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Ventricular septal defect

Ventricular septal defect
Classification & external resources
Echocardiographic image of a moderate ventricular septal defect in the mid-muscular part of the septum. The trace in the lower left shows the flow during one complete cardiac cycle and the red mark the time in the cardiac cycle that the image was captured. Colours are used to represent the velocity of the blood. Flow is from the left ventricle (right on image) to the right ventricle (left on image). The size and position is typical for a VSD in the newborn period.
ICD-10 Q21.0
ICD-9 745.4
DiseasesDB 13808
MeSH C14.240.400.560.540

A ventricular septal defect (VSD) is a defect in the ventricular septum, the wall dividing the left and right ventricles of the heart.

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 alger children.[1][2]

Congenital VSDs are collectively the most common congenital heart defects.[3]  



A VSD can be detected by cardiac auscultation. Classically, a VSD causes a pathognomonic holo- or pansystolic murmur. Auscultation is generally considered sufficient for detecting a significant VSD. The murmur depends on the abnormal flow of blood from the left ventricle, through the VSD, to the right ventricle. If there is not much difference in pressure between the left and right ventricles, then the flow of blood through the VSD will not be very great and the VSD may be silent. This situation occurs a) in the fetus (when the right and left ventricular pressures are essentially equal), b) for a short time after birth (before the right ventricular pressure has decreased), and c) as a late complication of unrepaired VSD. Confirmation of cardiac auscultation can be obtained by non-invasive cardiac ultrasound (echocardiography). To more accurately measure ventricular pressures, cardiac catheterization, can be performed.


During ventricular contraction, or systole, some of the blood from the left ventricle leaks into the right ventricle, passes through the lungs and reenters the left ventricle via the pulmonary veins and left atrium. This has two net effects. First, the circuitous refluxing of blood causes volume overload on the left ventricle. Second, because the left ventricle normally has a much higher systolic pressure (~120 mm Hg) than the right ventricle (~20 mm Hg), the leakage of blood into the right ventricle therefore elevates right ventricular pressure and volume, causing pulmonary hypertension with its associated symptoms. This effect is more noticeable in patients with larger defects, who may present with breathlessness, poor feeding and failure to thrive in infancy. Patients with smaller defects may be asymptomatic.


  Treatment is either conservative or surgical. Smaller congenital VSDs often close on their own, as the heart grows, and in such cases may be treated conservatively. In cases necessitating surgical intervention, a heart-lung machine is required and a median sternotomy is performed. Percutaneous endovascular procedures are less invasive and can be done on a beating heart, but are only suitable for certain patients. Repair of most VSDs is complicated by the fact that the conducting system of the heart is in the immediate vicinity.

Epidemiology and Etiology

VSDs are the most common congenital cardiac anomalies. They are found in 30-60% of all newborns with a congenital heart defect, or about 2-6 per 10000 births. It is debatable whether all those defects are true heart defects, or if some of them are normal phenomena, since most of the trabecular VSDs close spontaneously.[4] Prospective studies give an prevalence of 2-5 per 100 births of trabecular VSDs that closes shortly after birth in 80-90% of the cases.[5] [6].

Congenital VSDs are frequently associated with other congenital conditions, such as Down syndrome.[7]

A VSD can also form a few days after a myocardial infarction[8] (heart attack) due to mechanical tearing of the septal wall, before scar tissue forms, when macrophages start remodeling the dead heart tissue.

See also


  1. ^ Ambumani P, Kuruchi Srinivasan. Ventricular Septal Defect, General Concepts. URL: Accessed on December 5, 2005.
  2. ^ Eidem BW. Ventricular Septal Defect, Muscular. URL: Accessed on April 13, 2006.
  3. ^ Hoffman JI, Kaplan S. The incidence of congenital heart disease. J Am Coll Cardiol. 2002 Jun 19;39(12):1890-900. PMID 12084585.
  4. ^ Meberg A, et al: Increasing incidence of ventricular septal defects caused by improved detection rate. Acta Pædiatrica 1994; 83: 653-657.
  5. ^ Hiraishi S, Agata Y, Nowatari M, Oguchi K, et. al. Incidence and natural course of trabecular ventricular septal defect: Two-dimensional echocardiography and color Doppler flow image study. J Pediatr 1992;120:409-15.
  6. ^ Roguin N, Du ZD, Barak M, Nasser N, Hershkowitz S, Milgram E. High prevalence of muscular ventricular septal defect in neonates. J Am Coll Cardiol 1995 November 15;26(6):1545-8
  7. ^ Wells GL, Barker SE, Finley SC, Colvin EV, Finley WH. Congenital heart disease in infants with Down's syndrome. South Med J. 1994 Jul;87(7):724-7. PMID 8023205.
  8. ^ Bruckheimer E. Ventricular septal defect. Medical Encyclopedia -, URL: Accessed on December 5, 2005.
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Ventricular_septal_defect". A list of authors is available in Wikipedia.
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