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J Thorac Cardiovasc Surg 2005;129:217-219
© 2005 The American Association for Thoracic Surgery

Brief Communications

Inhaled nitric oxide does not improve systemic oxygenation after bidirectional superior cavopulmonary anastomosis

^a Department of Cardiology, Children's Hospital, and Department of Pediatrics, Harvard Medical School, Boston, Mass
^b Department of Critical Care Medicine and Division of Cardiology, Hospital for Sick Children Toronto, Toronto, Ontario, Canada

Received for publication April 5, 2004; accepted for publication April 13, 2004.

^* Address for reprints: Ian Adatia, MBChB, University of California at San Francisco Children's Hospital, 505 Parnassus Ave, Room M-655, San Francisco, CA 94143-0106 (E-mail: iadatia@pedcard.ucsf.edu).

The first 20% of the full text of this article appears below.

Inhaled nitric oxide (NO) is a selective pulmonary vasodilator that decreases intrapulmonary shunt fraction.¹ We sought to determine whether inhaled NO would ameliorate hypoxemia after bidirectional superior cavopulmonary anastomosis (BCPA).

	Methods

 
The research and ethics review board approved the study, and the parents of all children gave informed and written consent. We included patients with systemic oxygen saturations of 75% or less after BCPA without venous decompressing collaterals or pulmonary disease. Patients were mechanically ventilated and studied on the first postoperative day in the intensive care unit. From a stable baseline, patients received a 15-minute trial of inhaled NO (80 ppm).² During the trial of inhaled NO, ventilator parameters and FIO₂ were unchanged. In 5 patients, cyclic guanosine monophosphate (cGMP) levels were measured.² One patient first received inhaled NO in the cardiac catheterization laboratory because of persistent hypoxemia after coil embolization of decompressing venous collaterals. This same patient was readmitted 7 months after BCPA with refractory hypoxemia as the . . . [Full Text of this Article]

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