Hypothermia for the treatment of postsurgical greatly accelerated junctional ectopic tachycardia.
Three infants developed greatly accelerated junctional ectopic tachycardia with a heart rate greater than 200 beats/min after open heart surgery. When the heart rate exceeded 200 beats/min for 5 hours, all the infants had congestive heart failure and clinical signs of low cardiac output. Conventional therapy (cardioversion, lidocaine, verapamil, digoxin and ice to face) has been shown in the past to be unsuccessful in controlling the heart rate. Because hypothermia is known to decrease automaticity of the heart, these patients were treated with induced hypothermia. The goal was to arbitrarily decrease the junctional ectopic rate to less than 180 beats/min to increase cardiac filling time. The duration of the junctional ectopic tachycardia greater than 180 beats/min ranged from 0.5 to 17 hours after cooling began. The duration of the hypothermia ranged from 4 to 24 hours. Spontaneous reversion to sinus rhythm occurred either during the hypothermia or shortly thereafter in all three patients. The blood pressure and urinary output remained stable during hypothermia. Hypothermia is an effective means of controlling the rate of greatly accelerated junctional ectopic tachycardia after open heart surgery in infants. Although hypothermia does not convert junctional ectopic tachycardia to sinus rhythm, it slows the rate to a more acceptable level, allowing the infants' survival and eventual recovery of sinus rhythm.
Bash
S E
SE
Department of Pediatrics, University of Illinois College of Medicine, Peoria 61637.
Shah
J J
JJ
Albers
W H
WH
Geiss
D M
DM
D004562:Electrocardiography; D005260:Female; D006330:Heart Defects, Congenital / Q000601:surgery*; D006339:Heart Rate; D006801:Humans; D007036:Hypothermia, Induced / Q000379:methods; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D011183:Postoperative Complications / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D013613:Tachycardia, Ectopic Junctional / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D013617:Tachycardia, Supraventricular / Q000628:therapy*