Mr. Jayesh Soni discusses congenital heart defects in children. He notes that approximately 8-12 children per 1000 are born with congenital heart defects. The document then describes the fetal circulation patterns and how they normally close after birth. It provides classifications for acyanotic and cyanotic heart defects and discusses specifics such as atrial septal defects (ASD), ventricular septal defects (VSD), signs/symptoms, diagnostic evaluations, and management including medical, interventional, and surgical options. Complications are also outlined.

1. Mr. Jayesh Soni
HOD Pediatrics
VCN Udaipur

2. 1. Umbilical arteries :- umbilical ligament (2 to 3
months)
2. Umbilical vein :- ligamentum teres
3. Ductus venosus :- ligamentum venosum
4. Ductus arteriousus :- ligamentum arteriosum
(1- 3 months)
5. Foramen ovale :- functional closure soon after
birth but anatomical closure occurs in about 1
year time (fossaovalis)

5. INCIDENCE:-
 Approximately 8 to 12 childern in 1000
are born with a congenital heart defect.
 Heart defects are among the most
common birth defect and are the
leading cause of birth defect-related
deaths.
 Right sided lesions are more common
in female, & left sided in males

6. ETIOLOGY:-
 90 % of cases is unknown.
 Heredity
 Consanguinous marriage
 Chromosomal abnormality – Trisomy 21(Down
syndrome), - Turner syndrome
 Other associated factors
- Teratogenic infections (Rubella)
- Teratogenic drug (thalidomide)
- Alcohol intake
- Radiation in 1st trimester of pregnancy
- Maternal IDDM
- High altitude
- Fetal hypoxia
- Birth asphyxia

7. CLASSIFICATION OF CHD :-
Obstruction of
blood from
ventricles
Increased pulmonary
blood flow
•Aortic stenosis
•Coarctation of aorta
•Pulmonary stenosis
•ASD
•VSD
•PDA
•AVC DEFECT
Acyanoti
c

8. CLASSIFICATION OF CHD :-
Mixed blood flow Decreased
pulmonary blood flow
• TGA
• Total anomalous
pulmonary venous
return
• Truncus arterious
• Hypoplastic left heart
syndrome
•TOF
•TA
Cyanotic

10. ACYANOTIC HEART DISEASES
If there is no abnormal communication
between pulmonary & systematic circulation
Or
If such connection is present, the pressure
forces the blood from arterial to venous side.
The blood supplies in the body is therefore
oxygenated & caynosis does not occurs.

12. ASD:
Atrial Septal defects are abnormal opening in
wall separating the right & left atria
….
More common in females, approx 17% of all
cases in congenital cardiac defects..

13. TYPES :-
1. Ostium primum - opening at lower
end of septum
2. Ostium secundum - opening at
centre of septum
3. Sinus venosus - opening at top of
septum

15. PATHOPHYSIOLOGY:-
Shunting b/w Lt to Rt
Volume overload in Rt
side
Rt heart enlargement
Overload on pulmonary
vasculature
Pulmonary HTN RVF

16. CLINICAL MANIFESTATIONS
• Frequent chest infection
• Effort intolerance
• dyspnoea
• Bulging of chest
• Congestive heart failure
• Cardiac enlargement

17. DIAGNOSIS
• Physical examination: systolic murmur
• Chest x ray: RA & RV hypertrophy
• Echocardiography
• ECG

18. MANAGEMENT :-
Medical management
• Treatment of chest infection & infective
endocarditis
• Interventional therapy
- Percutaneous ASD closure
Surgical management
• Mostly by simple suture closure
• In larger defects pericardial or prosthetic
patch

20. PERCUTANEOUS ASD CLOSURE

21. NURSING MANAGEMENT :-
 Closely monitor vital signs, central venous
and intra-arterial pressures, and intake and
output.
 Watch for atrial arrhythmias.
 Give an antibiotic and an analgesic, as
ordered.
 Provide range-of-motion exercises and
coughing and deep-breathing exercises.

22. COMPLICATIONS
• Pulmonary hypertension
• Heart failure
• Atrial fibrillation
• Stroke from embolization
• Eisenmenger syndrome (reversal of the
shunt into a right-to-left shunt)
• Infective endocarditis
• Surgical complication

23. VENTRICULAR SEPTAL DEFECT
Accounts for 25 %of
all congenital heart
lesions. Also called
 Roger’s disease
 Interventricular
septal defect

24. Types of VSD:-
1. Membranous VSD 2. Muscular VSD

25. PATHOPHYSIOLOGY :-
Shunting of blood from Lt to Rt
Rv to pulmonary artery
Volume overload in the Rt side
Pulmonary HTN
Eisenmenger’s syndrome and hypertrophy of
muscle

26. SIGNS & SYMPTOMS :-
 Palpitation
 Frequent chest infection
 Feeding difficulties
 Tachycardia
 Excessive sweating associated with feeding
 Poor weight gain
 Failure to thrive
 Biventricular hypertrophy
 Congestive heart failure

27. DIAGNOSTIC EVALUATION
•Auscultation of heart sounds – harsh
systolic murmur sound.
•Chest X-ray :- enlargement of heart.
•ECG = biventricular hypertrophy.
•2-D-echocardiogram with colour
Doppler study.

28. MANAGEMENT OF VSD:-
• SMALL VSD
- all close spontaneously
* 50% by 2yrs
* 90% by 6yrs
* 100% during school yrs
Surgical intervention is usually
not necessary

29. • MODERATE TO LARGE VSDs :-
1. Medical Management:
a. CHF management: digoxin and diuretics
b. Avoid oxygen; oxygen is a potent pulmonary
vasodilator and will increase blood flow into the PA.
c. Increase caloric intake
2. Cardiac catheterization for placement of a
ventricular occlusion device for muscular defects

30. INDICATIONS for SURGERY
• Basic Indications for surgical closure
– Mid-large shunt
– Failure to thrive
– Continued CHF or
– Recurrent pulmonary infections
• SURGERY:- (Usually repaired before age 1)
a. One-stage approach: preferred surgical plan; patch closure
of VSD (an oval patch of knitted dacron by mattress suture
posteriorly).
b. Two-stage approach: first surgery is to band the PA to
restrict pulmonary blood flow; second surgery is to patch close
the VSD and remove the PA band.

31. Surgical
correction has
to be done
before
irreversible
damage to
pulmonary
vasculature
occurs.

33. COMPLICATIONS
• Congestive cardiac failure
• Infective endocarditis on rt.ventricular side
• Complete heart block
• Delayed growth & development in infancy
• Damage to electrical conduction system
during surgery (causing arrythmias)
• Pulmonary hypertension
• Eisenmenger's syndrome.