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Ann Thorac Surg 2006;81:1434-1435
© 2006 The Society of Thoracic Surgeons
Division of Pediatric Cardiology, Lucile Packard Childrens' Hospital, Stanford University School of Medicine, 750 Welch Rd, Suite 305, Palo Alto, CA 94304
(Email: gewright{at}stanford.edu).
In this retrospective review, Agarwal and colleagues [1] evaluated the effects of inhaled nitric oxide (iNO) in bidirectional Glenn patients who had elevated Glenn pressures immediately postoperatively. The effects of iNO on Glenn pressures, systemic perfusion, and respiratory indices were assessed. The study demonstrated that in a majority of these patients iNO lowered superior vena cava pressures and improved systemic perfusion and gas exchange. In the subset of patients who did not benefit from iNO, anatomic obstruction or ventricular dysfunction was subsequently noted, and those patients underwent further operative interventions.
This study provides a basis for stepwise evaluation of postoperative Glenn patients with significantly elevated Glenn pressures and diminished clinical cardiac output. An early trial of iNO is warranted to determine whether hemodynamics are compromised due to elevated pulmonary vascular resistance (PVR). If the Glenn pressure does not fall to at least 17 mm Hg, then anatomic obstruction or ventricular dysfunction is likely, and an echocardiogram followed by cardiac catheterization is indicated. This series also suggests that there is a role for iNO in successfully getting patients with borderline preoperative pulmonary artery pressure and PVR through the immediate postoperative period after a Glenn procedure. Use of iNO empirically to come off cardiopulmonary bypass and in the early postoperative period may eliminate a detrimental period of low cardiac output for such patients, particularly for those who have long bypass times. Although not examined in this study, patients with elevated PVR preoperatively may benefit most by the complete avoidance of cardiopulmonary bypass during the Glenn procedure when possible.
These results are thought provoking, because prior similar work looking at iNO in postoperative Glenn patients has yielded equivocal findings. Notably in this study, all of the patients who had elevated Glenn pressures postoperatively had significantly higher pulmonary artery pressures and pulmonary vascular resistance at preoperative catheterization. The postoperative Glenn pressures in these patients were more elevated than those of the patients in prior study populations. There may be a subset of single ventricle patients with altered endogenous nitric oxide synthesis or metabolism. In such patients with longstanding elevations in PVR, with additional endothelial dysfunction secondary to cardiopulmonary bypass, pulmonary blood flow may be limited postoperatively by pulmonary vasoconstriction. In those cases, as in this study, iNO may improve cardiac output and oxygenation through direct pulmonary vasodilation. On the other hand, exogenous nitric oxide may not provide much benefit in patients who do not have long-term alterations in pulmonary vascular tone. In those cases, iNO may have salutary effects on oxygenation only when there is intrapulmonary shunting.
This study helps to identify a subgroup of patients who benefit from iNO in the early postoperative period. Similar work is needed to identify which single ventricle patients with elevated PVR would respond to chronic therapies.
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