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Normal Cardiac Development Fetal Circulation Congenital Heart Defects Cardiac Transplantation
Septal Defects Right Heart Lesions Left Heart Lesions Anomalies of Arteries and Veins
Atrial Septal Defects Ventricular Septal Defects Atrioventricular Septal Defects Aortopulmonary Window Persistent Truncus Arteriosus

Ventricular septal defects (VSDs)

  • Ventricular septal defects are defined as a deficiency anywhere in the ventricular septum. They are the most common type of defect during childhood, making up to 20% of diagnosed congenital heart defects.
  • Anatomically, the ventricular septum can be divided into four regions based on the anterior and posterior extension of the septomarginal trabecularis. These include the inlet septum, trabecular septum, trabecular and outlet or infundibular septa (which make up the muscular septum), and the membranous septum. The division by section allows for classification of defects according to location (Soto, Becker, Moulaert, Lie, Anderson; 1980).

Perimembranous defects may occur in the inlet, trabecular, or infundibular regions. In these cases, part of the rim of the defect is formed by a portion of the cardiac central fibrous body.

Muscular defects may exist in any one of three areas. Inlet muscular defects are found in the areas between the trabecular and inlet septa, infundibular muscular defects between the infundibular and trabecular septa, and trabecular muscular defects in the infundibulum itself.

Subarterial infundibular defects are located in the areas normally formed by the infundibular septum with the non-muscular rim formed by the adjacent arterial valves.


  • Ventricular septal defects allow for left-to-right shunting beginning at birth when pulmonary resistance falls and systemic pressures increase. This leads to an increase in the amount of blood passing through the right ventricles, pulmonary arteries, and left atrium which leads to congestive heart failure as well as hypertension of all three structures.
  • Clinical manifestations vary depending on the sizes of the defects and the degrees of shunting that occurs. Clinical manifestations may develop within days after birth or take up to 6 months: i.e., depending on severities of the defects, the presence of additional cardiac defects, and/or the elicitation of other extracardiac anomalies.
  • Most infants are asymptomatic, as defects are often too small to allow for significant left-to-right shunting. Larger defects can manifest themselves as congestive heart failure, respiratory infections, tachypnea, dyspnea, and/or altered growth rates.
  • The management of a ventricular septal defect is dependent on both the size and location of the defect. In general, the majority of defects are small and thus can typically be managed conservatively: i.e., if the child reaches 6 months of age without evidence of pulmonary hypertension. Ventricular septal defects do not enlarge with age; instead, some are known to decrease in size and occasionally close spontaneously. Still, it is commonly recommended that larger defects be surgically closed within the first months of life.
    • Membranous defects tend to improve with time and may be managed conservatively; i.e., if pulmonary arterial pressures remains low.
    • Muscular defects may also close spontaneously, particularly if the lesions are small. Yet, if significant shunting and pulmonary hypertension occur, it is recommended that the defect be closed (either surgically or minimally invasively).
    • Defects in the infundibular region are typically large and unlike those in other areas of the septum, do not decrease in size. For these reasons, and the fact that aortic regurgitation is a frequent complication, it is recommended that infundibular lesions be surgically corrected.
    • Atrioventricular canal defects almost always require surgical intervention, because like the infundibular types, they are typically large and do not spontaneously decrease in size.