This presentation includes normal fetal heart anatomy and physiology and classification of heart diseases. In this ppt fallot's tetralogy, patent ductus arteriosus, coarctation of aorta, atrial septal defect are discussed in details. This presentation gives basic idea about the congenital diseases to the BPT students.

1. CONGENITAL HEART DISEASES
DR.SAMIR JADAV (PT)

2. FETAL HEART AND BLOOD CIRCULATION

3. FETAL HEART AND BLOOD CIRCULATION
▪ The growing fetus is fully dependent on a special organ
called the placenta for nourishment.
▪ A special cord called the umbilical cord links the placenta to
the fetus.
▪ The mother’s blood flows through a thin layer of cells in the
wall of the uterus, giving the fetus food and oxygen while
removing any wastes like carbon dioxide.
▪ There is actually no direct contact between the circulatory
systems of the mother and fetus.

4. FETAL HEART AND BLOOD CIRCULATION
▪ The fetus does not use its own lungs until birth, so its
circulatory system is different from that of a newborn baby.
▪ Before birth, the fetal heart does not have to pump blood
to the lungs to pick up oxygen.
▪ In the fetal heart, pulmonary artery and aorta is connected
by a blood vessel called the ductus arteriosus.
▪ In embryonic life lungs remain collapsed, and starts
working after birth.

5. FETAL HEART AND BLOOD CIRCULATION
▪ Blood flowing in the pulmonary artery bypasses the
collapsed lungs by ductus arteriosus and flows directly into
the aorta.
▪ After birth, the ductus closes and a separate pulmonary
artery and aorta form.
▪ The fetal heart also has an opening between the upper
chambers (the right and left atria) called the foramen
ovale.
▪ It lets blood flow directly from the right atrium to the left
atrium during fetal development, but closes after birth.

6. FETAL HEART AND BLOOD CIRCULATION
▪ So the ductus arteriosus and the foramen ovale are part of
the fetal circulatory system before birth but disappear
soon after birth.
▪ In most babies, these blood-flow routes naturally close up
shortly after birth, when the baby’s lungs and
cardiovascular system take over.
▪ Because the fetal heart has a circulatory system different
from the one the baby uses after birth, it may be days or
weeks before some congenital heart defects are found.

7. CLASSIFICATION
Heart
diseases
Congenital
heart disease
Acyanotic Cyanotic
Acquired
heart disease

8. ACYANOTIC CYANOTIC
Patent ductus arteriosus
Coarctation of aorta
Atrial septal defect
Ventricular septal defect
Fallot’s tetralogy
Transportation of great
vessels

9. FALLOT’S TETRALOGY
▪ a congenital malformation of the heart characterized
by an abnormal opening in the septum dividing the
ventricles, misplacement of the aorta so that it receives
blood from both ventricles instead of only the left
ventricle, narrowing of the pulmonary artery, and
enlargement of the right ventricle.

10. FALLOT’S TETRALOGY

11. Pathology
 Four features of tetralogy :-
i. Pulmonary stenosis : Obstruction of outflow tract of
RV.
ii. Ventricular septal defect
iii. Dextroposition of aorta
iv. Right ventricular hypertrophy
 The right ventricular obstruction increases right
ventricular systolic pressure equal to that of left ventricle.

12. Pathology
Due to, dextraposition of aorta, pulmonary obstruction and
septal defect, blood enters the aorta and produces
cyanosis.
Decrease blood flow in pulmonary artery thus limits
limits and ability to absorb oxygen.
Producers anoxia.
Chronic anoxia may produce compensatory
polycythemia and eventually clubbing of the
extremities.

13. Clinical features
▪ Dyspnea on exertion
▪ Clubbing of digits
▪ Heart of normal size
▪ A systolic Murmur
▪ Second pulmonic sound is is weak or absent
▪ Aortic second sound is is increased

14. Treatment
Operation is the only way to save child
Corrective operation
▪ Pulmonary artery obstruction is is corrected
 Ventricular septal defect and position of aorta is
corrected.
 Post OP PT Management
 Cardiac rehabilitation.

15. PATENT DUCTUS ARTERIOSUS
 Most common congenital abnormality.
 Once in every 4000 births.
 15 % of all cases of CHD.
 2 to 3 times more common in females.

16. PDA

17. Aetiology
▪ PDA develops from the 6th left aortic arch and is an
important normal fetal pathway connecting the left
pulmonary artery at its bifurcation to the aorta just
beyond the origin of left subclavian artery.
▪ Through to this channel blood bypasses the collapsed
lungs in in embryonic life so that blood flows directly
from the pulmonary artery into the aorta bypassing the
lungs.
▪ With the birth, the body starts respiration with
expansion of the lungs.

18. Aetiology
▪ The blood in the pulmonary artery passes to the lungs,
so the ductus arteriosus usually closes within a few
days and becomes fibrotic, which is then called
ligamentum arteriosum.
▪ It is said that changes in the oxygen tension of the
arterial blood exerts a direct stimulus on the closer of
the ductus.

19. Pathology
 As the pressure is higher in the aorta than the pulmonary
artery, blood will flow from the aorta to the pulmonary
artery.
 With this increase of blood in the lungs the pulmonary
vessels become dilated (pulmonary plethora) and their
pulsation becomes increased (hilar dance).
 This additional blood flow to the lungs will cause more
blood to the left side of the heart resulting in left
ventricular hypertrophy.

20. Clinical features
▪ Symptoms is directly proportional to the size of ductus.
▪ Many cases may remain asymptomatic, where few cases
present with serious heart failure during first year.
▪ Congestive heart failure in adult patients.
▪ It often appears during the first pregnancy in females.
Physical signs :
 Continuous murmur, often described as machinery
murmur.

21. Clinical features
▪ Murmur becomes highlighted in systole, diminished in
diastole.
▪ Best heard in 2nd intercostal space.
▪ Smaller ductus heard earlier.
▪ Pulse collapsing in nature.
▪ A wide pulse pressure in a large ductus.
▪ Thrusting left ventricular apical impulse.

22. Special investigations
Chest X-ray
 May be normal
Fluroscopy
 Hilar dance may be observed.
ECG
 Usually normal with small ductus.
 Will show left ventricular hypertrophy with large
ductus.

23. Special investigations
Cardiac catheterization
 Localises the shunt.
 Confirming the diagnosis.
Aortography
 Most definite diagnostic method.

24. Complications
Cardiac failure
Bacterial endocarditis
Aortic rupture
Myocardial ischemia
Pulmonary hypertension.
Right heart hypertrophy and failure.

25. Treatment
▪ Operation is carried out in babies over 2 to 3 years of age.
▪ Low risk, excellent result.
▪ Ligation of patent ductus.

26. COARCTATION OF AORTA
▪ It is second commonest
congenital malformation
after PDA.
▪ It consist 10 to 15 % of
CHD.
▪ Twice as frequent in males.

27. Aetiology
Narrowing of aorta immediately beyond the origin of left
subclavian artery very near to the position of ligamentum
arteriosum.
Most popular theory is, coarctation is an extension of the
fibrotic process which converts patent ductus into
ligamentum arteriosum.

28. Pathology
In most patients the constriction is about 2 to 4 cm in
length just below the origin of left subclavian artery.
Usually, the lumen becomes 1 to 3 millimeter in the
constricted area.
Distal to the coarctation, the aorta is usually dilated.
Two main types :-
I. Post ductal type
II. Pre ductal type

29. Pathology
As the ductus remains patent, deoxygenated blood pass
from the pulmonary artery into the aorta distal to the
coarctation.
So, the lower trunk and lower extremities becomes
cyanosed, whereas the head, neck and upper extremities
remain pink.
This is known as differential cyanosis.
Patient may have other cardiac lesions and mortality rate is
high.

30. Clinical features
Hypertension : above the obstruction
 Headache
 Dizziness
 Epistaxis
 Throbbing and pulsation of arteries of head, neck.
 Systolic murmur
 Chance of LVF
Hypotension : below the obstruction

31. Clinical features
Hypotension
▪ Weak femoral pulsation
▪ Cold lower extremities
▪ Intermittent claudication of the legs

32. Complications
▪ LVF
▪ Intracranial haemorrhage
▪ Intrathoracic haemorrhage
▪ Rupture of aorta (very rare)

33. Special investigations
▪ Chest radiograph
▪ ECG
▪ Cardiac catheterization
• For location and extent
 Aortography
• For location and extent

34. Treatment
Operation : ideal age is 5 to 7 years
Coarctation of aorta is excised and end-to-end
anastomosis of aorta is performed usually with a graft.
Post operative antibiotic for 3-4 days.
Discharge in 7-10 days.
Post op physiotherapy
 Cardiac rehab

35. ATRIAL SEPTAL DEFECT
▪ This defect allows blood to flow from left to right atrium, so
the right side of heart and lung overfilled, left side of heart
receives less blood.
▪ Three types :-
1) Secundum defect
2) Ostium primum defect
3) Anomalous drainage of pulmonary veins

36. 1) Secundum defect
▪ Commonest variety
▪ Defect is in center of the septum
▪ Embryologically failure to develop
Symptoms :
Uncommon in first few years of life
Fatigue
Palpitation
Exertional dyspnoea
A soft systolic murmur

37. 1) Secundum defect
Treatment :
 Direct suturing and closure of defect by continuous suture
with prolene.
 Operation is performed with heart lung machine.

38. 2) Ostium primum defect
▪ Associated with incomplete formation of mitral (bicuspid)
valve and tricuspid valve.
Treatment :- operative correction between 4 to 6 years
of age.

39. 3)Anomalous drainage of pulmonary veins
▪ This is due to failure of incorporation of sinus venosus into
the atrium proper.
▪ The pulmonary veins either enter into right atrium or vena
cava.
Treatment :-
• A single anomalous vein : no harmful and no require Rx.

40. 3)Anomalous drainage of pulmonary veins
• When require treatment; can be corrected by insertion of
prosthetic patch so that defect close and pulmonary veins
made to enter the left atrium.