Longstanding Cardiac Perforation by a Permanent Endocardial Pacing Electrode

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radiating to the axilla. There was no hepatomegaly or peripheral edema. Laboratory Data Hematocrit 37 percent; WBC 1l,OOO; blood sugar 146 mg percent; SGOT 110 karmen units; arterial pH 7.42; P02 70 mm Hg, PC02 66 mm Hg, O 2 saturation 94 percent; bicarbonate 41.5 mEq/L (room air). The remaining chemical determinations were normal. Chest roentgenogram showed left ventricular enlargement, dilatation of the aorta, calciflcation of the aortic knob, pulmonary vascular congestion and Kerley B lines. Electrocardiogram revealed complete atrioventricular block, atrial rate of 88 beats/min, ventricular rate of 40 per minute and a complete left bundle branch block pattern. An Elecath semi-floating bipolar temporary transvenous pacemaker electrode was inserted from an infraclavicular approach via the left subclavian vein with electrocardiographic monitoring at the bedside. Good initial blood return was noted following the subclavian puncture. Large positive P waves were noted during the electrode insertion, and with further advancement, a rapid transition to tall positive ventricular potentials was observed. The normal intracardiac electrocardiograph recording from the right atrium is commonly characterized by large biphasic P waves. Right ventricular endocardial recordings show deep QS and small P waves. The patient could be paced at an energy level of 2.0 milliamperes. A post-insertion electrocardiogram showed 1: 1 capture at 80 beats/min and complete left bundle branch block pattern. In the following hours, unreliable pacing ensued; the energy level was increased to 8 milliamperes with 1: 1 capture; diaphragmatic contractions were noted with each pacemaker discharge. Chest roentgenogram revealed the electrode to be lying outside the cardiac silhouette posteriorly along the heart border (Fig 1). Under fluoroscopic observation, a bipolar pacing electrode was inserted via the right median basilic vein and the original pacemaker electrode removed. Review of the videotape recordings of the removal show the pacemaker remaining external to the heart throughout its removal (Fig 1 ). DISCUSSION

Complications of temporary transvenous pacing via the subclavian vein from an infra- or supraclavicular approach have included partial pneumothorax, arterial puncture, myocardial perforation, bacteremia, infection at the insertion site, and malpositioning." Campo et a)3 have reported two instances of extraluminal pacer electrcde insertion from the supraclavicular approach. In the present report, the electrode was inserted from an infraclavicular approach. Because of the unusual position of the initial electrode, the possibility of anomalous venous structures was investigated by the injection of contrast material into the superior vena cava and left subclavian veins with visualization of normal anatomy. The electrode appeared to be extrinsic to the cardiac chambers along the posterior heart border between pericardium and pleura and presumably traversed directly through mediastinal structures due to inadvertent venous perforation at the insertion site. Although reliable pacing can be readily achieved at the bedside by this and similar techniques, temporary pacer electrodes should be introduced under fluoroscopic control whenever possible. Blind pacemaker insertion should be attempted only in extreme emergencies and

for lifesaving reasons, in which case catheter position should be documented by chest x-ray examination as soon as possible. This case illustrates one of the possible potential complications of pervenous pacemaker electrode insertion without fluoroscopic control. REFERENCES

1 Kimball JT, Killip T: A simple bedside method for transvenous intracardiac pacing. Am Heart J 70:35,1965 2 Escher DJW, Furman S, Solomon N: Transvenous emergency cardiac pacing. Ann New York Acad Sci 167:582, 1969 3 Campo IN, Garfield GJ, Escher DJW, et al: Complications of pacing by pervenous subclavian semiHoating electrodes including two extraluminal insertions (Abstract). Am J Cardiel 26:627, 1970

Longstanding Cardiac Perforation

by

a Permanent Endocardial Pacing Electrode* B. }. Hurwitz, M.B., F.C.C.P.

e.ci«,

and I.W.P. Obel, M.B., B.Ch.,

A case of longstanding (19 months) cardiac perforation by an endocardial pacing electrode is described, in which uninterrupted cardiac pacing has been accompanied by intermittent diaphragmatic pacing. Repositioning of the electrode was not performed. CASE REPORT

An 80-year-old white woman was first seen in April, 1970 because of syncopal attacks for the preceding two years. There was no history of angina pectoris or myocardial infarction. She was found to be in total heart block with a pulse rate of 32 per minute. Her blood pressure was 260/110. X-ray film of the chest showed mild cardiomegaly due to left ventricular enlargement. There was mild diabetes. On April 15, 1970, an Elema no. 588B endocardial electrode was passed via the right external jugular vein into the apex of the right ventricle. The diastolic pacing threshold was 1.3 volts. oo A Vitatron fixed rate pacemaker was attached for permanent pacing. Methyldopa controlled her hypertension and tolbutamide her diabetes. She returned home to Rhodesia, 1,000 miles distant. There she was seen regularly by an internist. She did not experience syncope and he did not notice any change in pulse or ECG. She was referred back to our clinic at four to six month intervals where she was examined and lead position, ECG and pacemaker output were checked. In November, 1970, at routine examination at our pacemaker clinic, the Vitatron power unit was found to be faulty and was electively replaced. Pacing failure had not occurred. The intra cardiac electrode remained in a good radiologic position in the apex of the right ventricle, and the pacing threshold was 1.2 volts. In August, 1971 her jugular venous pressure became raised ·From the Department of Medicine and Cardiac Clinic, Johannesburg Hospital and University of the Witwatersrand, Johannesburg, South Africa. ooThreshold Analyzer, Elema-Scholander, Stockholm, Sweden.

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LONGSTANDING CARDIAC PERFORATION BY PACING ELECTRODE and ankle edema was noted. This responded promptly to ethacrynic acid 50 mg daily, digoxin 0.25 mg daily and potassium supplements. At no time was there evidence of cardiac tamponade. In February, 1972 when the power unit was being electively replaced, it was noted that the diaphragm contracted intermittently. Cardiac pacing continued uninterrupted. She then admitted to having rhythmic contractions of the anterior abdominal muscles, especially when she lay on her left side. This, she said, had been present for one year, and because she was otherwise asymptomatic, she had not brought it to the attention of her medical attendants. Close questioning of her family, with whom she lived, verified the duration of this intermittent abdominal wall pacing. Measurement of spike potentials of each of the standard limb leads, impulse duration, and heart rate, on a calibrated oscilloscope'[ revealed no abnormality or change at any time. X-ray film showed the intracardiac electrode to be unchanged in a stable position at the inferior border of the right ventricle (Fig 1 and 2). Fluoroscopy showed pacing of the left dome of the diaphragm. This was most marked in full expiration with the patient either in the erect or in the prone position. On full inspiration diaphragmatic pacing was virtually obliterated. The diastolic pacing threshold was 2.9 volts at the time of replacement of the power unit and, although this was higher than previously, it was thought to be acceptable and the lead was not repositioned. Constant ECG monitoring over five days showed continuous cardiac pacing. She was closely observed at our clinic for the following month, during which time she was asymptomatic and all measurable parameters showed continued cardiac pacing in all positions, together with intermittent diaphragmatic pacing when she lay on her left side. She then returned home to be closely followed by her internist. Six months later the patient was well with continued normal cardiac pacing. tTektronix model2B67, Tektroniks, Inc., Beaverton, Oregon.

FIGURE 2. Lateral chest view showing endocardial electrode (February, 1972). DISCUSSION

FIGURE 1. Posteroanterior view showing endocardial electrode (February, 1972).

CHEST, VOL. 64, NO.3, SEPTEMBER, 1973

Since Furman and Schwedal' introduced intracardiac electrodes for cardiac pacing, the safety and effectiveness of this route has been repeatedly confirmed. A not uncommon complication of this procedure is penetration and perforation of the myocardium, occurring in from 210 percent of all cases. I • 1l The Elema 588B electrode, as used in this case, is a flexible lead with outer Silastic covering and a broad platinum tip. Perforation with this electrode is most unusual. Lagergren et al' 2 found no instance of perforation using this electrode in 305 consecutive cases observed for up to two years. Myocardial perforation usually presents with diaphragmatic or abdominal wall pacing, intennittent pacing or pacing failure. A change in the electrical axis of the pacing stimulus, pericardial friction rub and extracardiac auscultatory clicks- may also suggest the diagnosis. The right ventricular myocardium is only 4-5 mm thick and penetration of this wall by an electrode may be accompanied by little or no change in its position radiologically, although Ormond et altO describe a technique where better radiologic diagnosis follows close visualization of the epicardial fat pad. Diagnosis was made in our patient when anterior abdominal wall and diaphragmatic pacing confirmed radiographically occurred. There was no change in her

SAWAYAMA ET AL

368 heart rate or in impulse duration of the spike potentials of each of the standard limb leads. The radiologic position of the electrode indicated that it was not in close proximity to the phrenic nerve. The fact that diaphragmatic pacing was abolished by deep inspiration further suggests that it followed direct contact between the perforated pacing electrode and the diaphragm, and was not due to phrenic nerve stimulation. The important complications of myocardial perforation are failed pacing and hemorrhage with subsequent cardiac tamponade. Although the latter is frequently mentioned in the literature as a possible complication, it rarely occurs. 1 - 1 2 It has been recommended that a perforated electrode should be retracted and repositioned, or left in situ and a new one inserted." Since our patient had paced normally with myocardial penetration probably of more than one year's duration, we elected to leave the electrode where it was. Although this was a departure from conventional management, we made this decision in view of the radiologic stability of the electrode, and because of the only slight rise in the pacing threshold. Because the electrode remained in a radiologically stable position with uninterrupted cardiac pacing for more than one year, we considered further change unlikely. The rise in pacing threshold to 2.9 volts was well within the capabilities of the power unit. Furthermore, the diaphragmatic pacing did not trouble her, and repositioning of this electrode might thus have been simply meddlesome. Indeed, one might argue that after a year a track may well have formed around the perforated electrode and remanipulation in these circumstances would be more likely to cause bleeding than to prevent it. This is supported by the view of Kramer et al 2 who prefer to leave a perforated electrode in situ rather than to reposition it. . Careful close monitoring of the patient over one month, following discovery of perforation, revealed no abnormality in pacing. Although we only saw her at four to six month intervals at our clinic because she lived 1,000 miles distant, she was under the care of an internist in her home town, who was fully aware of her condition and who examined her regularly. Follow-up of this patient, once the diagnosis was known, was thus frequent, with due attention being given to all possible criteria of electrode movement and pacing failure. Any interruption in cardiac pacing would have been rapidly noted, and have been regarded as an indication to urgently change the pacing electrode. We have thus shown with follow-up of our patient that cardiac pacing had not failed over a period of at least 19 months and that the electrode was unchanged in position during this time. This case of uninterrupted cardiac pacing together with intermittent diaphragmatic pacing following perforation of a pacing catheter is unique in our experience. REFERENCES

Furman S, Schwedal JB: An intracardiac pacemaker for Stokes-Adamsseizures. N Engl J Med 261:943-8, 1959

2 Kramer DH, Moss AJ: Mechanisms and significance of Pacemaker-induced extracardiac sound. Am J Cardiol 25:367-71, 1970 3 Sykosch HJ: Special problems in cardiac stimulation: A review of 500 pacemaker patients. Geriatrics 24:78-84, 1969 4 Goldstein S, Moss AJ; Rivers RJ Jr, et al: Transthoracic and transvenous pacemakers: A comparative clinical experience with 131 implantable units. Br Heart J 32:35-45, 1970 5 Green GD, Forkes W, Bain WH, et al: Pacemaker lifetimes-a review and definitions, based on experience in Glasgow with Chardack-Greatbach (Medtronic) pacemakers. Am Heart J 80:414-21, 1970 6 Furman S, Escher DJ, Soloman N, et al: Experiences with myocardial and transvenous implanted cardiac pacemakers. Am J CardioI23:66-72, 1969 7 Macaulay MB, Wright JS: Transvenous cardiac pacing. Experience of a percutaneous supraclavicular approach. Br Med J 4:207-9,1970 8 Gotsman MS, Peller LW, Beck W, et al: Some problems of permanent artificial pacing. Br Med J 1:343-6, 1968 9 Marchand P, Jaros CG, Obel IW, et al: The problems of long term pacing of the heart. South African Med J 41:239, 1967 10 Ormond RS, Ruben6re M, Anbe DT, et al: Radiographic demonstration of myocardial penetration by permanent endocardial pacemakers. Radiology 98:35-7, 1971 11 Standen JR: The radiologist and the cardiac pacemaker. J Can Assoc Rad 22:203-13, 1970 12 Lagergren H, Johansson L, Schuller H, et al: 305 cases of permanent intravenous pacemaker treatment for AdamsStokes syndrome. Surgery 59:494-7,1966

Bronchial Asthma with "Crossed Splitting" of the Second Heart Sound* Toshitami Sawayama, M.D.; Hiroshi Katsume, M.D.; Masaru Tohara, M.D.; and Shoso Nezuo, M.D.

''Crossed sp6tting" of the second heart sound was recognized in the polygraphic tracing of a 75-year-old woman during recovery from an attack of acute bronchial asthma. This ausculatatory finding, not previously reported, is discussed in relation to probable hemodynamic changes associated with bronchial asthma.

T

he aortic component (A2) of the second heart sound (S2) normally precedes the pulmonic component (P2). Reversal of this relationship is well recognized in the presence of left ventricular malfunction, but has not been previously described in human subjects during primary disturbances of the pulmonary circulation, although it has been described during acute cor pulmonale ·From the Department of Cardiology, Kawasaki Medical School, Okayama, Japan Reprint requests: Dr. Sawayama, Department of Cardiology, Kawasaki Medical School and Hospital, Nakasange, Okayama, Japan 700. Reprint requests: Dr. Sawayama, Department of Cardiology, Kawasaki Medical School and Hospital, Nakasange, Okayama, Japan 700

CHEST, VOL. 64, NO.3, SEPTEMBER, 1973