TAILIEUCHUNG - Ebook Visual guide to neonatal cardiology: Part 2
Part 2 book “Visual guide to neonatal cardiology” has contents: Coarctation of the aorta, vascular rings and pulmonary slings, double outlet right ventricle, double outlet left ventricle, single ventricle and biventricular hearts with hypoplasia of one ventricle, patent ductus arteriosus, and other contents. | 260 42 Coarctation of the Aorta Hitesh Agrawal 1 , John W. Bokowski 2 , and Damien Kenny 3 1 Texas Children’s Hospital, Houston, TX, USA 2 Rush Center for Congenital and Structural Heart Disease, Chicago, IL, USA 3 Our Lady’s Children’s Hospital, Crumlin, Dublin, Ireland Pathophysiology The aortic arch and its branches develop during the fourth to eighth weeks of gestation. Abnormalities in the development of left fourth and sixth embryonic aortic arch are thought to be implicated. Various theories have been proposed to explain how coarctation develops. Ductal theory states that ductal tissue surrounds the aortic arch in a circumferential fashion, thus causing narrowing of the aorta when ductal tissue constricts. This is supported by the fact that coarctation most commonly occurs at the site of ductal insertion and often manifests after ductal closure. However, aortic coarctation (CoA) can occur away from the insertion of ductus arteriosus, which cannot be explained solely by ductal theory. Developmental theory hypothesizes that coarctation develops as a result of hemodynamic disturbances that reduce the volume of blood flow through the fetal aortic arch, and it may be that CoA cannot be explained by a single pathophysiologic mechanism. Clinical Manifestation Newborns with CoA are usually asymptomatic at birth, when the ductus arteriosus is open, or if the narrowing is mild. After ductal closure, newborns present with dusky color, poor feeding, tachypnea, and often in a shock-like state if severe coarctation is present. Cases with milder degrees of narrowing may be missed until childhood or adulthood and can be brought to attention by the presence of an ejection systolic click from an associated aortic valve anomaly or a systolic ejection murmur in the aortic area, a continuous murmur arising from collateral formation, upper extremity hypertension, and diminished or delayed femoral pulses. Prior to ductal closure, a difference in pulse oximetry between the .
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