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Ventricular Septal Defect

Ventricular septal defect (VSD) is a common congenital heart defect where there is an abnormal opening in the wall separating the two lower chambers of the heart. VSDs account for 30% of congenital heart defects and occur in about 1 in 500 live births. Small VSDs that are less than 3mm in diameter often close on their own without any treatment and are asymptomatic. Large VSDs greater than the size of the aortic valve can cause heart failure, breathing issues, and failure to thrive in infants and require surgical repair between 3-6 months of age to prevent lung damage from pulmonary hypertension. The long-term prognosis for VSDs is generally good if repaired, but Eisenmenger

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159 views3 pages

Ventricular Septal Defect

Ventricular septal defect (VSD) is a common congenital heart defect where there is an abnormal opening in the wall separating the two lower chambers of the heart. VSDs account for 30% of congenital heart defects and occur in about 1 in 500 live births. Small VSDs that are less than 3mm in diameter often close on their own without any treatment and are asymptomatic. Large VSDs greater than the size of the aortic valve can cause heart failure, breathing issues, and failure to thrive in infants and require surgical repair between 3-6 months of age to prevent lung damage from pulmonary hypertension. The long-term prognosis for VSDs is generally good if repaired, but Eisenmenger

Uploaded by

ChianChuan Wee
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
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Ventricular septal defect:

 Common, accounting for 30% of all cases, 1/500 births.


 This is a defect anywhere in the ventricular septum, usually
o Perimembranous (adjacent to the tricuspid valve) -67%
o Muscular (completely surrounded by muscle)
 Most conveniently be considered according to the size of the lesion.

Small VSD:
 Defect smaller than the aortic valve in diameter, perhaps up to 3mm.

Clinical features:

 Asymptomatic
 May have thrill at lower sterna edge.
 Loud pansystolic murmur at lower left sterna edge.
 Quiet pulmonary second sound

Investigations:

1. Echocardiography
 Demonstrates the precise anatomy of the defects.
 It’s possible to assess it’s hemodynamic effects by Doppler echocardiograph
2. CXR & ECG
 Normal, no findings.

Management:

 Most of these lesions will close spontaneously


This is ascertained by the:
 Disappearance of murmur
 Normal ECG
 Normal echocardiogram

 Whilst the VSD is present, prevention of bacterial endocarditis is attempted by:


 Maintaining good dental hygiene
 Antibiotic prophylaxis before dental extraction or any other operation where there will
be bleeding.
Large VSDs:
 Defects are the same size or bigger than the aortic valve.

Clinical features:

 Heart failure with breathlessness and failure to thrive after 1 week old
 Recurrent chest infections

 Active precordium
 Soft pansystolic murmur or no murmur
 Apical mid-diastolic murmur- from increased flow across the mitral valve after blood has
circulated through the lungs.
 Loud pulmonary second sound (P2) – due to raise pulmonary arterial diastolic pressure.

 Heart failure- tachypnoea, tachycardia, enlarged liver.

Investigation:

1. CXR
 Cardiomegaly
 Enlarged pulmonary arteries
 Increased pulmonary vascular markings
 Pulmonary oedema

2. ECG
 Biventricular hypertrophy by 2months of age
 Signs of pulmonary hypertension

3. Echocardiography
 Demonstrates: anatomical defects, haemodynamic effects and severity of pulmonary
hypertension.

Management:

1. Drug therapy for heart failure


 Diuretics
 Captopril

2. Surgical repair, usually performed at 3-6months of age in order to:


 Manage heart failure
 Manage failure to thrive
 Prevent permanent lung damage from pulmonary hypertension and high blood flow.
**there is always some degree of pulmonary hypertension in children with large left to right shunt. This
damage the lungs as in increased pulmonary blood flow and pulmonary hypertension will ultimately lead
to irreversible damage of the pulmonary capillary vascular bed.

This pulmonary vascular disease usually becomes established in the second year of life.

But, Eisenmenger’s syndrome with cyanosis due to intracardiac shunting from right to left, rarely evolves
until the second decades.

Prognosis:

Long term prognosis is good.

Except in the case of Eisenmenger’s syndrome, which many patients die in the second or third decade of
life.

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