Ann Thorac Surg 1996;62:583-585
© 1996 The Society of Thoracic Surgeons
Case Report
Successful Management of Junctional Tachycardia by Hypothermia After a Fontan Operation
Toshihide Asou, MD,
Hideaki Kado, MD,
Yuichi Shiokawa, MD,
Kouji Fukae, MD,
Hisataka Yasui, MD
Department of Cardiovascular Surgery, Fukuoka Children's Hospital, Fukuoka, Japan
Accepted for publication March 13, 1996.
 |
Abstract
|
|---|
We report herein the findings of a 2-year-old boy in whom junctional tachycardia developed 2 days after he underwent a modified Fontan operation and thereafter was successfully treated by hypothermia without paralyzing and artificially ventilating the patient. Chlorpromazine was useful in achieving moderate hypothermia by surface cooling without producing any unfavorable effects associated with topical cooling.
|
Introduction
|
|---|
Junctional tachycardia is one of the most challenging arrhythmias after open heart operations [1, 2]. When it is encountered in convalescing patients who have undergone the Fontan operation, they often become seriously ill because of a low cardiac output due to the loss of sinus rhythm and atrioventricular synchrony [3]. Moderate hypothermia is known to be one of the most useful treatments for junctional tachycardia after pediatric open heart operations [3–6]. Most reports [3–6], however, have shown that patients need to be mechanically ventilated and paralyzed to achieve moderate hypothermia. On the other hand, mechanical ventilation may impede the pulmonary blood flow during Fontan circulation. We present herein a pediatric patient in whom moderate hypothermia was smoothly achieved during treatment for junctional tachycardia in a spontaneously breathing condition by the use of chlorpromazine, which acts as both a sedative and a vasodilator [7].
A 2-year-old boy with a right isomeric heart, who had previously received a bidirectional cavopulmonary shunt, underwent a modified Fontan procedure that included reconstruction of the total cavopulmonary connection and repair of the common atrioventricular valve regurgitation. After a 2-day uneventful postoperative course with a stable sinus rhythm, junctional ectopic tachycardia suddenly developed in the ward. The heart rate reached 210 beats/min within 3 hours of onset. An electrocardiogram showed a narrow QRS morphologic configuration and atrioventricular dissociation at an atrial rate of 140 beats/min. Although rapid atrial pacing at a rate of 230 beats/min revealed ventricular captures, overdrive suppression with rapid atrial pacing failed to convert the junctional tachycardia into a sinus rhythm. Conventional medications including adenosine, digoxin, propranolol, and verapamil were only able to induce a small and transient reduction of the heart rate. We then started surface cooling by placing a heat-exchanging blanket under the patient and ice packs around the neck and the flanks. We used chlorpromazine to sedate and vasodilate the patient to achieve smooth cooling. Chlorpromazine was constantly administered at a rate of 0.34 mg•kg-1•h-1 during hypothermia.
Hypothermia was remarkably effective, as shown in Figure 1
. The heart rate was controlled when the rectal temperature reached 34°C. During cooling, the heart rate demonstrated a linear correlation with the body temperature of the patient. Sinus rhythm eventually returned 10 hours after the initiation of hypothermia. The central venous pressure returned to an acceptable level immediately after conversion of the cardiac rhythm to a sinus rhythm. An echocardiogram revealed an ejection fraction of 0.55, whereas it had been 0.35 at the onset of junctional tachycardia. Neither metabolic nor respiratory acidosis developed during hypothermia. Both the blood pressure and urinary output remained stable. No side effects associated with hypothermia were observed. After 24 hours of moderate hypothermia, the patient was rewarmed without any further episodes of junctional tachycardia. The patient thereafter demonstrated an uneventful course.
View larger version (24K):
[in this window]
[in a new window]
|
Fig 1. . Hourly changes in heart rate (HR), body temperature, and central venous pressure (CVP). The heart rate reached greater than 200 beats/min within 3 hours after the onset of junctional tachycardia. Surface cooling was effectively initiated 10 hours after the onset of junctional tachycardia. The heart rate was thus lowered to less than 150 beats/min 6 hours after the initiation of hypothermia.
|
|
|
Comment
|
|---|
Junctional tachycardia is one of the most challenging arrhythmias and can be fatal after pediatric open heart operations [1, 2]. Antiarrhythmic drugs tend to have little effect on this arrhythmia [1, 2]. Hypothermia has been reported to be an alternative treatment for postoperative junctional tachycardia [3–6]. Most patients reported, however, were paralyzed and ventilated to achieve hypothermia [3–6]. We successfully applied hypothermia in the management of junctional tachycardia without paralyzing and artificially ventilating the patient who had undergone a modified Fontan operation, because the positive airway pressure associated with mechanical ventilation was considered to potentially impede the pulmonary blood flow due to the Fontan physiology in this patient. Careful attention, however, should be paid to the successful institution of hypothermia by surface cooling. First of all, it is essential to administer a sedative to prevent patients from either responding or demonstrating natural reflexes to the stress caused by hypothermia through the autonomic nerves. Second, a vasodilator should be used to cool the whole body evenly. The wider the gap between the central and peripheral body temperature becomes, the more ventricular arrhythmias tend to occur. Therefore, because chlorpromazine acts as both a sedative and a vasodilator [7], it is extremely useful in achieving hypothermia by surface cooling without producing any unfavorable effects.
|
Footnotes
|
|---|
Address reprint requests to Dr Asou, Department of Cardiovascular Surgery, Fukuoka Children's Hospital, 2-5-1 Tojin-machi, Chuo-ku, Fukuoka 810, Japan.
|
References
|
|---|
- 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]
- Gillette PC. Diagnosis and management of postoperative junctional ectopic tachycardia. Am Heart J 1989;118:192–4.[Medline]
- Balaji S, Sullivan I, Deanfield J, James I. Moderate hypothermia in the treatment of resistant automatic tachycardias in children. Br Heart J 1991;66:221–4.[Abstract/Free Full Text]
- Bash SE, Shah JJ, Albers WH, Geiss DM. Hypothermia for the treatment of postsurgical greatly accelerated junctional ectopic tachycardia. J Am Coll Cardiol 1987;10:1095–9.[Abstract]
- Sholler GF, Walsh EP, Mayer JE, Saul JP, Gamble WJ, Lang P. Evaluation of staged treatment protocol for postoperative rapid junctional tachycardia [Abstract]. Circulation 1988;78(Suppl 2):597.
- Pfammatter JP, Paul T, Ziemer G, Kallfelz. Successful management of junctional tachycardia by hypothermia after cardiac operations in infants. Ann Thorac Surg 1995;60:556–60.[Abstract/Free Full Text]
- Ishikawa S, Otsuka M, Iwao H, et al. Effects of intravenous infusion of chlorpromazine on hemodynamics and neurohormone in young children with congenital heart disease [Abstract]. Circulation 1991;84(Suppl 2):384.
This article has been cited by other articles:
|
|
|
|
 
Y. Iwata, J. W. Newburger, D. Zurakowski, and R. A. Jonas
Postoperative Hypothermia and Blood Loss After the Neonatal Arterial Switch Procedure
Ann. Thorac. Surg.,
November 1, 2007;
84(5):
1627 - 1632.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. Taniguchi, T. Takahashi, K. Toda, H. Matsue, Y. Shudo, H. Shintani, M. Mitsuno, and Y. Sawa
Left ventricular mass: impact on left ventricular contractile function and its reversibility in patients undergoing aortic valve replacement
Eur. J. Cardiothorac. Surg.,
October 1, 2007;
32(4):
588 - 595.
[Abstract]
[Full Text]
[PDF]
|
|
|
Top
Abstract
Introduction
