Acynotic heart defects
Ventricular septal defect (VSD)
Incidence and pathophysiology:
VSDs account for approximately 25% of all CHD.
VSD is the most common congenital cardiac lesion and is
often accompanied by other cardiac defects.
The lesion consists an abnormal opening between the right
and left ventricle which may vary in size from a miniscule
hole to complete absence of the septum, resulting in a
common ventricle.
Altered hemodynamics:
The degree of left to right shunting through the VSD depends on the size
of the defects and the pulmonary vascular resistance compared with the
systemic vascular resistance
The pulmonary vascular system is high in the newborn.
Over the first few weeks of life, the resistance decreases.
As this occurs, an increased amount of blood shunts left to right of the
VSD level.
The pulmonary vascular circulation receives increased pulmonary blood
flow. With large defects the pulmonary arteries are exposed to systemic
pressure, causing pulmonary hypertension and over time, progressive
pulmonary disease.
Manifestations:
Signs and symptoms vary with the size of the defect and
the presence of associated cardiac lesions.
Clinical symptoms are usually not seen at birth because of
continued high pulmonary vascular resistance in the
newborn.
Infants with moderate to large defects will become
symptomatic within the first few weeks of life.
Children with small defects will remain asymptomatic.
Clinical manifestations:
tachypnea, dyspnea.
Poor growth.
Palpable thrills.
Systolic murmur at left lower sternal border.
Shortness of breath.
Failure to gain weight.
Fast heart rate.
Pounding heart.
Frequent respiratory infections.
Diagnosis:
1. Chest X –:
- Cardiomegally of varying degrees present.
- Pulmonary vascular marking increase.
2. ECG:
i. Small VSD , ECG is normal.
ii. Moderate VSD, left ventricular hypertrophy( LVH) and occasional left atrial
hypertrophy(LAH) may be seen.
iii. Large defect, shows biventricular hypertrophy(BHV) with or without LAH.
3. Echocardiogram- used to make a definite diagnosis.
4. Cardiac catheterization( rarely needed, unless there are concerns of high blood
pressure in the lungs, in which case surgery to close the defect is generally not
recommended).
5. MRI of the heart- used to find out how much blood is getting to the lungs.
Therapeutic management:
Therapeutic management:
20 -80% of all VSDs closed spontaneously.
1. Many small lesions do not require surgical intervention.
2. If there is aortic valve regurgitation related to VSD
position near the valve and even if the defect is small,
surgery is indicated to reduce the progression of valve
insufficiency.
3. Antibiotic prophylaxis is indicated for all VSDs.
Medical management:
1. Infants who develop CHF- digoxin, diuretics, ACE inhibitors
to reduce afterload.
2. Nutritional supplements are added to infants milk to
increase caloric intake. NGT feeding or gastrostomy tube
feeding for infants who are unable to breast feed.
3. Avoid exposure to respiratory infections.
Surgical management:
Most VSD are closed by surgery but muscular defects by
devices placed at cardiac catheterization.
Surgery is usually done at 3-6 months of age for:
a. Managing heart failure and failure to thrive.
b. Prevent permanent lung damage from pulmonary
hypertension and high blood flow.
Complications:
Congestive heart failure.
Growth failure, especially in infancy.
Bacterial endocarditis.
Eisenmenger complex.
Pulmonary artery hypertension.
Aortic regurgitation.
Sub aortic obstruction.
