Atrial septal defect

useful for nursing students in their child health nursing, medical surgical nursing.

2. Common congenital malformation
Acyanotic:Acyanotic:
a.a.Atrial septal defectAtrial septal defect
b.b.Ventricular septal Ventricular septal
defectdefect
c.c.PDAPDA
d.d.Coarctation of Coarctation of
AortaAorta
Cyanotic:Cyanotic:

a.a.TOFTOF
b.b.Transposition of Transposition of
great vesselsgreat vessels
c.c.Tricuspid atresiaTricuspid atresia

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

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

5. 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

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

7. 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

9. Pathophysiology
Increased left atrial pressure(0
2
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

10. Clinical Features
In majority remains asymptomatic
Systolic murmer best heard over 2
nd
& 3
rd

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

12. A hyperdynamic impulse of the right
ventricle may be palpated at the lower left
sternal border
Split S
2
Cyanosis in later stages
Cardiomegaly
Pulmonary vascular emboli
Echo shows right ventricular volume
overload
Cardiac catheterization shows increased
0
2
content in blood

13. 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.

14. Management
•Medical
Furosemide 1mg/kg BD
Digoxin 5 mg/kg BD
Potassium chloride 1meq/kg BD
Antibiotics

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

16. 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 O
2
demand
8.Psychological support
9.Prevention of infection

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

19. 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.

20. 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.

21. 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 )

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

23. 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

24. Eisenmengers syndrome

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

26. Cardiac failure and its symptoms
Cyanosis seen on exertion specially
while crying
Prominence of left precordium
Digital clubbing
Poor exercise tolerance
S
2
is split

28. Diagnostic evaluation
•Hematology for polycythemia
•Electrocardiography
•Echocardiography/ doppler
•Radiographic findings
•Cardiac catheterization for 0
2
saturation

29. 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

30. •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

32. Complication
•Residual VSD
•Conduction defects
•Infection

33. 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%