Runaway Pacemaker with Demonstration of Supernormal Period of Excitation * Udipi R. Shettigar, M.D.; Robert E. Kreiger, M.D.; Ronald Krone, M.D.; and Alexander S. Geha, M.D., F.C.C.P.
This report documents the presence of supernormal conduction in the normal heart. A 26-year-old woman with congenital heart block treated with a fixed-rate permanent pacemaker returned to the hospital with evidence of pacemaker failure. Pacemaker spikes occurred regularly at a rate of 140 per minute, eliciting ventricular responses only when they occurred during the supernormal period of the cardiac cycle. Telemetric cardiac monitoring revealed complete pacemaker capture, at a rate of 140 per minute when the patient was walking. FoDowing replacement of the pulse generator, the pacemaker performed effectively.
T
he supernormal recovery phase in cardiac muscle follows the vulnerable portion of the refractory period, and represents the time when the heart muscle will respond to subliminal stimulus, which cannot evoke a response at any other time in the cardiac cycle. Adrian," in 1920, coined the term "supernormal phase" and demonstrated such a phenomenon on both nerve and cardiac muscle of a frog. Subsequently, although several authors found a similar period of excitability in the mammalian ventricle and in isolated Purkinje fibers, other investigators were unable to demonstrate it. In 1960, Soloff and Fewell- first demonstrated the supernormal period in the human heart, while pacing with subthreshold stimuli. Since then, several authors 2 , 6 , 1 have reported this in patients with electronic pacemakers. A patient similar to ours was reported by Parker and Kaplan'" in 1971; however, in our patient there was also a demonstration ·From the Division of Cardiology, Department of Medicine, The Jewish Hospital of St. Louis, Washington University School of Medicine, St. Louis. Reprint requests: Dr. Kleiger, 216 South Kingshighway, St.
Louis 63110
of occasional periods of one to one ventricular response to pacemaker discharges following a ventricular response to pacemaker discharge in the supernormal period. This phenomena was observed only when the patient was walking. Our patient also had a runaway pacemaker, which is an uncommon complication of permanent cardiac pacing. CASE
REPoRT
A 26-year-old housewife was first seen by a physician in 1957 when she was nine years old, with a diagnosis of complete heart block. The patient' was asymptomatic until she was 19 years of age, when she first experienced dizzy spells and syncopal attacks. A fixed-rate epicardial permanent pacemaker was implanted. Since then the pulse generator bas been replaced twice. In 1969 a transvenous bipolar (Medtronic 586OC) fixed-rate pacemaker set at a rate of 80 per minute was inserted. The patient subsequently was lost to follow-up. In May of 1972 she came to the emergency room of Jewish Hospital with a one-day history of dizziness, fatigue and intermittent palpitations. The electrocardiogram revealed complete heart block and a junctional rhythm at a rate of 50 per minute. The pacemaker spikes appeared regularly at a rate of 140 per minute, eliciting a ventricular response, whenever pacemaker spikes fell between 0.50 to 0.64 second after the QRS. Figure 1 shows a representative response occurring with a pacemaker stimulus .52 seconds after the QRS. Telemetric cardiac monitoring revealed occasional runs of one to one ventricular response which occurred only when the patient was walking (Fig 2). These runs seemed to be initiated by pacemaker spikes falling in the supernormal period of the regular beats but, unfortunately, the onset of such periods could not be documented on paper. There were no appreciable fluctuations in pacemaker spike amplitude during the period of observation. Analysis of x-ray film findings showed 99 percent battery deflection. The output was two volts. The patient underwent replacement of the pulse generator one day following admission to the hospital (Medtronic 590, set at a rate of 82 per minute), and bas remained asymptomatic to date. DISCUSSION
A supernormal period of enhanced excitability is a property of cardiac muscle that has been observed experimentally in cold-blooded animals and in mammalian as well as human hearts. Katz and Pick 12 have sug-
FIGURE 1. Electrocardiogram of 26-year-old woman with congenital heart block. Pacemaker bas failed and pacemaker spikes are occurring at 140 per minute. Rhythm is junctional with complete block. Pacemaker spikes elicit response occurring at end of T wave (see beats marked X). This period represents supernormal period.
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RUNAWAY PACEMAKER 227
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·H .'. FIGURE 2. Pacemaker spikes occurring regularly at rate of 140 per minute, eliciting one to one ventricular response, noted several times when patient was walking.
gested that supernormal periods are not demonstrable in the normal myocardium, but can be shown in a depressed myocardium. Feldman" was not able to demonstrate supernormal excitability in any of the ten patients he studied. In Feldman's patients the basic cardiac rhythm was maintained by a pacemaker, while a second pacemaker catheter in the right ventricle discharged subliminal impulses at various intervals. However, other authors" have been able to demonstrate the existence of supernormal periods of excitability in their patients when the myocardium was stimulated by varying the amplitude and timing of the stimulus. With the advent of flxed-rate permanent transvenous pacemakers as a method of treatment for heart block, several instances of competitive pacing have resulted and occasionally demonstrated supernormal periods. 4,1,9,lo Dressler et al" studied five patients with pacemaker failure for the existence of supernormal periods of myocardial excitability. They found that supernormal periods of excitability consisted of at most two phases: one, the "phase of high supernonnality," in which every subthreshold stimulus elicited a response; and second, the "phase of low supernormality," during which some subthreshold stimuli were effective, while others were not. Our patient demonstrated these findings as well. A subliminal stimulus falling between 0.50 to 0.56 second after the QRS, elicited a response 100 percent of the time, whereas a stimulus falling between 0.56 to 0.64 second after the QRS elicited a response only some of the time. However, this distinction between high and low supernormal periods of excitability was not present at all times. This variability probably could be attributed to the spontaneous and physiologic alterations in the ventricular threshold for excitability. It is evident from these several reports that supernormal periods can exist anytime between the nadir of the T wave and the initial portion of U waves and may have a duration of 40 to 150 msec, In our patient, the supernormal period of excitability was demonstrated when the failing pacemaker was discharging subliminal stimuli at a runaway rate of 140 per minute. The demonstration of one to one ventricular response to subliminal pacemaker stimuli when the patient was walking is an interesting phenomenon and has not been previously reported. The explanation for this response is not clear. It is most likely due to the lowering of the ventricular threshold for
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excitation during physical exertion by release of endogenous catecholamines or an alteration of autonomic tone. There was no indication of any increase in the pacemaker stimuli strength when ventricular response occurred. Preston et aIlS studied threshold changes in 14 patients with implanted pacemakers. They have demonstrated the lability of the myocardial threshold in man, and the susceptibility of threshold to manipulation by physiologic activity and pharmacologic agents. Epinephrine, methylprednisolone, or potassium chloride in Ringer's solution lowered the threshold. A solution of insulin, aldosterone, potassium in 5 percent dextrose, and 3 percent sodium chloride increased the threshold. Three physiologic variables, eating, sleeping and exercise produced signi6cant changes in the threshold. Elevation of the threshold was accompanied by sleeping or consumption of a large meal. On the other hand, even mild exercise caused significant lowering of the threshold level. Preston, et al,13 postulated that spontaneous physiologic changes in the level were related to changes in the sympathetic tone. Walker et al lO,12 have reported two patients with pacemaker generator failure in whom subliminal pacemaker stimuli elicited a ventricular response when potassium was administered, even if the serum potassium were normal. This suggested the administration of potassium as a method of restoring myocardial responsiveness to a partially exhausted pacemaker until a replacement can be implanted. Runaway pacemakers are an uncommon complication of permanent cardiac pacing, Wallace et al 15 have recently reviewed 44 cases of runaway pacemakers, with an overall mortality of 34 percent. Runaway pacing has been reported in each of five types of pulse generators: fixed rate, variable rate, synchronous, stand-by and demand. It has been found to occur at any time during the life span of a pacemaker, and has been observed from as early as two days to as late as 36 months following implantation. The runaway rate may range anywhere from llO to 900 per minute. Twenty-three percent of reported patients reviewed by Wallace et al 16 had a runaway pacemaker rate of between 150 to 300 per minute. Usually, the amplitude of the pacing impulse decreases as the rate increases, resulting in a loss of effective pacing. Most runaway pacemakers have been due to pacemaker electronic component failure such as failure of capacitors, transistors, or transformers or wire
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fracture. Battery failure is an uncommon cause of runaway pacemakers.ts-F and it does not usually cause a runaway rate greater than 130 per minute. Treatment urgently requires replacement of the pacemaker generator. Our patient represented a case of runaway pacemaker due to battery failure. The existence of a supernormal period of excitability was shown. A change iri threshold during activity was demonstrated by episodes of one to one ventricular response to subliminal pacemaker stimuli when the patient was walking. The mechanism of the lowered threshold is uncertain but may represent response to the endogenous release of catecholamines or change in autonomic tone.
1 Adrian ED: The recovery process of excitable tissues. J Physiol (Pt. 1) 54: I, 1920 2 Soloff LA, Fewell IW: Super normal phase of ventricular excitation in man. Its bearing on genesis of ventricular premature systoles and a note on atrioventricular conduction. Am Heart J 59:869, 1960 3 Tavel ME, Fish C: Repetitive ventricular arrhythmia resulting from artificial internal pacemaker. Circulation 30:493, 1964 4 Linenthal AJ, Zoll PM: Quantitative studies of ventricular refractory and super normal periods in man. Trans Assoc Am Physicians 75:285, 1962 5 Feldman DS: Excitability of human heart on endocardial stimulation. Clin Res 11: 166, 1963 6 Dolara A, Camilli L: Super normal excitation and conduction. Electrocardiographic observations during subthreshold stimulation in two patients with implanted pacemaker. Am J Cardio121:746, 1968 7 Dressler W, Jones S, Swartz J: Super normal phase of myocardial excitability in man. Circulation 32 (Suppl 2) : 79, 1965 8 Burchell HG: Analogy of electronic pacemaker and ventricular parasystolic with observations on refractory period, super normal phase, and synchronization. Circulation 27:878,1963 9 Burchell HB, Connolly DC, Ellis FH Jr: Indication for and results of implanting cardiac pacemakers. Am J Med 37:764,1964 10 Walker WJ, Elkins JT, Wood LW: Effect of potassium response to a subthreshold cardiac pacemaker. N Eng! J Med 271:597, 1964 11 Dick A, Langendorf R, Katz LN: The super normal phase of atrioventricular conduction. 1. Fundamental mechanism. Circulation 26:388, 1962 .12 Katz LN, Pick A: Clinical Electrocardiography. (Pt 1) The Arrhythmias. Philadelphia, Lea and Febiger, 1956 .13 Preston TA, Fletcher RD, Luecher BR, et al: Changes in myocardial threshold. Physiologic and pharmacologic factors in patients with implanted pacemaker. Am Heart J 74:235-242, 1967 14 Surawiez: Measure of ventricular excitability threshold by hyperpotassemia. JAMA 191:1049, 1965 15 Wallace WA, Abelmann WH, Norman JC: Runaway demand pacemaker. A report, in vitro reproduction and review. Ann Thorac Surg 9:209-220, H170 16 Chardack W, Gage AA: Two years clinical experience with implantable pacemaker for complete heart block. Chest 43:225, 1963
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17 Furman S, Escher JW, Lister J, et al: A comprehensive scheme for management of pacemaker malfunction. Ann Surg 163:611-620, 1966 18 Parker DP, Kaplan MA: Demonstration of super normal period in the intact human heart as a result of pacemaker failure. Chest 59:461, 1971
Empyema Due to Actinomycoses naeslundi* Monroe S. Karetzky, M.D., F.C.C.P.,oo and Julius W. Garoey, M.D.t
A case of pulmonary actinomycosis due to Actinomyces naeslundi in a 20-year-old woman is described. She is the first patient in whom this agent has been shown to be pathogenic for man. The resnIting empyema responded to therapy but decortication was required.
A israeli.
ctinom ycosis in man is caused by Actinomyces 1 , 2 It is a rare entity but with the recognition of the importance of obtaining anaerobic cultures, it may be expected to be seen with increasing frequency." Actinomyces naeslundi, like A israeli, is a saprophytic member of the normal mouth flora, but the organism is facultative rather than anaerobic and has never been found to be pathogenic.vs This paper presents the first clinical report of actinomycosis due to A naeslundi. CASE REPORT
A 20-year-old woman had been in good health until seven days prior to hospitalization when she developed shortness of breath, dyspnea on exertion and orthopnea accompanied by fever, shaking chills and night sweats. Three days prior to admission she began to have a productive cough, and pleuritic pain over the left posterior thorax. One month prior to her illness she was in an automobile accident but denied head trauma or loss of consciousness. On admission, she was noted to be tachypneic and dehydrated. Her pulse rate was l00/minute, with blood pressure of 130/80 mm Hg, a respiratory rate of 20/minute and a temperature of 101.6°F, orally. Examination of the mouth revealed poor dental hygiene with partial upper and lower edentia. Physical examination of her chest showed consolidation on the left. Significant laboratory findings included a hematocrit value of 32 percent and a white blood cell count of 14,OOO/ml with a marked shift to the left. Chest x-ray films showed pleural effusion on the left, and after needle thoracentesis yielded pus, a chest tube was inserted. Thirteen hundred ml of pus o From the Departments of Medicine and Surgery, Morrisania Hospital, Bronx, N.Y. "Director of Pulmonary Division, Morrisania Hospital; Assistant Professor of Medicine, Albert Einstein College of Medicine. . tDirector of Thoracic Surgery, Morrisania Hospital; Assistant Professor of Surgery, Albert Einstein College of Medicine. Reprint requests: Dr. Karetzkll, Montefiore-M01risania Affiliation, 168th and Gerard, Bronx 10452
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