Ventricular septal defect

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**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).
ICD-10	Q 21.0
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.^[1]^[2]

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

diagram of a healthy heart and one with VSD

1 Diagnosis
2 Pathophysiology
3 Treatment
4 Epidemiology and Etiology
5 See also
6 References
7 External links

[edit] Diagnosis

A VSD can be detected by cardiac auscultation. Classically, a VSD causes a pathognomonic holosystolic 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.

[edit] Pathophysiology

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.

[edit] Treatment

A nitinol device for closing muscular VSDs, 4 mm diameter in the centre. It is shown mounted on the catheter into which it will be withrawn during insertion.

Treatment is either surgical or conservative. Smaller congenital VSDs often close on their own, as the heart grows, and are thus treated conservatively. Open surgical procedures require a heart-lung machine and are done with a median sternotomy. 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.

[edit] Epidemiology and Etiology

VSDs are the most common congenital cardiac anomalies. They are found in 30% of all newborns with a congenital heart defect, or about 2-3 per 1000 births.

Congenital VSDs are frequently associated with other congenital conditions, such as Down syndrome.^[4]

A VSD can also form a few days after a myocardial infarction^[5] (heart attack) due to mechanical tearing of the septal wall, before scar tissue forms, when macrophages start remodeling the dead heart tissue.

[edit] See also

[edit] References

^ Ambumani P, Kuruchi Srinivasan. Ventricular Septal Defect, General Concepts. eMedicine.com. URL: http://www.emedicine.com/ped/topic2402.htm. Accessed on December 5, 2005.
^ Eidem BW. Ventricular Septal Defect, Muscular. eMedicine.com. URL: http://www.emedicine.com/ped/topic2543.htm. Accessed on April 13, 2006.
^ Hoffman JI, Kaplan S. The incidence of congenital heart disease. J Am Coll Cardiol. 2002 Jun 19;39(12):1890-900. PMID 12084585.
^ 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.
^ Bruckheimer E. Ventricular septal defect. Medical Encyclopedia - MedlinePlus.org, URL: http://www.nlm.nih.gov/medlineplus/ency/article/001099.htm. Accessed on December 5, 2005.