The document discusses various acyanotic heart diseases including atrial septal defect (ASD), ventricular septal defect (VSD), patent ductus arteriosus (PDA), coarctation of aorta, pulmonary stenosis, and aortic stenosis. It provides details on the pathophysiology, clinical features, investigations, and management of each condition. Key points include that ASD is the most common congenital heart disease, VSD has a pansystolic murmur at the lower left sternal edge, PDA causes a continuous murmur and loud P2 with pulmonary hypertension, coarctation causes hypertension and rib notching on CXR, and large defects can lead to pulmonary hypertension and

1. ACYANOTIC HEART DISEASE
Dr.B.BALAGOBI

2. ACYANOTIC HEART DISEASE
• VSD:Commonest congenital heart disease
• PDA
• PS
• ASD
• Coarcation of aorta
• AS
• AVD

3. ATRIAL SEPTAL DEFECT.
• 2 common types
– Ostium secundum defect:midseptum.(common,defect in foramen
ovale);Usually presents in adult life,Spontaneous closure is unlikely,Need Sx
– Ostium primum defect:low in the septum.(Usually presents in first year)
associated with other endocardial cushion defects (cleft AV valves, inlet type VSD
• Pathophysiology:
– L-R shunt-increased flow across Rt heart-RV & PA enlargement.
• Clinical features:
– Asymptomatic
– slow wt gain(FTT)
– frequent LRTI,No risk of infective endocarditis in ostium secondum ASD
• Diagnosis:
– Right ventricular heave(Due to RVH)
– Soft long ejection systolic murmur due to increased blood flow
across the pulmonary valve at 3rd IC space
– fixed wide split S2,large ASDincreased blood flow across
tricupid valve  Mid diastolic murmur

4. Auscultation in ASD
•Increased flow across the
pulmonary valve produces a systolic
ejection murmur and fixed splitting
of the second heart sound
•Increased flow across the TV
produces a diastolic rumble at the
mid to lower right sternal border.

5. Investigations:
• CXR:
– enlarged heart
– Enlarged PA
– increased pulmonary vascular markings,Central plethra
• ECG:
– Right axis in secundum defect
– hallmark of primum defect is extreme Left axis deviation
– RVH,RBBB
• ECHO:RVH,valve anatomy,flow direction.
• Treatment:(indicated if symptoms+,RV overload)
– Device closure during cardiac cathetrization
– surgical closure.

6. ASD: Therapy
• Percutaneous Closure
– only for secundum (contra in others)
– adequate superior/inferior rim around ASD
– no R-L shunting
• Surgical Closure
– Good prognosis:
• closure age < 25, PA pressure <40
• If >25 or PA>40, decreased survival due to
CHF, stroke, and afib

7. Atrial Septal Defect

8. Atrial Septal Defect

9. Atrial Septal Defect

10. VENTRICULAR SEPTAL DEFECT.
• Most common CHD (32%),Often one component of another
more complex congenital heart lesion.
• Pathophysiology:
– Lt-Rt shunt as long as pulmonary vascular resistance is lower than
systemic resistance,if reverse shunt reverses.
• Large defects lead to pul.hypertension-Eissenmenger syndrome.
• Clinical features: depend on size of the defect
– asymptomatic
– growth failure
– recurrent LRTI
– congestive heart failure
– SOB,cyanosis(Eissenmenger),Risk of infective endocarditis+
• Diagnosis:
– parasternal thrill
– pansystolic murmur at lower left sternal edge(Loud if small defect,if large VSD
 increase flow across pulmonary valve ejection systolic murmur
– loud p2.(Pulmonary HT)

12. Ventricular Septal Defect

13. Investigations
• CXR:
– cardiomegaly,enlarged LA&LV.
– Enlarged PA,increased pulmonary vascular markings
– Pulmonary oedema
• ECG:
– extreme leftt axis is charecteristic,biventricular hypertrophy.
• ECHO:chamber size & pressures.
• Cardiac catheter:O2 content,PA pressure,size & no of
defects.

14. MANGEMENT OF VSD
• Majority close spontaneously before 1 year of
age;less than 10% require surgery.
• 2 types of VSD
– Perimembranous(90%)
– Muscular(More likely close spontaneously)
• Treatment:
– Surgical closure before pulmonary vascular changes
become irreversible.(if symptoms + like FTT,Features
of Pul HT Loud P2,RVH)
– Endocarditis prophylaxis
– Heart failure Mx:ACEI,digoxin,diuretics.

15. Eisenmenger’s Syndrome
• Final common pathway for all significant LR
shunting in which unrestricted pulmonary
blood flow leads to pulmonary vaso-occlusive
disease (PVOD); RL shunting/cyanosis
devleops
• Generally need Qp:Qs >2:1

17. Eisenmenger: Treatment
• Sxs +polycythemia  phlebotomy
– Careful if microcytosis, strongest predictor of
cerebrovascular events
• RULE OUT CORRECTABLE DISEASE
• Once diagnosis established, avoid aggressive testing
as many patients die during cardiovascular
procedures
• Diuretics prn, oxygen
• Definitive: Heart Lung transplant
– Prostacyclin therapy may delay, expensive

18. PATENT DUCTUS ARTERIOSUS.
• Connection between PA & descending aorta,Common in preterm
• Pathophysiology:
– Lt-Rt shunt,reverses if pulmonary resistance increases-RV
enlargement.If PDA is large Eissenmenger syndrome can develop.
• Clinical features:
– depend on size & direction of flow
– slow growth,LRTI,SOB,cyanosis.
• Diagnosis:
– bounding pulse
– continous murmur/Machinery murmur
– loud S2.(Pul HT)

20. Investigations
• CXR:cardiomegaly,increased pul vascularity.
• ECG:Lt or biventricular hypertrophy.
• ECHO:2D visualises PDA,doppler shows turbulance.
• Cardiac catheter:PA pressures & O2 sats.
• Treatment:
– Endocardial prophylaxis as long as patent
– Indomethacin:a prostaglandin E1 inhibitor may close a PDA.
• Surgical:ligation /coil/clipping/division

21. Patent Ductus Arteriosis

22. Patent Ductus Arteriosis

23. Coarctation of Aorta
• Narrowing in proximal descending aorta usually just beyond the
origin of Left subclavian artery.
• May be long/tubular but most commonly discrete ridge
• Blood flow to the lower body maintained through collateral vessels
• 98% of all coarctations at segment of aorta adjacent to ductus arteriosus.
• Natural hx:
– poor prognosis if unrepaired
– High BP in UL & Low BP in LL
– Systemic HypertensionLVF,Aortic Aneurysm/dissection,ICH
– murmur (continuous or systolic murmur heard in back or SEM/ejection click of
bicuspid AV)
– weak/delayed LL pulses
– Rib notching on CXR is pathognomonic
• Associated with
– Turner’s syndrome
– Subarachinoid haemorrhage

25. Rib notching

26. Coarctation Repair
• Surgical correction
1) Patch aortoplasty with
removal of segment and
end to end anastomosis
or subclavian flap repair
2) bypass tube grafting
around segment

27. Pulmonary Stenosis
• No symptoms in mild or moderately severe
lesions.
• Cyanosis and RVH, right-sided heart failure in
patients with severe lesions.
• High pitched systolic ejection murmur maximal in
second left interspace.
• Ejection click often present.
• Oligaemic lung fields(Reduced pulmonary
vascular marking)

28. Pulmonary Stenosis

29. Valvular Aortic Stenosis
• Most common type, usually asymptomatic in
children.
• May cause severe heart failure in infants.
• Prominent left ventricular impulse, narrow
pulse pressure.
• Harsh systolic murmur and thrill along left
sternal border, systolic ejection click.

30. Valvular Aortic Stenosis

31. Duct dependent Heart disease
• Some babies with CHD will depend on the
circulation through PDA ,when duct close they
become critically ill.
• Causes
– R/S:TA,PA,Critical PS
– L/S:COA,Critical AS,Hypoplastic left heart disease
– TPGV
• Treatment
– Prostaglandin infusion  keep the duct open.

32. Which of the following are non
cyanotic heart disease?
A. ASD
B. Pulmonary atresia
C. Large VSD
D. Truncus arteriosis
E. Aortic stenosis

33. T/F ASD?
A. Ostium Primum type is the commonest
B. Ostium secondum type gets infective
endocarditis
C. Children are usually symptomatic during
early childhood
D. Is most common congenital heart disease occurs in
Rubella
E. Usually close spontaneously
F. Is the commonest acyanotic heart disease

34. T/F regarding ASD?
A. Associated with RBBB
B. Cause parasternal heave indicates pulmonary
hypertension
C. Associated with recurrent respiratory tract
infection
D. Murmur is due to left to right flow throw the
defect
E. Cause variable split in second heart sound
F. Is rare in adults

35. T/F VSD?
A.Perimembrous type is commoner
B. Never cause infective endocarditis
C. Loudness of murmur is proportional
to the severity
D.Usually close spontaneously
E. Cause left ventricular hypertrophy.

36. T/F regarding VSD?
A. Cause pansystolic murmur that is best heard
at left lower sternal edge
B. Right to left shunt occurs in uncomplicated
VSD
C. Soft S2 is heard if there is a pulmonary
hypertension
D. Occurs in Down syndrome
E. Recurrent LRTI is due to pulmonary
congestion

37. T/F PDA?
A. Associated with congenital rubella
B. Cause small volume pulse
C. Is an indication for the antibiotic
prophylaxis against infective
endocarditis
D. If left untreated cause pulmonary
hypertension
E. In a full term baby is likely to close.

38. T/F regarding PDA?
A. Is a acyanotic heart disease
B. Cause plethoric lung field in CXR
C. Common in premature babies
D. May be seen in babies with cyanotic heart
disease
E. May cause heart failure

39. T/F large uncomplicated PDA is
associated with ?
A. Cyanosis
B. Clubbing
C. Normal P2
D. Wide pulse pressure
E. Recurrent LRTI

40. T/F COA?
A. Cause hypertension
B. Cause systolic murmur at the inter scapular
area
C. Cause bounding femoral pulse
D. Associated with Turners syndrome
E. Rib notching seen in CXR

41. T/F Patent ductus arteriosus?
A. Is a feature of congenital rubella
B. In a full term ,baby is likely to close
spontaneously
C. Associated with small volume pulse.
D. Is an indication for antibiotic prophylaxis against
infective endocarditis
E. Loud P2 indicates pulmonary hypertension

42. T/F which of the following are the
complications of the left to right shunt,
A. Recurrent LRTI
B. Cerebral abscess
C. Pulmonary hypertension
D. CCF
E. Hypercyanotic episodes