RESUMEN
Persistence of the fetal circulation is a recently recognized cause of severe cyanosis in newborn full term infants. Abnormally elevated pulmonary vascular resistance apparently stimulated by hypoxia, acidosis, and/or hyperviscosity results in cyanosis due to large right-to-left shunts through persistent fetal channels (patent foramen ovale and patent ductus arteriosus). Initial chest radiographs demonstrate clear lungs, decreased, normal, or mildly prominent pulmonary vascularity, and normal to moderately enlarged cardiac silhouettes. Angiocardiography, when required to rule out cyanotic congenital heart disease, demonstrates normal intracardiac anatomy, normal great vessel relationships, and right-to-left shunting across the patent foramen ovale and patent ductus arteriosus. Significant tricuspid regurgitation occurs in some of these infants, associated with variable right ventricular dilatation; the left ventricle is normal. The majority of babies with this condition ultimately survive. Treatment consists of intensive care including oxygen therapy and correction of acidosis. Vasodilators such as tolazoline may be helpful.