CARDIAC DEVELOPMENT



Congenital heart disease results from altered embryonic development or failure of the rudimentary portion of a structure ever to be formed. Abnormal development of one structure in turn may hinder the development of another portion of the circulatory system (for example, abnormal development of the mitral valve may lead to abnormal formation of the left ventricle).
The fetus’ circulation essentially places the pulmonary and systemic systems in parallel rather than in series as in the adult. Oxygenated blood from the umbilical vein passes into the portal venous system and subsequently into the inferior vena cava and is shunted preferentially across the patent foramen ovale to the left heart to perfuse the coronary arteries, head, and upper trunk. Blood returning from the upper portions of the body arrives at the right atrium via the superior vena cava, and most proceeds through the tricuspid valve to the right ventricle and pulmonary artery. However, only a small proportion of this blood goes into the pulmonary arterial tree; most is shunted via the patent ductus arteriosus to the descending aorta. Note that many congenital lesions that cause intracardiac shunts (for example, tetralogy of Fallot) or markedly abnormal cardiac outflow (for example, transposition of the great arteries) would not cause any difficulty during fetal development.
At birth the pulmonary vascular resistance decreases markedly owing to the inflation of the lungs and the increase in oxygen tension to which the pulmonary vessels are exposed. Systemic vascular resistance rises when the umbilical cord is clamped, removing the low-resistance placental circulation. Left atrial pressure rises, which in turn closes the foramen ovale. The increase in arterial Po2 along with alterations in prostaglandins causes the ductus arteriosus to close functionally within 10 to 15 hours. Many congenital heart lesions may not become apparent until cyanosis develops after closure of the foramen ovale or ductus arteriosus.





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