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J Thorac Cardiovasc Surg 1997;113:435-442
© 1997 Mosby, Inc.

SURGERY FOR CONGENITAL HEART DISEASE

INHALED NITRIC OXIDE IN PATIENTS WITH CRITICAL PULMONARY PERFUSION AFTER FONTAN-TYPE PROCEDURES AND BIDIRECTIONAL GLENN ANASTOMOSIS

Received for publication April 4, 1996 revisions requested May 24, 1996; revisions received Sept. 16, 1996 accepted for publication Sept. 20, 1996. Address for reprints: A. Gamillscheg, MD, Department of Pediatric Cardiology, Children's Hospital, University of Graz, Auenbruggerplatz 30, A-8036 Graz, Austria.

Abstract

Objective: The aim of this study was to evaluate the effects of inhaled nitric oxide in patients with critical pulmonary perfusion after Fontan-type procedures and bidirectional Glenn anastomosis. Methods: Inhaled nitric oxide (mean 4.1 ± 0.7 ppm, 1.5 to 10 ppm) was administered in 13 patients (mean age 5.6 ± 1.6 years, 1.5 to 17 years) with critical pulmonary perfusion (central venous pressure >20 mm Hg or transpulmonary pressure gradient >10 mm Hg) in the early postoperative period after total cavopulmonary connection (n = 9) or after bidirectional Glenn anastomosis (n = 4). Results: In patients after total cavopulmonary connection inhaled nitric oxide therapy decreased central venous pressure by 15.3% ± 1.4% (p = 0.0001) and transpulmonary pressure gradient by 42% ± 8% (p = 0.0008) and increased mean systemic arterial and left atrial pressures by 12% ± 3.6% (p = 0.011) and 28% ± 8% (p = 0.007), respectively. Arterial and venous oxygen saturations improved by 8.2% ± 1% (p = 0.005) and 14% ± 4.3% (p = 0.03), respectively. In patients after bidirectional Glenn anastomosis inhaled nitric oxide therapy resulted in a decrease of central venous pressure by 22% ± 1% and of the transpulmonary pressure gradient by 55% ± 6% and improved arterial and venous oxygen saturations by 37% ± 29% and 11% ± 3%, respectively. Mean systemic arterial and left atrial pressures remained nearly unchanged. No toxic side effect was observed in Conclusion: Inhaled nitric oxide may play an important role in the management of transient critical pulmonary perfusion caused by reactive elevated pulmonary vascular resistance in the early postoperative period after Fontan-type operations and bidirectional Glenn anastomosis.

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