Rebound Pulmonary Hypertension After Inhalation of Nitric Oxide
Section snippets
Patients
Between January 1, 1992, and January 1, 1995, 20 patients with isolated TAPVC presented to Children's Hospital for operative repair. Anomalous pulmonary venous drainage was supracardiac in 9 patients, infracardiac in 8, to the coronary sinus in 2, and mixed in 1. All infants had repair during cardiopulmonary bypass using deep hypothermic circulatory arrest. Postoperatively, 9 of 20 patients demonstrated pulmonary hypertension, defined as a mean pulmonary artery pressure (mPAP) of 25 mm Hg or
Results
The hemodynamic changes after the 15-minute trial of NO are displayed in Table 2. Nitric oxide decreased mPAP in all 9 patients (35.6 ± 2.4 to 23.7 ± 2.0 mm Hg; p = 0.008), for a 32% ± 5% reduction (Fig. 1). Pulmonary vascular resistance decreased by 41% ± 7% in all 6 patients in whom it could be calculated (11.5 ± 2.0 to 6.4 ± 1.0 U · m2; p = 0.03) (Fig. 2). There were no significant changes in right or left atrial pressure heart rate, cardiac index, systemic blood pressure, or systemic
Comment
Pulmonary hypertension occurred commonly among infants after repair of TAPVC and was present in 88% of patients with an infradiaphragmatic drainage pattern. Inhaled NO significantly and selectively decreased pulmonary artery pressure in all hypertensive patients. The average reduction in pulmonary vascular resistance was 41%. Although the effect of inhaled NO on hemodynamic indices has been reported after operations for congenital heart disease 4, 5, 6, 13, this study describes the acute and
Acknowledgements
We thank the cardiac surgeons at Children's Hospital whose technical skill made this study possible: Richard A Jonas, John E. Mayer, Frank L. Hanley, Redmond P. Burke, and Pedro J. del Nido. We are grateful to Aldo R. Castañeda for his critical review of the manuscript.
This study was supported in part by a grant-in-aid award from Children's Hospital.
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