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Congenital Heart Defects
By- kajal Sansoya
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
Congenital heart defects
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
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.
Congenital heart defects
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.
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.
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
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.
Complications
• Cardiac failure
• Infective endocarditis
• Paradoxial embolism
• Pulmonary hypertension
• Rupture of ductus
Management
• Surgical ligation
• Transcatheter occluding devices
• Video assisted thoracoscopic clip closure
• Drug- indomythacin, iburoprofen
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
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.
• 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.
Congenital heart defects
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)
Clinical features
• More in females
• Palpations and fatigue
• Recurrent respiratory failure
• Retard growth & development
• Dyspnoea
• Cardiac failure
• Atrial fibrilization
• Paradoxial embolism
• arrhythmias
Sign & symptoms
• Hyperdynamic precordium
• Visible & palpable pulmonary artery pulsations
• Systolic thrills
• S1 is loud, S2 is widely spilt & fixed
• Mid-diastolic murmur
• Ejection systolic murmur
• Pulmonary hypertension
• Pansystolic murmur of mitral regurgitation,
tricuspid regurgitation
Investigation
• X-rays- enlargement of heart & pulmonary artery,
increase vascular markings
• ECG- Rt. Atrial enlargement, Rt. Ventricular
hypertrophy
Right axis deviation in ostium secundum
Left axis deviation in ostium prinum
Prolonged intervals of PR
• ECHO- RV dilation, RV hypertrophy, pulmonary
artery dilation
• Cardiac catherisation
Complication
• CHF
• Atrial fibrilization
• Pulmonary hypertension
• Eisenmenger’s syndrome
• Infective endocarditis
• Paradoxial embolism
Management
• Treatment of infection
• Surgical closure of defect
• Transcatheter septal occluder
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.
Congenital heart defects
Haemodynamics
• Blood flow from LV- RV then to pulmonary
artery. Overload on right side results in
reversal of shunt R-L and pulmonary
hypertension.
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
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
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
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
Congenital heart defects
• 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.
• 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.
Cyanotic spell
 Babies lips & skin will appear more blue than
usual and their breathing may deeper and
faster.
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
Investigation
X-rays
ECG
ECHO
Cardiac cartheterisation
Thank you
Happy reading 

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Congenital heart defects

  • 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.
  • 11. Complications • Cardiac failure • Infective endocarditis • Paradoxial embolism • Pulmonary hypertension • Rupture of ductus
  • 12. Management • Surgical ligation • Transcatheter occluding devices • Video assisted thoracoscopic clip closure • Drug- indomythacin, iburoprofen
  • 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
  • 19. Sign & symptoms • Hyperdynamic precordium • Visible & palpable pulmonary artery pulsations • Systolic thrills • S1 is loud, S2 is widely spilt & fixed • Mid-diastolic murmur • Ejection systolic murmur • Pulmonary hypertension • Pansystolic murmur of mitral regurgitation, tricuspid regurgitation
  • 20. Investigation • X-rays- enlargement of heart & pulmonary artery, increase vascular markings • ECG- Rt. Atrial enlargement, Rt. Ventricular hypertrophy Right axis deviation in ostium secundum Left axis deviation in ostium prinum Prolonged intervals of PR • ECHO- RV dilation, RV hypertrophy, pulmonary artery dilation • Cardiac catherisation
  • 21. Complication • CHF • Atrial fibrilization • Pulmonary hypertension • Eisenmenger’s syndrome • Infective endocarditis • Paradoxial embolism
  • 22. Management • Treatment of infection • Surgical closure of defect • Transcatheter septal occluder
  • 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