CASE REPORTS
Inhibition of Bipolar Demand Pacemaker
by Diaphragmatic Myopotentials
S. SERGE BAROLD, M.B., LING S. ONG, M.D., MICHAEL D. FALKOFF, M.D.,
AND ROBERT A. HEINLE, M.D.
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SUMMARY This report describes inhibition of a normally functioning bipolar demand pulse generator by diaphragmatic myopotentials. Transient pacemaker suppression occurred repeatedly with
deep respiration, straining, the Valsalva maneuver, coughing, sneezing and laughing. When the magnet was applied, none of these
maneuvers inhibited the pacemaker. Extensive investigations ruled
out an intermittent electrode problem such as a wire fracture or insulation break.
Sensing of diaphragmatic myopotentials should be considered in
the differential diagnosis of unexplained pacemaker pauses.
INHIBITION OF DEMAND PACEMAKERS by
musculoskeletal potentials has been reported to occur only
with unipolar pacing systems.1 14 Mymin et al.,2 however,
described one case of apparent suppression of a bipolar unit
by myopotentials but gave no details about the mechanism
of interference. Peter et al.", recently described transient
inhibition of a unipolar demand pacemaker during deep
respiration and suggested, without direct -proof, that the
pacemaker was suppressed by myopotentials associated with
respiration.
We describe in this report transient inhibition of a bipolar
demand pacemaker by diaphragmatic myopotentials. This
unusual type of interference became apparent only with active contraction of the diaphragm such as deep respiration,
straining, Valsalva maneuver, coughing, sneezing, and
laughing.
paced (delivery) refractory period of the generator, suggesting partial recycling from a signal of marginal amplitude for
sensing." Chest X-ray revealed good electrode position and
no evidence of perforation. We considered the abnormality
benign and indeed the patient became asymptomatic and
returned to work.
For several years on regular follow-up visits, the ECG
continued to show conducted sinus rhythm with right bundle
branch block and left anterior hemiblock so that evaluation
of pacemaker function necessitated application of the
magnet. We electively replaced the pulse generator on
4/26/73. The chronic threshold for bipolar pacing was 3.5
mA measured with an external 5880A Medtronic pulse generator. The unipolar ventricular electrogram displayed normal intracavitary morphology and neither the unipolar
(from tip and proximal electrodes) nor bipolar electrograms
registered the artifacts commonly seen with an intermittent
wire fracture;'7 the amplitude of the P wave was less than
0.25 mV. A new Medtronic demand pulse generator (Model
5842) was implanted. Ventricular capture occurred only
after application of the magnet.
A 24-hour Holter recording in January 1975 revealed normal pacing and sensing, except for a single pause considered to represent T wave sensing. We failed to detect
further irregularity until 5/2/75 several months after the
start of transtelephone monitoring. The patient now
appeared to be pacemaker dependent and the SS interval
occasionally lengthened to less than two automatic intervals. Application of the magnet again resulted in consistently regular SS intervals. The patient remained well and
was followed at weekly intervals over the telephone. We
finally rejected the diagnosis of T-wave sensing in January
1977 when the SS interval lengthened to more than twice the
automatic interval. The patient returned for evaluation and
a long ECG showed normal pacing during spontaneous
respiration. The automatic interval was unchanged. There
was no pacemaker sound or twitching of the diaphragm or
intercostal muscles. Deep inspiration unmasked the abnormality and caused irregular and occasionally prolonged inhibition of the pacemaker. Transient suppression was consistently reproducible with deep respiration, straining, the
Valsalva maneuver, coughing, sneezing, and laughing (figs.
2, 3). Inhibition occurred both in the supine and sitting posi-
Case Report
A 61-year-old male was admitted to the Genesee Hospital on 11/6/70 with recurrent syncope and dizziness for
several months. The electrocardiogram (ECG) showed normal sinus rhythm, left anterior hemiblock, and complete
right bundle branch block. Continuous monitoring revealed
Mobitz type II atrioventricular (A-V) block soon complicated by prolonged asystole with a Stokes-Adams attack
only a few hours after admission. A permanent transvenous
pacemaker was implanted using a Medtronic demand pulse
generator (model 5842) and a 5818 bipolar electrode. The
threshold for bipolar pacing was 0.7 mA measured with an
external 5840 Medtronic pulse generator. Over the next
three days the ECG showed occasional prolongation of the
spike to spike (SS) interval to less than 2 automatic intervals (fig. 1). We interpreted these pauses as either sensing of
the T-wave or voltage afterpotential (or both) because application of the magnet over the pulse generator consistently
restored regular pacing."6 Some of the prolonged SS intervals were less than the sum of the automatic interval and the
From the Division of Cardiology, Department of Medicine, The Genesee
Hospital and University of Rochester School of Medicine and Dentistry,
Rochester, New York.
Address for reprints: Dr. S. Serge Barold, The Genesee Hospital, 224 Alexander Street, Rochester, New York 14607.
Received March 21, 1977; revision accepted May 20, 1977.
679
VOL 56, No 4, OCTOBER 1977
CIRCULATION
680
A
FIGURE 1. Electrocardiograms recorded two
days after implantation of pulse generator in
1970. A and B) The pacemaker appears to recycle
from a signal related to the T wave. C) The SS interval lengthens by only 160 msec which is less
than the delivery (paced) refractory period of this
particular pulse generator (about 250 msec). This
suggests partial recycling from a marginal signal
for sensing (i.e., voltage near the sensitivity of the
pulse generator).
B
C
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tions. None of these maneuvers could inhibit the pacemaker
when the magnet was applied. Very long rhythm strips with
the magnet did not produce evidence of an intermittent wire
fracture because the spike did not change in size (in leads
usually unaffected by respiration) and the SS interval
remained normal and never doubled suddenly.'8 The magnet was then removed and the following tests were performed during spontaneous respiration; a) raising of the
arms;9, 20 b) bending and turning of the trunk; c) isometric
exercise techniques to produce musculoskeletal potentials
capable of suppressing unipolar demand pacemakers.", 813 The SS intervals remained normal during
all these procedures.
The size and direction of the pacemaker spikes in the 12lead paced ECG had not changed since 1970. The implanted
pulse generator was removed with the tentative diagnosis of
an intermittent wire fracture near the distal end of the pacing catheter. The permanent electrode was immediately connected to an external 5880A Medtronic pulse generator
because the patient was pacemaker dependent. Neither the
5880A Medtronic pulse generator nor an old 5840 model
(both on full demand sensitivity) could be inhibited by any of
the maneuvers that previously suppressed the implanted
pacemaker. These external pacemakers were tested both
during bipolar and unipolar pacing (the latter with the tip
and proximal electrodes in turn functioning as the cathode).
We measured the pacing thresholds with a model 209A
Cordis Pacer Systems Analyzer (PSA) delivering a 1 msec
constant voltage pulse. The results did not suggest a wire
fracture or insulation break (table 1). Bipolar and unipolar
pacing with a 10 volt constant voltage output did not stimulate the left hemidiaphragm. With the Cordis PSA unit connected to the permanent electrode, we repeated all the
maneuvers that had suppressed the implanted pacemaker.
These consistently inhibited the PSA unit during bipolar and
unipolar demand pacing, the latter with the tip as the
cathode (figs. 4, 5). There was no inhibition when the proximal electrode became the cathode. During some of the long
period of inhibition the special sensing light on the Cordis
PSA flashed several times indicating that more than one signal was being detected by the unit. Unipolar and bipolar
fixed rate pacing with the Cordis PSA unit showed no inhibition.
The ventricular electrograms of spontaneous beats could
not be recorded as there was no underlying rhythm. We,
therefore, recorded the voltage waveform from the two pacemaker terminals during demand pacing with the Cordis
PSA unit. The following arrangements were evaluated: 1)
bipolar pacing (fig. 4); 2) unipolar pacing with the tip as the
cathode (fig. 5); 3) unipolar pacing with the proximal electrode as the cathode. Very long recordings were obtained on
an Electronics for Medicine Recorder (filter settings: 1-500
Hz). Inhibition only occurred with 1) and 2) and the pacemaker waveform did not show the characteristic sudden
changes in voltage seen with an intermittent wire fracture.2"
Finally, the waveforms were recorded on a Hewlett-Packard
storage oscilloscope and then all the inhibiting maneuvers
were repeated during bipolar and unipolar demand pacing.
It then became evident that the inhibiting maneuvers created
electrical noise from musculoskeletal artifacts, some of
which were of sufficient amplitude to be sensed by the demand pacemaker (figs. 4, 5).
A maxilith bipolar pulse generator (Cardiac Pacemakers,
Inc.) with a lesser sensitivity (narrow band) was then connected to the permanent electrode. Before closing the pacemaker pocket, we repeated all the inhibiting maneuvers, and
the SS interval now remained absolutely constant. The
patient has continued to be completely asymptomatic.
Several Holter recordings taken over the next few weeks
with instructions to take deep breaths, cough, laugh, sneeze
intermittently, revealed regular pacing and sensing of ventricular extrasystoles without a single period of inhibition.
We tested the technical characteristics of the explanted
pulse generator with two commercially available pacemaker analyzers which revealed normal function according
TABLE 1. Threshold Measurements with Cordis Threshold
Analyzer (1 msec constant voltage pulse)
Pacing mode
Voltage
(volts)
Bipolar
at 5 volts
5
Threshold
2.2
Unipolar: Tip As Cathode
at 5 volts
a
Current
(mA)*
Inhibition
of Cordis
PSAt
during deep
Impedance respiration,
(ohms)
etc.
11.2
446
Yes
4.8
458
Yes
11.6
431
451
Yes
Yes
360
386
No
No
Threshold
2.8
6.2
Proximal
Electrode
as
Cathode
Unipolar:
at 5 volts
Threshold
3
1.7
13.9
4.4
*90 msec after onset of pulse.
tCordis Pacing System Analyzer. Sensitivity
in duration).
msec
1
mV (square
wave
45
PACEMAKER INHIBITION BY MYOPOTENTIALS/Barold et al.
681
A
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900
3420
900
900 1460 900
FIGURE 2. A) Prolonged inhibition of bipolar demand pacemaker during a maximal inspiratory effort. B) Temporary
inhibition during coughing (intervals in msec). Leads I, II and III were recorded simultaneously.
to specifications. A 209A Cordis Pacing System Analyzer
(PSA) revealed a sensitivity of 1.6 mV (using a rectangular
voltage pulse having a 45 msec duration and a rise time of
less than 2 msec). A Medtronic 5300 PSA revealed normal
sensing function (i.e., sensed R wave test signals: standard
4mV, 45 msec square wave signals).
Discussion
Prolongation of the pacemaker spike to spike (SS) interval during deep respiration and the various maneuvers de-
scribed in this report should always raise the suspicion of an
intermittent electrode problem (wire fracture or insulation
break) near the tip of the catheter inside the heart.'6 18, 21
The preoperative diagnosis of an intermittent electrode
problem was unlikely in our case because application of the
magnet did not produce ineffectual or attenuated pacemaker spikes and sudden doubling of the SS interval,'8
though the absence of these findings cannot positively rule
out the diagnosis. Indeed, an intermittent wire fracture may
occasionally present as a pure sensing problem if its timing
ljl e<:: ~1-: l--l: mWX
'I~~~~~~~M
'!
FIGURE 3. A ) Apparent T wave sensing during a moderately increased inspiratory effort. B) Slightly increased inspiratory effort causes partial recycling of the pulse generator suggesting sensing of a signal close to the sensitivity of the demand circuit. The delivery (paced) refractory period of this particular pulse generator is about 250 msec. Compare with
figure 1 (intervals in msec). Leads I. II, III were recorded simultaneously.
682
CIRCULATION
-
f
I seca-
Isec
-
VOL 56, No 4, OCTOBER 1977
I
2+m
FIGURE 4. Bipolar demand pacing. Storage os-
cilloscope recordings of the pacemaker waveform
directly from the two pacing terminals. Deep inspiration causes continuous noise with intermittent peaks as high as 2 m V causing inhibition seen
on the surface ECG.
2mv
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t
-Isec -
always allows the fractured ends to be in contact whenever
the pacemaker delivers its impulse.'6 18 In this situation,
momentary changes in resistance cause voltage changes
across the pacemaker terminals (false signals) with temporary inhibition22 and regular fixed rate pacing would
therefore occur with the magnet.
Measurements of electrode impedance may also be normal if there is electrical continuity whenever the pulse
generator fires. On this basis, we cannot agree with the conclusions of Peter et al.15 who felt that mere restoration of
regular pacing with the magnet ruled out an intermittent
wire fracture in their case of temporary inhibition of a unipolar demand pacemaker by myopotentials associated with
inspiration. Moreover, these workers did not confirm their
diagnosis by intracardiac recordings. We excluded an intermittent electrode problem in our case by recording the
magnified pacemaker waveform directly from the two pacing terminals simultaneously with the surface electrocardiogram. With an intermittent fracture, prolongation of the SS
interval would have coincided with sudden and large disruptions of the waveform characteristic of any transient electrode problem.2"
Mymin et al.2 described the apparent suppression of a
single bipolar pulse generator by muscle potentials presumably originating near the implantation site. The geometry of
the sensing electrode in a bipolar system makes this occurrence difficult to understand. A wire fracture or loose connection may also present with intermittent cessation of
f- I sec
I
2fv,41
1
FIGURE 5. Unipolar demand pacing (tip as
cathode). Storage oscilloscope recordings of the
pacemaker waveform directly from the two pac-
ing terminals. In bottom panel, during deep inspiration, there is continuous noise from
diaphragmatic myopotentials with peaks of about
2 m V causing pacemaker inhibition seen on the
surface ECG.
1b
2mv
-
sec
i
PACEMAKER INHIBITION BY
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pacing related to movement such as arm raising.1920 When
testing for muscle inhibition, if the baseline of the ECG becomes grossly blurred by artifacts, brief acceleration of the
spontaneous rhythm or the presence of ventricular extrasystoles may be invisible, and if sensed, the apparent pacemaker pause may be attributed to muscle inhibition
(pseudointerference).'2 Perhaps the case of Mymin et al.,2
with apparent suppression of a bipolar pulse generator, constitutes an example of pseudointerference or sensing of false
signals from a loose connection or wire fracture. In this
respect, an insulation leak close to skeletal muscle could
conceivably detect myopotentials and suppress a bipolar
pulse generator.'3' 20 We also ruled out an insulation problem in our case because the pacemaker spike did not change
in amplitude or direction over a period of seven years.23
The myopotential noise recorded in our patient was
similar to published recordings of skeletal muscle interfer3,7,24 25 The amplitude of the
ence of unipolar pacemakers.'
diaphragmatic myopotentials were variable and only those
above the sensitivity of the pulse generator could be sensed.
This explains why a pulse generator may respond to
myopotentials by inhibition rather than reversion to
asynchronous pacing, as it does with other types of more
uniform and continuous interference. Parker et al.26 demonstrated no sources of extracardiac voltage on the bipolar
ventricular electrogram of walking dogs with bipolar pacing
electrodes. These workers recorded only very small superimposed muscular signals (maximum 0.6 mV) in the unipolar ventricular electrogram. Pertinent to our observations,
these authors also observed one instance of nonmyocardial interference recorded on a bipolar ventricular electrode and this consisted of probable diaphragmatic
myopotentials of 0.8 mV during coughing with a corresponding 1.6 mV signal in the unipolar ventricular electrogram.26
The observations in our case clearly document inhibition
of a unipolar and bipolar demand pacing system by
diaphragmatic myopotentials. This type of interference
should be considered the differential diagnosis of unexplained pacemaker pauses.27
MYOPOTENTIALS/Barold et al.
makers by skeletal muscle potentials. JAMA 223: 527, 1973
3. Wirtzfeld A, Lampadius M, Schmuck L: The influence of muscle potentials on synchronized pacemakers. In Cardiac Pacing, Proceedings of the
4th International Symposium. Van Gorcum, Assen 1973, p 169
4. Schulten HK, Baldus 0, R6hrig FR, Smekal PV, Behrenbeck D, Hilger
HH: St6rbeeinflussung von implantiecten Herschrittmachern durch Elekund durch Muskelimpulse. Z Kardiologie 62: 889, 1973
trogerate
5. Godin JF, Guiheneuc P, Neimann JD, Dodinot B: Blocage des stimulateurs sentinelles par les potentiels musculaires. Arch Mal Coeur 67: 1317,
1974
6. Gribbin B, Abson CP, Clarke LM: Inhibition of external demand pacemakers during muscular activity. Br Heart J 36: 1210, 1974
von Herz7.Irnich W, de Bakker JMT, Bisping HJ:
schrittmachern.
Gegenmassnahmen. Biomedizinische Technik 19: 193, 1974
8. Ohm OJ, Bruland H, PedorsenOM, Woerness E: Interference effect of
myopotentials on function of unipolar demand pacemakers. Br HeartJ
36: 77, 1974
9. PauletJ, Courgeon P, Kerdiles Y, Pony PC, GouffaultJ: Leurre des
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10. Piller LW, Kennelly BM: Myopotentials inhibition of demand pacemakers. Chest 66: 418, 1974
Il. Smyth NPD, Alferness C, Shearon L, Rockland RH, Keshishian JM,
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S S Barold, L S Ong, M D Falkoff and R A Heinle
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Circulation. 1977;56:679-683
doi: 10.1161/01.CIR.56.4.679
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