Aortopulmonary transposition in the fetus: speculation on pathophysiology and therapy.
Fetuses with transposition and abnormalities of the foramen ovale and/or ductus arteriosus detected by ultrasound may develop severe hypoxemia postnatally. Higher than normal oxygen content in the pulmonary artery has been considered to be responsible. Patterns of blood flow in the normal fetus and the fetus with aortopulmonary transposition were reviewed. Well-oxygenated ductus venosus is preferentially directed through the foramen ovale into the left atrium. Normally this produces a higher oxygen content in the ascending aorta. In the fetus with transposition, pulmonary arterial oxygen content is higher. Pulmonary vascular resistance is decreased and the ductus arteriosus constricted. Increased pulmonary venous return to the left atrium tends to close the foramen ovale. Changes are more likely in the last trimester because sensitivity of the pulmonary circulation and ductus arteriosus increases. Severe ductus arteriosus constriction could result in pulmonary arterial hypertension and increased pulmonary arteriolar smooth muscle development. Variability of responses could be related to the proportion of umbilical venous blood passing through the ductus venosus. It is proposed that, in fetuses with evidence of abnormalities of the ductus arteriosus and/or the foramen ovale, methods to occlude the ductus venosus be developed to avoid progressive changes.
Rudolph
Abraham M
AM
Department of Pediatrics and Cardiovascular Research Institute, University of California, San Francisco, California 94143, USA. amrudolph@eartlink.net
D000818:Animals; D001011:Aorta / Q000002:abnormalities / Q000503:physiopathology; D004373:Ductus Arteriosus / Q000503:physiopathology; D005260:Female; D005315:Fetal Diseases / Q000503:physiopathology* / Q000628:therapy*; D046128:Fetal Therapies; D006346:Heart Septum / Q000503:physiopathology; D006801:Humans; D007231:Infant, Newborn; D008955:Models, Cardiovascular; D011247:Pregnancy; D011651:Pulmonary Artery / Q000002:abnormalities / Q000503:physiopathology; D011652:Pulmonary Circulation; D014188:Transposition of Great Vessels / Q000503:physiopathology* / Q000628:therapy*; D014655:Vascular Resistance