Significance of the Sinus-Node Recovery Time
By ONKAR S. NARULA, M.D., PHILIP SAMET, M.D.,
AND
ROGER P. JAVIER, M.D.
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SUMMARY
The phenomenon of postpacing depression of cardiac pacemakers was utilized to
evaluate the sinus-node function in 56 patients by analyzing the sinus-node recovery
time (SRT), that is, the interval between the last paced P wave and the following
sinus P wave. Corrected SRT (CSRT) is defined as the recovery interval in excess of
the sinus cycle (SRT -sinus cycle length). The SRT was measured following sinusnode suppression by (1) isolated premature beats (PABs) and (2) atrial pacing
(AP) at rates of 100 to 140/min for periods of 2 to 5 min at each level. Twentyeight patients had normal heart rates (group A), and 28 patients had sinus bradyeardia
(SB; group B). Ten of the 28 patients with SB were restudied after receiving atropine
(2 mg intravenously). The CSRT with PABs was similar in both group A and group
B patients and remained essentially unchanged after atropine despite a decrease in
sinus cycle length. The phenomenon of interpolated PABs was demonstrated in seven
of the 56 patients. In 27 of the 28 patients with normal heart rates (group A), the
CSRT with AP ranged from 110 to 525 msec and was essentially independent of
the rate and duration of AP. In the remaining one patient of group A, despite a
normal heart rate, the CSRT was prolonged (1810 msec) and directly dependent
on the rate and duration of AP. In 12 of the 28 patients with SB, the CSRT was
comparable to that in group A (<525 msec). In the remaining 16 patients with SB
(group B), the CSRT ranged from 560 to 3740 msec and was usually directly proportional to the rate and duration of AP. After atropine in most of the patients with
a prolonged CSRT, the CSRT remained abnormal whereas in others junctional escape
beats appeared first, followed eventually by normal sinus rhythm. In a single patient
with SB and an abnormal CSRT, restudy 7,i months later again showed a prolonged
CSRT indicating the reproducibility of the measurement. The CSRT with AP provides
a potentially useful clinical means of assessing the sinus-node function and thereby
aids in the diagnosis of the "sick sinus syndrome." It is stressed that AP was found
to be more reliable than PABs in eliciting an abnormal response. Furthermore, a
normal sinus (atrial) rate does not necessarily provide assurance of a normal sinusnode response to AP, that is, normal sinus-node function.
Additional Indexing Words:
Sinus-node function
Atrial pacing
Sinus bradyeardia
THE VARIOUS clinical and ECG manifestations of disorders of sinus-node
function include sinoatrial block, sinus pauses.
or sinus arrest, sinus bradyeardia, and the
brady-tachyarrhythmia syndrome. These constitute the sick sinus syndrome.' This syn-
Atropine
drome has been known ever since the
availability of suitable recording instruments
permitted differentiation from other forms of
bradyeardia. Although previously considered a
benign rhythm, it has gained clinical importance due to several reports ascribing StokesAdams attacks to this syndrome.2 4 Interest in
From the Division of Cardiology, Department of
Internal Medicine, Mount Sinai Hospital of Greater
Miami, Miami Beach, Florida, and the University of
Miami School of Medicine, Miami, Florida.
Presented in part at the 55th Annual Meeting of the
Federation of American Societies for Experimental
Biology, Chicago, Illinois, April 12-17, 1971.
Address for reprints: Dr. Onkar S. Narula, Division
of Cardiology, Department of Internal Medicine,
Mount Sinai Hospital of Greater Miami, 4300 Alton
Road, Miami Beach, Florida 33140.
Received July 1, 1971; revision accepted for
publication September 14, 1971.
140
Circulation, Volume XLV. January 1972
SINUS-NODE RECOVERY TIME
patients with sinus bradyeardia or sick sinus
syndrome has developed in view of available
effective pacemaker therapy.;
Sinus bradyeardia (SB) may be a manifes-
Downloaded from http://circ.ahajournals.org/ by guest on September 30, 2016
tation of one or more of the following three
mechanisms : 7 8 ( 1) interactions of parasympathetic and sympathetic systems on the sinusnode automaticity; (2) poor function of the
sinus node (SN) as an impulse generator; and
(3) depressed conduction of the generated
impulse from the sinus node to the atrium
with sinoatrial (SA) block.
Thus far, the adequacy of sinus-node
function has been reflected primarily by the
atrial rate during sinus rhythm. As yet, no
means are available to record selectively and,
if recorded, to validate the sinus-node
potentials in man.
The purpose of the present study is to
utilize the phenomenon of postpacing depression of cardiac pacemakers to evaluate the
sinus-node function by analyzing the sinusnode recovery time, that is, the interval
between the last paced P wave and the
following sinus P wave. The sinus-node
recovery time (SRT) was measured following
sinus-node suppression by (1) isolated premature atrial beats (PABs) and (2) atrial pacing
(AP), to provide quantitative measurements
in patients with normal and abnormal sinus
node. It should be stressed at the outset that
wve have used both AP and PABs to stress the
sinus node and have found AP to be a more
reliable means than PABs for use in the
diagnosis of the sick sinus syndrome.
Methods
Fifty-six patients (ranging in age from 16 to 90
years wvith mean age 61 vears) wvere studied.
Group A included 28 patients with normal heart
rates (table 1), and group B included 28
patients with sinus bradyeardia (SB; table 2).
Patients who showed a sinus rate of 55/mimi or
less on more than one occasion were included in
the SB group. The electrocardiographic findings
and the cardiac medications are given in tables
1 and 2.
None of these patients had had a recent
myocardial infarction, that is, within 8 to 10
weeks prior to the study, nor were anv in the
immediate postoperative period. All patients were
studied in the postabsorptive state and were
Circulation, Volumie XLV, January 1972
141
premedicated with 100 mg of pentobarbital
(Nembutal), administered intramuscularly 30
min prior to the study. One of these patients
(case 38) was restudied 73 montlhs later.
Sinus recovery time (SRT) was measured
during (1) premature atrial beats (PABs) and
(2) after right atrial pacing (AP). Bipolar
electrograms (BE) were recorded from the high
right atrium (RA) and the His bundle region
(BH), simultaneous with three standard ECG
leads (usually L-I, aVF, and V1). Right atrial
stimulation was achieved from the high RA
in the region of the sinus node. In the initial part
of the study, pacing sites in the right atrium and
stimulus strength were changed to assess the
effect of these factors, but no difference in the
SRT was observed. Premature atrial stimuli, 2
msec in duration and twice the diastolic
threshhold, were delivered after 12 to 14 sinuis
cycles. The entire atrial cycle -,,as scanined bv the
placement of progressivelv more prematuire atrial
beats. All recordings were made at paper speeds
of 100 to 200 mm/sec. After the entire atrial
cycle had been explored by PABs, atrial pacing
(AP) was performed at tvo or three different
heart rates, 100, 120, and 140/min for periods of
2 and 5 min at each level. AP levels of over
120/min wer e used only in selected patienits.
Between each atrial pacing level a rest period of 2
to 3 min vas given to alloxv the rhythm to return
to its basic levels. In our study, the sinus cvele
usuallv returned to its control levels in less thani 1
min. The blood pressure was monitored either via
an arterial needle or by a blood pressure cuff
throughout the studv.
In 10 of the 28 patients wvith sinus bradycardia,
stuidies wvere performed after atropine (2 mg)
wvas administer-ed intravenously. 'Measuremnents
xvere made 5 min after atropine administrationi to
assess the effect of vagal tone and of altering
sinus rate on the SRT. After atropine, the
stimulation sequence used xvith PABs durinlg
control study wvas repeated xvhereas atrial pacing
wvas repeated only at a single level of 120/mim for
2 or 5 min.
Definitions
In everv patient the intervals betwveen successive atrial depolarization were measured from the
bipolar atrial electrograms. During each test
cycle, the following intervals wvere measured: (1)
A1A1 which is defined as the interval between the
txvo atrial electrograms of sinus origin; (2)
average A1A1, xvhich is the average of 5 cycles
(A1A1) measured preceding the PABs or AP; (3)
A1A., the interval betxveen atrial electrograms of
sinus origin and the PAB; (4) A2A3, which is the
interval betwveen the PAB or the last atrial paced
P and the stucceedinig atrial electrogramii of sinus
142
NARULA ET AL
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SINUS-NODE RECOVERY TIME
143
Group A
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Case 24: Typical effect of prematurity (A1A.,) of PABs
on SRT (A.,A:) in group A patients. Initially there is
a progressive increase in prematurity up to approxi-
mately 75% of the sinuis cycle length. A further increase
Downloaded from http://circ.ahajournals.org/ by guest on September 30, 2016
in prematurity is accompanied by little lengthening of
SRT and a plateau effect is seen. At RP = atrial abso-
ltute refractory period.
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origin and is defined as SRT; (5) the corrected
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length (A1A1) ranged from 600 to 920 msee
(mean, 775). In all patients, as the A1A.,
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Case 41: Atypical effect of prematurity (A1A2) of
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Circulatioon, Volume XLV, January 1972
144
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SINUS-NODE RECOVERY TIME
147
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decrease in the A1A2 interval resulted in no
appreciable increase in CSRT but a plateau
effect was seen (fig. 1). This maximum effect
on lengthening of CSRT was usually observed
when A1A.2 ranged between 70 and 80% of the
sinus cycle (range, 65 to 90%). The maximum
CSRT following PABs was variable from
patient to patient and ranged from 100 to 370
msec (mean, 197 ± 70) or 12 to 41% of the
basic sinus cycle (table 1). The CSRT was
reproducible in each patient during a given
procedure.
Group B. The CSRT in 24 patients was similar to those in group A and ranged from 100
to 435 msec (mean, 226 ± 91) (table 2). A
single other patient (case 42) showed a
markedly prolonged CSRT (900 msec or 75%
of the sinus cycle). In the remaining three
patients (cases 36, 41, and 43), in contrast to
group A, the PABs were followed by a pause
(AA,3) essentially equal to the sinus cycle
length or CSRT ranged from 0 to 40 msec (fig.
2).
12 had CSRT comparable to that in group A
(<'525 msec) (fig. 6). In the remaining 16
patients the maximum CSRT ranged from 560
to 3740 msec (mean, 1880 + 1079; table 2).
In the latter 16 patients the CSRT was usually
directly dependent on the rate and duration of
AP and progressively increased with increase
in either of these two factors (fig. 7). In some
of these 16 cases, after the termination of AP,
the first sinus P was recorded without an
appreciably prolonged CSRT but with a
markedly prolonged second sinus cycle. In
some of the patients with SB and prolonged
CSRT, the postpacing depression persisted for
several sinus cycles before returning to control
levels. Most patients with SB and prolonged
CSRT were not receiving cardiac medications.
In patients with prolonged CSRT, the development of symptoms was avoided by turning
on the atrial pacemaker when the asystole,
due to the sinus pause, exceeded 4 sec. After
the cessation of AP, no acceleration in sinus
rate was observed for the following 15 sec.
After Atrial Pacing
After Atropine
Group A. In 27 of the 28 patients in group
A, the CSRT remained essentially unchanged
despite an increase in rate and duration of AP
from 100 to 140/min and from 2 to 5 min. A
slight fluctuation in CSRT in the range of + 20
to ± 50 msec could be observed between
different levels. A typical response to AP at
three different levels each for 2- and 5-min
duration is shown in figure 3. The range of
CSRT in these 27 patients was 100 to 525 msec
(mean, 260 + 98) or 15 to 59% of the sinus
cycle (table 1).
In the remaining one patient (case 28) with
a history of syncope and a normal heart rate,
the CSRT was prolonged and directly proportional to the rate of AP. The CSRT progressively increased with increase in rate of AP
from 100 to 120 to 140/min for 2 min at each
level and ranged from 1810 to 3710 and
beyond . msec, respectively (fig. 4). However, in this patient the CSRT with PABs was
320 msec and was similar to that of the other
27 patients in group A (fig. 5).
Group B. Of the 28 patients in this group,
WVith AP. Ten patients with SB (table 2)
wvere restudied after atropine. In tvo of these
10 patients (cases 50 and 56) with SB, the
control CSRT was not prolonged and remained unchanged after atropine. The other
eight patients had a control prolonged CSRT.
In four of the latter eight patients (cases 55,
39, 36, and 34), the CSRT after atropine was
1710, 620, 480, and 360 msec in contrast to
control levels of 1350, 2450, 1860, and 1420
msec, respectively. In the remaining four
patients (cases 30, 33, 37, and 38), junctional
escape beats at intervals of 1120, 2250, 1200,
and 4260 msec were the first to appear,
followed eventually by sinus rhvthm after
several cycles of junctional beats (fig. 8, lower
panel).
AWith PAB.s. The duration of CSRT (A2A: A1A1) or the recovery interval in excess of the
sinus cycle remained essentially unchanged
after atropine. The SRT (A.,Al) after PABs
shortened because of a decrease in basic sinus
cycle length (A1A1) and not because of any
decrease in the time required for the sinus
node to recover.
Cirt ulation, Volum-,Ae XLV, January 1972
NARULA ET AL.
148S
A
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830
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Figure 3
Case 5: Effect of iate ancd cluratio)i of atrial pacilg (AP) on1 SRT in paticltts tuiti normnal sinWis
functiot. (A to F) Despite a progressiue it2crease in1 AP ate.s frotmi 1(0) to 120, arnd to 140 olin
for 2 atnd 5 mmir at each pacing rate, the CSRT (A)A -A A,) is essentially the same from
panels A (295 trisec) to F (310 misec). This indicates that CSRT is indep)endenit of rate andl
durationt of AP, within limits, in patients with normal sinus function. After the cessation of AP,
the depressant effect persists for a fetw beats as showsn by prolonged cycle lengths. PI = pacing
imputlse. Time lines in this and suibsequent figtures are at 1-sec intervals.
Cuiiives are cotntint(otu.s from left hlalf to right half of that figuire.
After Spontaneotus Atrial Tachycardia
In one patient (case 18) with recurrent
spontaneous atrial tachycardia, CSRT was
measured during stable sinus rhythm by atrial
pacing (fig. 9, upper panel). At the end of the
study, the patient spontaneously developed
atrial tachycardia with an atrial cycle length
of 215 msec (fig. 8, lower panel). After atrial
tachycardia had persisted for 5 min, it was
terminated by rapid atrial stimulation
(400/min). The CSRT measured at the
termination of the tachycardia was essentially
the same as that after atrial pacing (100/min
for 2 min), despite its spontaneous origin and
a faster rate than AP (fig. 9).
Follow-uip
In one patient (ease 38) with a hiistory of
syncope, the CSRT was studied before and
after 712 months of a permanent pacemakel
implantation. The CSRT was markedly pro-
longed when first studied and remained
abnormal during the second study (fig. 8)
even at a slower AP rate.
Interpolated Premature Atrial Beats
In seven of the 56 patients, pacer-induced
interpolated PABs wvere observed. As the
PABs were induced at progressively increasing
prem-aturity, a level was reached at which
the subsequent interval (A.,A:1) suddenly
shortened and exhibited no compensatory
pause (A1A1 = A1A.. + A.,A:1) (fig. 10). This
phenomenon could be reproduced in a given
patient within a narrow range of the atrial
cycle. A decrease in prematurity from this
level resulted in sinus-node depression (increase in A2sA3) whereas an increase in
prematurity exhibited relative or absolute
refractoriness of the atrium. During relative
refractoriness, the interval between the pacing impulse and the atrial depolarization
Circulation, Volume XLV. Januar) 1972
SINUS-NODE RECOVERY TIME
AP =
1001min-
2 min-
|
!
Pi,
-
AP
1001min
149
<,
¢
q
835m
P-P 1065Smsec
880
840
-5 min
PI
P-P 1070 msec
840
890
lJ 810
AP = 120/min-2 min !
P/Ij
AP
120/min
820
5minq
Pi
--AP
900900
|
PlP 1170 msec
P-P 1160
j
msec
945
b
930
875
140/min-2 min 4
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PI1P
I6me
8708780
_AP 140/min-5 mninmPI,
l
l PP
1150 msec
830 870
87
1138
H. Bro, tt80069 3/20/71
lengthened or a phenomenon of atrial reentry
or repetitive atrial firing was exhibited for 2 to
3 beats. In these patients, the coupling
interval, at which interpolated PABs were
produced, ranged from 350 to 450 imsec and
was longer than the refractory period of the
underlying atrial myocardium.
Discussion
Sinus-Node Recovery Time
The function of the sinus node is not only to
generate the normal heart beat but also to
respond to physiologic influences. The present
study (by using atrial stimulation as a
provocative test) provides a potential clinically useful parameter to assess sinus-node
function. The sinus-node response is characterized by the duration of postpacing depression
or SRT. Gaskell9 first demonstrated the
depression of the intrinsic pacemaker activity
by driving the heart at a rate faster than the
dominant pacemaker. In a subsequent canine
study, Lange10 found that the sinus node was
less readily depressed than other pacemakers
when pacing was terminated. This phenomenon of overdrive suppression has been clinically observed and utilized especially in terminating supraventricular arrhythmias.11' 12
This study provides measurements of the
Circulation, Volume XLV, January 1972
CSRT with PABs and AP in patients both
with normal heart rate and with SB. The
range of CSRT with AP in all but one patient
(case 28) with normal heart rates was narrow
(110 to 525 msec), whereas in patients with
SB it was very wide (140 to 3730 msec). The
data show that patients with SB do not
comprise a homogeneous group (figs. 6 and 7)
and may or may not show an abnormal
response. The CSRT in the normal heart rate
group was usually independent of the duration and rate of AP (up to 140/min) whereas
in the majority of the patients with SB and an
abnormal response it was directly proportional to the duration and rate of AP. In the
patients with normal heart rates the beats
following AP showed a slight lengthening of
the sinus cycle length which usually lasted for
a short time with a progressive reversion to
control levels over 5 to 6 beats, whereas a
longer period was required in patients with
prolonged SRT. In an occasional case with SB,
the maximum postpacing depression was not
seen in the very first sinus P wave but in the
second sinus P wave which appeared after a
marked delay. Most of the patients with SB
and prolonged SRT were receiving no cardiac
medication. This indicates that the abnormal
SRT was not due to drugs. No overshoot or
1.50
@;s-#i!n S_+- @i~ ~ ~ ~ - J_-
NARULA ET AL.
A L-1
~
~
795
915~.~+
915
2 min
100/min
AP
890
9
V
BH
B
(BH!
t~~~
Ll
~
835
P-P 930 msec
~~~~~~~~A
PI;
W! .
780
*
ll
271
_I
120/min
AP
BE
c(BH)
2
---. A:
.\y
_
minI
P-P 960 ,sec.
900
li
0-
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3300
I
A
A
140/min
AP
BE
D (BH)
L-1
min
800
780
P-P 1060
810
msec
1
C Gol
-80603
800
4610 +
!
~~~~I
2 i6 70
14
Figure 4
Case 28: A p)atienit uLvith histort of spiycope and no docneiented SB or A-V contdnictiont defect
showed a p)rolongedI SRT. (A) Conitiol rhtjthrii stril) (L-1) dnring niormial sinus rhythmn. (B to
D) Sim7iiultanieo.us recordings of bip3olar electrogr,ani (BE) fronm tile area of the A-V jtictioni
(BH) atid ECG lead L-1. SRT after AP is markedly prolonged and lengthened progressively
(2710 to 4610 msec) weith p)rogre.ssite increase in AP tote from 100 to 140/mliuii.
acceleration of sinus rate sx as observed for
period up to 15 see after the terimination of
AP. These findings are in contrast to a sttidy
on dogs which showx ed that in presumablnormal dogs the SRT was directly proportional to the rate and duration of AP.1'" An
analysis of the data in the dog study1" shows
that the change in SRT with increase in rate
and duration of AP was usuallv small and in
the range of about 50 msec. This increase is
insignificant in view of the normal fluctluations
in SRT (range, +50 msec) between different
levels in our study. Recentlv reported x alues
of CSRT in patients with normal sinus rate are
comparable to that of onrs.l:3 However,
because of a limited number of patients (three
cases) with SB, that study did not showv that
a
patients with SB necessarily havre a proloiged
CSRT.1'
The temporary depression of pacemaker
automaticity subsequent to premature electrical stimulation has been demonstrated in
several experimental and clinical studies.11 14-16
Recently, Bonke and associates'1 studied the
factors determining the duration of the postextrasystolic pause following induced PABs
in the isolated right atrium of the rabbit. Their
study showed that the duration of the postex-
trasystolic pause increased progressively with
a progressive increase in prematurity of the
PABs up to a level approximately equal to 70%c
of the sinus cycle, beyond which a further increase in prematurity resulted in an essentially
plateau effect. Our findings support these obCircolation. Voluniie XLV. Januar48}1972
SINUS-NODE RECOVERY TIME
151
A~~~~~~~~~~~~~~~~~H
A (BH)
K
930
-
v
A
-
',
55
P8-A
850
1020;
[-1
---
,-
_
A-A 865 msec
____________
~~~~PIA3
Al
2
\
(BH)
1A
.
Pl-A
Downloaded from http://circ.ahajournals.org/ by guest on September 30, 2016
C
925
A-A 815
75
325
msec
L-1
aVF
1220
_
\
560
_
n-- - -
V,
,
_-J
5
C, Gol., #80603 2, 16/70
.1148
Figure 5
Case 28: Same patient as in Figure 4. Normal SRT with premature atrial beats (PABs). (A to
C) With a decrease in cotnpling interval (A1A.) from panels A to C, the SRT (A. A:) ranged
from 1105, to 1220, to 1220 mnsec, respectively, in contrast to the markedly long SRT after
AP (fig. 4 Ipanel D). This shows the inability of the PABs to differetntiate betwceeni a normal
and abnormal sitntns-node functioni. PI-A = the interual bettwcen the PI and the prematuire
atrial electrogranm (A.).
servations (fig. 1). With PABs, after atropine
administration, the absence of any change in
CSRT despite an increase in sinus rate indicates that the CSRT is independent of the
cycle length and vagal tone. Furthermore, it
explains the similar response to PABs in patients with normal heart rates and SB.
The mechanism of overdrive suppression
following AP is probably mediated in some
way through humoral responses. 18-2' This inability to abolish completely the postpacing
depression after atropine in this and other
studies"'. 13 suggests the role of factors other
than acetylcholine. It has been suggested22. 23
that driving stimuli. result in an increase in
extracellular K+ which leads to the suppression
by two mechanisms (1) a decrease in phase 4
depolarization and hence a decrease in
automaticity; (2) a decrease in the resting
Circulation, Volume XLV, January 1972
potential and in the amplitude of the action
potential which, in turn, may render it
ineffective as a stimulus for propagation.24 24
However, as yet this issue is unsettled.2'
In most of the patients, SB was not
to increased vagal tone as only
minimal acceleration in sinus rate was exhibited after atropine administration. In addition,
a prolonged CSRT remained abnormal despite
a decrease from the control levels and suggests
secondary
that the prolongation was mainly due to
a
poor function of the sinus node itself, although
vagal tone contributed to it.
The important question is what parameter
of the sinus-node function is reflected by this
response (postpacing depression): (1) Is it
due to a delay or block in sinoatrial conduction or (2) does the prolonged SRT indicate a
change in automatic capacity of the sinus
A2
NARULA ET AL.
152
AP =75/min
2 min
(BElL-1-_
(BH)
~~~~~A-A1350
1310
msec
A
-
_
_
1260l+i
)G_jD
....
.9W+,350g_>1
AP
2 min
100/min
A
,
3
BE
B (BH)
A,
A.
L-1
120i+A130
se
Downloaded from http://circ.ahajournals.org/ by guest on September 30, 2016
J.
A
130-
1
fA1
i
AP
C
120/min
2 min
BE
(BH)
AA1320
me
L-1
:I-,------1
..
.1l 778265
3 6 '70
------
1460
-
4
1220
R
Figure 6
Case 43: A patient with SB and a normal CSRT which is independent of the rate of AP.
(A to C) Simultaneous recordings of BE(BH) and ECG lead L-1. AP for 2 min at each level
with a rate of 75, 100, and 120/min shows a normal CSRT (A2A5 - A1A1 - 140 msec)
(panel C).
node as an impulse generator? The first
possibility is unlikely for the following reasons: (a) The presence of sinus rhythm (SR)
is an indication of intact sinoatrial conduction
whereas the existence of a compensatory
pause following the atrial stimulation (with
PAB and AP) is suggestive of conduction
from the atrium to the sinus node.17 (b) Atrial
pacing at a rate faster than SR should
decrease the refractory period (RP) of the
atrium, within limits, due to a decrease in
cycle length and thus facilitate conduction
from SN to RA. (c) Concealed conduction
from RA to SN with AP may delay SN to RA
conduction for one subsequent sinus cycle, but
longer delays (SRT) cannot be attributed to
this property. (d) Experimental work shows
that following atrial stimulation a shift in
impulse origin may occur from true pacemaker cells in the center of SN to latent
pacemaker cells situated at the periphery of
the SN.17 23 However, the conduction time
from the latter pacemakers to RA should be
shorter as opposed to that of the former.
Therefore, the second possibility, that is, a
change in the automaticity of the sinus
pacemaker cells (or decrease in the strength
of the sinus impulse) is the most likely
explanation for postpacing depression. This is
further supported by a recent editorial suggesting that sinus impulses, if subthreshhold,
may fail to excite the atrium and result in long
pauses with atrial asystole.26 This decrease in
automaticity may be secondary to shift in
pacemaker site from true to latent pacemaker
cells or direct depression of automaticity
Circulation, Volume XLV, January 1972
SINUS-NODE RECOVERY TIME
153
Control
A
__
AP
=
100/min
1670
1680
sl
P-P 1670 msec
-
Li
~PP
AP
120/min
P-P
1680
-1 -.
4
2 min
[~~~~~~~~~~~~~~~~~~~~~AI
c
1680
lliJl!TllrT
1
17i80
3870 msecl
2 min,
msecP
____________________T_
Downloaded from http://circ.ahajournals.org/ by guest on September 30, 2016
P-P 5410 msec
l---
_.
S~~~~~~
o.lLoomb,lm
33110
-T -
w
3010
1~~~~~-
L- r-0-
L1
-
r
~
A
--
260
-
..6-,S91696 3/16/71
Figure 7
Case 51: A patient with SB and an abnormal SRT. (A) Rhythm strip showing control sinuis
cycle length (1670 msec). (B and C) An increase in AP rate from 100 to 120/min for 2 min
at each level demonstrated a progressive increase in SRT from 3870 to 5410 msec. The severe
depressent effect is demonstrated even in the subsequent beats with markedly prolonged
sinnis cycle lengths.
mediated through humoral responses or alterations in electrolytes. Accordingly, the
quantitative data of SRT with AP in normal
patients probably provide a measure by which
the function of the sinus node as an impulse
generator can be assessed. The automatic capacity of the sinus node may be reflected by
the duration of (1) the sinus-node recovery
time after the termination of atrial pacing and
of (2) the depressant effect present in the
subsequent beats which show a longer sinus
cycle length as compared to the control sinus
cycles preceding AP.
It should be stressed that AP, rather than
PABs, is a more reliable method of differentiating between a normal and an abnormal sinusnode response. The CSRT following PABs was
usually similar in all patients (normal or SB)
and was in no way comparable to the
prolonged CSRT seen with AP in patients
with sick sinus (tables 1 and 2). Case 28 (figs.
4 and 5) is illustrative. This patient had a
Circulation, Volume XLV, January 1972
history of syncope and on admission showed
heart rates within the normal range without
any arrhythmias. The CSRT, although normal
during PABs, was grossly abnormal with AP.
Following the cessation of AP, a period of
asystole more than 4.5 see in duration was
noted. These findings are of clinical significance and suggest (1) that a normal sinus rate
is no assurance of normal sinus-node function
and (2) that all patients with SB may not have
a poor sinus node. They also may explain (3)
why some patients with SB and comparable
rates are stable and asymptomatic, whereas
others have syncopal or dizzy spells. The latter
group probably represent patients with bradytachy syndrome who manifest long periods of
asystole following supraventricular arrhythmias.
The majority of the patients with SB and a
markedly prolonged CSRT did not demonstrate escape of lower pacemakers, that is, the
A-V junctional or ventricular, during the
NARULA ET AL.
154
51370 AP =1201in
2 min
m-1i
BE
(BH)
A-A 1370
mse0
A1500
~1600
-----4000 -----
Downloaded from http://circ.ahajournals.org/ by guest on September 30, 2016
At,pine 2 mg
AP = 80min
2 min
1080
1/ 26/71
.
xz
L-1 AA 1080
10810
8- -
Control
BV~
BE e '
h
mon 5/
1590
1300
ho
AT
(BH)
BH
V
2o
miina 00me.(B
APe APat10/min
ler APatt 120/mmn
en.TeSTdspt
~
~ ~
~
toie(
~
r
{
-v
148
--46
A
waftgi
\ 'r
.
k
-1
-'
A A 1330
13801
'
~~~~~~B1
g dinsee nrvnul
for400me.(Bgtoiea2m)amiitrdintravkenouly
2 mmn was
prolonged (3450 msec).
Circulation, Volume XLV, January 1972
SINUS-NODE RECOVERY TIME
Downloaded from http://circ.ahajournals.org/ by guest on September 30, 2016
periods of asystole. In no case was the escape
of an ectopic atrial pacemaker seen. Concerning man, no control data are available to
indicate the normal escape interval of lower or
subsidiary pacemakers following suppression
by AP. Animal studies performed after crushing of the sinus node have suggested a greater
depression or longer recovery time of the A-V
junctional pacemakers than the sinus node.10
These findings cannot necessarily be applied
to man. The long periods of asystole without
the escape of lower pacemakers leads us,
however, to believe that the automatic capacity of these subsidiary pacemakers (especially A-V junctional) is also compromised in the
patients with abnormal sinus response or
prolonged SRT. In some of these cases when
SRT was reevaluated after atropine, junctional
pacemakers were the first to appear and were
followed subsequently by sinus rhythm.
Patient 38 (fig. 8) with SB when initially
studied showed markedly prolonged SRT. Because of the history of syncope, a permanent
pervenous demand pacemaker was implanted.
Seven and a half months later, a follow-up
study showed similarly prolonged SRT. Another patient, case 18 (fig. 9), showed
identical SRT with AP (at 100/min for 2 min)
and following termination of spontaneous
atrial tachycardia (280/min for 5 min). The
above findings demonstrate the reproducibility of SRT and support the clinical use of AP
for evaluation of sinus-node function. To test
the sinus-node function, we recommend that
the AP be initially used only at one level
(120/min for 2 min ). Demonstration of a
normal SRT would eliminate the need for a
second level since the SRT in patients with
normal sinus node is independent of rate and
duration of AP. However, if an abnormal SRT
is recorded with a single level, a second higher
level of AP showing further prolongation of
SRT may be employed as comfirmation.
Interpolated Beats
The phenomenon of interpolated beats has
been reported clinically.27 This was observed
in seven patients during our study (fig. 10).
The interpolated beats indicate the inability
of the PABs at that level of prematurity to
Circulation, Volume XLV, January 1972
155
depolarize the sinus pacemaker. The absence
of sinus-node depression may be the result of
(1) unidirectional conduction block from the
RA to SN because of the refractoriness of the
tissue at the periphery of the sinus node28 or
(2) the penetration of the premature impulse
into the sinus node during the absolutely
refractory period of the sinus pacemaker cells.
In these patients, atrial depolarization with a
further increase in prematurity of the PABs,
beyond that for interpolated PABs, indicates a
shorter refractory period for the right atrial
muscle than the sinus node or perinodal sinus
tissue.28 Previous studies from this laboratory
have demonstrated the presence of independent unidirectional blocks in conducting
tissues, that is, A-V node or His-Purkinje
system.29 30 Therefore, the demonstration of
interpolated beats and the presence of unidirectional block during conduction from RA
to SN does not permit the prediction of the
conduction capabilities from SN to RA, that is,
sinoatrial block. In addition, many patients
whose ECG pictures were compatible with
the diagnosis of sinus arrest or SA block did
not demonstrate this phenomenon of interpolated PABs. All the seven patients who
manifested interpolated PABs had normal
heart rates and a normal SRT during AP.
References
1. FERRER MI: Sick sinus syndrome in atrial disease.
JAMA 206: 645, 1968
2. BIRCHFIELD RI, MENEFEE EE, BRYANT GDM:
Disease of the sinoatrial node associated with
bradyeardia, asystole, syncope and with paroxysmal atrial fibrillation. Circulation 16: 20,
1957
3. FowLE NO, FENTON JC, CONWAY GF: Syncope
and cerebral dysfunction caused by bradyeardia without atrioventricular block. Amer Heart
J 80: 303, 1970
4. RAMUSSEN K: Chronic sino-atrial heart block.
Amer Heart J 81: 38, 1971
5. SILVERMAN LF, MANKIN HT, MCGOON DC:
Surgical treatment of an inadequate sinus
mechanism by implantation of a right atrial
pacemaker electrode. J Thorac Cardiovasc
Surg 55: 264, 1968
6. CLARKE M, EVANS DW, MILSTEIN BB: Sinus
bradyeardia treated by long term atrial pacing.
Brit Heart J 32: 458, 1970
7. EYSTER JAE, MEEK WJ: Cardiac irregularities in
NARULA ET AL.
156
_ A
A
A
A
Pacing 100/=3in
~~~~~~~~~A
A (RA)
r
AA 820
820
msec
805
BE (RA)~~~~~~~~~~~~~~~~~~~~~~~~~
(RA)
_
[-1 X: ;/7,
Downloaded from http://circ.ahajournals.org/ by guest on September 30, 2016
MElk,
686165
-rrrrrrrr r
r,
>!
ts,-i1A
/A'
A ,<,
3/2/71
3
8/25/70
3/2/71
ilk;igi
'I
BE
1X
!+
1
+
I
W'
A'
~
(RA)
A-A 215msec
J-RAS
BE
1
(RA)
400/min
k.~ 'lA
A;-/ RJ^;v- ~ys U; 2^-A
y
\A
215 msec
LA~~~~~~~~~~~~~~~~~~~~~~P
10 sec
~~~1A~~~~
i
BE
C
250
M,
Elk.,
#86165
190
190
215
Al~A
:340
A-A 1220 msec
1040
1010
1136
312/71
Figure 9
(Upper panel A to C) Case 18: Patient with paroxysmal supraventricular tachycardias and
a permanent ventricular demand pacemaker (QRS blocking). Simultaneous recordings of BE
from the right atrium (RA) and ECG lead L-1 during NSR show SRT of 1170 msec (C)
after AP at 100/min for 2 fin. Chest wall stimuli (CWS) are applied at the cessation of AP
to block the escape of the demand ventricular pacemaker.
(Lower panel) Rhythm strip (L-1) recorded from the same patient (case 18) prior to the
implantation of the permanent pacemaker (8/25/70) shows spontaneous onset and cessation of
Circulation, Volume XLV, January 1972
A1
SINUS-NODE RECOVERY TIME
157
Al
BE
208
K
A2
Al
J
A-A 810
!
ms
iRAi
30
A3
A
1090
P
820
A
BH V
I
I
B>E
Aw~~
ClV F
0l
v
-'----v
I_
_
_
_
_
_
__
_
_
_
_
_
jAl I
Al
A-A 830 ms
825
820
430
PI
jA3
A2
A
1
390
800
820
Downloaded from http://circ.ahajournals.org/ by guest on September 30, 2016
(RA)
B E- 'fI_
(BH)
I
n
L1
,_
OVF~~~
H G-
r
w
aV1- - - _ ___-~ ~ ~ ~ ~'
v
W
w
1153
133982 12 29 70
Figure 10
Case 16: Interpolated premature atrial beat. (A) Simultaneous recordings of BE(RA), BE(BH),
and three ECG leads (L-1, aVF, and V1). The premature atrial beat is followed by an expected
partially compensatory pause (A2A3) of 1090 msec. (B) The induced (PI) PAB is interpolated
and is not followed by any compensatory pause. The sum of A1A2 (430 msec) and A2A3 (390
msec) intervals is equal to the sinus cycle length (820 msec). The atrial beat following the
PAB is sinus in origin as indicated by the normal sequence of atrial activation from high
right atrium [BE(RA)] to the region of the A-V junction [BE(BH)] and the shape of the P
waves. At this coupling interval some beats were interpolated and some followed by a compensatory pause as in panel A.
morphine poisoning in the dog. Heart 4: 59,
1912
8. CUSHNEY AR: The irregularity of the mammalian
heart observed under aconite and an electrical
stimulation. Heart 1: 1-22, 1910
9. GASKELL WH: On the innervation of the heart
with special reference to the heart of tortoise: j
Physiol 4: 43, 1884
10. LANGE G: Action of driving stimuli
and extrinsic sources or in
pacemaker tissues. Circ Res 17:
11. PICK A, LANGENDoRF R, KATz LN:
from intrinsic
situ cardiac
449, 1965
Depression of
premature impulses.
Amer Heart J 41: 49, 1951
12. LISTER JW, COHEN LS, BERNSTEIN WH, SAMET
cardiac pacemakers by
SVT. (A) Again on 3/2/71 during the same study as in upper panel the patient spontaneously
developed atrial tachycardia (AT) with a cycle length (A-A) of 215 msec. (B and C) Five
minutes after the onset of AT, rapid atrial stimulation (RAS) was instituted at a rate of 400/min
for 10 sec. The cessation of RAS is followed by a normal sinus P wave with an SRT of
1220 msec which is essentially similar to that in the upper panel despite the spontaneous
origin of atrial tachycardia at a rapid rate (approximately 280/min) for longer duration as
opposed to AP at 100/min for 2 min only. At the cessation of AT, the demand ventricular
pacemaker escapes (VPI) simultaneously with the sinus P shown in BE(RA). This P and the
subsequent two P waves are not conducted because of a rate similar to that of the pacemaker
escape interval.
Circulation, Volume XLV, January 1972
NARULA ET AL.
158
P: Treatment of supraventricular tachycardias
by rapid atrial stimulation. Circulation 38:
1044, 1968
21.
13. MIANDEL W, HAYAKAWA H, DANZIG R, 'MARCUS
HS: Evaluation of sino-atrial node function in
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15.
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18.
19.
20.
man by overdrive suppression. Circullation 44:
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CUSHNEY AR: Stimulation of the isolated
ventricle, with special reference to the development of spontaneous rhythm. Heart 3: 257,
1911-1912
EcciiFs JC, HOFF HE: Rhythm of the heart beat;
2. Disturbance of rhythm produced by late
premature beats. Proc Roy Soc 115: 327,
1934
EYSTER JAE, MEEK WJ: Experiments on the
origin and conduction of the cardiac impulse.
Arch Intern Med (Chicago) 18: 775, 1916
BONKE FIM, BOU.MAN LN, VAN RIJN HE:
Change of cardiac rhythm in the rabbit after
an atrial premature beat. Circ Res 24: 533,
1969
HUTTER OF, TRAUT-WEIN W: Vagal and sympathetic effects on the pacemaker fibers of the
sinus venosus of the heart. J Gen Physiol 39:
715, 1956
WEST TC: Effects of chronotropic influences on
subthreshold oscillations in the sino-atrial node.
In Specialized Tissues of the Heart, edited by
A Paes de Carvalho, WC de Mello, BF
Hoffman. New York, Elsevier Publishing,
1961
VINCENzI FF, WEST C: Release of autonomic
mediators in cardiac tissue by direct subthresh-
22.
23.
24.
25.
26.
27.
28.
29.
30.
old electrical stimulation. J Pharmacol Exp
Ther 141: 185, 1963
GRODNER AS, LAHRTZ HG, POOL PE, BRAUNWALD
E: Neurotransmitter control of sino-atrial
pacemaker frequency in isolated rat atria and
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Circulation, Volunze XLV, January 1972
Significance of the Sinus-Node Recovery Time
ONKAR S. NARULA, PHILIP SAMET and ROGER P. JAVIER
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Circulation. 1972;45:140-158
doi: 10.1161/01.CIR.45.1.140
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