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

Transcription

1 Successful Management of Junctional Tachycardia by Hypothermia After Cardiac Operations in Infants Jean-Pierre Pfammatter, MD, Thomas Paul, MD, Gerhard Ziemer, MD, and Hans C. Kallfelz, MD Department of Pediatric Cardiology, Children's Hospital, and Division of Thoracic and Cardiovascular Surgery, Hannover Medical School, Hannover, Germany 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 critical 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 'unctional ectopic tachycardia is one of the most challenging arrhythmias encountered in pediatric cardiol- J ogy and in pediatric intensive care medicine. This dysrhythmia typically occurs in two settings: a chronic congenital form [1, 21, and in the early postoperative course after open heart operation in infants and children 13]. 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 I41. Postoperative junctional ectopic tachycardia is a selflimiting 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 lc antiarrhythmic agent, has been shown to be useful in postoperative junctional ectopic tachycardia [51. Moderate body surface hypothermia is an alternative treatment strategy for postoperative junctional ectopic tachycardia in the clinical setting, and Accepted for publication April I1, Address reprint requests to Dr Pfamrnatter, Department of Pediatric Cardiology, Children's ttospital, Ilannover Medical School, Konstantv- Gutschowstrasse, D Hannover, Germany. 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 I hour) lowered to 32 to 34 C in all 6 patients. This significantly lowered the tachycardia rate from 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. (Ann Thorac Surg 1995;60:556-60) 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 Patients Between June 1991 and February 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. Preoperatively all 6 infants were in stable sinus rhythm. Three patients were receiving digoxin preoperatively; they continued to receive intravenous digoxin in 1995 by The Society of Thoracic Surgeons (95)00425-K

2 Ann Thorac Surg PFAMMATTER ET AL ;60: HYPOTHERMIA IN JUNCTIONAL TACHYCARDIA Table 1. Patient Characteristics Reoccurrence Patient Age at Maximum HR Onset of JET Duration of of SR (days No. Sex Operation Diagnosis (beats/min) (h postop) Cooling (h) postop) Outcome 1 M 5 mo VSD, PHT Alive 2 M 3 mo VSD, PHT Alive 3 F 4 days VSD, CoA Alive 4 M 4 m o TOF Alive 5 M 4 mo TOF Alive 6 M 5 mo TOF Alive CoA - coarctation of the aorta; F lemale; M male; PHT pulmonary hypertension; SR = sinus rhythm; TOF - tetralogy of Fallot; VSD ventricular septal defect. the postoperative course. In the remaining 3 patients, digoxin administration was started routinely in the immediate postoperative period before junctional ectopic tachycardia developed. Digoxin serum levels were determined every 24 hours and remained within normal limits in all 6 patients. All patients were given intravenous furosemide (1 to 2 mg/kg per dose) as needed. Inotropic support consisted of dopamine (5 to 9 tzg" kg ' min ') in all patients with additional epinephrine in 2 infants (0.05 to 0.2 ttg.kg ~.min ~). All patients were on vasodilation with intravenous nitroglycerin (5 to 15 /zg. kg ~-min ~). As soon as the diagnosis of junctional ectopic tachycardia was established, inotropic support (ie, epinephrine and dopamine) was reduced to the lowest tolerable level. The study protocol had been approved by the hospital's scientific board. Informed consent was obtained from the parents. Methods DIAGNOSTIC CRITER[A. 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). TREATMENT PROTOCOL. The decision to start treatment of postoperative junctional ectopic tachycardia was based on the definition of a critical heart rate (180 to 200 beats/min) in the presence of the diagnostic criteria cited above. The objective was to begin early therapy to avoid low cardiac output failure (as judged on clinical grounds, without invasive cardiac output measurements) after inotropic and possible chronotropic agents had been reduced as mentioned above. 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 I to 1.5 mg/kg (2 patients) or as a continuous infusion of 300 mg/m 2 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 Ill!! Fi~,, ~. Surface electrocardio~am of patient 1 after onset of functional ectopic tachycardia 3 hours postoperatively. QRS complexes show right bundle-branch block morphology; ven~cular rate is 212 beats/rain. Atrioventn'cular dissociation is present with an atn'al rate qf 144 beats/rnin. Arrows indicate two consecutive clearly visible P waves. ls

3 558 PFAMMATTER E~[ AL Ann Thorac Surg HYPOTHERMIA INJUNCIIONAI IACHYCARDIA 1995;60: electrodes (routinely placed during operation) was successfully performed to further improve hemodynamics by restoring atrioventricular synchrony. All the patients were mechanicallv normoventilated, sedated (morphine 0.1 mg-kg ~' h ~) and paralyzed (vecuronium bromide, 0.1 to 0.2 mg.kg ~. h ~) 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 arted' 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 necessarv. Continuous electrocardiographic monitoring was maintained through the entire postoperative hospital stay. Before hospital discharge all patients had a 24-hour Holter monitor registered. Results 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 I 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/rain 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 ~tr was seen shortly after the initiation of hypothermia. Maximum HR before cooling ranged from 192 to 263 beats/rain with a mean of 219 beats/rain. 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/rain. This represents a significant (p < by paired t test) fall in HR bv a mean of 54 beats/rain (range, 34 to 83 beats/rain) (Fig 2). Before hypothermia was started, 3 patients showed oliguria (<0.5 ml of urine, kg ' h ~), a fall in arterial HR Fig 2. Change in heart rate (HR) within the first 4 hours after bey~inning qf body surface cooling. Zero indicates the time when the h qpothennia was started. blood pressure, or both. The remaining 3 patients were treated before any clinical sign of low cardiac output developed. These symptoms resolved within a few hours after introduction of hypothermia. The prolonged state of hypothermia was not associated with any serious side effects in any patient. In no case was significant metabolic acidosis or electrolyte imbalances observed. Besides temporary local redness the cooling procedure itself did not cause dermal injury. 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/rain). 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). During the whole postoperative hospital stay no infectious complications were observed in the 6 patients. This is of special importance as hypothermia is known for its potential to induce suppressed immune response. 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

4 Ann Thorac Surg PFAMMATTER ET AL ;60: HYPOTHERMIA IN JUNCTIONAL TACHYCARDIA HB A B C Fig 3. Variation in heart rate (HR~ during and after rewarming. (A time when rewarming was starte& all patients had a rectal temperature ~34 C at that time. B time when a rectal temperatore 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). were in stable sinus rhythm without antiarrhythmic treatment. Comment 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 effecl 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 I 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 hypothermiainduced 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

5 560 PFAMMATFER ET AL Ann Thorac Surg HYPOTHERMIA IN JUNCTIONAL TACHYCARDIA 1995;60: 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. 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: Paul T, Reimer A, Janousek J, Kallfelz HC. Efficacy and safety of propafenone in congenital junctional ectopic tachycardia. J Am Coil Cardiol 1992;20: 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: Gillette PG. Diagnosis and management of postoperative junctional ectopic tachycardia. Am Heart J 1989;118: Garson A, Moak JP, Smith RT, Norton JB. Usefulness of propafenone for control of postoperative junctional ectopic tachycardia. Am J Cardiol 1987;59: Bash SE, Jitendra JS, Albers WH, Geiss DM. Hypothermia for the treatment of postsurgical greatly accelerated junctional ectopic tachycardia. J Am Coll Cardiol 1987;10: Garson A, Gillette PG. Junctional ectopic taehycardia in children: electrocardiography, electrophysiology and pharmacologic response. Am J Cardiol 1979;44: Till JA, Slew YH, Rowland E. Histopathological findings in three children with His bundle tachycardia occurring subsequent to cardiac surgery. Eur Heart J 1992;13: Krongard E. Postoperative arrhythmias in patients with congenital heart disease. Chest 1984;85: Gillette PG, Garson A, Porter CJ. Junctional ectopic tachycardia: new proposed treatment by transcatheter His bundle ablation. Am Heart J 1983;106: 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: Hoffmann BF. Temperature effects on cardiac transmembrane potentials. In: Dripps RD, ed. Physiology of induced hypothermia. Washington, DC: National Academy of Sciences, 1956: Balaji S, Sullivan J, Deanfield J, James I. Moderate hypothermia in the management of resistant automatic tachycardias in children. Br Heart J 1991;66: Till JA, Rowland E. Atrial pacing as an adjunct to the management of postsurgical His bundle tachycardia. Br Heart J 1991;66: Rankin AC, Rae AP. Cardiac arrhythmias during rewarming of patients with accidental hypothermia. Br Med J 1984;289: Sholler GF, Walsh EP, Mayer JC, Saul JP, Gamble WJ, Lang P. Evaluation of staged treatment protocol for postoperative rapid junctional tachycardia [Abstract]. Circulation 1988; 78(Suppl 2):597.