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J Thorac Cardiovasc Surg 1996;112:1403-1405
© 1996 Mosby, Inc.
BRIEF COMMUNICATIONS |
Boston, Mass.
From the Departments of Cardiology and Cardiac Surgery, Children's Hospital, Pediatrics and Surgerry, Harvard Medical School, Boston, Mass.
Received for publication April 18, 1996 Accepted for publication April 24, 1996. Address for reprints: Ian Adatia, FRCP(C), Cardiology and critical Care Medicine, The Hospital for Sick Children, 555 University Ave., Toronto, M5G 1X88, Canada.
The neonatal pulmonary vasculature may be extremely labile. Remodeling of the vessel wall, functional maturation of the endothelial cell, differentiation of the smooth muscle cell, release of vasoactive mediators, and vessel recruitment all contribute to the successful transition to a mature pulmonary circulation.
1 In the child with pulmonary hypertensive congenital heart disease postnatal remodeling is abnormal. 2 Even if a neonatal cardiac operation is undertaken, endothelium-dependent pulmonary vascular relaxation may be impaired after cardiopulmonary bypass and the postoperative course may be complicated by transient pulmonary hypertension. 3
Inhaled nitric oxide has been demonstrated to provide safe selective pulmonary vasodilation after cardiac operations. 4,5 However, pulmonary vasospasm is not the only cause of elevated proximal pulmonary artery pressures. After operation in the neonate with complex congenital heart disease it may be difficult to differentiate between pulmonary vasoconstriction and anatomic obstruction to pulmonary blood flow. A definitive diagnosis may require transport of a sick newborn infant and invasive investigation of the condition.
Therefore we investigated the use of a trial of inhaled nitric oxide after operation in the neonate with pulmonary hypertension or excessive cyanosis to differentiate vasospasm from fixed anatomic obstruction to pulmonary blood flow.
Methods
Fifteen patients with a median age of 11 days (range 1 to 52 days) with pulmonary hypertension (defined as a mean pulmonary artery pressure >25 mm Hg) or with excessive cyanosis compatible with an elevated pulmonary vascular resistance after cardiac operation underwent challenge with nitric oxide. The characteristics of the patients are summarized in Table I.
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3 The Wilcoxon signed rank test was used to compare the change in hemodynamic parameters with nitric oxide. Values are expressed as mean plus or minus standard error.
The study was approved by the investigational review board. Written and informed consent was obtained from the parents.
Results
Nine of 15 patients showed a response with a fall in pulmonary artery pressure or a rise in systemic arterial oxygen saturation after an inhaled nitric oxide challenge. Six patients did not respond and all were found to have anatomic obstruction to pulmonary blood flow.
Eight of 10 patients who had undergone complete neonatal repair showed a response to inhaled nitric oxide with a significant fall in mean pulmonary artery pressure from 35 ± 4 to 26 ± 4 mm Hg (p < 0.05) and in pulmonary vascular resistance from 17 ± 6 to 10 ± 4 Um2 (p < 0.05). There was no clinically important change in other hemodynamic parameters. Only one of five patients with single ventricle and severe hypoxemia after initial palliative systemic–to–pulmonary artery shunt procedures responded with an immediate increase in systemic arterial oxygen tension from 19 to 45 mm Hg. He was treated with continuous low-dose nitric oxide therapy until resolution of pulmonary vasoconstriction occurred.
Two patients (Nos. 7 and 8) with proximal pulmonary artery hypertension (both had undergone right ventricular outflow tract reconstruction) showed no response to inhaled nitric oxide. Further investigation revealed an unobstructed proximal pulmonary anastomosis but hypoplastic branch pulmonary arteries with low distal pulmonary pressures (Fig. 1). Both patients were treated conservatively with subsequent successful balloon dilation of the branch pulmonary arteries. In four of five neonates with refractory cyanosis after receiving modified Blalock-Taussig shunts, systemic arterial oxygen saturation did not improve sufficiently (43% ± 11% before nitric oxide and 51% ± 8% with nitric oxide) in response to nitric oxide. All four subsequently were found to have stenotic systemic–to–pulmonary artery shunts. The shunts were revised in all with improvement in oxygenation and three of four have undergone subsequent operation with fenestrated total cavopulmonary anastomoses.
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In nine newborn patients with elevated pulmonary vascular resistance, inhaled nitric oxide reduced the pulmonary artery pressure and pulmonary vascular resistance selectively without adverse systemic effects, thus confirming pulmonary vasoconstriction as the cause of increased right ventricular afterload. However, in six patients with proximal pulmonary artery hypertension or refractory cyanosis, a postoperative challenge with inhaled nitric oxide failed to reduce pulmonary artery pressure or improve systemic oxygenation. All six patients were found to have anatomic obstruction to pulmonary blood flow. Thus the judicious use of a trial of inhaled nitric oxide may be of value to rule out pulmonary vasoconstriction and direct investigation toward reassessment of the surgical result.
Certain young children with transposition of the great arteries, truncus arteriosus, and single ventricle have labile pulmonary vascular beds with pulmonary vasoconstriction and hypertension. However, high proximal pulmonary artery pressures alternatively may indicate distal pulmonary artery stenosis. In patients with single ventricle, intense cyanosis after insertion of a Blalock-Taussig shunt may reflect systemic–to–pulmonary artery shunt obstruction. We do not propose that a trial of inhaled nitric oxide should replace or delay diagnostic procedures when anatomic obstruction to pulmonary flow is evident. However, in neonatal cases when there is genuine doubt, failure of the patient to show a response to nitric oxide should be regarded as strong evidence of anatomic and possibly surgically remediable obstruction.
We have reported here the use of a short challenge with inhaled nitric oxide after operation in the neonate with congenital heart disease and proximal pulmonary artery hypertension or excessive cyanosis. We have described how the results of such a challenge may be used advantageously to direct therapy in the patient with pulmonary vasoconstriction who shows response to nitric oxide or in the patient who shows no response with further investigation of surgically remediable obstruction to pulmonary blood flow.
References
This article has been cited by other articles:
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  R. W. Day, J. A. Hawkins, E. C. McGough, K. L. Crezee, and G. S. Orsmond Randomized controlled study of inhaled nitric oxide after operation for congenital heart disease Ann. Thorac. Surg., June 1, 2000; 69(6): 1907 - 1912. [Abstract] [Full Text] [PDF]
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 J. Soongswang, I. Adatia, C. Newman, J. F. Smallhorn, W. G. Williams, and R. M. Freedom Mortality in potential arterial switch candidates with transposition of the great arteries J. Am. Coll. Cardiol., September 1, 1998; 32(3): 753 - 757. [Abstract] [Full Text] [PDF]
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 S. C. Body and S. K. Shernan The Utility of Nitric Oxide in the Postoperative Period Seminars in Cardiothoracic and Vascular Anesthesia, March 1, 1998; 2(1): 4 - 30. [Abstract] [PDF]
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 A. Gamillscheg, G. Zobel, B. Rigler, and A. Beitzke Inhaled nitric oxide after Glenn and Fontan procedures J. Thorac. Cardiovasc. Surg., November 1, 1997; 114(5): 867 - 868. [Full Text]
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