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Atrial Excitability and Conduction
During Rapid Atrial Pacing
VANCE J. PLUMB, M.D., ROBERT B. KARP, M.D., THOMAS N. JAMES, M.D.,
AND ALBERT L. WALDO, M.D.
SUMMARY Using temporary atrial wire electrodes placed at selected atrial sites, rapid atrial pacing at
rates of up to 368 beats/min was used to study atrial excitability and conduction in seven patients who underwent open heart surgery. The threshold for atrial pacing was found to be an exponential function of pacing
rate (r = 0.55, p < 0.01), increasing threefold when the fastest pacing rates were compared with the slowest
pacing rates (p < 0.005). Atrial conduction times (measured from pacing to recording sites), prolonged dur-
ing rapid atrial pacing both for studies conducted before institution of cardiopulmonary bypass (p < 0.005)
and for those done 7 days postoperatively (p < 0.05). However, prolongation of conduction times always
depended on achievement of a critically rapid pacing rate. During rapid atrial pacing, we observed a high incidence of alternans of the atrial electrogram (17 of 42 studies). Thus, human atrial excitability, conduction
and electrogram morphology are not constant during pacing at rapid rates. Rather, at rapid pacing rates, there
is depression of atrial excitability, prolongation of atrial conduction times and alternation in electrogram
morphology. These findings have clinical relevance and theoretical implications for the understanding and
treatment of rapid atrial rhythms.
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bypass and on the seventh postoperative day. At the
time of the intraoperative study, two of the patients
had been receiving digoxin and two had been receiving propranolol. During induction and/or maintenance of anesthesia, three patients received scopolamine (0.4-0.5 mg) and all patients received
diazepam, morphine, nitrous oxide, halothane, fentanyl and pancuronium. At the time of the postoperative study, three patients were receiving digoxin, one
in combination with procainamide and one in combination with alpha-methyldopa. Four patients were
taking no cardioactive drugs at the time of postoperative study. The subjects gave informed consent for all
aspects of the study.
Patients who undergo open heart surgery at the
University of Alabama in Birmingham routinely have
a pair of Teflon-coated, stainless-steel wire electrodes
placed on the right atrial epicardium near the sulcus
terminalis. These wire electrodes are brought through
the anterior chest wall for use in the diagnosis and
treatment of postoperative arrhythmias in a manner
previously described.7 All patients in this study also
had another pair of wire electrodes placed on the
Bachmann's bundle (the anterior interatrial myocardial band) and another pair placed on the posteroinferior left atrium near the coronary sinus. The usual
technique of electrode placement was modified only
in that the electrodes were placed before cardiopulmonary bypass.
Using bipolar threshold stimuli, defined as the
minimal stimulus (mA) required to obtain and maintain constant atrial capture,8 each electrode site was
paced in turn at a constant basic rate just faster than
the spontaneous rate to measure a control conduction
time to each of the other electrode sites. The pacing
rate was then increased up to rates of 368 beats/min
(range 237-368 beats/min) in a stepwise fashion in increments of 5-10 beats/min. At each pacing rate, pacing was performed for brief periods (at least 15 beats),
the maximum pacing rate in each study being deter-
LITTLE is known about atrial excitability and conduction in man or experimental animals during rapid
atrial rhythms, particularly at rates greater than 200
beats/min. In our studies of rapid atrial pacing to interrupt atrial flutter in man," 2 unexpectedly high
stimulus strengths were often required to obtain atrial
capture. Other investigators have observed or
suggested that atrial conduction time is prolonged in
experimental models of atrial flutter.3`6 It is not clear
whether these incomplete observations are peculiar to
atrial flutter or are characteristic of any rapid atrial
rhythm. Learning more of the nature of atrial excitability and conduction during rapid atrial rhythms
should provide better understanding of rhythms such
as atrial flutter, atrial fibrillation, and ectopic (nonparoxysmal) atrial tachycardia. Therefore, we
designed a study of atrial excitability and conduction
in patients using fixed atrial wire electrodes.
Methods
Atrial pacing thresholds and atrial conduction times
were determined 42 times in seven patients. Five
patients were studied during open heart surgery and
seven after open heart surgery. Six of the seven
patients had aortocoronary artery saphenous vein bypass grafting and one had mitral valvuloplasty to correct mitral regurgitation due to mitral valve prolapse.
The patients were 52-64 years old. Studies were conducted intraoperatively before cardiopulmonary
From the Departments of Medicine and Surgery, University of
Alabama Medical Center, Birmingham, Alabama.
Supported by NHLBI program project grant HL11,310 and
SCOR in Ischemic Heart Disease 5P5OHL7667, a grant-in-aid from
the American Heart Association, and the Greater Birmingham
Foundation.
Address for correspondence: Vance J. Plumb, M.D., Department
of Medicine, University of Alabama Medical Center, Birmingham,
Alabama 35294.
Received April 10, 1980; revision accepted August 20, 1980.
Circulation 63, No. 5, 1981.
1140
ATRIAL EXCITABILITY AND CONDUCTION/Plumb et al.
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mined by clinical circumstances. For each increment
in pacing rate, both the stimulus threshold and the
conduction time from the pacing site to each of the
other two recording sites were measured. Between
each increment in pacing rate, the control pacing rate
was resumed. When the strength of the pacing
stimulus had to be increased to achieve capture, the
new stimulus strength was maintained upon return to
the basic (control) pacing rate, and the conduction
times at the basic (control) rate were determined at
this new stimulus strength. At the termination of the
study, the'threshold stimulus for pacing at the basic
(control) rate was determined again to insure'that the
initially determined threshold had not changed.
Atrial pacing was performed using a Medtronic
Model 1 349A battery-powered pacemaker, which
delivered a constant current stimulus of 2 msec duration. During atrial pacing, ECG leads I, II and III
were recorded simultaneously with the stimulus artifact and with the bipolar atrial electrograms from
each of the other two sites using an Electronics for
Medicine DR-12 switched-beam oscilloscopic recorder. These data were also simultaneously recorded on
magnetic tape (Honeywell model 5600) for later playback'and analysis. ECGs were recorded between a
bandpass of 0.1-500 Hz, and electrograms were recorded between a bandpass of 0.1-500 Hz or 12-500
Hz. The bipolar atrial wire electrodes were always
electrically isolated from ground and from the recording device. Conduction times were measured from the
stimulus artifact to the dominant deflection of the
atrial electrogram of each recording site using a vernier measuring device with an accuracy of 1 msec at a
paper recording speed of 100 mm/sec or using two
Hewlett-Packard Model 5300A Universal interval
counters. The latter were connected to two character
generators which printed out the measurements in
milliseconds on the Electronics for Medicine recorder.' The accuracy of the printed-out measurements was randomly cross-checked using the vernier
measuring device. To allow for a relatively constant
electrophysiologic state to develop, the first eight
paced beats were not included in any measurements.
To compare atrial conduction times at the various
atrial pacing rates, the time from each stimulus site to
each recording site at each of the several pacing rates
was expressed as the percent change in conduction
time compared with control:
conduction time (fast rate) - conduction time (basic rate) X 100
conduction time (basic rate)
The significance of conduction time prolongation was
analyzed by applying the Fisher-Behrens test of
significance for grouped data with unequal variance.9
Regression equations were computed for the mean
change in conduction times plotted as a function of
pacing rate. The slopes of the regression equations for
rates less than the critical pacing rate were then compared to the slopes for rates faster than the critical
rate using the Fisher-Behrens test. The mean pacing
threshold at the fastest rates was compared to the
1141
RELATIONSHIP OF PACING THRESHOLD TO RATE
S_]
0
(I,
z
LX
U1)
CC
z
0
CD
-
c
OD
120
165
300
255
210
ATRIAL PACING RATE (beats/min)
345
FIGURE 1. Comparison of the increase in threshold
(plotted as the natural logarithm) and the atrial pacing rate
for all studies. The solid line indicates the regression line and
the dotted line the standard error.
mean threshold at the basic pacing rate using the t test
for paired means of unequal variance, and the natural
logarithm of the fractional increase of threshold was
plotted as a function of the pacing rate.
Results
Pacing Threshold
In all studies, pacing threshold significantly increased (r = 0.55, p < 0.01) with increasing pacing
rates (fig. 1). The threshold rise ranged from 25-925%
when compared at the slowest and fastest rates (fig. 2).
The average threshold at the fastest rate was three
times that at the slowest rate (p < 0.0005). The same
magnitude of threshold increase was seen among
patients studied before cardiopulmonary bypass as
among those studied postoperatively. Figure 3 is an
example of pacing threshold determination during
atrial pacing at a rate of 330 beats/min. When an increase in pacing rate resulted in incomplete atrial capture (2:1 in this example), complete (1:1) capture
could be reestablished by increasing the pacing
stimulus strength.
The development of 2: 1 atrial capture was the most
frequent consequence of the rise in pacing threshold,
and was seen in 42 of 50 instances. Seven patients had
intermittent, irregular loss of atrial capture ("Mobitz
II"). One example of "Mobitz I' loss of atrial capture
was seen, manifested as atypical Wenckebach
periodicity with the greatest increase in conduction
time in the beat just preceding the dropped beat.
Conduction Times
Significant conduction time prolongation was seen
with increasing pacing rate in all patients, but only
after a critical pacing rate was achieved. Figure 4
-f1wUyWog7nl-t' 1J
VOL 63, No 5, MAY 1981
CIRCULATION
1142
p < 0.0005
* =
Prebypass
o =
Post op
Means
*
=
FIGURE 2. Pacing threshold at the slowest
pacing rate (range 102-125 beats/min) compared with the pacing threshold at the fastest
pacing rate (range 273-345 beats/min) for
each study.
E
c)
-J
0
U)
Li
I
cr.
I
14
5-
Fastest Pacing Rate
Slowest Pacing Rate
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conduction times prolong (p < 0.01). As the pacing
rate increases, so does the pacing threshold, from 8 to
shows atrial conduction time determination and illustrates the prolongation of conduction times noted
during critically rapid pacing (see also figure 3). Table
I is a list of the full range of pacing rates and corresponding conduction times for the entire study from
which figure 4 is taken. Figure 5 is from a representative study in which the percent change in conduction
time from the pacing site on Bachmann's bundle to the
recording site on the posterior left atrium is plotted
over the full range of pacing rates. Note that as the
pacing rate increases, conduction times are relatively
constant until a critical rate is reached, at which point
23 mA.
When the pacing threshold increased from 7 to 15
mA at a pacing rate of 300 beats/min, the increased
stimulus strength was associated with a decrease in the
control conduction times at the basic pacing rate of
103 beats/min (table 1). Because pacing threshold increased as rate increased, conduction times were
remeasured at the basic rate for each increase in
stimulus strength. As stimulus strength increased,
conduction times at the basic rate shortened (fig. 6).
1 sec-.
*
WS
ECG %
1
S
AEG ' 4
I
'
., 1 1111 1,1 .,1.1
11
(ST)
/1 -i
1.S
AEG
d
1,
_00 -0-01-11'lTr.~.m- W~
91r
1
'
'F
1'-1s
(BB)
1
12 mA
14mA
L 1. .I
7'
L 1.
n"ul~
A
1
I.
v
.
I
11
'
r
. .1.1. .. i
I
4
1.1
!I' 1'J* `
-
il I. 1.I
1-
1-
S-S 182 msec
(Rate 330 bpm)
FIGURE 3. ECG lead I recorded simultaneously with bipolar atrial electrograms (A EG) recorded from the
sulcus terminalis (ST) and Bachmann's bundle (BB) during pacing from the posteroinferior left atrium. At
the previous pacing rate of 320 beats/min, the atria were completely captured at a stimulus strength of 12
mA. However, when the pacing rate was abruptly increased from the control rate to 330 beats/min, there
was only 2:1 atrial capture. Illustrated are the last several beats of2:1 atrial capture as the stimulus strength
was being increased to 14 mA, at which point 1:1 atrial capture was obtained. Paper recording speed is 50
mm/sec. Time lines are at 1-second intervals. S = stimulus artifact.
ATRIAL EXCITABILITY AND CONDUCTION/Plumb et al.
1 143
ECG
I
S-S 210 msec
(Rate 285 bpmn)
* lsec s~~S
*
-~
S-S 585 msec
(Rate 103 bpm)
AEG
(BB)
72
74
74
75
75/
74
68
68
S
AEG
(PL A')
84
83
83
1
72
73
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FIGURE 4. ECG lead I recorded simultaneously with unfiltered bipolar atrial electrograms (AEG) from
Bachmann's bundle (BB) and the posteroinferior left atrium (PLA) during pacing from the sulcus terminalis.
Conduction times from the stimulus site to each recording site are shown (in msec) both at a pacing rate of
285 beats/min and at the basic pacing rate of 103 beats/min. Paper recording speed is 100 mm/sec. Time
lines are at 1-second intervals. S = stimulus artifact.
Maximal suprathreshold pacing (determined by the
pacing threshold at the fastest pacing rate) shortened
the conduction times during pacing at the basic rate by
an average of 6% (range 2-8%) from values observed
when pacing at basic rate using threshold stimuli.
In the one case where Bachmann's bundle was
paced before cardiopulmonary bypass, conduction
DEPENDENCE OF ATRIAL CONDUCTION AND
EXCITABILITY ON PACED RATE
+30
I
2 +20
z
0
U
o
z
I
(REPRESENTATIVE STUDY)
11.~~~~~
+10
0
Ii1 '
z
0
iI I {iil
1
t
tt
-101 8
9
mA
1114
mA mA
mA
1
lOC3
140
180
220
1
260
19
mA
23
mA
1
300
---v
340
PACED RATE (beats/m
FIGURE 5. The percent change (+ SD) in conduction time
and the pacing threshold are plotted as a function ofpacing
rate for a representative study. Note the constancy of conduction times until the pacing rate reached the critical rate
of 286 beats/min, when conduction times prolonged
markedly.
TABLE 1. Conduction Times-Representative
Site Sulcus Terminalis)
CT to BB
Stimulus
Pacing rate
(mseC - SD)
(mA)
(beats/min)
65 0.4
7
103
111
67 - 0.7
7
68 - 0.6
7
120
7
129
68- 0.7
69 0.6
7
141
69 -0.5
7
150
70 0.7
7
160
7
170
700 0.8
69 1.1
180
7
7
69 0.9
192
69 0.8
7
200
69 0.6
7
214
69 1.0
7
225
69 0.6
7
235
70 1.1
240
7
69 1.1
7
252
70 1.2
7
267
74 3.0
7
273
285
7
733 1.7
76 3.3
15
300
60 0.4
103
15
15
72- 1.2
311
Abbreviations: CT = conduction time;
mann's bundle; PLA = posteroinferior left
Study (Pacing
CT to PL
(mseC
SD)
68 0.7
68 1.0
68 1.1
69 1.8
71 3.0
70 1.8
69 - 0.8
70 -0.8
70 -1.9
69 0.5
70-1.4
71- 1.0
70 1.6
71 1.0
73 1.7
74 1.6
76 2.0
77 1.7
80 1.9
90
1.8
60 0.8
82 1.7
BB = Bachatrium.
ClIRCULATION
1144
+8
DEPENDENCE OF ATRIAL CONDUCTION
TIME ON STIMULUS STRENGTH
+4
TABLE 2. Critical Pacing Rate-Prebypass Studies
(REPRESENTATIVE STUDY)
Pt
0I
z
0
U
-4
z
0
-8
z
C-,
hIC
i
-12
i
-16
10
15
20
PACING STIMULUS STRENtGTH (mA)
25
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FIGURE 6. Comparison of the percent change in conduction time (± SD) at a constant pacing rate as the stimulus
strength is increased. Threshold for this pacing rate was 8
mA.
times to both distal recording sites decreased by
7-20% at intermediate pacing rates and increased at
very rapid pacing rates (fig. 7). This was the only time
we saw a significant conduction time decrease.
Studies Before Cardiopulmonary Bypass
Eleven of 13 studies showed significant conduction
time prolongation with increasing pacing rate. Conduction time prolongation in every study depended on
achieving a critically rapid pacing rate. The magnitude of this critical pacing rate varied among
patients, and in individual patients varied among the
various pacing sites (table 2).
Figure 8 shows the grouped data on conduction
time changes for patients studied before cardiopulmonary bypass (13 studies in five patients)
analyzed by the linear regression method for pacing
rates less than 240 beats/min and faster than 240
beats/min. There was a clear difference (p < 0.005) in
30
* =
*
z
0
U
20
=
BB
BB
-
VOL 63, No 5, MAY 1981
ST
PLA
1
2
2
3
3
6
6
6
7
7
7
Pacing
Recording
Critical rate
site
ST
ST
PLA
ST
ST
ST
PLA
PLA
PLA
BB
BB
site
BB
PLA
BB
BB
PLA
BB
ST
BB
ST
ST
PLA
(beats/min)
251
275
221
216
159
290
275
275
203
312
312
Mean
253.5
Abbreviations: ST = sulcus terminalis; BB = Bachmann's bundle; PLA = posteroinferior left atrium.
the slope of the slower vs the faster pacing rates, representing conduction time prolongation at the faster
rates. The choice of 240 beats/min as the critical pacing rate for the group is arbitrary, with individual
variation in the critical pacing rate. For example, the
circled data points show a study in which conduction
times began to prolong at a pacing rate of only 159
beats/min (from a patient with coronary artery disease).
Postoperative Studies
Conduction time prolongation at increasing pacing
rates showed greater variability in the postoperative
studies than in the studies performed before cardiopulmonary bypass. All patients still showed conduction time prolongation with increasing pacing rates,
but not invariably with each combination of pacing
and recording site. In only two patients did conduction time prolong regardless of pacing site or recording site. In two cases conduction times prolonged
to one distant site but not to the other site being
simultaneously recorded. In fact, in individual patients, the incidence of postoperative studies showing conduction time prolongation ranged from
25-100% (mean 77%). Table 3 shows for all post-
10
n
z
I
Ue
o
1=
'_ *
*
F---- ,3
TABLE 3. Postoperative Pacing Studies
-10
-201
140
180
220
260
300
340
ATRIAL PACING RATE (beats/min)
FIGURE 7. Percent change in conduction time (± SD) from
the pacing site on Bachmann's bundle (BB) to the sulcus terminalis (ST) and to the posteroinferior left atrium (PLA) in
patient 7. Conduction times decreased at pacing rates of
203-261 beats/min and increased at pacing rates over 300
beats/min.
% studies with
CT prolongation
100
PLA
66.7
ST
80
BB
80
ST
100
Abbreviations: ST = sulcus terminalis; BB = Bachmann's bundle; PLA = posteroinferior left atrium; CT =
conduction time.
Pacing site
ST
ST
PLA
PLA
BB
Recording site
BB
0
ATRIAL EXCITABILITY AND CONDUCTION/Plumb et al.
< 240 beats/min
Regression Line:
y = -1.115 + 0.013(x)
r =0.09
1
D 2 Data points
3 Data points
a 4 Data points
!
20
0J
10
0O
0
*
0
-10-
Rum~
120
150
y = -32.651 + 0.1i 30(x)
r
=
0.45
i~~~~~~~
*
*
0
z
0
L0
in
z
0
240 beats/min
Regression Line:
p < 0.005
* 1 Data point
z
0
>
1145
180
210
240
.S
270
300
330
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ATRIAL PACING RATE (beats/min)
FIGURE 8. Rate dependence ofconduction time for allprecardiopulmonary bypass studies. Rates less than
and equal to 240 beats/min are compared with rates greater than 240 beats/min.
the fastest rates that occurred in 22 of the 29 postoperative studies. The circled data points show a study
where conduction time prolongation began at a pacing rate of only 140 beats/min (from the patient with
mitral valve prolapse), illustrating the individual
variability of this phenomenon and the somewhat arbitrary nature of the choice of 240 beats/min as the
critical pacing rate for the group. Table 4 shows the
critical pacing rate for each postoperative study.
operative studies the incidence of conduction time
prolongation to each of the other two sites when each
site was paced.
The grouped data on conduction time changes for
all postoperative studies (29 studies in seven patients)
are shown in figure 9. Again, the linear regression
equation slopes are significantly different for the fast
pacing rates compared with the slow pacing rates
(p < 0.05), indicating conduction time prolongation at
LUJ
z
0
0
0
z
0
t 240 beats/min
Regression Line:
y = -0.203 ± 0.020 (x)
r = 0.13
501
p 0.05
1 Data point
40
D 2 Data points
1 3 Data points
& ' 4 Data
points
30
*
20 ^
0
CJ)
0
0
z
10-
0
0'
m
0
0
0
......
...
0;
> 240 beats/min
Regression Line:
y = -12.307 + 0.058 (x)
r = 0.15
00
............. ......
120
150
180
210
240
270
300
330
ATRIAL PACING RATE (beats/min)
FIGURE 9. Rate dependence of conduction time for all postoperative studies.
240 beats/min are compared with rates greater than 240 beats/min.
Rates less than and equal to
CIRCULATION
1146
VOL 63, No 5, MAY 1981
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immediately below the stimulating electrodes.'0"12 A
TABLE 4. Critical Pacing Rate-Postoperative Studies
~ ~,
Critical
Recordiantge~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ similar
explanation seems reasonable for our studies.
Critical rate
Pacing
Recording
of our study did not permit us to detect
design
The
(beats/min)
site
site
Pt
any supernormal phase of excitability such as has been
200
BB
1
ST
reported for canine atrium,'3 for the canine
140
BB
2
ST
Bachmann's bundle,'4 and for isolated specialized
162
atrial fibers.1" In one of our experiments, conduction
ST
2
PLA
times decreased by 7-20% while pacing Bachmann's
194
BB
2
PLA
bundle at intermediate rates (fig. 7), a finding that may
2a5
BB
3
ST
indicate a supernormal phase of conduction.'4 16
214
PLA
ST
3
The increase in atrial pacing threshold as the pacing
286
ST
BB
3
rate is increased has clear clinical implications and
222
may help explain certain problems in the clinical use
PLA
3
BB
of rapid atrial pacing to interrupt type I atrial flutter.
280
BB
4
ST
The
pacing threshold may be quite high at pacing rates
280
PLA
4
ST
and exceeding the atrial rate during type
approaching
280
ST
4
PLA
I atrial flutter (240-340 beats/min).2 The successful
330
ST
4
BB
interruption of type I atrial flutter by rapid atrial pac330
ing typically requires pacing rates substantially in ex4
PLA
BB
cess of the flutter rate,1 so further increases in
296
BB
ST
5
should be anticipated. In fact, the pacing
threshold
204
BB
ST
at very rapid pacing rates may sometimes
threshold
6
240
PLA
6
ST
exceed 20 mA,'7 the maximal current output of most
180
ST
6
PLA
commercially available pacemakers. It is reasonable
242
to suspect that some reported failures of pacing to inBB
6
PLA
6
7
7
7
ST
BB
BB
ST
ST
PLA
188
240
2233
290
PLA.k
ST
240.3
Mean
Abbreviations: ST = sulcus terminal[is; BB
bundle; PLA = posteroinferior left atriium.
=
Bachmann's
Electrical Alternans of the Atrial Electrogram
During rapid atrial pacing, electrical alternans
appeared in the atrial electrogram in 17 of 42 studies
(fig. 10). Electrical alternans is also present in figure 4
in the atrial electrogram recorded from the posterior
left atrium. Figure 10 represents an example of alternation of the conduction time intervals that accompanied the electrical alternans in six of 17 studies.
When the slower basic pacing rate was resumed, the
alternans was abolished (fig. 10). Eight times, the electrical alternans occurred in only one of the two simultaneous atrial electrograms
recorded from different
atrial sites (figs. 4 and 10).
Discussion
Atrial Excitability
The demonstration by our study that atrial excitability becomes depressed as the atrial pacing rate
is increased has not, to our knowledge, been described
in man. However, stimulus thresholds are known to
increase with increasing pacing rate in isolated guinea
pig ventricles'0 and isolated rat atria.1" 12 It has been
assumed that the rise in threshold is due to the stimuli
falling in the relative refractory period of the muscle
terrupt classic (type I) atrial flutter may have been
caused by using subthreshold stimuli.
Conduction Time Prolongation
We found that as the atrial pacing rate is increased,
atrial conduction time almost always prolongs, but
only after a critical rate is reached. Others have shown
that atrial conduction might prolong at rapid atrial
rates. Atrial conduction time has been reported to increase in dogs as the rate of atrial stimulation was increased beyond a critical rate.'8 Parallel decreases in
conduction velocity and the rate of rise of the action
potential have been reported during rapid stimulation
above a critical rate in isolated rabbit atria.'9 Similar
findings have been reported without changes in resting (diastolic) transmembrane potential.20 In isolated
rabbit atria, the conduction velocity during induced
circus movement tachycardia was shown to be much
slower than conduction in the same tissue paced at
slower rates.2" 22 Slow atrial conduction has been
demonstrated in a variety of models of canine atrial
flutter.3-5
Our experiments measured the conduction time
between two atrial sites, which is a function not only
of conduction velocity, but also of the length of the
pathway of conduction, the stimulus strength and
stimulus latency. Stimulus latency would be expected
to show approximately equal degrees of conduction
prolongation to all recording sites during stimulation
at a fixed site and would not be expected to be a function of rate. The four studies in which conduction
times prolonged to one distant site but not to another
simultaneously recorded site provide indirect evidence
against stimulus latency as an explanation of our
results.
We presume that the decrease in conduction times
1147
ATRIAL EXCITABILITY AND CONDUCTION/Plumb et al.
1 sec-b
ECG
1
,AS
I
S
AEG
(ST)
AEG
(B B)
I
I. I.
109 7 11
111 ll109 1 11
- 12
108
105 106 108
.,111.2.1,1
,1 .d
,~~~~~~~~~~V1
X
L10 108S13
L1n
1.
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S-S 212 msec
(Rate 283bpn)
77 6977
-I.
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-I
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S-S 480msec
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FIGURE 10. ECG lead I recorded simultaneously with bipolar atrial electrograms (AEG) recordedfrom the
sulcus terminalis (ST) and Bachmann's bundle (BB) during pacing from the posteroinferior left atrium. Conduction times from the pacing stimulus (S) to each recording site are shown (in msec) during rapid pacing at
283 beats/min and at the basic pacing rate of 125 beats/min, illustrating the alternation of conduction times
and atrial electrogram morphology noted during rapid atrial pacing. Paper recording speed is 50 mm/sec.
Time lines are at 1-second intervals.
at the basic pacing rate as the stimulus strength was
increased represents the activation of an increasingly
large area of atrial mass at the site of stimulation.23
The nonuniform decrease in conduction time at the
basic rate as suprathreshold pacing stimuli were used
may be related to variation in the absolute magnitude
of the increase in stimulus strength, to variation in
bipolar interelectrode distance, and to variation in the
nature of the myocardial tissues24 in contact with the
epicardial wires.
A lengthening of the pathway of impulse conduction
would also be manifest as conduction time prolongation. Since atrial refractoriness is known to be inhomogenous,3' 56 25, 26 an increase in rate might render
parts of the prior shortest path refractory, so that conduction via a new pathway would be longer. The
bipolar atrial electrogram morphology changes we
observed, however, were largely a change in the
amplitude of the atrial electrogram with preservation
of the form recorded simultaneously at two widely
spaced atrial sites, suggesting almost identical directions of atrial depolarization.
As the pacing rate increases, the stimulus may encroach upon phase 3 of the action potential, decreasing the takeoff potential of the propagated impulse
compared with pacing at slower rates and resulting in
a slowing of conduction velocity.27 28 Unfortunately,
in vivo atrial refractoriness has not been defined in
man for rates in excess of 150 beats/min.29 At even
faster rates the action potential duration and atrial
refractoriness may continue to shorten.26 However,
the tail of atrial refractoriness after 70% of repolarization may be very important in considering the
relationship of pacing rate and atrial conduction to
atrial refractoriness, and encroachment of the
stimulus on repolarization may be a cause for slowing
of conduction velocity and prolongation of conduction times.
Rapid atrial pacing at a critically rapid rate might
be associated with a relative depolarization of transmembrane resting potential apart from repolarization (phase 3) considerations. In fact, rate-dependent
rises in extracellular potassium concentration, which
decrease the resting transmembrane potential of
human atrium,30 have been reported during rapid
stimulation of isolated rabbit atria,31 and would be expected to decrease conduction velocity at rapid pacing rates, but do not explain why prolongation of conduction time depended on achievement of a critical
pacing rate.
Whatever the mechanism of prolongation of atrial
conduction times with faster rates, our studies suggest
a fundamental difference from the mechanism of the
rise in atrial pacing threshold with increasing rate.
First, the rate dependence of threshold was seen in
each study, in contrast to the conduction time
prolongation during rapid pacing which, while noted
in the majority of studies, was not always seen. Second, the rises of threshold and increases in conduction times did not occur concurrently (fig. 5). Third,
CIRCULATION
1148
the increase in threshold did not appear to depend
on
achievement of a critical pacing rate, whereas
prolongation of conduction did.
Electrical Alternans
Atrial electrical alternans
demonstrated in our
study during pacing at very rapid rates has also been
demonstrated during rapid atrial pacing in the dog,"'
induced by prior
during canine atrial arrhythmias
atrial electrical stimulation, 32-5 during aconitineinduced atrial arrhythmias,36 during spontaneous
canine atrial flutter,5 and in spontaneous human atrial
flutter." 2, Its mechanism has been attributed to
local change in conduction32 and to the stimulation
rates approaching the maximum frequency permitted
by the limiting refractory period of the tissue involved.35 These observations suggest that the presence
of electrical alternans is a function of rapid rate and is
independent of the underlying mechanism of the
rhythm.
as
17
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Theoretical Implications
Although the mechanism of rapid atrial
arrhythmias such as ectopic atrial tachycardia, atrial
flutter and atrial fibrillation is uncertain, it has been
proposed that conditions of slowed conduction and
diminished excitability are necessary for their
perpetuation.37 The present study suggests that since
slowed conduction and diminished excitability are an
intrinsic property of rapid atrial rates, rapid atrial
rhythms of whatever mechanism might tend to be selfsustaining.
Acknowledgment
We gratefully acknowledge the statistical assistance provided by
Roy Swatzell and Dr. Malcom Turner. We also thank Al Germann
for invaluable aid and BeaJudson for patient secretarial assistance.
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Boyd, 1949
10. Johnson EA, McKinnon MG: The differential effect of
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11. Landmark K: The action of promazine and thioridazine in
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calcium in different frequencies and strengths of stimulation on
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12. Refsum H, Landmark K: The effect of nifedipine on the effective refractory period and excitability of the isolated rat atrium
at different calcium levels and frequencies of stimulation. Acta
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13. Brooks CM, Orias 0, Gilbert JL, Siebens AA, Hoffman B,
Suckling EE: Excitability cycle of mammalian auricle. Am J
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14. Childers RW, Merideth J, Moe GK: Supernormality in
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15. Hogan PM, Davis LD: Electrophysiological characteristics of
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16. Agha AS, Castillo CA, Castellanos A ir, Myerburg Ri, Tessler
MP: Supernormal conduction in the human atria. Circulation
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17. Waldo AL, Wells JL
Plumb
Cooper TB, MacLean
WAH: Studies of atrial flutter following open heart surgery.
Annu Rev Med 30: 259, 1979
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Some effects of rhythmic stimulation of
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19. Yamagishi Sano T: Effect of temperature on pacemaker activity of rabbit sinus node. Am Physiol 212: 829, 1967
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The Nature of Atriosinus Conduction
During Rapid Atrial Pacing
in the Rabbit Heart
CHARLES R. KERR, M.D.,
AND
HAROLD C. STRAUSS, M.D., C.M.
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SUMMARY During clinical electrophysiologic investigations, the sinus node recovery time (SNRT)
lengthens as the atrial pacing rate increases; after reaching a maximum value, SNRT shortens with further increases in pacing rate. This phenomenon has been ascribed to the onset of atriosinus entrance block. In this
study we investigated the nature of atriosinus conduction during rapid atrial pacing and related changes in
SNRT to changes in conduction. In eight rabbit sinus node preparations, the crista terminalis was paced for 1
minute at cycle lengths ranging from 400 to 100 msec, while crista terminalis electrograms were recorded by
surface electrode and sinus node transmembrane action potentials were recorded by microelectrode. In all experiments SNRT prolonged progressively as the cycle length shortened until 2: 1 atriosinus block occurred; at
that point SNRT shortened. After correction for spontaneous cycle length, SNRT was inversely related to the
cycle length of action potentials recorded from the pacemaker site in the sinus node (r = -0.84), indicating
that SNRT depends on the number of impulses reaching the pacemaker site. In four experiments, the microelectrode was moved toward the crista terminalis in intervals of 50-100 ju, repeating the pacing sequence at
each site. The site of atriosinus block could be identified as the point at which action potential amplitude fell
rapidly. With progressively shorter cycle lengths, the site of block moved progressively farther from the pacemaker site in the sinus node. Therefore, the shortening of SNRT with rapid pacing may be explained by the
presence of atriosinus block and by a reduction in the number of impulses that reach the pacemaker site in the
sinus node.
RAPID ATRIAL PACING is frequently used to
sinus node automaticity in patients suspected of
having sinus node dysfunction. The duration of the
recovery cycle after a train of rapid atrial pacing is
called the sinus node recovery time (SNRT), and its
prolongation has been widely accepted as evidence of
sinus node dysfunction.'-' In general, as the rate of
atrial pacing is increased, the duration of the recovery
cycle increases until a maximum degree of suppresassess
From the Division of Cardiology, Department of Medicine, and
the Department of Pharmacology, Duke University Medical
Center, Durham, North Carolina.
Supported in part by USPHS grant HL19216, HL 07101 and
RR30, General Clinical Research Centers Program of the Division
of Research Resources, NIH.
Dr. Strauss is recipient of Research Career Development Award
1-K04-HL-00268, NIH.
Dr. Kerr is a Fellow of the Medical Research Council of Canada.
Address for correspondence: Charles R. Kerr, M.D., Division of
Cardiology, Vancouver General Hospital, 2775 Heather Street,
Vancouver, B.C. VSZ, 3J5.
Received May 20, 1980; revision accepted September 3, 1980.
Circulation 63, No. 5, 1981.
sion occurs; beyond this point the recovery cycle
shortens as the atrial pacing rate continues to be increased. In man, maximum suppression normally occurs at 118-130 beats/min.2 5, '6 The decrease in
SNRT at faster rates may be the result of block of impulses before they can reach and depolarize the sinus
node. Such a reduction in the rate of sinus node discharge would cause a reduction in sinus node suppression."7 10 In cases of sinus node dysfunction, atriosinus entrance block may occur at lower pacing rates,
so maximum sinus node recovery time may occur at
pacing rates lower than 1 18 beats/min.4' 6 9, 11, 12
Although the shortening of the SNRT at fast pacing rates has been well documented and the presence
of atriosinus block has been postulated to explain this
phenomenon, in vitro studies are required to corroborate these findings. In this study we used an
isolated sinus node preparation from the rabbit to
characterize atriosinus conduction during rapid atrial
pacing. In particular, we examined the nature and site
of block of retrogradely conducted impulses and the
relationship between the rate of pacing and SNRT.
Atrial excitability and conduction during rapid atrial pacing.
V J Plumb, R B Karp, T N James and A L Waldo
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Circulation. 1981;63:1140-1149
doi: 10.1161/01.CIR.63.5.1140
Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 1981 American Heart Association, Inc. All rights reserved.
Print ISSN: 0009-7322. Online ISSN: 1524-4539
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