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J Thorac Cardiovasc Surg 2002;124:16-19
© 2002 The American Association for Thoracic Surgery
Editorials |
From the Division of Cardiovascular Surgery, The Heart Institute for Children, Hope Children's Hospital, Oak Lawn, Ill.
Received for publication Jan 7, 2002. Accepted for publication Feb 8, 2002. Address for reprints: Bradley S. Allen, MD, The Heart Institute for Children, Hope Children's Hospital, 4440 West 95th St, Oak Lawn, IL 60453 (E-mail: Brad@THIC.com).
| The first 300 words of the full text of this article appear below. |
| Introduction |
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Repair of cyanotic congenital heart defects necessitating cardiopulmonary bypass (CPB) is becoming more frequent in infants and neonates. Despite apparently successful surgical correction, postoperative myocardial and pulmonary dysfunction continues to be a major contributor to morbidity and mortality and is more severe than after repair of acquired defects in adults with normoxic conditions.
1-3 The neonatal heart also has a reduced response to inotropic agents compared with the adult heart.
1,2 Thus, preservation of myocardial function in neonates during cardiac operations assumes even greater importance, because a perioperative insult is less well tolerated and more difficult to treat.
Congenital malformations of the heart frequently lead to physiologic abnormalities ("stress") that are quite different from those seen in the adult, and so the concerns during CPB are not necessarily the same. The most common preoperative stress in adults is ischemia, secondary to coronary artery disease, and the major concern is avoidance of a "regional" myocardial reperfusion injury with the reintroduction of blood.
4 In contrast, the most common preoperative stress in pediatric patients is hypoxia (cyanosis).
1,2 The major concern, therefore, is whether a reoxygenation injury (similar to a reperfusion injury) occurs with the abrupt reintroduction of oxygen. The occurrence of such an injury could be even more detrimental, as it would result in "global "damage, since hypoxia affects the entire body, not just the heart.
Acute hypoxia and acidosis may occur as a consequence of many congenital heart defects and can result in depletion of glycogen, adenosine triphosphate, and Krebs cycle intermediates, leading to myocardial dysfunction.
2,5,6 Significant acute hypoxia forces the myocardium to rely on anaerobic metabolism, and when acidosis is present, this further heightens these deleterious effects. Chronic hypoxia leads to cyanosis, a condition frequently encountered in infants and children undergoing cardiac operations. Despite compensatory mechanisms,
Related Article
J. Thorac. Cardiovasc. Surg. 2002 124: 105-112.
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