hypothesis. Although we do
not know whether the causative lesion for entrance
block in and around the sinus node is an anatomic or
physiologic barrier, it is probably related to considerable fibrosis in the approaches to the sinus node
and atrial myocardium."' 12
We could assess sinus node function in our patient,
although a maj'or part of the right and left atria were
in flutter and/ or fibrillation. The presence of an underlying sick sinus syndrome'31 is supported by (1) the
presence of sinus bradycardia; (2) dampened response
to atropine; (3) prolonged corrected sinus node
recovery time, and (4) secondary sinus node pauses
after overdrive suppression.
Segmental right atrial flutter-fibrillation is probably related to the presence of isolated islands of dissociated atrial activity. Impulses from the fibrillating
left atrium or parts of the right atrium could excite
other areas of the right atrium to produce regular activity, the latter depending on the frequency of
stimulation and refractory period of the right atrium.'
Variations in rates at sites of more regular atrial activity and transient degeneration to atrial fibrillation
support the latter possibility. However, as indicated
by Wells et al., the atrial activity suggestive of atrial
flutter and/or flutter-fibrillation may represent a type
I atrial fibrillation or type IV atrial fibrillation.'7' `
Atrial stimulation is one method for converting
atrial flutter to sinus rhythm."'-"' However, previous
studies have indicated a variable success rate in con-
verting flutter by atrial stimulation. 1' 20 Our inability
to convert atrial flutter to sinus rhythm may be related
to the presence of dissimilar atrial rhythms, as suggested by Zipes and DeJoseph,' or to the possibility
that dissimilar atrial rhythm may be one of the expression of atrial fibrillation.`7
Clinical Implications
Our findings and those previously reported'11 7' SUggest that (I) the ECG may not accurately reflect atrial
activity; (2) sinus rhythm may coexist with atrial
flutter and or fibrillation; and (3) it may be possible to
assess sinus node function and diagnose the presence
of sick sinus syndrome even in the presence of atrial
flutter-fibrillation if the area of the sinus node is
protected by entrance block. An underlying sick sinus
syndrome warrants a temporary pacemaker before
attempted conversion by DC shock.
Acknowledgment
The 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 and
dog. 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 of
atrial arrhythmias. Further observations on dissimilar atrial
rhythms. 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 longstanding atrial fibrillation. Chest 66: 172, 1974
86
CI RCULATION
Downloaded from http://circ.ahajournals.org/ by guest on April 29, 2017
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, 1958
7. Chung EK: A reappraisal of atrial dissociation. Am J Cardiol
28: 111, 1971
8. Waldo AL, Vitikainon KJ, Kaiser GA, Bowman FO, Malm
JR: Atrial standstill secondary to atrial inexcitability (atrial
quiescence). Circulation 46: 690, 1972
9. Legato MG, Ferrer MI: Intermittent intra-atrial block: its
diagnosis, incidence and implications. Chest 65: 243, 1974
10. Kramer M, Harriman RJ, Boxer R, Hoffman BF: Electrograms from the canine sinoatrial pacemaker recorded in vitro
and in situ. Am J Cardiol 42: 939, 1978
11. Kaplan MB, Langendorf R, Lev M, Pick A: Tachycardiabradycardia 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: electrophysiologic evaluation. In His Bundle Flectrocardiography and
Clinical Electrophysiology. Philadelphia, FA Davis, 1975, p
275
14. Mandel WJ, Hayakawa D, Danzig R, Marcus HS: Evaluation
15.
16.
17.
18.
19.
20.
21.
22.
VOL 63, No 1, JANUARY 1981
of sinoatrial node function in man by overdrive suppression.
Circulation 44: 59, 1971
Talano VJ, Euler D, Randall WC, Eshaghy B, Loeb HS, Gunnar RM: Sinus node dysfunction. An overview with emphasis
on anatomic and pharmacologic considerations. Am J Med 64:
773, 1978
Benditt DG, Strauss HC, Scheinman MM, Behar VS, Wallace
AG: Analysis of secondary pauses following termination of
rapid atrial pacing in man. Circulation 54: 436, 1976
Wells LJ Jr, Karp RB, Kouchoukos NT, Maclean WAH,
James TN, Waldo AL: Characterization of atrial fibrillation in
man: studies following open heart surgery. PACE 1: 426, 1978
Wells JL Jr, Maclean WAH, James TN, Waldo AL: Characterization of atrial flutter. Studies in man after open heart surgery using fixed atrial electrodes. Circulation 60: 665. 1979
Haft JI, Kosowsky BD, Lau SH, Stein E, Damato AN: Termination of atrial flutter by rapid electrical pacing of the
atrium. Am J Cardiol 20: 239, 1967
Zipes DP: The contribution of artificial pacemaking to understanding of pathogenesis of arrhythmias. Am J Cardiol 28: 21 1,
1971
Vergara GS, Hildner FJ, Schoenfeld CB, Javier RP, Cohen LS,
Samet P: Conversion of supraventricular tachycardia with
rapid atrial stimulation. Circulation 46: 788, 1972
Rosen K, Sinno MZ, Gunnar RM, Rahimtoola SH: Failure of
rapid atrial pacing in the conversion of atrial flutter. Am J Cardiol 29: 524, 1972
Coexistence of sick sinus rhythm and atrial flutter-fibrillation.
J A Gomes, P S Kang, M Matheson, W B Gough, Jr and N El-Sherif
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Circulation. 1981;63:80-86
doi: 10.1161/01.CIR.63.1.80
Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 1981 American Heart Association, Inc. All rights reserved.
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