Ventricular septal defect(VSD): Symptoms, Diagnosis, Complications & Treatments
Ventricular septal defect (VSD) is one of the most common congenital heart malformations. It may be present as a single anomaly but may be accompanied by other congenital cardiac anomalies.
It is divided into Perimembranous, Muscular, and Subarterial type. Perimembranous type is the most common type (70%). Subarterial type is indications for surgical treatment regardless of defect size. Because defects appear near the LVOT, they can cause aortic valve prolapse and ultimately cause aortic regurgitation.
The clinical manifestations of VSD depend on the size of the defect and the pulmonary blood flow. However, in moderate to large VSD, symptoms such as tachypnea, poor oral intake, poor weight gain, and tachycardia are present. In moderate to large VSDs, murmurs can also be heard. Low-pitched pansystolic murmur may appear at the lesion site and mid-diastolic rumbling murmur may appear at apex. Also, as blood flow to the pulmonary blood vessels increases, the size of P2 increases. LV hypertrophy and pulmonary angiographic findings can be observed on chest x-ray.
Confirmation is achieved through echocardiography. Through this, the position of the lesion can be confirmed and the amount of the short circuit can be confirmed.
Small VSDs usually close naturally within 1 year of life (30-50%). However, large VSDs that are asymptomatic have a poor prognosis, and cardiopulmonary transplantation is the only treatment that leads to Eisenmenger syndrome.
Complications include eisenmenger syndrome, aortic regurgitation in the subarterial type, and infective endocarditis.
The direction of treatment is to treat Congestive heart failuare (CHF congestive heart failure) and to prevent Eisenmenger syndrome. We aim at two big things. In the case of congestive heart failure, diuretics and digoxin are used to alleviate symptoms. In diuretics, common diuretics and K sparing diuretics are used to maintain electrolyte balance. (Ex. Furosemide + spironolactone), Eisenmenger syndrome should be diagnosed as soon as possible and the surgical treatment should be decided if the amount of short circuit is large.
<Indication for surgical treatment>
- No response to medical therapy (ex.diuretics, digoxin)
- Large defect with pulmonary hypertension (but, pulmonary resistance <8 wood unit / m2
- Qp / Qs & gt; 1.5 to 2 (& gt; 2y-o)
- Subarterial type
In contrast, eisenmenger syndrome refers to a syndrome in which pulmonary hypertension leads to anatomic changes in the pulmonary artery when the heart disease (ex VSD) with severe left and right shunts is not treated. If the pulmonary artery pressure increases significantly, the blood flow into the right ventricle due to the left and right shorts can not escape into the pulmonary artery, resulting in congestion in the right ventricle, which eventually escapes through the defect. In other words, excessive pressure is applied to the right ventricle, resulting in RV hypertrophy, as well as a rightward short-circuit in the right ventricle that moves the blood flow to the left ventricle. The appearance of the right eye shorts can be seen through cyanosis.
It is important that VSD should not be treated surgically if Eisenmenger syndrome is present. If you fill the defect in this situation, the blood flow in the right ventricle will become stagnant without getting out of the pulmonary artery or defect, which will lead to heart failure. Therefore, the only solution for Eisenmenger syndrome is cardiac transplantation, and it is important to surgically treat VSD before this syndrome appears.
It is divided into Perimembranous, Muscular, and Subarterial type. Perimembranous type is the most common type (70%). Subarterial type is indications for surgical treatment regardless of defect size. Because defects appear near the LVOT, they can cause aortic valve prolapse and ultimately cause aortic regurgitation.
The clinical manifestations of VSD depend on the size of the defect and the pulmonary blood flow. However, in moderate to large VSD, symptoms such as tachypnea, poor oral intake, poor weight gain, and tachycardia are present. In moderate to large VSDs, murmurs can also be heard. Low-pitched pansystolic murmur may appear at the lesion site and mid-diastolic rumbling murmur may appear at apex. Also, as blood flow to the pulmonary blood vessels increases, the size of P2 increases. LV hypertrophy and pulmonary angiographic findings can be observed on chest x-ray.
Confirmation is achieved through echocardiography. Through this, the position of the lesion can be confirmed and the amount of the short circuit can be confirmed.
Small VSDs usually close naturally within 1 year of life (30-50%). However, large VSDs that are asymptomatic have a poor prognosis, and cardiopulmonary transplantation is the only treatment that leads to Eisenmenger syndrome.
Complications include eisenmenger syndrome, aortic regurgitation in the subarterial type, and infective endocarditis.
The direction of treatment is to treat Congestive heart failuare (CHF congestive heart failure) and to prevent Eisenmenger syndrome. We aim at two big things. In the case of congestive heart failure, diuretics and digoxin are used to alleviate symptoms. In diuretics, common diuretics and K sparing diuretics are used to maintain electrolyte balance. (Ex. Furosemide + spironolactone), Eisenmenger syndrome should be diagnosed as soon as possible and the surgical treatment should be decided if the amount of short circuit is large.
<Indication for surgical treatment>
- No response to medical therapy (ex.diuretics, digoxin)
- Large defect with pulmonary hypertension (but, pulmonary resistance <8 wood unit / m2
- Qp / Qs & gt; 1.5 to 2 (& gt; 2y-o)
- Subarterial type
In contrast, eisenmenger syndrome refers to a syndrome in which pulmonary hypertension leads to anatomic changes in the pulmonary artery when the heart disease (ex VSD) with severe left and right shunts is not treated. If the pulmonary artery pressure increases significantly, the blood flow into the right ventricle due to the left and right shorts can not escape into the pulmonary artery, resulting in congestion in the right ventricle, which eventually escapes through the defect. In other words, excessive pressure is applied to the right ventricle, resulting in RV hypertrophy, as well as a rightward short-circuit in the right ventricle that moves the blood flow to the left ventricle. The appearance of the right eye shorts can be seen through cyanosis.
It is important that VSD should not be treated surgically if Eisenmenger syndrome is present. If you fill the defect in this situation, the blood flow in the right ventricle will become stagnant without getting out of the pulmonary artery or defect, which will lead to heart failure. Therefore, the only solution for Eisenmenger syndrome is cardiac transplantation, and it is important to surgically treat VSD before this syndrome appears.
