Malfunctioning Electrocardiographic Monitor Simulating Sinus Arrest

Malfunctioning Electrocardiographic Monitor Simulating Sinus Arrest

Malfunctioning Electrocardiographic Monitor Simulating Sinus Arrest* A ltzhak Kronzon, M.D.; Michael Schloss, M.D.; and George Bear, M.D. A 64-year...

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Malfunctioning Electrocardiographic Monitor Simulating Sinus Arrest*

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ltzhak Kronzon, M.D.; Michael Schloss, M.D.; and George Bear, M.D.

A 64-year-old patient was admitted to the hospital with a history of two syncopal episodes. The results of the physical examination, resting electrocardiogram and Hisbundle study were all normal. Study with a 24-hour ECG monitor (Holter) was at first interpreted as demonstrating periods of sinus arrest. However, more careful examination revealed that these actually represented transient speeding of the monitor tape, perhaps secondary to a semiconductor malfunction. Such monitor malfunction may stimulate severe rhythm disturbances.

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the Department of Medicine ( Division of Cardiology), New York University Medical Center, New York. Reprint requests: Dr . Kronzon, New York University Medical Cent er, 550 First Avenue, New York City 10028

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Hg. The carotid pulses were normal and equal, there was no jugular venous distention, and the lungs were clear. Examination of the heart showed the point of maximal impulse in the fifth intercostal space in the midclavicular line, the heart sounds were normal, and there were no murmurs. Findings from the rest of the phy sical examination were entirely within normal limits . The electrocardiogram revealed normal sinus rhythm, with an axis of 0· . There wer e no atrioventricular or intraventricular conduction abnormalities. The chest roentgenogram was normal; and the results of additional laboratory stu dies as described above, an echocardiogram, and urinary catecholamine stu dies were all within normal limits . Bundle of His recording was performed on the fourth hospital day and demonstrated normal atrio-His and H isventricle intervals. Atrial pacing with an attempt to suppress the sinus node was performed. With atrial pacing rates of up to 150 per minute, the sinus node recovery time was within normal limits . Twenty-four hour monitoring with an electrocardiographic monitor (Holter) was then performed. During the entire period of monitoring, the patient was asymptomatic. In reviewing the 24-hour tapes, the initial impression was suggestive of periods of sinus arre st with a duration up to six

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A 64-year-old man was admitted to New York University Hospital for evaluation of syncopal episodes. The patient was doing well until two year s prior to this admission when he had a sudden dizzy spell while crossing the street and fainted a few seconds later . He was then hospitalized and monitored for three days ; no arrhythmia was detected. Investigations to elucidate the cause of his syncopal ep isodes included a glucos e tolerance test , serial electrocardiograms and enzyme studies, blood cell counts, and a neurologic work-up. Th e results of these were all entirely normal. A syncopal episode occurred three days prior to this admission. Physical examination revealed a well-nourished, well-developed man in no distress. The heart rate was 60 beats per minute and regular, and the blood pre ssure was 120/80 mm

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FIGURE 2. Transient speeding of monitor (Holter) tape occurring during P-R interval (third beat, strip A) , during T wave (second beat, stri p B), and during entire PQRST com plex (strip C) .

CASE REPORT

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n patients presenting with syncopal e p isod es, a cardiologic evaluation is fr equently undertaken to determine the etiology. In the presence of a normal resting ele ctro ca rd io gra m , continuous monitoring has been found to be a useful tool in evaluating transient ECG changes. Howev er, technical problems with mechanical malfunction ma y rarely simulate rhythm disturbances . This report demonstrates such a case.

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FIGURE 1. Two rhythm strips from 24-hour recording simulating periods of sinus arrest with duration of 2 sec (A) and 6.2 sec (B).

582 KRONZON, SCHLOSS, BEAR

CHEST, 68: 4, OCTOBER, 1975

seconds (Fig lA and 1B) . More careful examination of the tapes, however , showed th at the se episodes were due to sudden transient speeding of the monitor tape. When the speeding was limit ed to th e T-P segme nt, the recording simulated sinus arres t. How ever , at various times during the recording, th e speeding could be see n to be limited to the PR interval ( Fig 2A ) or to the T wave (Fig 2B) or to the entire PQRST complex ( Fi g 2C ). The entire phenomenon was, therefore, inte rpreted as an artifact due to transient speed ing of the monitor tape. Repeated recordings with another monitor (Holter ) were entirely normal. The malfunctioning monitor was examined by the manufacturers. During the investigation, the y could not locate the site of the malfunction. However, it was assumed that due to a temporary malfunction of the semiconductor, the full 9 v of the battery, rather than 4.2 v, were transmitted to the monitor's motor, thus increasing its speed. DISCUSSION

Continuous recording by an electrocardiographic monitor is now being accepted as a reliable method for identifying transient arrhythmias and other electrocardiographic changes.t -" In the case report presented, malfunction of a monitor (Holter) simulated the appearance of abnormalities in cardiac rhythm. The mis interpretation of monitor recording malfunction may result in mismanagement of the patients and even perhaps implantation of pacemakers when not actually in dicated. We are not aware of such cases having been previously reported, and one must assume that monitor mechanical malfunction simulating such arrhythmias is a rare event. The purpose of this report is to call attention to this possibility and hopefully prevent its recurrence. REFERENCES

Gilson JS, Holter NJ, Glas scock WR : Clinical observations using the electrocardiocorder ASVEP continuous electrocardiographic system. Am J CardioI14:204-217, 1964 2 Corday E, Bazika V, Lang TW, et al : Detection of phantom arrhythmias and evanescent electrocardiographic abnormalities : Use of prolonged direct electrocardiocording. JAMA 193 :79-83, 1965

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h emodec tomas commonly a rise from th e carotid bodies and are usually b enign. The occurrence of this tumor in the mediastinum and a fatal course a re exceedingly rare. H ence, the following case is reported. CASE REpORT

A man aged 20 years was hospitalized on May II , 1973 for progressive brachial neuralgia of six months' duration. Clinical examination revealed dulln ess and diminish ed breath sounds in the right infraclavicular region . Th ere was no evide nce of a primary neoplasm in the neck or abdomen. A roentgenogram of the chest showed a rounded opacity in the right upper chest with erosion of th e first rib ( Fig I ) . The white blood cell count was 9,650 / cu mm, Th e differ ential count was 64 percent polymorphonuclear leukoc ytes, 34 percent lymphocytes, 2 percent eosinophils, and 2 percent rnonocytes, The hemoglobin level was 14.3 gm/l00 ml, and the erythrocytic sedimentation rate was 49 rum/hr. Th e levels of serum electrolytes, blood urea, and blood glucose, as well as the bleeding time , clotting time, and urinalysis results were normal. The patient's blood group was O. The result s of barium meal and intravenous pyelogram stud ies were normal, Right thoracotomy on May 13, 1973 revealed an extrapleur al mass in the apex of the chest. The tumor was very vascular and was found to be infiltra ting the brachial plexus. As much tumor tissue as possible was resected. Th e excised specimen was a poorly circumscribed, lobulated vascular tumor, 3 X 3 in, with areas of necrosis. Th e tumor was composed of large cells arrayed in an organoid pattern with groups of five to ten cells sepa rated by strands of Bbrocollagenous tissue containing small blood vessels (Fig 2 ). Th e blood vessels showed no endothelial prolifer ation . The cells were large epithelioid type with polyhedral and irregular shapes. The cytoplasm was abundant and eosinophilic, with occasional vacuolations. The nucl ei were single and large with vesicular to deep-staining properties. Mitotic figllTes were occasionally seen . The cells were weakly chromaffin-positive, and the PAS stain was negative. There was reticulin around the blood vessels and in the stroma separating the groups of cells. Th ere were no rosettes, neurohl asts, or ganglion cells. The classic organoid pattern and epithe lial cell appearance, with no evidence to suggest a secondary neoplasm, led to the diagnosis of chemodectoma. Th e immediate postoperative cour se was uneventful, Th e pati ent was given cobalt therapy, but the brachial neuralgia persisted, and a mass appea red in the supraclavicular area.

Malignant Mediastinal Chemodectoma * Solomon Victor , M.B., F.C.C.P.; K. Vijay Anand, M.B., B.S., P. Andappan, M.S.; Sarasa Bharathy, M.D.; Subba Rao, M.D .; and K. C. Reddy, M.S.

A 20-year-old man with a posterior mediastinal mass and erosion of the rib proved to have a malignant chemodectoma. The case is of interest because of the rare location and malignant fatal course. °From Vijaya Hospital, Madras, India. Reprint requests: Dr. Victor , A72 Kilpauk Garden Colony, Madras, South India 600 010

CHEST, 68: 4, OCTOBER, 1975

FIGURE 1. Chest roentgenogram showing mass in right upp er lung field.

MALIGNANT MEDIASTINAL CHEMODECTOMA 583