Ventricular Septal Defect – Diagnosis And Treatment

Ventricular Septal Defect – Diagnosis And Treatment

Ventricular septal defect is a anatomically parietal defect, single or multiple, located in the interventricular septum. This defect may be isolated or associated with other cardiac malformations. It is a congenital heart malformation with left-right shunt and increased pulmonary flow.

Interventricular septum that separates the left ventricle of the right ventricle has four areas: membranous septum, inlet septum, trabecular septum and outlet septum. Lack of development of one component leads to septal ventricular defect in that area. Being classified according to their anatomical location and to their frequency, ventriculare septal defects are:

1. Perimembranos ventricular septal defect – the most common variant, is located near the tricuspid valve and is representing approximately 70-80% of all ventricular septal defects.
2. Muscular ventricular septal defect – single or multiple (“swiss cheese”), about 15% of all ventricular septal defects.
3. Infundibular ventricular septal defect – represent  5-7% of all ventricular defects and  can lead to aortic valve damage by their anatomical proximity.
4. Atrioventricular septal defect –  this type of ventricular septal defect is located in the area of atrioventricular ceiling.

Ventricular Septal Defect

Pathophysiology:

Hemodynamic changes are depending on: size of the defect, the location of the defect, lung pressure, left ventricular ejection resistance. According to these features exist:

• Small restrictive ventricular septal defect, with reduced shunt and with  pulmonary blood flow pressure / systemic blood flow pressure ratio of 1.5;
•  Moderate ventricular septal defect with moderate shunt, with pulmonary blood flow pressure / systemic blood flow pressure ratio between 1.5 and 2.5;
• Large ventricular septal defect with large shunt and pulmonary blood flow pressure / systemic blood flow pressure ratio greater than 2.5. In this case exist a significant increase pressure in the right ventricle, right atrium and will appear high blood pressure that leads to a increased resistance in  pulmonary veins and will appear vascular obstructive pulmonary disease with Eisenmenger syndrome, when the shunt reverses and becomes a right-left shunt and will appear cyanosis and congestive heart failure.

Ventricular Septal Defect

Symptoms:

It is unusual that a ventricular septal defect to give symptoms in the immediately postnatal period.

Children with small ventricular septal defect with trivial shunt are asymptomatic, discovered incidentally on clinical examination. Ventricular septal defect with moderate or large shunt, leading to installation of heart failure phenomena in the first months of life. This children presents: hepatomegaly, tachypnea, tachycardia, dyspnea, fatigue and sweating, are underweight and lung infections are common. Children with large unrestricted ventricular septal defect, will develop Eisenmenger syndrome.

Clinical examination detect on auscultation a characteristic systolic murmur and trill. In unrestricted, large ventricular septal defect, systolic murmur may be less expressive, despite the severity of the disease.

Diagnosis:

Diagnosis of ventricular septal defect is confirmed by laboratory investigations:

1. ECG. Small ventricular defects have normal ECG. Large ventricular septal defects show signs of ventricular hypertrophy and overload of the right atrium.
2. Cardiothoracic radiography. In small ventricular septal defect the radiography is normal. In large defects appear cardiomegaly and overload of pulmonary circulation.
3. Echocardiography . Bidimensional and color Doppler echocardiography reveal ventricular septal defect,  the shunt location and its direction. Interventricular septum is a complex structure with curved appearance and echo examination can miss many of ventricular defects.
4. Cardiac catheterization. Itis done only when there are discrepancies between
   echocardiographic examination and clinical manifestations. Can measure the pressures in heart cavities, and oxygen saturation in blood gases, can determine pulmonary pressure, vascular resistances. Also, can test the reversibility of pulmonary vascular disease. Can detect small muscular septal defects or other abnormalities that escaped to echo exam.

Ventricular Septal X-Ray

Natural evolution:

The determining factor of natural evolution is the size of ventricular septal defect. The small muscular ventricular defect may close spontaneously in the first months of life. Large ventricular septal defects, are leading to congestive heart failure and often require surgical closure during the first year of life. Children with large ventricular septal defects and increased pulmonary vascular resistance, with Eisenmenger syndrome can not be operated. Those who have moderately increased vascular resistance and with left-right shunt, may benefit from surgery.

Treatment:

Medical treatment, is prophylactic to prevent infectious endocarditis. Once installed congestive heart failure, drug therapy with cardiac tonics, diuretic and oxygen therapy, trying to improve the symptoms.

Interventional closure. The device is placed by percutaneous approach in specific sites, to close the parietal defect without affecting surrounding structures (tricuspid valve in particular). It is recommended in cases with small muscular ventricular septal defect, single or multiple, which has a higher surgical risk.

Surgery. Surgical indication is based on several factors: age, size of defect, location, direction and magnitude of the shunt and pulmonary vascular resistances. About 30% of infants with ventricular septal defect and severe symptoms are requiring closure of the defect in the first year of life. In children diagnosed with large ventricular septal defect, around the age of 4-6 weeks, 80% of these defects will reduce their size or will close spontaneously with the developing of cardiac structures. After one year of age, only a third of ventricular septal defects can close spontaneously.

Ventricular Septal Defect

Perioperative mortality is close to zero when the intervention is made early, before the onset of complications. Postoperative complications are: residual defects with significant shunt (technical defect or incomplete diagnosis), tricuspid regurgitation and atrioventricular block.

Banding of the pulmonary artery. Is generally recommended primary ventricular septal defect closure, regardless of age. Only in situations with multiple muscular septal defects, banding of the pulmonary artery is generally recommended and will be done at the age of 3-5 years.