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VSD is an acyanotic congenital heart defect, aka a left-to-right shunt, so there are no signs of cyanosis in the early stage. However, an uncorrected VSD can increase pulmonary resistance leading to the reversal of the shunt and corresponding cyanosis. [4]
Eisenmenger syndrome or Eisenmenger's syndrome is defined as the process in which a long-standing left-to-right cardiac shunt caused by a congenital heart defect (typically by a ventricular septal defect, atrial septal defect, or less commonly, patent ductus arteriosus) causes pulmonary hypertension [1] [2] and eventual reversal of the shunt into a cyanotic right-to-left shunt.
An acyanotic heart defect, is a class of congenital heart defects. In these, blood is shunted (flows) from the left side of the heart to the right side of the heart, most often due to a structural defect (hole) in the interventricular septum. [1] People often retain normal levels of oxyhemoglobin saturation in systemic circulation.
Voila—two separate chambers. If these don’t fuse though, then a gap is left between the two chambers, in other words, a ventricular septal defect, or VSD. The majority of cases are caused by a defect in the membranous portion of the septum.
This gives the infant time to grow, increasing the size of, and thereby the ease of operation on, the heart, as well as the ease of recovery. Infants will generally require surgery within three to six months, however, they may be able to go up to two years before the operation becomes necessary, depending on the severity of the defect.
Levo-Transposition of the great arteries (also known as Levo-TGA, congenitally corrected TGA, double discordance, or ventricular inversion) is a rare, acyanotic heart defect in which the primary arteries are transposed, with the aorta anterior and to the left of the pulmonary artery, and the morphological left and right ventricles with their ...
An uncorrected left-to-right shunt can progress to a right-to-left shunt; this process is termed Eisenmenger syndrome. [3] This is seen in Ventricular septal defect, Atrial septal defect, and patent ductus arteriosus, and can manifest as late as adult life. This switch in blood flow direction is precipitated by pulmonary hypertension due to ...
The mechanism of many of the risks and complications related to failure of the Glenn bidirectional shunt is thought to be thrombosis. Right-side dominant circulation, elevated pulmonary vascular resistance, and prolonged operative and recovery time are the major factors that increase the risk of complications and failure.