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Ventricular septal defect
A ventricular septal defect (VSD) is a defect in the ventricular septum, the wall dividing the left and right ventricles of the heart. It is a common congenital heart defect. The extent of the opening may vary from pin size to complete absence of the ventricular septum, creating one common ventricle. The ventricular septum consists of an inferior muscular and superior membranous portion and is extensively innervated with conducting cardiomyocytes.
The membranous portion, which is close to the atrioventricular node, is most commonly affected in adults and older children in the United States. It is also the type that will most commonly require surgical intervention, comprising over 80% of cases.
Membranous ventricular septal defects are more common than muscular ventricular septal defects, and are the most common congenital cardiac anomaly.
Ventricular septal defect is usually symptomless at birth. It usually manifests a few weeks after birth.[citation needed]
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.
The restrictive ventricular septal defects (smaller defects) are associated with a louder murmur and more palpable thrill (grade IV murmur). Larger defects may eventually be associated with pulmonary hypertension due to the increased blood flow. Over time this may lead to an Eisenmenger's syndrome the original VSD operating with a left-to-right shunt, now becomes a right-to-left shunt because of the increased pressures in the pulmonary vascular bed.
Congenital VSDs are frequently associated with other congenital conditions, such as Down syndrome. Congenital heart disease, particularly VSDs, is the number one cause of death for children with Down syndrome ages birth to two.
A VSD can also form a few days after a myocardial infarction (heart attack) due to mechanical tearing of the septal wall, before scar tissue forms, when macrophages start remodeling the dead heart tissue.
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Ventricular septal defect
A ventricular septal defect (VSD) is a defect in the ventricular septum, the wall dividing the left and right ventricles of the heart. It is a common congenital heart defect. The extent of the opening may vary from pin size to complete absence of the ventricular septum, creating one common ventricle. The ventricular septum consists of an inferior muscular and superior membranous portion and is extensively innervated with conducting cardiomyocytes.
The membranous portion, which is close to the atrioventricular node, is most commonly affected in adults and older children in the United States. It is also the type that will most commonly require surgical intervention, comprising over 80% of cases.
Membranous ventricular septal defects are more common than muscular ventricular septal defects, and are the most common congenital cardiac anomaly.
Ventricular septal defect is usually symptomless at birth. It usually manifests a few weeks after birth.[citation needed]
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.
The restrictive ventricular septal defects (smaller defects) are associated with a louder murmur and more palpable thrill (grade IV murmur). Larger defects may eventually be associated with pulmonary hypertension due to the increased blood flow. Over time this may lead to an Eisenmenger's syndrome the original VSD operating with a left-to-right shunt, now becomes a right-to-left shunt because of the increased pressures in the pulmonary vascular bed.
Congenital VSDs are frequently associated with other congenital conditions, such as Down syndrome. Congenital heart disease, particularly VSDs, is the number one cause of death for children with Down syndrome ages birth to two.
A VSD can also form a few days after a myocardial infarction (heart attack) due to mechanical tearing of the septal wall, before scar tissue forms, when macrophages start remodeling the dead heart tissue.