Elsevier

The Annals of Thoracic Surgery

Volume 62, Issue 6, December 1996, Pages 1759-1764
The Annals of Thoracic Surgery

Rebound Pulmonary Hypertension After Inhalation of Nitric Oxide

https://doi.org/10.1016/S0003-4975(96)00542-5Get rights and content

Abstract

Background. We describe the hemodynamic response to initiation and withdrawal of inhaled nitric oxide (NO) in infants with pulmonary hypertension after surgical repair of total anomalous pulmonary venous connection.

Methods. Between January 1, 1992, and January 1, 1995, 20 patients underwent repair of total anomalous pulmonary venous connection. Nine patients had postoperative pulmonary hypertension and received a 15-minute trial of inhaled NO at 80 parts per million. Five of these patients received prolonged treatment with NO at 20 parts per million or less.

Results. Mean pulmonary artery pressure decreased from 35.6 ± 2.4 to 23.7 ± 2.0 mm Hg (mean ± standard error of the mean) (p = 0.008), and pulmonary vascular resistance decreased from 11.5 ± 2.0 to 6.4 ± 1.0 U · m2 (p = 0.03). After prolonged treatment with NO, pulmonary artery pressure increased transiently in all patients when NO was discontinued.

Conclusions. After operative repair of total anomalous pulmonary venous connection, inhaled NO selectively vasodilated all patients with pulmonary hypertension. Withdrawal of NO after prolonged inhalation was associated with transient rebound pulmonary hypertension that dissipated within 60 minutes. Appreciation of rebound pulmonary hypertension may have important implications for patients with pulmonary hypertensive disorders when interruption of NO inhalation is necessary or when withdrawal of NO is planned.

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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