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Catheter-induced arrhythmias
Catheter-induced
arrhythmias
Panos C. Voukydis M.D., Ph.D Stafford I. Cohen, M.D. Boston, Mass.
It is frequently stated that intracardiac foreign bodies such as an electrode catheter, a central venous line, or a pulmonary artery catheter that migrates to the’ventricle may give genesis to arrhythmias.lB2 Such arrhythmias are difficult to treat if their origin is not promptly recognized The present report describes six cases of catheter-induced arrhythmias that occurred in the Medical Intensive-Care Unit of the Beth Israel Hospital during a period of eight months. Materials, techniques and clinical observations
During eight consecutive months, 72 flowdirected pulmonary artery catheters and 80 temporary transvenous ventricular pacemakers were introduced in 106 patients admitted to the Medical Intensive-Care Unit, The criterion for insertion of pulmonary artery catheters was acute myocardial infarction with unstable hemodynamics including cardiogenic shock and hypotension in patients with acute or chronic respiratory problems. The criteria for insertion of temporary ventricular pacemakers were as follows: complete heart block, second degree A-V block associated with Stokes-Adams attacks, new bifascicular or trifascicular block in the presence of an acute myocardial infarction, ventricular ectopic activity requiring ventricular overdrive suppression, and hypotension in conjunction with a very slow supraventricular rate. In addition, patients undergoing intra-aortic balloon counterpulsation routinely received a ventricular transvenous pacing electrode and a flow-directed pulmonary artery catheter. The flow-directed catheters were usually inserted via a cutdown to From the Department of Medicine, Medical School, Boston, Mass. Received
for publication
Reprint Brookline
requests: Dr. Ave., Boaton,
588
March
Beth
Israel
Hospital
and
Israel
Hospital,
Harvard
11, 1974.
P. C. Voukydis, Mass. 02215.
Beth
330
an arm vein and they were advanced to the pulmonary artery under pressure control or under fluoroscopic control. The temporary electrodes were usually inserted via the transfemoral route and were advanced to the right ventricular apex under fluoroscopic control. On a few occasions, an arm vein was used for insertion of the electrode. Introduction of a flow-directed catheter into the right ventricle was only rarely associated with ventricular ectopic activity. In contrast, introduction of the temporary electrode into the right ventricle was usually associated with ventricular ectopic activity in the form of ventricular ectopic beats or, rarely, short runs of ventricular tachycardia. In the latter event, the electrode was withdrawn to the right atrium and then repositioned. The electrode placement was considered to be satisfactory when threshold for stimulation was less than 1.5 ma. and there was no catheter-induced ventricular ectopic activity. Five patients with temporary pacemakers and one with a flow-directed pulmonary artery catheter developed ventricular ectopic activity within several hours to three days following the catheter placement. Case 1. A 43-year-old man was referred from another hospital for treatment of an extensive anterior myocardial infarction. Upon admission he was mildly hypotensive and his electrocardiogram (ECG) showed evidence for a new right bundle branch block and left posterior hemiblock that did not exist in the tracing submitted from the referring hospital. A flow-directed catheter was placed in the pulmonary artery and an electrode was advanced to the apex of the right ventricle and connected to a standby pacemaker. The mild hypotension was treated successfully with volume replacement. Two hours later, ventricular ectopic activity appeared which, within one hour, evolved into continuous bigeminy with nonfixed coupling (Fig. 1, A 1
November,
1974, Vol. 88, No. 5, pp. 588-592
Catheter-induced
prcur
arrhythmias
off
Fig. 1. Case 1. Pacing catheter-induced bigeminy in a 43-year-old man suffering from an acute myocardial in. farction. A; when the pacer is off every conducted beat is followed by an ectopic beat. The coupling interval varies continuously between 0.30 and 0.42 sec. The atria1 rate is 120. B; now the pacer is turned on at a rate of 111. The paced beats have a configuration very similar to the ectopic beats of strip A. Note the retrograde Pwave immediately after the peak of R.
Fig. 2. Case 3. Continuous strip, monitor lead. Catheter-induced ectopic activity and ventricular flutter-fibrillation. There are three types of beats. Beats a are probably of nodal origin. Beats b and c are interpolated bifocal ventricular ectopic beats. The ectopic activity degenerates into short runs of ventricular flutter-fibrillation three times. The electrode was removed from the ventricle while the bottom line of the strip was being taken. Note the atria1 ectopic beat following the first nodal beat after the last ventricular ectopic beat.
despite adequate treatment with lidocaine. A chest x-ray revealed that the intracardiac catheters had maintained their initial positions. Tntravenous procainamide was then administered. The patient received 1 Gm. of the drug during a two-hour period with no significant improvement. The pacemaker was then activated and a rhythm strip revealed that the paced beats had a configuration very similar to the ventricular ectopic beats. (Fig. 1, B 1. The threshold for stimulation had increased from 0.3 ma. to 0.5 ma. The diagnosis of catheter-induced arrhythmia was confirmed with cessation of ectopic activity when the electrode was withdrawn. Case 2. A 68-year-old retired physician was admitted for syncope. Physical examination revealed mild pulmonary edema. The ECG showed complete heart block with a nodal rhythm, rate 54, and signs of an acute inferior myocardial infarction. A flow-directed catheter
American
Heart Journal
was placed in the pulmonary artery and an electrode was placed in the right ventricle and connected to a demand pacemaker. Several hours later, ventricular ectopic activity appeared at a frequency of 10 to 15 beats per minute, which had a varying coupling interval and remained unresponsive to treatment. The pacemaker was then activated and the ventricles were continuously stimulated. The paced beats had the same configuration as the spontaneous ectopic beats. The diagnosis of catheter-induced arrhythmia was made. The electrode was repositioned with cessation of the ventricular ectopic activity. Case 3. A 73-year-old woman was admitted following a syncope spell. Her ECG revealed an idioventricular rhythm at a rate of 35. A ventricular electrode was inserted and connected to a demand pacemaker set to be inhibited by a rate above 50 per minute. On the third hospital
589
Voukydis
and Cohen
Fig. 3. Case 6. Continuous strip, Lead VI. Catheter-induced isorhythmic dissociation in a 67-year-old man with acute myocardial infarction and papillary muscle dysfunction. There are four kinds of beats. Beats a are wide (QRS = 0.16 sec.) and are always preceded by a P-wave and a P-R interval varying between 0.04 and 0.08 sec. Beats b have a completely different configuration and are not preceded by P-waves. Beats care always preceded by a P-wave and a P-R interval of 0.16 sec. Beats dare similar in configuration to beats a, but are not preceded by P-waves and appear to be interpolated between two a beats. The a beats cannot be the result of a repetitively firing ventricular ectopic focus, because the R-R interval varies widely. Fluoroscopy showed that the flowdirected catheter was displaced inside the right ventricle with a large loop in the right atrium. Every atrial contraction caused a forward thrust of the catheter. Thus it appears that the a beats were catheter-induced.
day, the pacemaker was not sensing properly and was turned off while a repositioning of the electrode was planned in the same day. A few hours later, ventricular ectopic activity was noted with coupling intervals varying between 0.44 and 0.52 sec. In spite of an infusion of lidocaine, the ectopic activity increased. There were salvos of 2 to 3 ventricular ectopic beats followed by three short runs of ventricular flutter which terminated spontaneously (Fig. 2). The pacing wire was withdrawn to the right atrium and all ectopic activity ceased. Case 4. A 66-year-old patient, in cardiogenic shock following an acute anterior myocardial infarction, was being treated with the intra-aortic balloon pump (IABP). As part of our established routine, he had placement of a flow-directed pulmonary artery catheter and a transvenous ventricular electrode. On the second day of counterpulsation, ventricular ectopic activity was noted at a rate of 10 to 12 ventricular ectopic beats per minute. The pacing threshold was found unchanged and the paced beats, although exhibiting a left bundle branch block pattern, had a distinctly different configuration from the ectopic beats. Lidocaine treatment was started and was ineffective. It was then noted that the ectopic beats occurred during deep inspiration. Fluoroscopy showed that the electrode formed an excessive loop inside the right ventricle during inspiration. The wire was withdrawn to the right atrium and the ectopic activity ceased. Case 5. A 54-year-old woman was admitted
590
with an acute inferior myocardial infarction. On the second hospital day she exhibited Mobitz Type II A-V block and a temporary transvenous pacemaker was inserted and placed on standby demand mode. Twelve hours later, the pacemaker started sensing erratically with resulting intermittent competition between the intrinsic rhythm and the pacemaker rhythm. When the pacer was turned off, it was noted that there were frequent ventricular ectopic beats with the same configuration as the paced beats. The diagnosis of catheter-induced arrhythmia was then considered. Repositioning of the pacing wire resulted in abolition of the ectopic activity and proper sensing. Case 6. A 67-year-old man was admitted for treatment of an acute myocardial infarction. Physical examination revealed a moderate degree of left ventricular failure and a new apical systolic murmur. A flow-directed catheter was placed into the pulmonary artery for monitoring of the “wedge” pressure. On the third hospital day, marked ventricular ectopic activity was noted which at times appeared to be an accelerated idioventricular rhythm with isorhythmic dissociation (Fig. 3). Therapeutic doses of lidocaine and procainamide failed to suppress the ectopic activity. It was then noted that the damped pressure tracing from the flow-directed catheter assumed a right ventricular pressure configuration after it was flushed. Fluoroscopy showed the tip of the catheter to be in the right ventricle and a large loop in the right atrium. Rv-
November,
1974, Vol. 88, No. 5
Catheter-indzwed
ery the cal the lar
atria1 contraction caused a forward thrust of catheter, which presumably caused mechanistimulation of the right ventricle. Removal of catheter resulted in cessation of the ventricuectopic activity.
Discussion
It is well-established that intraventricular catheters may cause ventricular ectopic activity or even ventricular tachycardia.‘, 2 This is illustrated dramatically by Case 3 of the present paper (Fig. 2). It is equally true, that an arrhythmia may occur independent of an intracardiac foreign body. Incorrect diagnosis of arrhythmia from an intraventricular catheter may lead to its unnecessary removal, thereby resulting in deprivation of a potentially lifesaving measure. It seems that establishing the basis for criteria that can help diagnose a catheter-induced arrhythmia might be of assistance to the staff of intensive-care units. Arrhythmias which are induced during catheter placement are very frequent. Paulk and Hurst4 had nine cases of ventricular fibrillation occur during pacemaker placement among 43 patients with complete heart block. Rutherford, McCann, and O’Donovar9 noted frequent ventricular ectopic beats and two cases of ventricular tachycardia during placement of polyethylene catheters in the pulmonary artery in a series of 28 patients. The use of flow-directed catheters, in contrast, is associated with lower incidence of ventricular ectopic activity.60ur experience with bedside flow-directed pulmonary artery catheterization is in agreement. It appears, however, that placement of the catheter under pressure guidance alone may result in excessive loops of catheter within the right ventricle or, more commonly, the right atrium. Our experience with placement of transvenous electrodes in the right ventricle under fluoroscopic control has indicated that uncomplicated ventricular ectopic activity can be expected during placement. Fortunately, the arrhythmias are only transient and we have not had to use electric shock to terminate an abnormal rhythm. The diagnosis of arrhythmias that are induced during catheter placement should be as obvious as the remedy. Our present series shows that the incidence of late catheter-induced arrhythmias is approximately 6 per cent. It appears, however, that this relatively high frequency is related to
American
Heart Journal
arrhythmias
temporary electrodes and pulmonary artery catheters. Permanent electrodes have not been reported to cause mechanically induced ventricular ectopic activity, despite the relatively high incidence of catheter dislodgement7 I1 The cases of catheter-induced arrhythmias herein presented illustrate the potential complexity of these arrhythmias. They also give a number of useful clues from which diagnostic principles can be constructed. In all cases, the arrhythmia developed following the placement of catheters, a fact which should arouse the suspicion of a catheterinduced arrhythmia. Another clue is ineffectiveness of anti-arrhythmics, especially when given in high doses. An additional aid to diagnosis is demonstration of displacement of the catheter from the initial position. If the catheter in question is a pacing wire, additional information can be obtained by noting ineffective sensing and an increase in pacing threshold. Erratic sensing and an increased threshold are probably due to a displacement of the catheter. It is also very useful to activate the pacemaker and compare the paced beats with the ectopic beats; if they are similar, the chances are that the ectopic beats are mechanically induced by the catheter. Another observation of the present series is the presence of widely varying coupling intervals. Cases 4 and 6 were unusual, the former showing ectopic activity only during inspiration, whereas the latter demonstrated a very complicated arrhythmia that could not be explained on the basis of known principles. Three cases similar to our Case 6 have been presented by Massumi and Ali. I2 The principles and criteria for diagnosis of catheter-induced arrhythmias can be summarized as follows: (1) the arrhythmia begins after a catheter has been placed m the right ventricle. The presence of dislodged catheters, excessive intracardiac loops of catheters, central displacement of central venous lines, or intracardiac fragments of polyethylene catheters should be sought by careful inspection of a chest x-ray taken after the arrhythmia has begun. (2) If the catheter in question is an electrode, usually there is a concomitant failure to sense properly and the threshold may increase. The paced beats usually look very much like the ectopic beats. (3) The ectopic beats have, in general, a left bundle branch block configuration. If they appear in the form of bigeminy, the coupling interval may vary widely. (4) High doses of anti-arrhythmic medications
591
Voukydis
and Cohen
may be ineffective. (5) Occasionally, the arrhythmias are complicated and hard to explain on the basis of established principles. (6) Finally, the ultimate test for diagnosis of a catheter-induced arrhythmia is cessation of the arrhythmia following removal or repositioning of the catheters. Summary
Catheter-induced arrhythmias, which occurred several hours to several days following successful placement of temporary transvenous right ventricular electrodes or flow-directed pulmonary artery catheters were observed in six out of 106 patients. The arrhythmias took the form of ventricular bigeminy, ventricular tachycardia and, in one instance, isorhythmic dissociation. These arrhythmias were resistant to high doses of antiarrhythmic medication. The diagnosis can be suspected by noticing an excessive catheter loop or an altered catheter position in the chest x-ray or by observing faulty sensing, erratic pacing, or an increased threshold for ventricular stimulation. Corroborative evidence can be obtained from the electrocardiogram, where the catheter-induced depolarizations usually take a left bundle branch block pattern and the coupling interval of the ectopic beats may vary widely. Some pacing catheter-induced beats resemble the paced beats in configuration. In other cases, the rhythm cannot be explained by established principles. The diagnosis of catheter-induced arrhythmia is confirmed when the arrhythmia ceases following removal or repositioning of the catheter.
592
REFERENCES
1. Lown, B., Temte, J. V., and Arter, W. J.: Ventricular tachyarrhythmias. Clinical aspects, Circulation 47: 1364,1973. 2. Lown, B., and Kosowsky, B. D.: Artificial cardiac pacemakers, N. Engl. J. Med. 383:1023, 1970. 3. Bloomfield, D. A.: Techniques of nonsurgical retrieval of iatrogenic foreign bodies from the heart, Am. J. Cardiol. 27~538, 1971. 4. Paulk, E. A., and Hurst, J. W.: Complete heart block in acute myocardial infarction. A clinical evaluation of the intracardiac bipolar catheter pacemaker, Am. J. Cardiol. 17:695, 1966. 5. Rutherford, B. D., McCann, W. D., and G’Donnovan, T. P. B.: The value of monitoring pulmonary artery pressure for early detection of left ventricular failure following myocardial infarction, Circulation 43:655, 1971. 6. Ganz, W. W., Forester, J. S., Chouette, D., et al.: A new flow-directed catheter technique for measurement of pulmonary artery and capillary wedge pressure without fluoroscopy, Am. J. Cardiol. 25:96, 1970. 7. Gonklin, E. F., Gregory, J., Grace, W. J., et al.: Use of the permanent transvenous pacemaker in 168 consecutive patients, AM. HEART J. 82:4,1971. 8. Legergren, H., Jobensson, L., Lendengren, J., et al.: One hundred cases of treatment for Adams-Stokes syndrome with permanent intravenous pacemaker, J. Thorac. Cardiovasc. Surg. 50:710, 1965. 9. Furman, S., and Escher, D. J. W.: Ventricular synchronous and demand pacing, AM. HEART J. 76:445, 1968. 10. Goldstein, S., Moss, A. J., Rivers, R. J., et al.: Transthoracic and transvenous pacemakers. A comparative clinical experience with 131 implantable units, Br. Heart J. 32:35, 1970. 11. Green, G. D., Forbes, W., Shaw, G. B., et al.: A four-year review of cardiac pacing in Glasgow: 181 Medtronic generators implanted in 127 patients, AM. HEART J. 83:265, 1972. 12. Massumi, R. D., and Ali, N.: Accelerated isorhythmic ventricular rhythms, Am. J. Cardiol. 28:170, 1970.
November, 1974, Vol. 88, No. 5
arrhythmias
Panos C. Voukydis M.D., Ph.D Stafford I. Cohen, M.D. Boston, Mass.
It is frequently stated that intracardiac foreign bodies such as an electrode catheter, a central venous line, or a pulmonary artery catheter that migrates to the’ventricle may give genesis to arrhythmias.lB2 Such arrhythmias are difficult to treat if their origin is not promptly recognized The present report describes six cases of catheter-induced arrhythmias that occurred in the Medical Intensive-Care Unit of the Beth Israel Hospital during a period of eight months. Materials, techniques and clinical observations
During eight consecutive months, 72 flowdirected pulmonary artery catheters and 80 temporary transvenous ventricular pacemakers were introduced in 106 patients admitted to the Medical Intensive-Care Unit, The criterion for insertion of pulmonary artery catheters was acute myocardial infarction with unstable hemodynamics including cardiogenic shock and hypotension in patients with acute or chronic respiratory problems. The criteria for insertion of temporary ventricular pacemakers were as follows: complete heart block, second degree A-V block associated with Stokes-Adams attacks, new bifascicular or trifascicular block in the presence of an acute myocardial infarction, ventricular ectopic activity requiring ventricular overdrive suppression, and hypotension in conjunction with a very slow supraventricular rate. In addition, patients undergoing intra-aortic balloon counterpulsation routinely received a ventricular transvenous pacing electrode and a flow-directed pulmonary artery catheter. The flow-directed catheters were usually inserted via a cutdown to From the Department of Medicine, Medical School, Boston, Mass. Received
for publication
Reprint Brookline
requests: Dr. Ave., Boaton,
588
March
Beth
Israel
Hospital
and
Israel
Hospital,
Harvard
11, 1974.
P. C. Voukydis, Mass. 02215.
Beth
330
an arm vein and they were advanced to the pulmonary artery under pressure control or under fluoroscopic control. The temporary electrodes were usually inserted via the transfemoral route and were advanced to the right ventricular apex under fluoroscopic control. On a few occasions, an arm vein was used for insertion of the electrode. Introduction of a flow-directed catheter into the right ventricle was only rarely associated with ventricular ectopic activity. In contrast, introduction of the temporary electrode into the right ventricle was usually associated with ventricular ectopic activity in the form of ventricular ectopic beats or, rarely, short runs of ventricular tachycardia. In the latter event, the electrode was withdrawn to the right atrium and then repositioned. The electrode placement was considered to be satisfactory when threshold for stimulation was less than 1.5 ma. and there was no catheter-induced ventricular ectopic activity. Five patients with temporary pacemakers and one with a flow-directed pulmonary artery catheter developed ventricular ectopic activity within several hours to three days following the catheter placement. Case 1. A 43-year-old man was referred from another hospital for treatment of an extensive anterior myocardial infarction. Upon admission he was mildly hypotensive and his electrocardiogram (ECG) showed evidence for a new right bundle branch block and left posterior hemiblock that did not exist in the tracing submitted from the referring hospital. A flow-directed catheter was placed in the pulmonary artery and an electrode was advanced to the apex of the right ventricle and connected to a standby pacemaker. The mild hypotension was treated successfully with volume replacement. Two hours later, ventricular ectopic activity appeared which, within one hour, evolved into continuous bigeminy with nonfixed coupling (Fig. 1, A 1
November,
1974, Vol. 88, No. 5, pp. 588-592
Catheter-induced
prcur
arrhythmias
off
Fig. 1. Case 1. Pacing catheter-induced bigeminy in a 43-year-old man suffering from an acute myocardial in. farction. A; when the pacer is off every conducted beat is followed by an ectopic beat. The coupling interval varies continuously between 0.30 and 0.42 sec. The atria1 rate is 120. B; now the pacer is turned on at a rate of 111. The paced beats have a configuration very similar to the ectopic beats of strip A. Note the retrograde Pwave immediately after the peak of R.
Fig. 2. Case 3. Continuous strip, monitor lead. Catheter-induced ectopic activity and ventricular flutter-fibrillation. There are three types of beats. Beats a are probably of nodal origin. Beats b and c are interpolated bifocal ventricular ectopic beats. The ectopic activity degenerates into short runs of ventricular flutter-fibrillation three times. The electrode was removed from the ventricle while the bottom line of the strip was being taken. Note the atria1 ectopic beat following the first nodal beat after the last ventricular ectopic beat.
despite adequate treatment with lidocaine. A chest x-ray revealed that the intracardiac catheters had maintained their initial positions. Tntravenous procainamide was then administered. The patient received 1 Gm. of the drug during a two-hour period with no significant improvement. The pacemaker was then activated and a rhythm strip revealed that the paced beats had a configuration very similar to the ventricular ectopic beats. (Fig. 1, B 1. The threshold for stimulation had increased from 0.3 ma. to 0.5 ma. The diagnosis of catheter-induced arrhythmia was confirmed with cessation of ectopic activity when the electrode was withdrawn. Case 2. A 68-year-old retired physician was admitted for syncope. Physical examination revealed mild pulmonary edema. The ECG showed complete heart block with a nodal rhythm, rate 54, and signs of an acute inferior myocardial infarction. A flow-directed catheter
American
Heart Journal
was placed in the pulmonary artery and an electrode was placed in the right ventricle and connected to a demand pacemaker. Several hours later, ventricular ectopic activity appeared at a frequency of 10 to 15 beats per minute, which had a varying coupling interval and remained unresponsive to treatment. The pacemaker was then activated and the ventricles were continuously stimulated. The paced beats had the same configuration as the spontaneous ectopic beats. The diagnosis of catheter-induced arrhythmia was made. The electrode was repositioned with cessation of the ventricular ectopic activity. Case 3. A 73-year-old woman was admitted following a syncope spell. Her ECG revealed an idioventricular rhythm at a rate of 35. A ventricular electrode was inserted and connected to a demand pacemaker set to be inhibited by a rate above 50 per minute. On the third hospital
589
Voukydis
and Cohen
Fig. 3. Case 6. Continuous strip, Lead VI. Catheter-induced isorhythmic dissociation in a 67-year-old man with acute myocardial infarction and papillary muscle dysfunction. There are four kinds of beats. Beats a are wide (QRS = 0.16 sec.) and are always preceded by a P-wave and a P-R interval varying between 0.04 and 0.08 sec. Beats b have a completely different configuration and are not preceded by P-waves. Beats care always preceded by a P-wave and a P-R interval of 0.16 sec. Beats dare similar in configuration to beats a, but are not preceded by P-waves and appear to be interpolated between two a beats. The a beats cannot be the result of a repetitively firing ventricular ectopic focus, because the R-R interval varies widely. Fluoroscopy showed that the flowdirected catheter was displaced inside the right ventricle with a large loop in the right atrium. Every atrial contraction caused a forward thrust of the catheter. Thus it appears that the a beats were catheter-induced.
day, the pacemaker was not sensing properly and was turned off while a repositioning of the electrode was planned in the same day. A few hours later, ventricular ectopic activity was noted with coupling intervals varying between 0.44 and 0.52 sec. In spite of an infusion of lidocaine, the ectopic activity increased. There were salvos of 2 to 3 ventricular ectopic beats followed by three short runs of ventricular flutter which terminated spontaneously (Fig. 2). The pacing wire was withdrawn to the right atrium and all ectopic activity ceased. Case 4. A 66-year-old patient, in cardiogenic shock following an acute anterior myocardial infarction, was being treated with the intra-aortic balloon pump (IABP). As part of our established routine, he had placement of a flow-directed pulmonary artery catheter and a transvenous ventricular electrode. On the second day of counterpulsation, ventricular ectopic activity was noted at a rate of 10 to 12 ventricular ectopic beats per minute. The pacing threshold was found unchanged and the paced beats, although exhibiting a left bundle branch block pattern, had a distinctly different configuration from the ectopic beats. Lidocaine treatment was started and was ineffective. It was then noted that the ectopic beats occurred during deep inspiration. Fluoroscopy showed that the electrode formed an excessive loop inside the right ventricle during inspiration. The wire was withdrawn to the right atrium and the ectopic activity ceased. Case 5. A 54-year-old woman was admitted
590
with an acute inferior myocardial infarction. On the second hospital day she exhibited Mobitz Type II A-V block and a temporary transvenous pacemaker was inserted and placed on standby demand mode. Twelve hours later, the pacemaker started sensing erratically with resulting intermittent competition between the intrinsic rhythm and the pacemaker rhythm. When the pacer was turned off, it was noted that there were frequent ventricular ectopic beats with the same configuration as the paced beats. The diagnosis of catheter-induced arrhythmia was then considered. Repositioning of the pacing wire resulted in abolition of the ectopic activity and proper sensing. Case 6. A 67-year-old man was admitted for treatment of an acute myocardial infarction. Physical examination revealed a moderate degree of left ventricular failure and a new apical systolic murmur. A flow-directed catheter was placed into the pulmonary artery for monitoring of the “wedge” pressure. On the third hospital day, marked ventricular ectopic activity was noted which at times appeared to be an accelerated idioventricular rhythm with isorhythmic dissociation (Fig. 3). Therapeutic doses of lidocaine and procainamide failed to suppress the ectopic activity. It was then noted that the damped pressure tracing from the flow-directed catheter assumed a right ventricular pressure configuration after it was flushed. Fluoroscopy showed the tip of the catheter to be in the right ventricle and a large loop in the right atrium. Rv-
November,
1974, Vol. 88, No. 5
Catheter-indzwed
ery the cal the lar
atria1 contraction caused a forward thrust of catheter, which presumably caused mechanistimulation of the right ventricle. Removal of catheter resulted in cessation of the ventricuectopic activity.
Discussion
It is well-established that intraventricular catheters may cause ventricular ectopic activity or even ventricular tachycardia.‘, 2 This is illustrated dramatically by Case 3 of the present paper (Fig. 2). It is equally true, that an arrhythmia may occur independent of an intracardiac foreign body. Incorrect diagnosis of arrhythmia from an intraventricular catheter may lead to its unnecessary removal, thereby resulting in deprivation of a potentially lifesaving measure. It seems that establishing the basis for criteria that can help diagnose a catheter-induced arrhythmia might be of assistance to the staff of intensive-care units. Arrhythmias which are induced during catheter placement are very frequent. Paulk and Hurst4 had nine cases of ventricular fibrillation occur during pacemaker placement among 43 patients with complete heart block. Rutherford, McCann, and O’Donovar9 noted frequent ventricular ectopic beats and two cases of ventricular tachycardia during placement of polyethylene catheters in the pulmonary artery in a series of 28 patients. The use of flow-directed catheters, in contrast, is associated with lower incidence of ventricular ectopic activity.60ur experience with bedside flow-directed pulmonary artery catheterization is in agreement. It appears, however, that placement of the catheter under pressure guidance alone may result in excessive loops of catheter within the right ventricle or, more commonly, the right atrium. Our experience with placement of transvenous electrodes in the right ventricle under fluoroscopic control has indicated that uncomplicated ventricular ectopic activity can be expected during placement. Fortunately, the arrhythmias are only transient and we have not had to use electric shock to terminate an abnormal rhythm. The diagnosis of arrhythmias that are induced during catheter placement should be as obvious as the remedy. Our present series shows that the incidence of late catheter-induced arrhythmias is approximately 6 per cent. It appears, however, that this relatively high frequency is related to
American
Heart Journal
arrhythmias
temporary electrodes and pulmonary artery catheters. Permanent electrodes have not been reported to cause mechanically induced ventricular ectopic activity, despite the relatively high incidence of catheter dislodgement7 I1 The cases of catheter-induced arrhythmias herein presented illustrate the potential complexity of these arrhythmias. They also give a number of useful clues from which diagnostic principles can be constructed. In all cases, the arrhythmia developed following the placement of catheters, a fact which should arouse the suspicion of a catheterinduced arrhythmia. Another clue is ineffectiveness of anti-arrhythmics, especially when given in high doses. An additional aid to diagnosis is demonstration of displacement of the catheter from the initial position. If the catheter in question is a pacing wire, additional information can be obtained by noting ineffective sensing and an increase in pacing threshold. Erratic sensing and an increased threshold are probably due to a displacement of the catheter. It is also very useful to activate the pacemaker and compare the paced beats with the ectopic beats; if they are similar, the chances are that the ectopic beats are mechanically induced by the catheter. Another observation of the present series is the presence of widely varying coupling intervals. Cases 4 and 6 were unusual, the former showing ectopic activity only during inspiration, whereas the latter demonstrated a very complicated arrhythmia that could not be explained on the basis of known principles. Three cases similar to our Case 6 have been presented by Massumi and Ali. I2 The principles and criteria for diagnosis of catheter-induced arrhythmias can be summarized as follows: (1) the arrhythmia begins after a catheter has been placed m the right ventricle. The presence of dislodged catheters, excessive intracardiac loops of catheters, central displacement of central venous lines, or intracardiac fragments of polyethylene catheters should be sought by careful inspection of a chest x-ray taken after the arrhythmia has begun. (2) If the catheter in question is an electrode, usually there is a concomitant failure to sense properly and the threshold may increase. The paced beats usually look very much like the ectopic beats. (3) The ectopic beats have, in general, a left bundle branch block configuration. If they appear in the form of bigeminy, the coupling interval may vary widely. (4) High doses of anti-arrhythmic medications
591
Voukydis
and Cohen
may be ineffective. (5) Occasionally, the arrhythmias are complicated and hard to explain on the basis of established principles. (6) Finally, the ultimate test for diagnosis of a catheter-induced arrhythmia is cessation of the arrhythmia following removal or repositioning of the catheters. Summary
Catheter-induced arrhythmias, which occurred several hours to several days following successful placement of temporary transvenous right ventricular electrodes or flow-directed pulmonary artery catheters were observed in six out of 106 patients. The arrhythmias took the form of ventricular bigeminy, ventricular tachycardia and, in one instance, isorhythmic dissociation. These arrhythmias were resistant to high doses of antiarrhythmic medication. The diagnosis can be suspected by noticing an excessive catheter loop or an altered catheter position in the chest x-ray or by observing faulty sensing, erratic pacing, or an increased threshold for ventricular stimulation. Corroborative evidence can be obtained from the electrocardiogram, where the catheter-induced depolarizations usually take a left bundle branch block pattern and the coupling interval of the ectopic beats may vary widely. Some pacing catheter-induced beats resemble the paced beats in configuration. In other cases, the rhythm cannot be explained by established principles. The diagnosis of catheter-induced arrhythmia is confirmed when the arrhythmia ceases following removal or repositioning of the catheter.
592
REFERENCES
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November, 1974, Vol. 88, No. 5