Congenital Heart Disease - VSD

1. Presentation by M.Rafi HAMIDI
Supervised by Prof. NAJMI, Head of Thoracic Surgery

3. Common congenital malformation
Acyanotic:
a. Atrial septal defect
b. Ventricular septal
defect
c. PDA
d. Coarctation of
Aorta
Cyanotic:
a. TOF
b. Transposition of
great vessels
c. Tricuspid atresia

4. Atrial Septal defect
• ASD is the abnormal opening between the
atrium, and it is a left to right shunt

5. Types
• 3 types:
 Secundum
 Primum
 Sinus venosus

6. Types
• Primum – affects the lower part of the
septum
• Secundum – common, affects the upper
part of the septum
• Sinus venosus – affects the upper part
and may be associated with abnormalities
of superior vena cava

7. Classification by size
ASDs can be
• Small (3 to <6 mm)
• Medium (6 to <12 mm)
• Large (>12 mm)

8. Incidence
• Sex - female : male = 3:1
• 1/1500 live births
• Ostium secundum counts for 7% of CHD’s
• 100% ASD’s 3mm in diameter
• Most of the secundum are associated with Holt-
Oram’s syndrome.
• Holt–Oram syndrome is a disorder that
affects bones in the arms and hands (the
upper limbs) and may also cause heart
problems

10. Pathophysiology
Increased left atrial pressure(02
nated
blood)

Left to right shunt ( no cyanosis)

Burden on right side of the heart

Increased pulmonary blood flow

Pulmonary stenosis / pulmonary HTN

Right ventricular hypertrophy

Right atrial pressure

Right to left shunt

cyanosis

11. Clinical Features
In majority remains asymptomatic
Systolic murmer best heard over 2nd & 3rd
ICS
Dysrrythmias
Increased fatigability
In older children recurrent chest infection,
breathlessness, & bulging of the chest due
to enlargement of right ventricle
Growth failure in some children

13. A hyperdynamic impulse of the right
ventricle may be palpated at the lower left
sternal border
Split S2
Cyanosis in later stages
Cardiomegaly
Pulmonary vascular emboli
Echo shows right ventricular volume
overload
Cardiac catheterization shows increased
02 content in blood

14. Diagnostic measures
• Chest X-Ray
• ECG
• MRI heart
• Cardiac catheterization
• Intracardiac imaging: with special catheters that
are typically placed in the venous system and
advanced to the level of the heart. Involves only
mild sedation.

15. Management
• Medical
Furosemide 1mg/kg BD
Digoxin 5 g/kg BD
Potassium chloride 1mq/kg BD
Antibiotics

16. Surgical closure
1. Cardiopulmonary bypass
2. Purse-string closure
3. Knitted Dacron patch

17. Nursing management
1. Identify symptoms
2. Carry out investigations
3. Monitor potassium levels
4. Intake output chart
5. Vital signs
6. Timely administrations of medications
7. Provide rest to decrease O2 demand
8. Psychological support
9. Prevention of infection

19. Complications
• Pulmonary hypertension & over circulation
• Heart failure
• Atrial dysrrhythmias
• Stroke

20. Prognosis
• With a small to moderate atrial septal
defect, a person may live a normal life
span without symptoms.
• Larger defects may cause disability by
middle age because of increased blood
flow and shunting of blood back into the
pulmonary circulation.

21. Ventricular Septal defect
• Abnormal opening between the ventricles
• It can be single pin hole opening to absence of
membrane
• Results in left to right shunt, ultimately right to
left shunt.

22. Types
• Membranous
• Muscular- swiss cheese
• (Perimembranous- lie in the LV outflow
tract just below the aortic valve.
• Infundibular- These defects lie beneath the
pulmonic valve )

23. Incidence
• VSD accounts for 25% of CHD’s
• Seen in 2-6 / 1000 live births
Etiology
• unknown

24. Pathophysiology
Blood from left ventricle right ventricle pulmonary artery

Increased pulmonary resistance

Increased pressure in right ventricle

Right ventricular hypertrophy

Enlargement of right ventricle

Enlargement of right atrium

Eisenmengers syndrome

Cyanosis

25. Eisenmengers syndrome

26. Clinical features
• Pan systolic Murmur
• In large VSD’s
Dyspnoea
Tachypnea
Feeding difficulties
Poor growth
Profuse perspiration
Recurrent pulmonary infections

27. Cardiac failure and its symptoms
Cyanosis seen on exertion specially
while crying
Prominence of left precordium
Digital clubbing
Poor exercise tolerance
S2 is split

29. Diagnostic evaluation
• Hematology for polycythemia
• Electrocardiography
• Echocardiography/ doppler
• Radiographic findings
• Cardiac catheterization for 02 saturation

30. Management
• Small defects no surgical correction but to
prevent bacterial endocarditis precautions
to be taken
• Moderate to large defects surgical closure
is needed
< 6 months: high risk for surgery usually
open heart surgery is done

31. • 6 to 24 months: in case of pulmonary
hypertension surgery is indicated to
prevent development of hypertensive
vascular disease
• >24 months: depends on pulmonary
vascular resistance
• Surgical interventions done for small
defects are Purse String closure n for
large defects Knitted Dacron patch
• Clamshell type catheter occlusion devices
are tested For closing of apical VSD

33. Complication
• Residual VSD
• Conduction defects
• Infection

34. Prognosis
• Risk depends on
Location of defect
Number of defects
Other associated cardiac defects
 Single membrane defect have low
mortality <5%
 Multiple defects have a risk of >20%