Search

Background. Apnea is associated with prostaglandin E1 infusion (PGE1) used in the palliation of ductal-dependent congenital heart lesions. Hypothesis. Aminophylline is a central respiratory stimulant and will decrease the incidence of PGE1-associated apnea and the need for intubation for apnea in infants with ductal-dependent congenital heart disease. Methods. Informed consent was obtained for all patients. In a prospective, double-blinded, placebo-controlled study, newborn infants with ductal-dependent congenital heart disease were randomized to receive either aminophylline or placebo during initiation and maintenance of PGE1, which was started at 0.01 μg/kg/min and increased to 0.03 μg/kg/min. Aminophylline was given as a bolus dose of 6 mg/kg before or during initiation of PGE1, and continued at 2 mg/kg dose every 8 hours for 72 hours. Serum aminophylline levels were checked at 18 and 36 hours. The primary study endpoint was intubation for apnea, with a secondary endpoint of apnea, as defined as acute cessation of breathing with associated hypoxia and bradycardia. Results. The study evaluated 42 infants. The 2 groups were similar for gestational age, weight, hematocrit, and use of sedation. In the aminophylline group, serum levels were 7.6 ± 1.2 μg/mL. No significant side effects of aminophylline were seen. Infants receiving aminophylline (n = 21) were less likely to have apnea (2 vs 11) or be intubated for apnea (0 vs 6). Length of postoperative stay and survival to discharge were similar between the 2 groups. Conclusions. Aminophylline was effective for the prevention of apnea and intubation for apnea associated with PGE1 in infants with ductal-dependent congenital heart disease.

Twenty-three successive patients with 27 different episodes of sustained atrial flutter were treated with atrial pacing for conversion of the tachyarrhythmia; 15 patients with 16 episodes of atrial flutter underwent intracardiac right atrial pacing and eight patients with 11 episodes of atrial flutter were treated with transesophageal atrial pacing. Ten of sixteen episodes (63%) and eight of 11 episodes (73%) were successfully converted using intracardiac and transesophageal techniques, respectively. Mean flutter cycle length for all 27 episodes was 219 ms (mean heart rate 274 beats per minute); successful pacing conversion cycle length (n = 15) was 72% of the flutter cycle length. Hemodynamic, electrophysiologic, and roentgenographic data were not predictive of conversion by either technique. Induction of localized atrial fibrillation or failure to meet critical pacing criteria may explain pacing failures. Based on this experience, a trial of transesophageal atrial pacing for acute conversion of any episode of atrial flutter in children prior to direct current cardioversion is recommended.

To determine the acute and chronic effects of vasodilator therapy in children, vasodilator therapy was evaluated in 13 children (aged 0.2 to 14.5 years) with severe left ventricular dysfunction or mitral regurgitation. In seven children, nitroprusside increased cardiac index by an average of 33% (P < .01) and increased stroke index by 29% (P < .01). In eight children, hydralazine caused a 31% increase in cardiac index (P < .01) and a 27% increase in stroke index (P < .02). Ten children received chronic oral vasodilator therapy and were followed for 5.7 ± 1.4 (SEM) months. Early clinical improvement was observed in every child. Symptoms of heart failure diminished in all, and five children became entirely asymptomatic. A significant (P < .05) improvement was noted in growth velocity, respiratory rate, heart size, and incidence of gallop rhythm after 1 month of therapy. The duration of the beneficial response to vasodilator therapy varied considerably, however, and significant improvement for the group was not found after 1 month. Four children had sustained clinical improvement for 6 months or longer, but the others experienced recurrent heart failure within 1 to 4 months.