Ventricular septal defect
Updates to Article Attributes
Ventricular septal defects (VSD) represent defects in the interventricular septum that allow allow a haemodynamic communication between the right and left ventricles. It typically results in a left to right shunt.
Epidemiology
They represent one of the most common congenital cardiac anomalies and may be associated with up to 40% of such anomalies 1. They are considered the most common congenital cardiac abnormality diagnosed in children and the second most common diagnosed diagnosed in adults 9. The estimated incidence is at ~1 in 400 births 6.
Pathology
Classification according to location
- membranous/perimembranous (most common: 80-90%)
- inlet/inflow
- outlet/subarterial
- muscular/trabecular
Associations
A VSD can occur on its own but frequently tends to occur with other cardiovascular associations:
- cardiovascular associations
-
extra cardiac associations
- aneuploidic/chromosomal anomalies
- other syndromic anomalies: there are several and include
Radiographic features
Plain film
The chest radiograph can can be normal with a small VSD. Larger VSDs may show cardiomegaly (particularly left atrial enlargement although the right and left ventricle can also be enlarged). A large VSD may also show features of pulmonary arterial hypertension, pulmonary oedema, pleural effusion and/or increased increased pulmonary vascular markings.
Ultrasound: echocardiography
Allows direct visualisation of the septal defect which can be easily easily seen in the four chamber view. A perimembranous VSD can seen as a septal dropout in the area adjacent to the tricuspid septal leaflet and below the right border of the aortic annulus. Small isolated VSD's can be difficult to detect prenatally.
CT
CTA with ECG-gating allows direct visualisation of the defect. Large VSDs may be seen on
contrast CT
MRI
May also show added functional information (e.g. quantification/shunt severity) in addition to anatomy. Some muscular defects can give a "Swiss cheese" appearance owing to their complexity.
Treatment and prognosis
The prognosis is good for small VSDs which show a high spontaneous intra-uterine or post-natal closure rate. VSD's usually do not cause any haemodynamic compromise in utero due to right and left ventricular pressures being very similar during that period.
Complications
- Eisenmenger phenomenon with shunt reversal (i.e. L to R becomes R to L)
- cardiac failure
-<p><strong>Ventricular septal defects</strong> <strong>(VSD)</strong> represent defects in the <a href="/articles/intraventricular-septum">interventricular septum</a> that allow a haemodynamic communication between the <a href="/articles/right-ventricle">right</a> and <a href="/articles/left-ventricle">left ventricles</a>. It typically results in a left to right shunt.</p><h4>Epidemiology</h4><p>They represent one of the most common <a href="/articles/congenital-heart-disease">congenital cardiac anomalies</a> and may be associated with up to 40% of such anomalies <sup>1</sup>. They are considered the most common congenital cardiac abnormality diagnosed in children and the second most common diagnosed in adults<sup> 9</sup>. The estimated incidence is at ~1 in 400 births <sup>6</sup>.</p><h4>Pathology</h4><h5>Classification according to location</h5><ul>- +<p><strong>Ventricular septal defects</strong> <strong>(VSD)</strong> represent defects in the <a href="/articles/intraventricular-septum">interventricular septum</a> that allow a haemodynamic communication between the <a href="/articles/right-ventricle">right</a> and <a href="/articles/left-ventricle">left ventricles</a>. It typically results in a left to right shunt.</p><h4>Epidemiology</h4><p>They represent one of the most common <a href="/articles/congenital-heart-disease">congenital cardiac anomalies</a> and may be associated with up to 40% of such anomalies <sup>1</sup>. They are considered the most common congenital cardiac abnormality diagnosed in children and the second most common diagnosed in adults<sup> 9</sup>. The estimated incidence is at ~1 in 400 births <sup>6</sup>.</p><h4>Pathology</h4><h5>Classification according to location</h5><ul>
-</ul><h4>Radiographic features</h4><h5>Plain film</h5><p>The chest radiograph can be normal with a small VSD. Larger VSDs may show cardiomegaly (particularly <a title="Left atrial enlargement" href="/articles/left-atrial-enlargement">left atrial enlargement</a> although the right and left ventricle can also be enlarged). A large VSD may also show features of <a title="Pulmonary arterial hypertension (PAH)" href="/articles/pulmonary-hypertension-1">pulmonary arterial hypertension</a>, <a title="Pulmonary oedema" href="/articles/pulmonary-oedema">pulmonary oedema</a>, <a title="Pleural effusion" href="/articles/pleural-effusion">pleural effusion</a> and/or increased pulmonary vascular markings.</p><h5>Ultrasound: echocardiography</h5><p>Allows direct visualisation of the septal defect which can be easily seen in the four chamber view. A perimembranous VSD can seen as a septal dropout in the area adjacent to the tricuspid septal leaflet and below the right border of the aortic annulus. Small isolated VSD's can be difficult to detect prenatally.</p><h5><strong>CT</strong></h5><ul><li>allows direct visualisation of the defect on contrast CT</li></ul><h5><strong>MRI</strong></h5><p>May also show added functional information (e.g. quantification/shunt severity) in addition to anatomy. Some muscular defects can give a "Swiss cheese" appearance owing to their complexity.</p><h4>Treatment and prognosis</h4><p>The prognosis is good for small VSDs which show a high spontaneous intra-uterine or post-natal closure rate. VSD's usually do not cause any haemodynamic compromise in utero due to right and left ventricular pressures being very similar during that period.</p><h5>Complications</h5><ul>- +</ul><h4>Radiographic features</h4><h5>Plain film</h5><p>The chest radiograph can be normal with a small VSD. Larger VSDs may show cardiomegaly (particularly <a href="/articles/left-atrial-enlargement">left atrial enlargement</a> although the right and left ventricle can also be enlarged). A large VSD may also show features of <a href="/articles/pulmonary-hypertension-1">pulmonary arterial hypertension</a>, <a href="/articles/pulmonary-oedema">pulmonary oedema</a>, <a href="/articles/pleural-effusion">pleural effusion</a> and/or increased pulmonary vascular markings.</p><h5>Ultrasound: echocardiography</h5><p>Allows direct visualisation of the septal defect which can be easily seen in the four chamber view. A perimembranous VSD can seen as a septal dropout in the area adjacent to the tricuspid septal leaflet and below the right border of the aortic annulus. Small isolated VSD's can be difficult to detect prenatally.</p><h5><strong>CT</strong></h5><p>CTA with ECG-gating allows direct visualisation of the defect. Large VSDs may be seen on non-gated studies.</p><h5><strong>MRI</strong></h5><p>May also show added functional information (e.g. quantification/shunt severity) in addition to anatomy. Some muscular defects can give a "Swiss cheese" appearance owing to their complexity.</p><h4>Treatment and prognosis</h4><p>The prognosis is good for small VSDs which show a high spontaneous intra-uterine or post-natal closure rate. VSD's usually do not cause any haemodynamic compromise in utero due to right and left ventricular pressures being very similar during that period.</p><h5>Complications</h5><ul>
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