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Phasic pacemaker failure
J. ELECTROCARDIOLOGY, 6 (3)267-269, 1973
Phasic Pacemaker Failure BY G1NES SANZ, M.D.,* GLEN R. VAN LOON, M.D., Ph.D., F.R.C.P.(C) t AND LEONARD SCHWARTZ, M.D., F.R.C:P.(c).**
had no further episodes of dizziness or syncope. From October 12 to 15, 1971, he experienced three episodes of lightheadedness and was readmitted to hospital on October 15. The electrocardiogram revealed occasional non-captured pacemaker spikes. The P. A. and lateral chest xray confirmed that the electrode tip was in the apex of the right ventricle and pacemaker function was not altered by changes in position. It was noticed that the non-conducted artifacts followed the P waves with an almost constant P-spike interval, between 280 and 320 msecs. (Fig. 1 and 2). The patient was monitored and during the first five hours 301 non-captured spikes were observed always at the same interval after the P wave. When the pacemaker spike did not bear this relationship to atrial depolarization, consistent pacemaker capture was present. Also, occasional pacemaker artifacts following the P wave by 280 to 320 msecs did capture the ventricle. After the fifth hour the number of non-captured artifacts suddenly increased and non-captured spikes not related to P waves occurred quite frequently. On October 19, 1971, the patient was taken to the Operating Room and the pacemaker voltage threshold was found to be 5.0 mA. The pacemaker electrode was removed and inspection of the electrode revealed that it had been severed completely, immediately adjacent to its connection to the battery. A new unipolar electrode was inserted and the threshold tested at .6 mA. The new electrode was connected to the original battery pack. For the remainder of the admission there was consistent pacemaker capture. No further evidence of pacemaker failure has been detected in a twelve month follow-up.
SUMMARY A case of pacemaker failure in relation to atrial depolarization is presented. The possible mechanisms of this rather unusual phenomenon are discussed. A transitory change in excitability threshold following atrial depolarization is the most likely explanation. Danzig 1 reported a case of phasic exit block of a functional pacemaker related to atrial depolarization which could best be explained by the phenomenon of Wedensky inhibition. This report describes a case of intermittent failure of a ventricular pacemaker apparently related to atrial depolarization. Wedensky inhibition offers a suitable explanation if complete atrio-ventricular block existed at the time of pacemaker failure. However, if atrio-ventricular block was not complete, then concealed conduction into the pacemaker parasystolic focus represents a valid alternate explanation. CASE
REPORT
An 84-year-old man was admitted to the Toronto General Hospital on August 31, 1971, with a history of recurrent syncope. The electrocardiogram showed complete atrio-ventricular block with no supraventricular capture. The QRS complexes were wide (0.14 sees) and the idioventricular rate was 33/min. A permanent transvenous Stanicor Cordis pacemaker was inserted via a cephalic vein. The threshold was found to be 1.2 mA. He was discharged on September 10, 1971, and for the next four and a half weeks he was well and
DISCUSSION From: Cardiovascular Unit and Department of Medicine, Toronto General Hospital, Toronto, Ontario. *Fellow in Cardiology, Toronto General Hospital. *Assistant Professor, University of Toronto, Staff Phy sician, Toronto General Hospital. **Associate in Medicine, 'University of Toronto, Staff Physician, Toronto General Hospital. Reprint requests to: Dr. Leonard Schwartz, Toronto General Hospital, 101 College Street, Toronto 101, Ontario, Canada.
During the initial five hours of monitoring following pacemaker failure this patient demonstrated a constant relationship between the noncaptured pacemaker spikes and the preceding P waves. The 301 noncaptured artifacts followed the P wave by 280 to 320 msecs. The 40 msecs interval represents less than 5% of the duration of this patient's cardiac cycle and suggests that this was not a random phenomenon. There are three 267
268
S A N Z ET A L
,~
,/1
li r
/ L
2
/
aVL
i
/
/
i
aVF -~ ~ z - ~ . _ r
/
/
/
Fig. 1. Leads 1, 2, AVL, AVF and V6 of the surface electrocardiogram, showing pacemaker rhythm and occasional noncaptured spikes (indicated by arrows) followingthe P waves by a 280-320 msec interval.
L2
Fig. 2. Continuous monitor recording (lead 2, paper speed 10 mm/sec). The arrows show the non-captured spikes. possible explanations which could account for the relationship between P waves and noncaptured artifacts :l 1. Movement of the pacemaker electrode by atrial contraction displacing the pacemaker tip from the ventricular wall resulting in phasic pacemaker failure; 2. Decremental conduction of the atrial electrical impulse through the conduction system and
depolarization of the ventricular tissue around the pacemaker electrode but without propagation to the remainder of the ventricle; 3. A decrease in the right ventricular excitability threshold following atrial depolarization, in the presence of complete atrio-ventricular block, with the pacemaker stimulus becoming temporarily subthreshold (i.e. true Wedensky inhibition). J. ELECTROCARDIOLOGY, VOL. 6, NO. 3, 1973
PHASIC PACEMAKER FAILURE
Pacemaker movement resulting from atrial contraction is an unlikely explanation for the events of this case. It has been established that atrial contraction begins 65 msec after the onset of the P wave. 2 One would expect noncaptured pacemaker artifacts to occur during or immediately following atrial contraction, that is, between 65 and approximately 200 msecs after the onset of the P wave. In the present case, during the period of partial pacemaker failure, pacemaker spikes occurring at this interval after the P wave consistently captured the ventricle. Only pacemaker spikes occurring at a longer interval from the P wave (280-320 msecs) were noncaptured and from the above discussion the mechanical aspects of atrial contraction would not be expected to effect these spikes. Decremental conduction has previously been invoked by Preston 3 to account for cases of atrial induced pacemaker failure. Obviously, for this mechanism to be operative, some degree of atrioventricular conduction must be present at the time of pacemaker failure. At no time during the monitoring of this patient was there any atrioventricular capture. However, atrio-ventricular capture only signifies atrial impulses which have reached the ventricle in above threshold strength. Subthreshold stimuli might penetrate the A-V conducting tissue, depolarize the myocardium around the pacemaker tip and render it temporarily refractory to the artificial pacemaker stimulus. In such cases, pacemaker capture would fail to occur. The P-pacemaker artifact interval of 280-320 msecs is consistent with this mechanism. With P-artifact intervals of less than 280 msecs, the artificial pacemaker stimulus would precede the arrival of the atrial impulse and, therefore, pacemaker capture occurred. Presumably, in instances when the P-artifact interval exceeded 320 msec, the myocardial refractoriness produced by the conducted atrial impulse had dissipated and the myocardium was again excitable. If, however, at the time of phasic pacemaker failure absolutely no atrio-ventricular conduction was present, then decremental conduction is not a plausible explanation and it is necessary to invoke a mechanism that would be operative in the presence of total atrio-ventricular block. In 1903, Wedensky,4 using a nerve-muscle preparation in which he had produced a zone of total conduction block, demonstrated that electrical impulses arriving at this blocked zone could change the excitability of the nerve beyond the block. Usually, excitability was enhanced and a subthreshold stimulus became threshold (Wedensky facilitation). However, decreased excitability might occur and in such a case the threshold J. ELECTROCARDIOLOGY,VOL. 6, NO. 3, 1973
269
stimulus became temporarily subthreshold (Wedensky inhibition). Wedensky inhibition offers a possible explanation for the sequence of events in this case. For the first five weeks after its insertion the pacemaker functioned adequately. Then, the electrode partially broke adjacent to its connection to the battery. As a result, the unit developed a high resistance and delivered a low intensity impulse which was usually threshold but became subthreshold during the excitability changes following the P wave (Wedensky inhibition). The pacemaker dysfunction was phasic and the heart rate, except rarely, did not slow significantly. The episodes of dizziness prior to admission were likely due to transitory changes in excitability resulting in a greater number of subthreshold stimuli. The interval between the P wave and the following nonconducted pacemaker artifact was within the limits previously published for the Wedensky phenomenon? Finally, the pacemaker electrode severed completely and total nonphasic pacemaker failure occurred. Therefore, two possible mechanisms exist to explain the atrial related phasic pacemaker failure in this case. Without more sophisticated studies of atrio-ventricular conduction, it is not possible to determine which is the more likely mechanism in this patient. However, in either case pacemaker failure was ultimately due to either high resistance in the electrode or low battery output and not to malposition of the pacemaker tip. Therefore, the management of a case of phasic pacemaker failure when the nonconducted pacemaker spikes follow the preceding P wave by a certain critical time interval should be directed toward testing and appropriately correcting one of the former two possibilities.
REFERENCES 1. Danzig, R., and Diamond, G.: Increase in threshold to ventricular activation related to atrial contrac tion. Am. Heart J. 82: 531, 1971. 2. Braunwald, E., Fishman, A. P., and Cournand, A.: Time relationship of dynamic events in the cardiac chambers, pulmonary artery and aorta in man. Circ. Res. 4: 00, 1956. 3. Preston, T. A.: Atrial phasic inhibition of implanted cardiac pacemakers. Circulation 28: VI-158, 1968. 4. Wedensky, N. E.: Die erregung, hemmung undo narcose. Pfluger. Arch. Ges. Physiol. 100: 1, 1903. 5. Fisch, C., and Greenspan, K.: Editorial - - Wedensky observations. Circulation 35: 819, 1967.
Phasic Pacemaker Failure BY G1NES SANZ, M.D.,* GLEN R. VAN LOON, M.D., Ph.D., F.R.C.P.(C) t AND LEONARD SCHWARTZ, M.D., F.R.C:P.(c).**
had no further episodes of dizziness or syncope. From October 12 to 15, 1971, he experienced three episodes of lightheadedness and was readmitted to hospital on October 15. The electrocardiogram revealed occasional non-captured pacemaker spikes. The P. A. and lateral chest xray confirmed that the electrode tip was in the apex of the right ventricle and pacemaker function was not altered by changes in position. It was noticed that the non-conducted artifacts followed the P waves with an almost constant P-spike interval, between 280 and 320 msecs. (Fig. 1 and 2). The patient was monitored and during the first five hours 301 non-captured spikes were observed always at the same interval after the P wave. When the pacemaker spike did not bear this relationship to atrial depolarization, consistent pacemaker capture was present. Also, occasional pacemaker artifacts following the P wave by 280 to 320 msecs did capture the ventricle. After the fifth hour the number of non-captured artifacts suddenly increased and non-captured spikes not related to P waves occurred quite frequently. On October 19, 1971, the patient was taken to the Operating Room and the pacemaker voltage threshold was found to be 5.0 mA. The pacemaker electrode was removed and inspection of the electrode revealed that it had been severed completely, immediately adjacent to its connection to the battery. A new unipolar electrode was inserted and the threshold tested at .6 mA. The new electrode was connected to the original battery pack. For the remainder of the admission there was consistent pacemaker capture. No further evidence of pacemaker failure has been detected in a twelve month follow-up.
SUMMARY A case of pacemaker failure in relation to atrial depolarization is presented. The possible mechanisms of this rather unusual phenomenon are discussed. A transitory change in excitability threshold following atrial depolarization is the most likely explanation. Danzig 1 reported a case of phasic exit block of a functional pacemaker related to atrial depolarization which could best be explained by the phenomenon of Wedensky inhibition. This report describes a case of intermittent failure of a ventricular pacemaker apparently related to atrial depolarization. Wedensky inhibition offers a suitable explanation if complete atrio-ventricular block existed at the time of pacemaker failure. However, if atrio-ventricular block was not complete, then concealed conduction into the pacemaker parasystolic focus represents a valid alternate explanation. CASE
REPORT
An 84-year-old man was admitted to the Toronto General Hospital on August 31, 1971, with a history of recurrent syncope. The electrocardiogram showed complete atrio-ventricular block with no supraventricular capture. The QRS complexes were wide (0.14 sees) and the idioventricular rate was 33/min. A permanent transvenous Stanicor Cordis pacemaker was inserted via a cephalic vein. The threshold was found to be 1.2 mA. He was discharged on September 10, 1971, and for the next four and a half weeks he was well and
DISCUSSION From: Cardiovascular Unit and Department of Medicine, Toronto General Hospital, Toronto, Ontario. *Fellow in Cardiology, Toronto General Hospital. *Assistant Professor, University of Toronto, Staff Phy sician, Toronto General Hospital. **Associate in Medicine, 'University of Toronto, Staff Physician, Toronto General Hospital. Reprint requests to: Dr. Leonard Schwartz, Toronto General Hospital, 101 College Street, Toronto 101, Ontario, Canada.
During the initial five hours of monitoring following pacemaker failure this patient demonstrated a constant relationship between the noncaptured pacemaker spikes and the preceding P waves. The 301 noncaptured artifacts followed the P wave by 280 to 320 msecs. The 40 msecs interval represents less than 5% of the duration of this patient's cardiac cycle and suggests that this was not a random phenomenon. There are three 267
268
S A N Z ET A L
,~
,/1
li r
/ L
2
/
aVL
i
/
/
i
aVF -~ ~ z - ~ . _ r
/
/
/
Fig. 1. Leads 1, 2, AVL, AVF and V6 of the surface electrocardiogram, showing pacemaker rhythm and occasional noncaptured spikes (indicated by arrows) followingthe P waves by a 280-320 msec interval.
L2
Fig. 2. Continuous monitor recording (lead 2, paper speed 10 mm/sec). The arrows show the non-captured spikes. possible explanations which could account for the relationship between P waves and noncaptured artifacts :l 1. Movement of the pacemaker electrode by atrial contraction displacing the pacemaker tip from the ventricular wall resulting in phasic pacemaker failure; 2. Decremental conduction of the atrial electrical impulse through the conduction system and
depolarization of the ventricular tissue around the pacemaker electrode but without propagation to the remainder of the ventricle; 3. A decrease in the right ventricular excitability threshold following atrial depolarization, in the presence of complete atrio-ventricular block, with the pacemaker stimulus becoming temporarily subthreshold (i.e. true Wedensky inhibition). J. ELECTROCARDIOLOGY, VOL. 6, NO. 3, 1973
PHASIC PACEMAKER FAILURE
Pacemaker movement resulting from atrial contraction is an unlikely explanation for the events of this case. It has been established that atrial contraction begins 65 msec after the onset of the P wave. 2 One would expect noncaptured pacemaker artifacts to occur during or immediately following atrial contraction, that is, between 65 and approximately 200 msecs after the onset of the P wave. In the present case, during the period of partial pacemaker failure, pacemaker spikes occurring at this interval after the P wave consistently captured the ventricle. Only pacemaker spikes occurring at a longer interval from the P wave (280-320 msecs) were noncaptured and from the above discussion the mechanical aspects of atrial contraction would not be expected to effect these spikes. Decremental conduction has previously been invoked by Preston 3 to account for cases of atrial induced pacemaker failure. Obviously, for this mechanism to be operative, some degree of atrioventricular conduction must be present at the time of pacemaker failure. At no time during the monitoring of this patient was there any atrioventricular capture. However, atrio-ventricular capture only signifies atrial impulses which have reached the ventricle in above threshold strength. Subthreshold stimuli might penetrate the A-V conducting tissue, depolarize the myocardium around the pacemaker tip and render it temporarily refractory to the artificial pacemaker stimulus. In such cases, pacemaker capture would fail to occur. The P-pacemaker artifact interval of 280-320 msecs is consistent with this mechanism. With P-artifact intervals of less than 280 msecs, the artificial pacemaker stimulus would precede the arrival of the atrial impulse and, therefore, pacemaker capture occurred. Presumably, in instances when the P-artifact interval exceeded 320 msec, the myocardial refractoriness produced by the conducted atrial impulse had dissipated and the myocardium was again excitable. If, however, at the time of phasic pacemaker failure absolutely no atrio-ventricular conduction was present, then decremental conduction is not a plausible explanation and it is necessary to invoke a mechanism that would be operative in the presence of total atrio-ventricular block. In 1903, Wedensky,4 using a nerve-muscle preparation in which he had produced a zone of total conduction block, demonstrated that electrical impulses arriving at this blocked zone could change the excitability of the nerve beyond the block. Usually, excitability was enhanced and a subthreshold stimulus became threshold (Wedensky facilitation). However, decreased excitability might occur and in such a case the threshold J. ELECTROCARDIOLOGY,VOL. 6, NO. 3, 1973
269
stimulus became temporarily subthreshold (Wedensky inhibition). Wedensky inhibition offers a possible explanation for the sequence of events in this case. For the first five weeks after its insertion the pacemaker functioned adequately. Then, the electrode partially broke adjacent to its connection to the battery. As a result, the unit developed a high resistance and delivered a low intensity impulse which was usually threshold but became subthreshold during the excitability changes following the P wave (Wedensky inhibition). The pacemaker dysfunction was phasic and the heart rate, except rarely, did not slow significantly. The episodes of dizziness prior to admission were likely due to transitory changes in excitability resulting in a greater number of subthreshold stimuli. The interval between the P wave and the following nonconducted pacemaker artifact was within the limits previously published for the Wedensky phenomenon? Finally, the pacemaker electrode severed completely and total nonphasic pacemaker failure occurred. Therefore, two possible mechanisms exist to explain the atrial related phasic pacemaker failure in this case. Without more sophisticated studies of atrio-ventricular conduction, it is not possible to determine which is the more likely mechanism in this patient. However, in either case pacemaker failure was ultimately due to either high resistance in the electrode or low battery output and not to malposition of the pacemaker tip. Therefore, the management of a case of phasic pacemaker failure when the nonconducted pacemaker spikes follow the preceding P wave by a certain critical time interval should be directed toward testing and appropriately correcting one of the former two possibilities.
REFERENCES 1. Danzig, R., and Diamond, G.: Increase in threshold to ventricular activation related to atrial contrac tion. Am. Heart J. 82: 531, 1971. 2. Braunwald, E., Fishman, A. P., and Cournand, A.: Time relationship of dynamic events in the cardiac chambers, pulmonary artery and aorta in man. Circ. Res. 4: 00, 1956. 3. Preston, T. A.: Atrial phasic inhibition of implanted cardiac pacemakers. Circulation 28: VI-158, 1968. 4. Wedensky, N. E.: Die erregung, hemmung undo narcose. Pfluger. Arch. Ges. Physiol. 100: 1, 1903. 5. Fisch, C., and Greenspan, K.: Editorial - - Wedensky observations. Circulation 35: 819, 1967.