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Ann Thorac Surg 1995;60:556-560
© 1995 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

Successful Management of Junctional Tachycardia by Hypothermia After Cardiac Operations in Infants

Department of Pediatric Cardiology, Children's Hospital, and Division of Thoracic and Cardiovascular Surgery, Hannover Medical School, Hannover, Germany

Accepted for publication April 11, 1995.

	Abstract

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

 
Background. Junctional ectopic tachycardia is an early postoperative complication after intracardiac repair of congenital heart disease, especially in infants. Because of the high ventricular rate and the usually poor response to antiarrhythmic drugs, this condition is associated with a high morbidity and mortality. The purpose of this study was to assess the safety and efficacy of moderate body surface hypothermia in the treatment of postoperative junctional ectopic tachycardia in infants.

Methods. Six consecutive infants with postoperative junctional ectopic tachycardia (mean age at operation, 14 weeks) were treated with surface cooling. The decision to start treatment was based on the definition of a crit- ical heart rate (180 to 200 beats/min) in the presence of junctional ectopic tachycardia diagnosed according to established criteria. Moderate hypothermia (rectal temperature between 32° and 34°C) was achieved by placing ice bags on the child's body surface. The patients were sedated, mechanically ventilated, and paralyzed.

Results. Mean interval between diagnosis of tachycardia and initiation of hypothermia was 4 hours. Rectal temperature was rapidly (within 1 hour) lowered to 32° to 34°C in all 6 patients. This significantly lowered the tachycardia rate from 219 ± 27 beats/min to 165 ± 25 beats/min (mean ± standard deviation; p < 0.001). Three patients with signs of low cardiac output had restoration of stable hemodynamics once the tachycardia rate had been decreased by hypothermia. Cooling was maintained for a period of 24 to 88 hours (mean, 59 hours). No serious side effects were observed.

Conclusions. Early institution of moderate hypothermia by body surface cooling was a safe and efficient measure to control ventricular rate in infants with postoperative junctional ectopic tachycardia.

	Introduction

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

 
Junctional ectopic tachycardia is one of the most challenging arrhythmias encountered in pediatric cardiology and in pediatric intensive care medicine. This dysrhythmia typically occurs in two settings: a chronic congenital form [1, 2], and in the early postoperative course after open heart operation in infants and children [3]. Because of the hemodynamic impairment due to the high heart rate (HR) and the loss of atrioventricular synchrony and because of the usually poor response to conventional antiarrhythmic treatment, this condition is associated with considerable morbidity and mortality [4]. Postoperative junctional ectopic tachycardia is a self-limiting tachycardia [4], which usually subsides within 48 to 72 hours. Treatment therefore is focused on reduction of the tachycardia rate to improve cardiac output during this period of often severe hemodynamic compromise. Recently, propafenone, a class Ic antiarrhythmic agent, has been shown to be useful in postoperative junctional ectopic tachycardia [5]. Moderate body surface hypothermia is an alternative treatment strategy for postoperative junctional ectopic tachycardia in the clinical setting, and was reported for the first time in a small series of infants in 1987 [6]. In this report we describe our experience with this form of therapy in 6 infants with postoperative junctional ectopic tachycardia.

	Patients and Methods

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

 
Patients
Between June 1991 and February 1994 6 infants had postoperative junctional ectopic tachycardia and all were treated by moderate surface hypothermia. Details of the patients are shown in Table 1. Mean age at operation was 14 weeks (range, 4 days to 5 months). Mean weight at operation was 4.6 kg (range, 2.7 to 6.7 kg). Five patients were male and 1 was female. Three children suffered from tetralogy of Fallot, 2 had a ventricular septal defect, and 1 patient had ventricular septal defect and coarctation. In all patients a corrective operation was performed including patch closure of a ventricular septal defect as the most obvious common feature of surgical procedures. The operations were performed using deep hypothermic circulatory arrest and hypothermic cardiac arrest without cardioplegic solution in all patients.

Methods
DIAGNOSTIC CRITERIA.
Diagnosis of postoperative junctional ectopic tachycardia was based on the following criteria [4]: (1) QRS complex configuration during tachycardia similar to QRS complex morphology during early postoperative sinus rhythm (usually complete right bundle-branch block configuration), (2) atrioventricular dissociation with atrial depolarization at a lower rate than ventricular depolarization, (3) no effect on tachycardia of overdrive atrial or ventricular pacing (tested in all patients) or by external cardioversion (performed without success in 1 patient), and (4) a ``warming-up'' phenomenon with a steady increase in HR to pathologic levels at the beginning of the dysrhythmia (Fig 1).

View larger version (34K): [in this window] [in a new window]   Fig 1. . Surface electrocardiogram of patient 1 after onset of junctional ectopic tachycardia 3 hours postoperatively. QRS complexes show right bundle-branch block morphology; ventricular rate is 212 beats/min. Atrioventricular dissociation is present with an atrial rate of 144 beats/min. Arrows indicate two consecutive clearly visible P waves.

Treatment initially consisted of intravenous propafenone as the first-line therapy in the first 4 consecutive patients of the study. Propafenone was given as boluses of 1 to 1.5 mg/kg (2 patients) or as a continuous infusion of 300 mg/m² per day (2 patients) once the diagnosis of postoperative junctional ectopic tachycardia was established according to the criteria cited above. If this therapy did not show a significant decrease in HR within 30 minutes, treatment was changed to hypothermia. In the last 2 patients hypothermia was introduced as the first-line therapy early in the course of the tachycardia.

Hypothermia was initiated immediately after failure of propafenone in 4 infants. In the remaining 2 children, hypothermia was started upon diagnosis of postoperative junctional ectopic tachycardia. The goal was a rectal body temperature of 32° to 34°C obtained by surface cooling. This was achieved with ice bags, wrapped up in cotton to avoid skin damage, which were preferentially placed in the inguinal or frontal region, and additionally or alternatively under the back. Once a rectal temperature of 34°C was reached, the ice bags were removed, as it was observed that temperature further continued to decrease to between 32° and 33°C. The skin was closely watched clinically for possible signs of skin damage induced by cooling. After reduction of tachycardia rate by hypothermia sequential atrial–ventricular pacing by epicardial electrodes (routinely placed during operation) was successfully performed to further improve hemodynamics by restoring atrioventricular synchrony.

All the patients were mechanically normoventilated, sedated (morphine 0.1 mg • kg^-1 • h^-1) and paralyzed (vecuronium bromide, 0.1 to 0.2 mg • kg^-1 • h^-1) during hypothermia to prevent shivering. Blood gases, glucose, and electrolytes were monitored closely and corrected if necessary. Parenteral nutrition was given from the third postoperative day on. Arterial and right atrial pressures were continuously monitored by radial artery and right atrial line, respectively. Once the patients were in a clinically stable condition for at least 24 hours, rewarming of patients was achieved within 1 to 3 hours by taking away ice bags and by using heating lights if necessary. Continuous electrocardiographic monitoring was maintained through the entire postoperative hospital stay. Before hospital discharge all patients had a 24-hour Holter monitor registered.

	Results

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

 
During the study period 8 infants (among approximately 170 infants operated on with cardiopulmonary bypass during the same period) had development of junctional ectopic tachycardia in the early postoperative course. In 2 of them ventricular rates were between 140 and 160 beats/min and the tachycardia resolved within 3 days without the need for intervention.

In the other 6 patients treatment was necessary due to the high ventricular rates. In these patients operation had been performed as preoperatively planned. Postoperative echocardiographic evaluation did not reveal significant residual lesions.

Onset of postoperative junctional ectopic tachycardia was documented between 1 and 42 hours postoperatively (mean, 12 hours; median, 7.5 hours). Propafenone, when given as antiarrhythmic treatment of first choice, did not significantly influence HR in any of the 4 patients in whom it was used (HR fell from a mean of 225 beats/min to a mean of 218 beats/min; p = not significant). Therefore, propafenone was judged to be insufficient. Hypothermia was initiated within a mean of 4 hours after diagnosis of postoperative junctional ectopic tachycardia had been established. Mean rectal temperature of the 6 patients at initiation of treatment was 37.4°C (range, 37.0° to 37.7°C). Cooling down to a rectal temperature of 32° to 34°C was rapidly achieved (within 1 hour) in all patients. Duration of cooling ranged from 24 to 88 hours (mean, 59 hours).

In all patients a significant fall in HR was seen shortly after the initiation of hypothermia. Maximum HR before cooling ranged from 192 to 263 beats/min with a mean of 219 beats/min. Within 4 hours after initiation of cooling HR was reduced to a range of 141 to 205 beats/min with a mean of 165 beats/min. This represents a significant (p < 0.001 by paired t test) fall in HR by a mean of 54 beats/min (range, 34 to 83 beats/min) (Fig 2).

View larger version (17K): [in this window] [in a new window]   Fig 2. . Change in heart rate (HR) within the first 4 hours after beginning of body surface cooling. Zero indicates the time when the hypothermia was started.

Once the patients had been cooled the rate of postoperative junctional ectopic tachycardia remained at a stable level without secondary tachycardia peaks. No other therapeutic interventions were undertaken during the initial critical phase of cooling. Rewarming was not associated with other dysrhythmias or with a significant increase in HR (Fig 3). At the time of rewarming, all the patients still had a predominant accelerated junctional rhythm/slow junctional ectopic tachycardia with ventricular rates between 130 and 160 beats/min (mean, 144 beats/min). Although the tachycardia was still present, hypothermia or other medical management was not required any more due to the slow heart rate. Predominant sinus rhythm reoccurred at a mean of 5.5 days postoperatively (range, 3 to 10 days).

View larger version (14K): [in this window] [in a new window]   Fig 3. . Variation in heart rate (HR) during and after rewarming. (A = time when rewarming was started; all patients had a rectal temperature <34°C at that time. B = time when a rectal temperature of 36°C was reached. C = 12 hours after the start of rewarming. Rectal temperature was greater than 37°C in all patients at that time).

All patients survived the tachycardia and are well and without any neurologic deficit. Heart rhythm was checked on an outpatient basis by 24-hour Holter monitors at 3 months postoperatively and then at 6-month intervals. Three of the patients showed premature atrial contractions (<1% of QRS complexes), and 1 patient showed short runs of supraventricular tachycardia at the time of postoperative hospital discharge. Subsequent 24-hour Holter monitors were normal. At a mean follow-up of 12 months (range, 2 to 32 months) all 6 patients were in stable sinus rhythm without antiarrhythmic treatment.

	Comment

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

 
Postoperative junctional ectopic tachycardia (also called His bundle tachycardia) is one of the most challenging problems in the early course after open heart operations in infants, especially after correction of tetralogy of Fallot or ventricular septal defect alone, but operation for any form of congenital heart disease can be involved.

Junctional ectopic tachycardia is characterized by a fast junctional rhythm with atrioventricular dissociation. Its pathophysiologic mechanism is enhanced automaticity [7]. The causative factors that lead to this arrhythmia are not clearly understood. It is hypothesized that disruption of conduction tissue by mechanical irritation during operation results in an arrhythmogenic focus [8]. Because of atrioventricular dissociation and the high HR this rhythm disturbance may be associated with critically impaired hemodynamics, often causing poor outcome [9]. As postoperative junctional ectopic tachycardia is a self-limiting tachycardia, which usually subsides within 2 to 3 days [4], its management is focused on reducing the tachycardia rate during this period, thus allowing the patient's survival during the phase of severe hemodynamic compromise. As postoperative junctional ectopic tachycardia has been shown to be mainly resistant to conventional antiarrhythmic drugs, alternative therapeutic strategies including transcatheter [10] or surgical [11] ablation of the bundle of His have been proposed.

In 1987 propafenone was reported as a promising new therapeutic option in the treatment of postoperative junctional ectopic tachycardia [5]. In addition, propafenone has been shown to be effective in patients with the congenital form of junctional ectopic tachycardia [2]. Problems with the use of propafenone are related to the negative inotropic effect, which may limit the use of the drug in this setting. Until 1991, propafenone had been used as the single agent in 3 patients with postoperative junctional ectopic tachycardia in our institution. Of these patients, 2 had a benign course and survived (1 patient with a sufficient response to propafenone, the other patient not responding to propafenone but with tachycardia rates not exceeding 200 beats/min). The last patient, a 4-year-old boy after a modified Fontan operation, finally died. The promising results of the first studies on the use of moderate body surface hypothermia in pediatric patients with postoperative junctional ectopic tachycardia encouraged us to the start the protocol presented.

Hypothermia is known to suppress cellular automaticity [12]. On the basis of this effect the application of moderate hypothermia in infants with postoperative junctional ectopic tachycardia proved to be a valuable alternative method in the first series reported. Hypothermia successfully slowed the heart rate and resulted in survival in all 3 infants in that series [6]. Confirmation of these first optimistic results came from two other institutions. In one study 6 pediatric patients with low cardiac output due to postoperative junctional ectopic tachycardia were treated with moderate hypothermia. Four infants survived; 2 older children after Fontan-type operations died [13]. In another study cooling was attempted in 10 children and was successful in 8. Of these 5 survived. In the survivors mean interval between occurrence of tachycardia and inititation of cooling was 1 hour; in those patients who died, it was 9 hours [14].

In our patients hypothermia was initiated early in the evolution of junctional ectopic tachycardia. As soon as the diagnosis was clearly established and after propafenone had failed to slow significantly the tachycardia rate within 30 minutes, cooling was started irrespective of the hemodynamic state of the patients and irrespective of the tachycardia rate (already at rates less than 200 beats/min in 2 patients). A significant effect of the reduction of epinephrine and dopamine dose on the rate of the tachycardia seems unlikely because the dose of these inotropic agents was reduced (if possible) during the warming-up phase of the tachycardia. During the initial phase of hypothermia, dosage of inotropic agents and vasodilators was not changed in any of the 6 patients.

In the present study, induction and maintenance of hypothermia was achieved in all patients and proved to be a safe procedure. Most of the patients exhibited an increase in blood pressure and urinary output. Cold diuresis as a reason for improved urinary output secondary to renal tubular absorption impairment seems unlikely but cannot be excluded because the urine of the patients in the hypothermic state had not been examined during the present study. Side effects such as metabolic acidosis were not encountered [6] because hypothermia-induced peripheral vasoconstriction could successfully be managed with vasodilator therapy. Reflex tachycardia was not observed while vasodilators were administered. Shivering was avoided by relaxation. During cooling and rewarming serious dysrhythmias such as atrial flutter or ventricular ectopy can theoretically occur [15]. This, however, was not observed in our study population.

The concomitant administration of digoxin during hypothermia is unlikely to have affected the course of the tachycardia. All the patients had been given intravenous digoxin already before the evolution of junctional ectopic tachycardia, and the dosage was not changed during tachycardia. Several reports have shown the failure of digoxin to influence the rate of junctional ectopic tachycardia [5, 16]. Whether routine use of digoxin postoperatively (which has now been abandoned) contributed to this arrhythmia cannot be excluded.

Moderate hypothermia by surface cooling is a promising and safe approach to management of postoperative junctional ectopic tachycardia in infants. It is not a causative treatment. By reducing the tachycardia rate, however, it allows survival until spontaneous resolution of the dysrhythmia occurs.

The limitations inherent in this study are those of the clinical investigation of one treatment modality in a small number of patients and without a control group. As it was the purpose to assess the efficacy of hypothermia, no comparisons with the effectiveness of propafenone in the treatment of this condition can be made. Due to the small number of patients presented, no comments on what mortality would be if a larger group of patients were treated with hypothermia can be made.

Our experience suggests that moderate hypothermia can be considered the treatment of choice for junctional ectopic tachycardia after open heart operations in infants. Ideally cooling should be started before the patients show signs of hemodynamic deterioration. In case of failure of hypothermia to improve the hemodynamic situation, catheter ablation of the bundle of His should be considered as the last resort.

	Footnotes

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

 
Address reprint requests to Dr Pfammatter, Department of Pediatric Cardiology, Children's Hospital, Hannover Medical School, Konstanty-Gutschowstrasse, D-30623 Hannover, Germany.

	References

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

 

1. Villain E, Vetter VL, Garcia JM, Herre J, Cifarelli A, Garson A. Evolving concepts in the management of congenital junctional ectopic tachycardia. Circulation 1990;81:1544–9.[Abstract/Free Full Text]
2. Paul T, Reimer A, Janousek J, Kallfelz HC. Efficacy and safety of propafenone in congenital junctional ectopic tachycardia. J Am Coll Cardiol 1992;20:911–4.[Abstract]
3. Grant JW, Serwer GA, Armstrong BE, Oldham HN, Anderson PAW. Junctional tachycardia in infants and children after open heart surgery for congenital heart disease. Am J Cardiol 1987;59:1216–8.[Medline]
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9. Krongard E. Postoperative arrhythmias in patients with congenital heart disease. Chest 1984;85:107–13.[Free Full Text]
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11. Gillette PG, Garson A, Hesslein PS. Successful surgical treatment of atrial–junctional and ventricular tachycardia unassociated with accessory connections in infants and children. Am Heart J 1981;102:984–91.[Medline]
12. Hoffmann BF. Temperature effects on cardiac transmembrane potentials. In: Dripps RD, ed. Physiology of induced hypothermia. Washington, DC: National Academy of Sciences, 1956:302–26.
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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Gerhard Ziemer Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Pfammatter, J.-P. Articles by Kallfelz, H. C. Search for Related Content PubMed PubMed Citation Articles by Pfammatter, J.-P. Articles by Kallfelz, H. C.