CASE REPORTS Asymptomatic Left Ventricular Aneurysm A Sequela of Blunt Chest Trauma HERBERT A. BERKOFF, M.D., GEORGE G. ROWE, M.D., ANDREW B. CRUMMY, M.D., AND DONALD R. KAHN, M.D. SUMMARY A routine chest X-ray taken four months after blunt chest trauma revealed a left ventricular aneurysm in a totally asymptomatic patient. At surgery a thin-walled, clot-filled aneurysm was successfully removed. This case demonstrates the need for careful
follow-up of all patients sustaining blunt chest trauma even though the initial cardiac evaluation may be negative. Our feeling that all such aneurysms should be treated surgically is further reinforced by our operative findings.
CARDIAC ANEURYSMS as sequelae of nonpenetrating chest injuries are rare. We recently treated successfully an asymptomatic left ventricular aneurysm which was fortuitously discovered four months after blunt chest trauma. The asymptomatic aneurysm was found only because of a routine chest X-ray and was not associated with either initial or later electrocardiographic abnormalities. It showed signs of rapid enlargement and contained friable clot at the time of surgery. Case Report A 24-year-old man was in an automobile accident on January 31, 1976. While driving, he was struck broadside on the left by another automobile which was traveling at very high speed. When seen at a nearby hospital he was hypotensive but arousable with direct stimulation. He had extensive maxillofacial injuries and a tender distended abdomen. A chest X-ray showed fractures of the left posterior fourth and sixth ribs and a slight increase in alveolar density throughout the lung compatible with pulmonary contusion (fig. 1). The cardiac contour was normal. An electrocardiogram on admission was unremarkable. Later, a left hemothorax necessitated insertion of a chest tube, and because of increasing difficulties in clearing secretions, a tracheostomy was done. A splenectomy was performed because of a ruptured spleen. He recovered rapidly and six days later he had operative reduction of multiple facial fractures. He was discharged on 2/13/76 and rapidly resumed his previous level of activity which included moderately strenuous athletics. Four months later he was hospitalized for dental work. A routine chest X-ray revealed a localized convexity on the anterolateral aspect of the cardiac silhouette. Fluoroscopy confirmed that the bulge was pulsatile and suggested the diagnosis of a cardiac aneurysm. He was transferred to the University of Wisconsin Medical Center for further evaluation and treatment.
He was asymptomatic and appeared healthy with a blood of 120/64 and a pulse of 80. Cardiac examination showed a precordial lift and widely split pulmonary second sound. A grade II/IV short systolic murmur was present medial to the cardiac apex. His ECG was normal and unchanged. An X-ray cardiac series was obtained (fig. 2A and B). In the frontal projection there was a bulge along the cardiac border just below the region of the left atrial appendage. In the right oblique projection, the bulge was noted to be located anteriorly. We concurred with the diagnosis of cardiac aneurysm. Right and left heart catheterization with coronary arteriograms demonstrated normal hemodynamics except that the left ventricular end-diastolic pressure was 18 mm Hg. A cine left ventriculogram showed that a localized aneurysm arose from the anterolateral aspect of the left ventricle approximately 3 cm below the aortic valve. There appeared to be several small openings through the wall of the ventricle into the aneurysmal sac which distended ominously in systole (fig. 3A and B). The adjacent coronary arteries were displaced but patent and no other abnormalities were identified. The impression was that there was a thin-walled pseudoaneurysm arising from the left ventricle. On May 19, cardiopulmonary bypass was instituted exposing only the right side of the heart. When the aneurysm was visualized, it was found to be totally nonadherent to surrounding structures so we inferred that it was true aneurysm. It measured 3.5 cm in its greatest diameter and expanded on the surface of the ventricle just inferior to the aortic valve. A small hemorrhagic area at the apex of the aneurysm appeared to be very thin (fig. 4). The left anterior descending coronary artery was approximately 1.5 cm away, but its first diagonal branch was displaced medially at the base of the aneurysm. After the sump had been placed in the left ventricle, the aorta was cross-clamped and the aneurysm incised. A moderate amount of clotted material was loosely adherent to the wall of the aneurysm. The base of the aneurysm was traversed by bands of ventricular musculature which explained the angiographic appearances of multiple orifices. The aneurysm was excised, leaving a funnel-shaped defect with a single, 1.8 cm opening into the ventricle. The aneurysm sac was trimmed to firm fibrous edges and the pressure
From the University of Wisconsin Center for Health Sciences, Madison, Wisconsin. Address for reprints: Herbert A. Berkoff, M.D., Department of Surgery, University of Wisconsin Hospitals, 1300 University Avenue, Madison, Wisconsin 53706. Received September 13, 1976; revision accepted October 14, 1976.
545 Downloaded from http://circ.ahajournals.org/ by guest on March 7, 2015
546
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ClIRCULATION
defect was closed using stitches through pledgets taking care to avoid the coronary vessels. The remainder of the ventricular wall contracted well and no other defects were identified. The patient's recovery was uneventful, and he was discharged on the eighth postoperative day. Discussion Traumatic contusion of the heart is relatively common and directly related to the severity of the blunt trauma. Kirsch' has stated that nearly 25% of patients subjected to blunt chest trauma have some degree of myocardial contusion, while others have indicated an even higher incidence.2 3 Usually there is clinically complete recovery with minimal residual scarring. However, in some cases, softening and fibrotic replacement of the contused myocardium are followed by thinning of the scar which leads to dilatation and aneurysm formation. This process may produce a true aneurysm within days or the process may take a number of years. Parmley et al. and others3 I have shown the coronary arteries to be relatively resistant to blunt trauma. Therefore, coronary thrombosis secondary to trauma is an unusual cause of an aneurysm. Conversely, penetrating trauma to the heart may result immediately in a pulsating hematoma which forms a pseudoaneurysm limited by the pericardium. Although a standard PA and lateral chest X-ray will not disclose every aneurysm, it is the best screening procedure. Any change in cardiac contour should be further evaluated with oblique views and fluoroscopy. Cardiac catheterization with angiocardiography and ventriculography are required to clarify ventricular functional capacity and to completely
delineate the aneurysm identifying its points of origin and relations with the coronary arteries and other structures. Aneurysms can be asymptomatic but some produce
7
AY Q176
...I
7 MP
8 FE BRUARY 976 FIGURE 1. A portable AP chest film taken during the initial hospitalization shows the cardiac silhouette to be normal. At this point, the pulmonary contusion had cleared.
7
FI(;URti 2. Top) The PA film of a cardiac series, taken 14 weeks later, showed an abnormal cardiac contour, with a bulge along the upper left cardiac border. Bottom) The right antero-obliqueprojection showed the abnormality to be located anteriorly. The impression was that the patient had a pseudoaneurysm of the left ventricle.
Downloaded from http://circ.ahajournals.org/ by guest on March 7, 2015
POSTTRAUMATIC LV
AN'EURYSM/Berkpfl"
Rowe Cru my, Kahn
547
definitesignsaMsymptoms. No-n-specificsymptonissuchas dvspnea, precor la] discomfbrt, or pain .may be experienced.
Abnormalities of heart sounds with murmurs; rubs, or gallop rhythms may be present. Nonspecific electrocardiogra h4c findin s, usually STJ wave changes suggestive of subendocardj'al in'ury or iseherma may be fbund. Emboli may result from dissemination of thronibi ftom within the aneurysm. Congestive h art fallure may be a major 4
problem, especially with large aneurysms. Then, extensive mvocardial destruction may result in Po r ventricular contraction or systolic expansion of the aneurvsm .may absorb
mudh of the ventricular stroke volume. Potential-ly lethal arrbvthmias and rupture of the aneurysm are maj r h zards, Limited experience with traumatic cardiac aneurysms a le makes it d u t .to gener i owever the aneurysm is well localized and its relationship with the coronary arteries makes resection possible, sur erv should be strongly considcred, even in asymp omatic cases. This Is especially true if the aneurysm shows systolic expansion, is thin walled or contains clots, This view is supported by the composite data, ftom the literature indicating survival in 1 1 of 12 operative subjects aiid death in at least 13 of 17 nonoptoo
erative
patjents.'."
Our patient demonstrates several unusual and disqu'ieting features. First, his asymptornatic aneurysm was fbund only because of a routine chest .ray 15 weeks after hj's -trauma. Second, his electrocatdiogram never showed any abnormal1w ties. T r t e aneurysm was ve t in ts apex rup" ture mav have been imminent. Fourth, it contained a moderate amount of ftiable clot Which was loosely adheront to the wall so that the threat of embolization was real, .
Downloaded from http://circ.ahajournals.org/ by guest on March 7, 2015
548
CIRCULATION
The patient played strenuous games of paddleball shortly after his injury. Whether this was a factor in the development of the aneurysm is moot. However, it does raise the consideration of exercise restriction in patients who are considered to have myocardial contusion. Because of the potentially lethal complications, repair should be undertaken promptly after diagnosing an aneurysm similar to the one reported here. Pupello et al.9 reported problems at operation because the edges of a sixweek-old aneurysm were friable and difficult to handle. However, in our patient, the aneurysm was 151/2 weeks old and had a tough fibrous wall making placement of all stitches relatively easy. Maturity of the repair process within the injured tissues may enhance surgical repair, but delay increases the possibility of a major catastrophe. We stress the importance of following patients with cardiac injury closely. It is important to realize that myocardial injury may be unrecognized especially in the presence of major trauma to other organs, and only with
VOL 55, No 3, MARCH 1977
routine follow-up chest X-rays can disasters of omission be avoided. The limited literature on the subject, while lacking statistical validity, strongly indicates surgery for this lesion. References I. Kirsch M: The treatment of acute traumatic rupture of the aorta: A 10year experience. Ann Surg 184: 308, 1976 2. Parmley LF, Manion WC, Mattingly TW: Nonpenetrating traumatic injury of the heart. Circulation 18: 371, 1958 3. De Muth WE Jr, Baue AE, Odem JA: Contusions of the heart. J Trauma 7: 443, 1967 4. Hawkes SZ: Traumatic rupture of the heart and intrapericardial structures. Am J Surg 27: 503, 1935 5. Glancy DL, Yarnell P, Roberts WC: Traumatic left ventricular aneurysm: cardiac thrombosis following aneurysmectomy. Am J Cardiol 20: 428, 1967 6. Singh R, Nolan SP, Schrank JP: Traumatic left ventricular aneurysm: two cases with normal coronary angiograms. JAMA 234: 412, 1975 7. Sakurai J, Salvadore L, Litwak R, Pereyo JA: Left ventricular aneurysm due to blunt trauma. NYS J Med 75: 2367, 1975 8. Killen DA, Gobbel WG Jr, France R, Vix VA: Post-traumatic aneurysm of the left ventricule. Circulation 39: 101, 1969 9. Pupello DF, Daily PO, Stinson EB, Shumway NE: Successful repair of left ventricular aneurysm due to trauma. JAMA 211: 826, 1970
Fluoroscope-Generated Electromagnetic Interference in an External Demand Pacemaker Report of a Case CAROL J. LEEDS, R.N., CCRN, MASOOD AKHTAR, M.D., AND ANTHONY N. DAMATO, M.D. SUMMARY Electromagnetic interference presented as inhibition and resetting of the demand circuitry of a ventricular-inhibited temporary external pacemaker in a 70-year-old man undergoing surgical implantation of a permanent bipolar pacemaker generator and lead. The arrhythmia was found to -be due to oversensing of waveforms modulated to simulate myocardial potentials emitted by a faulty
fluoroscopy unit used in the vicinity of external temporary transvenous pacing equipment. The documentation of this disruption of pacemaker rhythm reinforces the need for continuous monitoring of patients treated with external demand pacemakers and for the careful maintenance of all electrical equipment.
THE VENTRICULAR-INHIBITED DEMAND PACEMAKER is engineered to sense the R wave of ventricular myopotentials and reset to avoid competitive rhythms. The nondiscriminatory nature of these demand circuitries is well established. Oversensing of physiologic signals, "afterpotentials," "false signals," and signals from electromag-netic fields can cause various pacemaker'-3 arrhythmias. This report deals with the effect of electromagnetic interference (EMI) on an external demand temporary pacemaker caused by a faulty fluoroscopy unit, a previously unsuspected source.
Case Report
From the Cardiology Department, U.S. Public Health Service Hospital, Staten Island, New York. Supported in part by the Bureau of Medical Services, National Heart, Lung, and Blood Institute Project HL 12536-06. Address for reprints: Carol J. Leeds, R.N., CCRN, Cardiology Department, USPHS Hospital, Staten Island, New York 10304. Received September 7, 1976; revision accepted October 4, 1976.
A 70-year-old man with complete atrioventricular block and a ventricular escape rate of 37 was catheterized for temporary transvenous ventricular pacing. A #6F, USCI quadripolar electrode catheter was percutaneously inserted into an antecubital vein and positioned fluoroscopically in the right ventricle. The distal electrode pair was connected to a Medtronic Model 5880A External Demand Pacemaker set at an automatic pacing interval (S-S) of 850 msec with the sensitivity control at maximum. The stimulus output was adjusted to 2 ma, 1.4 ma greater than the ventricular pacing threshold. A permanent ventricular-inhibited demand pacemaker (Medtronic 5950) and bipolar endocardial lead (Medtronic 6904-58) were implanted surgically the following day. During the procedure, the surface and the intracardiac electrograms (proximal electrode pair of the temporary catheter) were monitored on an Electronics for Medicine oscilloscopic
Downloaded from http://circ.ahajournals.org/ by guest on March 7, 2015
Asymptomatic left ventricular aneurysm: a sequela of blunt chest trauma. H A Berkoff, G G Rowe, A B Crummy and D R Kahn Circulation. 1977;55:545-548 doi: 10.1161/01.CIR.55.3.545 Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 1977 American Heart Association, Inc. All rights reserved. Print ISSN: 0009-7322. Online ISSN: 1524-4539
The online version of this article, along with updated information and services, is located on the World Wide Web at: http://circ.ahajournals.org/content/55/3/545
Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published in Circulation can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial Office. Once the online version of the published article for which permission is being requested is located, click Request Permissions in the middle column of the Web page under Services. Further information about this process is available in the Permissions and Rights Question and Answer document. Reprints: Information about reprints can be found online at: http://www.lww.com/reprints Subscriptions: Information about subscribing to Circulation is online at: http://circ.ahajournals.org//subscriptions/
Downloaded from http://circ.ahajournals.org/ by guest on March 7, 2015
follow-up of all patients sustaining blunt chest trauma even though the initial cardiac evaluation may be negative. Our feeling that all such aneurysms should be treated surgically is further reinforced by our operative findings.
CARDIAC ANEURYSMS as sequelae of nonpenetrating chest injuries are rare. We recently treated successfully an asymptomatic left ventricular aneurysm which was fortuitously discovered four months after blunt chest trauma. The asymptomatic aneurysm was found only because of a routine chest X-ray and was not associated with either initial or later electrocardiographic abnormalities. It showed signs of rapid enlargement and contained friable clot at the time of surgery. Case Report A 24-year-old man was in an automobile accident on January 31, 1976. While driving, he was struck broadside on the left by another automobile which was traveling at very high speed. When seen at a nearby hospital he was hypotensive but arousable with direct stimulation. He had extensive maxillofacial injuries and a tender distended abdomen. A chest X-ray showed fractures of the left posterior fourth and sixth ribs and a slight increase in alveolar density throughout the lung compatible with pulmonary contusion (fig. 1). The cardiac contour was normal. An electrocardiogram on admission was unremarkable. Later, a left hemothorax necessitated insertion of a chest tube, and because of increasing difficulties in clearing secretions, a tracheostomy was done. A splenectomy was performed because of a ruptured spleen. He recovered rapidly and six days later he had operative reduction of multiple facial fractures. He was discharged on 2/13/76 and rapidly resumed his previous level of activity which included moderately strenuous athletics. Four months later he was hospitalized for dental work. A routine chest X-ray revealed a localized convexity on the anterolateral aspect of the cardiac silhouette. Fluoroscopy confirmed that the bulge was pulsatile and suggested the diagnosis of a cardiac aneurysm. He was transferred to the University of Wisconsin Medical Center for further evaluation and treatment.
He was asymptomatic and appeared healthy with a blood of 120/64 and a pulse of 80. Cardiac examination showed a precordial lift and widely split pulmonary second sound. A grade II/IV short systolic murmur was present medial to the cardiac apex. His ECG was normal and unchanged. An X-ray cardiac series was obtained (fig. 2A and B). In the frontal projection there was a bulge along the cardiac border just below the region of the left atrial appendage. In the right oblique projection, the bulge was noted to be located anteriorly. We concurred with the diagnosis of cardiac aneurysm. Right and left heart catheterization with coronary arteriograms demonstrated normal hemodynamics except that the left ventricular end-diastolic pressure was 18 mm Hg. A cine left ventriculogram showed that a localized aneurysm arose from the anterolateral aspect of the left ventricle approximately 3 cm below the aortic valve. There appeared to be several small openings through the wall of the ventricle into the aneurysmal sac which distended ominously in systole (fig. 3A and B). The adjacent coronary arteries were displaced but patent and no other abnormalities were identified. The impression was that there was a thin-walled pseudoaneurysm arising from the left ventricle. On May 19, cardiopulmonary bypass was instituted exposing only the right side of the heart. When the aneurysm was visualized, it was found to be totally nonadherent to surrounding structures so we inferred that it was true aneurysm. It measured 3.5 cm in its greatest diameter and expanded on the surface of the ventricle just inferior to the aortic valve. A small hemorrhagic area at the apex of the aneurysm appeared to be very thin (fig. 4). The left anterior descending coronary artery was approximately 1.5 cm away, but its first diagonal branch was displaced medially at the base of the aneurysm. After the sump had been placed in the left ventricle, the aorta was cross-clamped and the aneurysm incised. A moderate amount of clotted material was loosely adherent to the wall of the aneurysm. The base of the aneurysm was traversed by bands of ventricular musculature which explained the angiographic appearances of multiple orifices. The aneurysm was excised, leaving a funnel-shaped defect with a single, 1.8 cm opening into the ventricle. The aneurysm sac was trimmed to firm fibrous edges and the pressure
From the University of Wisconsin Center for Health Sciences, Madison, Wisconsin. Address for reprints: Herbert A. Berkoff, M.D., Department of Surgery, University of Wisconsin Hospitals, 1300 University Avenue, Madison, Wisconsin 53706. Received September 13, 1976; revision accepted October 14, 1976.
545 Downloaded from http://circ.ahajournals.org/ by guest on March 7, 2015
546
VOL 55, No 3, MARCiA 1977
ClIRCULATION
defect was closed using stitches through pledgets taking care to avoid the coronary vessels. The remainder of the ventricular wall contracted well and no other defects were identified. The patient's recovery was uneventful, and he was discharged on the eighth postoperative day. Discussion Traumatic contusion of the heart is relatively common and directly related to the severity of the blunt trauma. Kirsch' has stated that nearly 25% of patients subjected to blunt chest trauma have some degree of myocardial contusion, while others have indicated an even higher incidence.2 3 Usually there is clinically complete recovery with minimal residual scarring. However, in some cases, softening and fibrotic replacement of the contused myocardium are followed by thinning of the scar which leads to dilatation and aneurysm formation. This process may produce a true aneurysm within days or the process may take a number of years. Parmley et al. and others3 I have shown the coronary arteries to be relatively resistant to blunt trauma. Therefore, coronary thrombosis secondary to trauma is an unusual cause of an aneurysm. Conversely, penetrating trauma to the heart may result immediately in a pulsating hematoma which forms a pseudoaneurysm limited by the pericardium. Although a standard PA and lateral chest X-ray will not disclose every aneurysm, it is the best screening procedure. Any change in cardiac contour should be further evaluated with oblique views and fluoroscopy. Cardiac catheterization with angiocardiography and ventriculography are required to clarify ventricular functional capacity and to completely
delineate the aneurysm identifying its points of origin and relations with the coronary arteries and other structures. Aneurysms can be asymptomatic but some produce
7
AY Q176
...I
7 MP
8 FE BRUARY 976 FIGURE 1. A portable AP chest film taken during the initial hospitalization shows the cardiac silhouette to be normal. At this point, the pulmonary contusion had cleared.
7
FI(;URti 2. Top) The PA film of a cardiac series, taken 14 weeks later, showed an abnormal cardiac contour, with a bulge along the upper left cardiac border. Bottom) The right antero-obliqueprojection showed the abnormality to be located anteriorly. The impression was that the patient had a pseudoaneurysm of the left ventricle.
Downloaded from http://circ.ahajournals.org/ by guest on March 7, 2015
POSTTRAUMATIC LV
AN'EURYSM/Berkpfl"
Rowe Cru my, Kahn
547
definitesignsaMsymptoms. No-n-specificsymptonissuchas dvspnea, precor la] discomfbrt, or pain .may be experienced.
Abnormalities of heart sounds with murmurs; rubs, or gallop rhythms may be present. Nonspecific electrocardiogra h4c findin s, usually STJ wave changes suggestive of subendocardj'al in'ury or iseherma may be fbund. Emboli may result from dissemination of thronibi ftom within the aneurysm. Congestive h art fallure may be a major 4
problem, especially with large aneurysms. Then, extensive mvocardial destruction may result in Po r ventricular contraction or systolic expansion of the aneurvsm .may absorb
mudh of the ventricular stroke volume. Potential-ly lethal arrbvthmias and rupture of the aneurysm are maj r h zards, Limited experience with traumatic cardiac aneurysms a le makes it d u t .to gener i owever the aneurysm is well localized and its relationship with the coronary arteries makes resection possible, sur erv should be strongly considcred, even in asymp omatic cases. This Is especially true if the aneurysm shows systolic expansion, is thin walled or contains clots, This view is supported by the composite data, ftom the literature indicating survival in 1 1 of 12 operative subjects aiid death in at least 13 of 17 nonoptoo
erative
patjents.'."
Our patient demonstrates several unusual and disqu'ieting features. First, his asymptornatic aneurysm was fbund only because of a routine chest .ray 15 weeks after hj's -trauma. Second, his electrocatdiogram never showed any abnormal1w ties. T r t e aneurysm was ve t in ts apex rup" ture mav have been imminent. Fourth, it contained a moderate amount of ftiable clot Which was loosely adheront to the wall so that the threat of embolization was real, .
Downloaded from http://circ.ahajournals.org/ by guest on March 7, 2015
548
CIRCULATION
The patient played strenuous games of paddleball shortly after his injury. Whether this was a factor in the development of the aneurysm is moot. However, it does raise the consideration of exercise restriction in patients who are considered to have myocardial contusion. Because of the potentially lethal complications, repair should be undertaken promptly after diagnosing an aneurysm similar to the one reported here. Pupello et al.9 reported problems at operation because the edges of a sixweek-old aneurysm were friable and difficult to handle. However, in our patient, the aneurysm was 151/2 weeks old and had a tough fibrous wall making placement of all stitches relatively easy. Maturity of the repair process within the injured tissues may enhance surgical repair, but delay increases the possibility of a major catastrophe. We stress the importance of following patients with cardiac injury closely. It is important to realize that myocardial injury may be unrecognized especially in the presence of major trauma to other organs, and only with
VOL 55, No 3, MARCH 1977
routine follow-up chest X-rays can disasters of omission be avoided. The limited literature on the subject, while lacking statistical validity, strongly indicates surgery for this lesion. References I. Kirsch M: The treatment of acute traumatic rupture of the aorta: A 10year experience. Ann Surg 184: 308, 1976 2. Parmley LF, Manion WC, Mattingly TW: Nonpenetrating traumatic injury of the heart. Circulation 18: 371, 1958 3. De Muth WE Jr, Baue AE, Odem JA: Contusions of the heart. J Trauma 7: 443, 1967 4. Hawkes SZ: Traumatic rupture of the heart and intrapericardial structures. Am J Surg 27: 503, 1935 5. Glancy DL, Yarnell P, Roberts WC: Traumatic left ventricular aneurysm: cardiac thrombosis following aneurysmectomy. Am J Cardiol 20: 428, 1967 6. Singh R, Nolan SP, Schrank JP: Traumatic left ventricular aneurysm: two cases with normal coronary angiograms. JAMA 234: 412, 1975 7. Sakurai J, Salvadore L, Litwak R, Pereyo JA: Left ventricular aneurysm due to blunt trauma. NYS J Med 75: 2367, 1975 8. Killen DA, Gobbel WG Jr, France R, Vix VA: Post-traumatic aneurysm of the left ventricule. Circulation 39: 101, 1969 9. Pupello DF, Daily PO, Stinson EB, Shumway NE: Successful repair of left ventricular aneurysm due to trauma. JAMA 211: 826, 1970
Fluoroscope-Generated Electromagnetic Interference in an External Demand Pacemaker Report of a Case CAROL J. LEEDS, R.N., CCRN, MASOOD AKHTAR, M.D., AND ANTHONY N. DAMATO, M.D. SUMMARY Electromagnetic interference presented as inhibition and resetting of the demand circuitry of a ventricular-inhibited temporary external pacemaker in a 70-year-old man undergoing surgical implantation of a permanent bipolar pacemaker generator and lead. The arrhythmia was found to -be due to oversensing of waveforms modulated to simulate myocardial potentials emitted by a faulty
fluoroscopy unit used in the vicinity of external temporary transvenous pacing equipment. The documentation of this disruption of pacemaker rhythm reinforces the need for continuous monitoring of patients treated with external demand pacemakers and for the careful maintenance of all electrical equipment.
THE VENTRICULAR-INHIBITED DEMAND PACEMAKER is engineered to sense the R wave of ventricular myopotentials and reset to avoid competitive rhythms. The nondiscriminatory nature of these demand circuitries is well established. Oversensing of physiologic signals, "afterpotentials," "false signals," and signals from electromag-netic fields can cause various pacemaker'-3 arrhythmias. This report deals with the effect of electromagnetic interference (EMI) on an external demand temporary pacemaker caused by a faulty fluoroscopy unit, a previously unsuspected source.
Case Report
From the Cardiology Department, U.S. Public Health Service Hospital, Staten Island, New York. Supported in part by the Bureau of Medical Services, National Heart, Lung, and Blood Institute Project HL 12536-06. Address for reprints: Carol J. Leeds, R.N., CCRN, Cardiology Department, USPHS Hospital, Staten Island, New York 10304. Received September 7, 1976; revision accepted October 4, 1976.
A 70-year-old man with complete atrioventricular block and a ventricular escape rate of 37 was catheterized for temporary transvenous ventricular pacing. A #6F, USCI quadripolar electrode catheter was percutaneously inserted into an antecubital vein and positioned fluoroscopically in the right ventricle. The distal electrode pair was connected to a Medtronic Model 5880A External Demand Pacemaker set at an automatic pacing interval (S-S) of 850 msec with the sensitivity control at maximum. The stimulus output was adjusted to 2 ma, 1.4 ma greater than the ventricular pacing threshold. A permanent ventricular-inhibited demand pacemaker (Medtronic 5950) and bipolar endocardial lead (Medtronic 6904-58) were implanted surgically the following day. During the procedure, the surface and the intracardiac electrograms (proximal electrode pair of the temporary catheter) were monitored on an Electronics for Medicine oscilloscopic
Downloaded from http://circ.ahajournals.org/ by guest on March 7, 2015
Asymptomatic left ventricular aneurysm: a sequela of blunt chest trauma. H A Berkoff, G G Rowe, A B Crummy and D R Kahn Circulation. 1977;55:545-548 doi: 10.1161/01.CIR.55.3.545 Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 1977 American Heart Association, Inc. All rights reserved. Print ISSN: 0009-7322. Online ISSN: 1524-4539
The online version of this article, along with updated information and services, is located on the World Wide Web at: http://circ.ahajournals.org/content/55/3/545
Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published in Circulation can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial Office. Once the online version of the published article for which permission is being requested is located, click Request Permissions in the middle column of the Web page under Services. Further information about this process is available in the Permissions and Rights Question and Answer document. Reprints: Information about reprints can be found online at: http://www.lww.com/reprints Subscriptions: Information about subscribing to Circulation is online at: http://circ.ahajournals.org//subscriptions/
Downloaded from http://circ.ahajournals.org/ by guest on March 7, 2015
