Membranous VSDs are located near the heart valves. These VSDs can close at any time.

Membranous VSDs are located near the heart valves. These VSDs can close at any time.
Muscular VSDs are found in the lower part of the septum. They're surrounded by muscle, and most close on their own during early childhood.
Inlet VSDs are located close to where blood enters the ventricles. They're less common than membranous and muscular VSDs.
Outlet VSDs are found in the part of the ventricle where blood leaves the heart. These are the rarest type of VSD.

1. Congenital heart disease DR : SANAIHSAN

2. A congenital cardiac malformation occurs in about 1% of live births. There is an overall male predominance, although some individual lesions (e.g. atrial septal defect and persistent ductus arteriosus) occur more commonly in females. A  congenital heart defect  ( CHD ), also known as a  congenital heart anomaly  or  congenital heart disease , is a problem in the structure of the heart that is present at birth

3. Aetiology The aetiology of congenital cardiac disease is often unknown, but recognized associations include: maternal prenatal rubella infection (persistent ductus arteriosus, and pulmonary valvular and arterial stenosis) maternal alcohol abuse (septal defects) maternal drug treatment and radiation ,genetic abnormalities (e.g. the familial form of atrial septal defect and congenital heart block) chromosomal abnormalities (e.g. septal defects and mitral and tricuspid valve defects are associated with Down’s syndrome (trisomy 21) or coarctation of the aorta in Turner’s syndrome

4. Ventricular septal defect (VSD) VSD is the most common congenital cardiac malformation (1 in 500 live births).  A  ventricular septal defect (VSD) is a birth defect of the heart in which there is a hole in the wall (septum) that separates the two lower chambers (ventricles) of the heart It occurs as an isolated abnormality or in association with other anomalies.

5. Classification Membranous VSDs are located near the heart valves. These VSDs can close at any time. Muscular VSDs are found in the lower part of the septum. They're surrounded by muscle, and most close on their own during early childhood. Inlet VSDs are located close to where blood enters the ventricles. They're less common than membranous and muscular VSDs. Outlet VSDs are found in the part of the ventricle where blood leaves the heart. These are the rarest type of VSD.

6. Pathophysiology Left ventricular pressure is higher than right ventricular pressure;  Blood therefore moves from left to right  Increases pulmonary blood flow  When pulmonary blood flow is very large, progressive obliteration of the pulmonary vasculature eventually causes the pulmonary arterial pressure to equal the systemic pressure (Eisenmenger’s complex).  Consequently, the shunt is reduced or reversed (becoming right-to-left) and central cyanosis  & Clubbing develops

7. Clinical features A moderate VSD produces fatigue and dyspnoea with cardiac enlargement and a prominent apex beat.  There is often a palpable systolic thrill at the lower left sternal edge. A loud ‘tearing’ pansystolic murmur is heard at the same position.  A large VSD eventually causes pulmonary hypertension Displaced Apex Beat Palpable P2 smaller defect produce loud murmur(PANSYSTOLIC MURMUR)

8. Investigations A small VSD produces no abnormal X-ray or ECG findings. ■ Chest X-ray shows a prominent pulmonary artery owing to increased pulmonary blood flow in larger defects. In Eisenmenger’s complex the radiological signs of pulmonary hypertension (i.e. ‘pruned’ pulmonary arteries) can be seen. Cardiomegaly occurs when a moderate or a large VSD is present. ECG shows features of both left and right ventricular hypertrophy. ■ 2-D echocardiography and CW Doppler can assess the size and location of the VSD, and its haemodynamic consequences. ■ CMR is increasingly being used.

9. Treatment Moderate and large VSDs should be surgically repaired before the development of severe pulmonary hypertension. Infective endocarditis prophylaxis is used.

10. Atrial septal defect (ASD) Clinical features: Most children with ASD are asymptomatic, although they are prone to pulmonary infection. Some complain of dyspnoea and weakness. Right heart failure and atrial fibrillation may develop to become the initial presentation in adult life. The physical signs of ASD reflect the volume overloading of the right ventricle . A right ventricular heave can usually be felt.

11. It is two to three times more common in women than in men. There are two main types of ASD, ostium secundum (75%), ostium primum (15%) and sinus venosus (10%). The common form is the ostium secundum defect, which involves the fossa ovalis in the atrial mid-septum. Communication at the level of the atria allows left-to-right shunting of blood.

12. Above the age of 30 years there may be an increase in pulmonary vascular resistance, which gives rise to pulmonary hypertension. Atrial arrhythmias, particularly atrial fibrillation, are common at this stage. Investigations: Chest X-ray: reveals a prominent pulmonary artery and pulmonary plethora. There may be noticeable right ventricular enlargement.

13. ECG usually shows some degree of right bundle branch block (because of dilatation of the right ventricle) and right axis deviation. Echocardiogram is usually abnormal if a significant defect is present. Indirect evidence includes right ventricular hypertrophy and pulmonary arterial dilatation, and abnormal motion of the interventricular septum. Subcostal views may demonstrate the ASD Flow disturbance can be assessed by colour Doppler. ■ CMR can provide additional information.

14. Treatment A significant ASD should be repaired before the age of 10 years or as soon as possible if first diagnosed in adulthood. There is a good result from surgery with osteum secundum ASD unless pulmonary hypertension has developed. Angiographic closure is now possible with significantly lower risk using a transcatheter clam shell device