Diagnosis and management of junctional ectopic tachycardia

Diagnosis and Management of Junctional Ectopic Tachycardia Farhan Sheikh, MBBS, Maninderdip Uppal, MD, Matthew Farina, MD, and John J. Wilson, MD ' U N C T I O N A L E C T O P I C tachycardia (JET) is an infrequent complication occurring in children undergoing cardiac operations. The incidence has been reported to be between 7% and 13%. ~,2 Fortunately, it is a rare form o f tachyarrhythmia, because its diagnosis carries a poor prognosis, reaching a mortality o f up to 50%. 3 Therefore, early recognition and treatment are of paramount importance. JET is characterized by a narrow complex tachycardia with complete atrioventricular (AV) dissociation or retrograde 1:1 ventriculoatrial conduction. The sinus rate is slower than the ventricular rate, and the P waves often may not be discernible. Ventricular rates may exceed 300 beats/min but are frequently over 200 beats/rain. The QRS complex is generally unchanged. This report describes the case o f a 26-week-old male infant who developed postoperative JET after repair o f ventricular septaI defect (VSD) and pulmonic stenosis.

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CASE REPORT A male child of an uncomplicated 39-week gestation pregnancy was noted at birth to have a murmur, which was diagnosed on follow-up echocardiogram as subvNvular pulmonic stenosis in addition to the VSD. Doppler gradient across the right ventricular outflow tract (RVOT) was 44 mmHg. The child was electively scheduled for surgery to repair these congenital lesions. At 26 weeks of age the child was admitted to the hospital weighing sixteen pounds. He was receiving 0.025 mg of digoxin twice daily. He had no known drug allergies. His physical examination showed no abnormalities apart from a loud systolic murmur. Results of routine laboratory tests were within normal limits. Preoperative electrocardiogram showed a sinus rhythm of 142 beats/min (Fig 1). The child was taken to the operating room and had an uneventful inhalation induction and maintenance with halothane/O2 and muscle relaxation with pancuronium. A double-lumen central venous catheter was placed in the right internal jugular vein, and a left 20-gauge (G) radial artery catheter was placed without incident after intubation. Continuous electrocardiogram (ECG), SpO2, arterial pressures, esophagem temperatures, and central venous pressures were monitored throughout and recorded as being within normal limits. After adequate heparinization, the child was placed on cardiopulmonary bypass (CPB). Operative procedure included closure of 1.0 × 1.5 cm VSD with a patch graft and subvalvular stenotic muscle resection. The child was weaned successfully and uneventfully from CPB without any inotropic support. There was no postoperative RVOT gradient documented by catheter pullback across the pulmonary artery to the right ventricle. Arterial blood gas analyses before, during, and after CPB were within normal limits. Similarly, urine output was noted to be adequate throughout. The child was placed on the ventilator and started on a morphine drip, 0.03 mg/kg. Initial hemodynamics on arrival in the 1CU were a mean arterial pressure (MAP) of 60 mmHg, a pulse of 141 beats/min, central venous pressure (CVP) of 12 mmHg, left atrial pressure (LAP) of 5 mmHg, and a temperature of 36.5°C. The patient remained in stable condition for severn hours. However, 6 hours later, the patient's heart rate had increased to 187 beats/min with MAP of 72 mmHg, CVP of 19 mmHg, and LAP of 1 mmHg. The patient was diagnosed with JET (Fig 2). Hypothermia was initiated, and the temperature was decreased to 33°C. The patient was digitalized; all metabolic abnormalities were optimized, and the patient was sedated with additional boluses of morphine. Urine output was maintained with furosemide. With initial therapy of cooling and Journal of Cardiothoracic and Vascular Anesthesia,

digitalization, the heart rate decreased to 160 beats/rain and the blood pressure remained stable. Ten hours later, the patient converted from a slow JET rate of 150 beats/rain to sinus rhythm of 142 beats/min. At this time, the temperature was allowed to rise to 37°C, but the patient's ECG reverted back to bursts of JET. The patient continued to have short bursts of JET with heart rates over 200 beats/rain over the next 48 hours. Hypothermia was reinstituted. On postoperative day (POD) 3, the patient continued to have bursts of accelerated JET to 280 bpm, with MAP decreasing to 30 to 50 mmHg (Fig 3). Procainamide was added to the therapy with stabilization of heart rate to 120 to 140 beats/rain. Hypothermia was also continued during this time. On POD 8, he remained in sinus rhythm, and procainamide was weaned. He was extubated on POD 9. Thereafter, the patient's hospital stay was complicated by catheter sepsis; however, he remained in sinus rhythm and was discharged on POD 20.

DISCUSSION Postoperative JET is a tachyarrhythmia usually observed in the postoperative period in children who have undergone repair of congenital cardiac defects, such as tetralogy o f Fallot and VSD. A high incidence appears to be related to surgery in the region o f the bundle o f His. Its m e c h a n i s m appears to result from enhanced automaticity within the bundle o f His from cellular damage or stretching involved in the repair. 4,5 The onset is early, and most develop within 24 hours of surgery. There are several principles o f treatment. Cardiac output must be increased. Patients should be adequately volume resuscitated and have adequate hematocrit ( > 35%). Metabolic abnormalities should be looked for and appropriately corrected. AV pacing just above the JET rate to restore AV synchrony, if possible, can also increase the cardiac output. Digoxin increases cardiac output, contractility, and is vagotonic; therefore, it should also be given.a Another important principle o f treatment is to increase vagal tone and decrease adrenergic tone. Drugs used frequently in cardiac surgery, ie, pancuronium, barbiturates, and meperidine, are vagolytic and can cause an increase in the inherent junctional rate in cardiac cells. Sympathomimetic drugs such as dopamine, isoproterenol, dobutamine, epinephrine, and norepinephrine also may increase the rate. 6 Therefore, treatment begins with removal or minimal dosages o f all drugs that can cause an increase in heart rate. This may not be an easy task, especially if the patient has a poor cardiac function; however, alternative drugs that have less vagolytic or chronotropic action, such as vecuronium or phosphodiesterase inhibitors (milrinone), could be used. Adrenergic tone also can be reduced by adequately sedating

From the Department of Anesthesiology, A-131, Department of Pediatric Cardiology, Albany Medical Center Hospital, Albany, NY 12208. Address reprint requests to Farhan Sheikh, MBBS, Department of Anesthesiology, Albany Medical Center Hospital, 47 New Scotland Ave, Albany, NY 12208. Copyright © 1997 by W.B. Saunders Company 1053-0770/97/1102-001753.00/0 Key words: cardiac arrhythmias, junctional ectopic tachycardia, cardiac surgery, congenital heart disease

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and paralyzing these patients with drugs such as sufentanil/ fentanyl and vecuronium. If the cardiac output and blood pressure are good or blood pressure is elevated, ~3-blockers have been attempted. 7,8 However ~3-blockers should be used cautiously, because they may decrease contractility and worsen hemodynamics. Systemic cooling should be started immediately. Systemic hypothermia (32°C to 34°C) appears to be important in reducing and controlling the rate because hypothermia has been reported to slow the heart rate by depressing automaticity.9 It also decreases the body's oxygen consumption, thereby reduc-

Fig 1. P r e o p e r a t i v e electrocard i o g r a m (lead II} s h o w s sinus r h y t h m of 142 b e a t s / m i n .

ing myocardial work. Cooling should be maintained until patients are judged to be stable for a period of at least 24 hours. 9 Most incidences of JET respond to the above measures; however, greatly accelerated JET ( > 200 beats/min) usually progresses to a low cardiac output state and congestive heart failure if protracted for more than several hours. Drug therapy used in this circumstance remains controversial with no good standardized treatment. Type 1C antiarrhythmics agents (flecainide, encainide, propafenone) have been used with some success. 1,4,10Amiodarone, a class 3 antiarrhythmic, also has been used by some investigators. Amiodarone was given until sinus

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rhythm returned or when sufficient slowing of JET occurred to allow for stable hemodynamics. Despite the apparent control of heart rate in this patient with procainamide and hypothermia, s procainamide should be used with caution as it may actually

worsen JET because of vagolysis and decrease in cardiac output. 11 Finally, ablation of the His bundle has had some success in grave situations.12 However, it remains controversial and limited to selected centers.

REFERENCES

1. Grant JW, Serwer GA, Armstrong BE, et al: Junctional tachycardia in infants and children after open heart surgery for congenital heart disease. Am J Cardio159:1216-1218, 1987 2. Raja R Hawker RE, Chaikitpingo A, et al: Amiodarone management of junctional ectopic tachycardia after cardiac surgery in children. Br Heart J 72:261-265, 1994 3. Garson A: Texas Children's Hospital, Letter to Mathew Farina. 1984, Jan 27.2 leaves 4. Garson A, Gillette PC: Junctional ectopic tachycardia in children: Electrocardiography, electrophysiology and pharacological response. Am J Cardio144:298-302, 1979 5. Gillette PC: The mechanisms of supraventricular tachycardia in children. Circulation 54:133-139, 1976 6. Braunstein PW, Sade RM, Gillette PC: Life-threatening postoperative junctional ectopic tachycardia. Ann Thorac Surgery 53:726-728, 1992

7. Garson A, Moak JR Smith RT, Norton JB: Usefulness of intravenous propafenone for control of postoperative junctional ectopic tachycardia. Am J Cardiol 59:1422-1424, 1987 8. Sholler GE Walsh EP, Mayer JE, et al: Evaluation of staged treatment protocol for postoperative rapid junctional tachycardia. Circulation 78:2320, 1988 (abstr) 9. Bash SE, Shah JJ, Albers WH, Geiss DM: Hypothermia for the treatment of postsurgical greatly accelerated junctional ectopic tachycardia. J Am Coll Cardiol 10:1095-1099, 1987 10. Paul T, Reminer A, Janousek J, Kallfelz HC: Efficacy and safety of propafenone in congenital junctional ectopic tachycardia. Am Coll Cardio120:911-914, 1992 11. Gillette PC: Diagnosis and management of postoperative junctional ectopic tachycardia. Am Heart J 118:192-194, 1989 12. Gillette PC, Garson A, Porter CJ, et al: Junctional automatic ectopic tachycardia: New proposed treatment by transcatheter HIS bundle ablation. Am Heart J 106:609-623, 1983