1. The document discusses various types of acyanotic congenital heart disease including ventricular septal defect (VSD), atrial septal defect (ASD), patent ductus arteriosus (PDA), and coarctation of aorta. 2. It provides details on the classification, symptoms, diagnosis, and treatment options for each condition. 3. The conditions are characterized by shunting of blood between the left and right sides of the heart without cyanosis, and can cause heart failure if left untreated.

1. ACYANOTIC CONGENITAL
HEART DISEASE
MANJU MULAMOOTTIL

2. ACYANOTIC CONGENITAL HEART DISEASE
The condition of acyanotic heart defect occurs
when shunting (flowing) of blood occurs from
the left side of the heart to the right side of the
heart due to a structural defect . Patients retain
normal levels of oxyhemoglobin saturation in
systemic circulation.

3. CLASSIFICATION
•Common shunt lesions
• Ventricular septal defect(VSD)
• Atrial septal defect(ASD)
• Patent ductus arteriosus(PDA)
•Common stenotic lesions
• Coarctation of aorta.

4. SIGNS AND SYMPTOMS
• Shortness of breath
• Congested cough
• Diaphoresis
• Fatigue
• Frequent respiratory infections
• Tachycardia
• Tachypnoea
• Respiratory distress
• Mild cyanosis (in right sided heart failure)
• Poor growth and development (from increased energy spent on breathing)

5. VSD
• VSD is a defect in the ventricular septum , the wall dividing the left
and right ventricles of the heart .
• The ventricular septum consists of an inferior muscular and superior
membranous portion and is extensively innervated with conducting
cardiomyocytes
• Membranous ventricular septal defects are more common than
muscular ventricular septal defects, and are the most common
congenital cardiac anomaly

6. PATHOPHYSIOLOGY
• During ventricular contraction, or systole, some of the blood from
the left ventricle leaks into the right ventricle, passes through the
lungs and re enters the left ventricle via the pulmonary veins and left
atrium.
• This has two net effects. First, the circuitous refluxing of blood
causes volume overload on the left ventricle. Second, because the left
ventricle normally has a much higher systolic pressure
(~120 mmHg) than the right ventricle (~20 mmHg), the leakage of
blood into the right ventricle therefore elevates right ventricular
pressure and volume, causing pulmonary hypertension with its
associated symptoms.
• In serious cases, the pulmonary arterial pressure can reach levels
that equal the systemic pressure. This reverses the left to right shunt,
so that blood then flows from the right ventricle into the left
ventricle, resulting in cyanosis, as blood is by-passing the lungs for

7. VSD

9. CLASSIFICATION
• The classification is based on the location of the VSD on the right ventricular surface of the inter
ventricular septum and is as follows
• Type 1 (Subarterial) (Supracristal) (Conal septal defect) (Infundibular)
Found in 5-7% of patients, more in Asians related to the pulmonary valve
• Type 2 (Perimembranous) (Paramembranous) (Conoventricular)
Most common variety found in 70%
• Type 3 (Inlet) (AV canal type)
Commonly associated with atrioventricular septal defect, found in about 5%
• Type 4 (Muscular)
Located in the muscular septum, found in 20%. Can be sub classified again based on the location into
anterior, apical, posterior and mid
• Type 5: Gerbode (Left ventricular to right atrial communication)
Due to absence of Atrioventricular septum.

10. SYMPTOMS AND SIGNS
• No signs of cyanosis in the early stage.
• however uncorrected VSD can increase pulmonary resistance leading to
the reversal of the shunt and corresponding cyanosis.
• Signs
• Pansystolic murmur along lower left sternal border.
• Palpable thrill( palpable turbulence of blood flow)
• Larger VSDs may cause a parasternal heave
• Displaced apex beat (the palpable heartbeat moves laterally over time, as
the heart enlarges.
• Fail to thrive
• Tachypnoea

11. DIAGNOSIS
1 Auscultation – Pansystolic murmur
2 ECHO
3 x-ray chest

13. TREATMENT
• Smaller congenital VSDs often close on their own, as the heart
grows, and in such cases may be treated conservatively.
• Ventricular septum defect in infants is initially treated
medically with cardiac glycosides (e.g., digoxin10-20 µg/kg per
day), loop diuretics (e.g., furosemide 1–3 mg/kg per day) and
ACE inhibitors (e.g., captopril 0.5–2 mg/kg per day
• VSD Device closure

14. • VSD closure
• Indications
1. Failure of congestive cardiac failure to respond to
medications
2. VSD with pulmonic stenosis
3. Large VSD with pulmonary hypertension
4. VSD with aortic regurgitation
Surgical treatment

15. ASD
Atrial septal defect (ASD) is a congenital heart defect in which
blood flows between the atria (upper chambers) of the heart.
Normally, the atria are separated by a dividing wall, the
interatrial septum. If this septum is defective or absent, then
oxygen-rich blood can flow directly from the left side of the heart
to mix with the oxygen-poor blood in the right side of the heart,
or vice versa. This can lead to lower-than-normal oxygen levels
in the arterial blood that supplies the brain, organs, and tissues.

16. PATHOPHYSIOLOGY
In case of a large ASD , which may result in a clinically
remarkable left-to-right shunt, blood will shunt from
the left atrium to the right atrium. This extra blood from
the left atrium may cause a volume overload of both
the right atrium and the right ventricle. If untreated, this
condition can result in enlargement of the right side of
the heart and ultimately heart failure.

17. PATHOPHYSIOLOGY
If the ASD is left uncorrected, the pulmonary hypertension
progresses and the pressure in the right side of the heart will
become greater than the left side of the heart. This reversal of the
pressure gradient across the ASD causes the shunt to reverse;
a right-to-left shunt will exist. This phenomenon is known
as Eisenmenger's syndrome. Once right-to-left shunting occurs,
a portion of the oxygen-poor blood will get shunted to the left
side of the heart and ejected to the peripheral vascular system.
This will cause signs of cyanosis

20. TYPES OF ASD
1. Ostium secondum – most common type comprises 6–10% of all
congenital heart diseases
1. The secundum atrial septal defect usually arises from an
enlarged foramen ovale, inadequate growth of the septum secundum,
or excessive absorption of the septum primum. Ten to twenty percent
of individuals with ostium secundum ASDs also have mitral valve
prolapse
2. If the ostium secundum ASD is accompanied by an acquired mitral
valve stenosis, that is called Lutembacher's syndrome.
2. Patent foramen ovale – it is a remnant of the fetal foramen ovale
3. Ostium primum – commonly classified as an atrioventricular septal defect
4. Sinus venosus ASD - the defect in the septum involves the venous inflow
of either the superior vena cava or the inferior vena cava

21. SYMPTOMS AND SIGNS
• Dyspnoea on exertion
• Fatigue
• Swelling of feet
• Frequent lung infections
• palpitation
• Auscultation – systolic ejection murmur
• Fixed splitting of S2

23. DIAGNOSIS
Diagnosis in children
• Most individuals with a significant ASD are diagnosed in
utero or in early childhood with the use of ultrasonography or
auscultation of the heart sounds during physical examination.
• X-ray chest
• Echo
• ECG – incomplete right bundle branch block

24. TREATMENT
• Percutaneous device closure
• surgical closure

25. PDA
•Patent ductus arteriosus (PDA) is a congenital disorder in
the heart wherein a neonate's ductus arteriosus fails to
close after birth.
• The ductus arteriosus is a normal fetal blood vessel that
closes soon after birth. In a PDA, the vessel does not close
and remains "patent" (open) resulting in irregular
transmission of blood between two of the most important
arteries close to the heart, the aorta and the pulmonary
artery.

26. PDA
PDA is common in neonates with persistent respiratory
problems such as hypoxia, and has a high occurrence in
premature children. In hypoxic newborns, too little
oxygen reaches the lungs to produce sufficient levels of
bradykinin and subsequent closing of the DA. Premature
children are more likely to be hypoxic and thus have PDA
because of their underdeveloped heart and lungs.

29. SYMPTOMS AND SIGNS
•Dyspnoea
•Tachycardia
•Poor growth
•Respiratory problems
•Continuous machine like murmur on auscultation
•Left subclavicular thrill
•Bounding pulse
•Widened pulse pressure

30. DIAGNOSIS
• Auscultation- continuous machine like murmur
• X-ray chest – cardiomegaly
• Echo

32. TREATMENT
• Medical management
• NSAID(inhibitors of PG synthesis) such as indomethacin have
been used to close PDA , because PGE1 is responsible for the
ductus to keep patent.
• PDA device closure
• Surgical closure

33. COARCTATION OF AORTA
• Coarctation of aorta, or aortic narrowing is a congenital
condition whereby the aorta narrows in the area where
the ductus arteriosus (ligamentum arteriosum after
regression) inserts. Aortic coarctation is considered when a
section of the aorta is narrowed to an abnormal width.
• The word “coarctation” means narrowing. Coarctations
are most common where the aorta—the major artery
leading away from the heart—arches toward the abdomen
and legs.

34. COARCTATION OF AORTA
• The aortic arch may be small in babies with coarctation.
When a patient has a coarctation, the left ventricle has to
work harder. Since the aorta is narrowed, the left ventricle
must generate a much higher pressure than normal in
order to force enough blood through the aorta to deliver
blood to the lower part of the body. If the narrowing is
severe enough, the left ventricle may not be strong enough
to push blood through the coarctation, thus resulting in
lack of blood to the lower half of the body.

36. CLASSIFICATION
•Preductal - The narrowing is proximal to the ductus
arteriosus
•Ductal Coarctation: The narrowing occurs at the
insertion of the ductus arteriosus.
•Postductal coarctation: The narrowing is distal to the
insertion of the ductus arteriosus

37. SYMPTOMS AND SIGNS
• Symptoms may be absent with mild coarctation.
• Difficulty breathing
• Poor apetite or trouble feeding
• Failure to thrive
• Dizziness or shortness of breath
• Fainting or near fainting episodes
• Chest pain
• Fatigue
• Leg pain with exercise
• Arterial hypertension in the arms with low blood pressure in the lower
extremities
• Weak pulses in the femoral arteries

38. DIAGNOSIS
1. X-ray –post stenotic dilation of the aorta
results in figure 3 sign
2. MR or CT angiography
3. Cardiac catheterization

40. TREATMENT
• Conservative if asymptomatic
• Surgical resection of the narrow segment if there is arterial
hypertension.
• 1. Aortic resection with end to end anastomosis
• 2. Patch aortoplasty
• 3. L subclavian flap angioplasty
• 4 . Bypass graft repair
• 5. Balloon angioplasty