This document provides information on various congenital heart defects including patent ductus arteriosus (PDA), atrial septal defect (ASD), ventricular septal defect (VSD), and tetralogy of Fallot. It describes the anatomy and physiology of each condition, their signs and symptoms, diagnostic testing, potential complications, and treatment options. The key points are: PDA, ASD, and VSD can cause left-to-right or right-to-left blood shunts depending on pulmonary pressures. Tetralogy of Fallot is characterized by four defects that cause deoxygenated blood to mix with oxygenated blood, leading to cyanosis. Surgical closure of defects or transcatheter
2. Introduction
• Congenital heart defects(CHD) , defect in
structure of heart or great vessels that is
present at birth
• Most common CHD are, ASD , VSD, PDA, TOF
• ASD- aterial septal defect
• VSD- ventricular septal defect
• PDA- patent ductus arterious
• TOF- tetralogy of fallot
4. Shunt in fetal circulation
1. Ductus venosus- vessel bring blood from
umblicial vein to IVC
2. Foramen ovalve- allow blood to go from RA
to LA.
3. Ductus arterious- allow blood to go from
pulmonary artery to aorta
5. Patent ductus arteriosus
• Ductus arteriosus is functional in foetus and
diverts de-saturated blood from main
pulmonary artery into descending aorta and
placenta for oxygenation.
• It closes by birth, but in PDA this is not close
thus causes blood to begin flow in opposite
direction.
7. Haemodynamics
• Since the pressure in aorta is higher than
pulmonary artery there will be continuous flow of
blood from aorta to pulmonary artery THIS IS
LEFT TO RIGHT SHUNT.
• When pulmonary hypotension develops, this
blood flow diminishes initially in diastole .
• Later, with development of EISENMENGER’S
syndrome , the blood flow is reversed. THIS IS
RIGHT TO LEFT SHUNT.
• Now , blood flow form pulmonary artery to aorta.
8. Eisenmenger’s syndrome
• Exchange of blood between lower 2 chambers
of heart. Thus, increase pressure in left
ventricle to pulmonary artery .
• Increase pressure in right ventricle to
pulmonary & aorta , because of increase
pressure in RV, RV has to pump more blood
• More blood is delivered to pulmonary & lungs
this may also cause CHD.
• Results in cynosis along with central or
periphery clubbing.
9. Clinical features
• Retardation in growth& development
• Dyspnoea
• Collapsing pulse
• Wider pulse pressure
• Apex beat is shifted downward
• Continuous thrills at upper sternal edge
• First heart sound is loud
• Machinery murmur
• Pulmonary hypertension
• Central cynosis &clubbing
10. Investigations
• X-rays shows- increase vascular markings
along with enlarged left atrium and ventricle
• ECG- left atrial enlagrement , left ventricular
hypertrophy
• ECHO- blood flow through ductus arteriosus.
13. Arterial septal defect
• ASD is defect in the inter-arterial septa. Based
on location of defect it can be classified into
three types.
OSTIUM SECUNDUM
OSTIUM PRIMUM
SINUS VENOSUS
14. Definition
• ASD is congenital heart defect in which blood
flows abnormally between two atria of heart.
• Normally, the atria is separated by a wall
called inter-arterial septum, but it remain
open in ASD
• OSTIUM SECUNDUM- commonest type of
ASD, involves the FORAMEN OVALE in mid-
septal region.
15. • OSTIUM PRIMUM- rare type of ASD. It occurs
near the AV valve .The AV valve may also be
deformed
• SINUS VENOSUS-rare type of ASD, it occurs in
highly in atrial septum near the entry of SVC &
is almost associated always with partial
abnormal pulmonary venous return.
17. Haemodynamics
• In ASD, blood is shunted from LA to RA then to
RV.
• The RV output & pulmonary blood flow is
increased. This leads to progressive
enlargement of RA and RV and pulmonary
arteries.
• Eventually, pulmonary hypertension appears
with reversal of shunt. (R-L shunt)
18. Clinical features
• More in females
• Palpations and fatigue
• Recurrent respiratory failure
• Retard growth & development
• Dyspnoea
• Cardiac failure
• Atrial fibrilization
• Paradoxial embolism
• arrhythmias
23. Ventricle septal defect
• The inter-ventricular septum has a
membranous & muscular portion. VSD implies
a defect in the inter-ventricular septum. Most
of VSD are “pre-membranous” –at junction of
membranous & muscular portions.
• VSD occur as a result of incomplete separation
of ventricles.
• Muscular defect is uncommon
• VSD may be associated with ASD, PDA or
pulmonary stenosis.
25. Haemodynamics
• Blood flow from LV- RV then to pulmonary
artery. Overload on right side results in
reversal of shunt R-L and pulmonary
hypertension.
26. Clinical features
• CHF
• Recurrent respiratory infection
• Hyperdynamic precodium
• Apex beat shifted downwards
• Systolic thrill at 3 or 4 inter-costal space
• Harsh pansystolic murmur
• Pulmonary hypertension
• Eisenmenger syndrome
27. Investigations
• X-rays- cardiomegaly, increase pulmonary
vascular markings, left atrial enlargement
• ECG- normal in small defect, left. Ventricular
hypertrophy in small- moderate, biventricular &
right ventricular hypertrophy in moderate- large
defect, left atrial enlargement, intra-ventricular
conduction defect, right bundle branch block
• ECHO- access lesion and size of VSD as well as
blood flow across it.
• Cardiac catheterisation- access pulmonary
vascular resistance
28. Management
• Small VSD require no treatment
• Operation in moderate- large defect with L-R
shunt
• Large defect with severe pulmonary markings
are not indicate for surgery. These are indicate
for lung transplant
29. Tetralogy of fallot
• TOF made up of 4 heart problems. It results in
cyanotic or blue babies. These 4 defects are
VSD
Overriding aorta
Pulmonary stenosis
Right ventricular hypertrophy
31. • VSD- allow oxygen rich blood mix with
deoxygenated blood
• Overriding aorta- aorta has moved forward
directly over the hole between the ventricles.
This allows deoxygenated blood from RV to
flow into the aorta
• Pulmonary stenosis- pulmonary artery is
narrowed & pulmonary valve doesn’t open all
the way. As a result less blood reaches to
lungs causes cyanosis.
32. • Right ventricular hypertrophy- wall of right
ventricle is thicker than normal. This happen
because right ventricular has to work hard to
pump blood through the narrow pulmonary
valve.
33. Cyanotic spell
Babies lips & skin will appear more blue than
usual and their breathing may deeper and
faster.
34. Clinical features
Dyspnoea, fatigue, hypoxic spell on excretion
Cyanotic spell during feeding, crying, fever or
exercise due to systemic vaso-dilation
producing increase R-L shunt across VSD