DETAILS ABOUT CHD

1. ACYNOTIC
HEART DISEASE

2. ANATOMY OF THE HEART
• The Heart Valves Four types of valves regulate
blood flow through your heart:
• The tricuspid valve
• The pulmonary valve
• The mitral valve
• The aortic valve

5. ATRIAL SEPTAL DEFECT

8. DEFINITION
“An atrial septal defect (ASD) is a hole in the wall (septum) between the
two upper heart chambers (left and right atria).” An atrial septal
defect is among the most common types of congenital heart diseases.

9. INCIDENCE
• 1 child per 1500 live births.
• ASD make up 30 to 40% of all congenital heart disease that is seen in
adults.
• The ostium secundum atrial septal defect accounts for 7% of all
congenital heart lesions.
• This lesion shows a female preponderance, with a male : female ratio of
1:2

10. CAUSES
• The cause of most congenital heart defects is unknown, but
rapid progress is being made in identifying the genetic basis
of many congenital heart lesions.
• Genetics and environmental factors probably play a role.

11. • Rubella infection. Becoming infected with rubella (German measles)
while pregnant can increase the risk of fatal heart defects.
• Drug or alcohol use or exposure to certain substances. Use of certain
medications, alcohol or drugs such as cocaine during pregnancy can
harm the developing fetes.
RISK FACTORS

12. There are three types of atrial septal defect (ASD)
1. Ostium primum (ASP 1)-: Opening at lower end of septum; may be
associated with mitral valve abnormalities.
2. Ostiumsecundum(ASP 2)-: Opening near center of septum
3. Sinus venosus defect-:Opening near junction of superior vena Gaya
and right atrium; may be associated with partial anomalous
pulmonary venous connection
TYPES

14. • ASYMPTOMATIC
• DECREASE EXERCISE
• DYSPNOEA
CLINICAL FEATURE
•

15. Signs and symptoms of large or long-standing
atrial septal defects may include:
• Shortness of breath, especially when exercising
• Fatigue
• Swelling of legs, feet or abdomen
• Heart palpitations or skipped beats
• Frequent lung infections
• Bluish skin color

16. DIAGNOSIS
• Cardiac examination
• ECG
• X RAY
• Echocardiogram

17. • Echocardiogram. This is a commonly used test to
diagnose an atrial septal defect. And, some atrial
septal defects are found during an echocardiogram
done for another reason. In echocardiography, sound
waves produce a video image of the heart. It allows
doctor to see heart's chambers and measure their
pumping strength. This test also checks heart valves
and looks for any signs of heart defects.
TESTS AND DIAGNOSIS

18. 1 Chest X-ray. An X-ray
image helps doctor to see
the condition of heart and
lungs. An X-ray may
identify conditions other
than a heart defect that may
explain signs or symptoms.

19. 2 Electrocardiogram (ECG). This test records the
electrical activity of heart and helps identify heart
rhythm problems.
Individuals with atrial septal defects may have a
prolonged PR interval.The prolongation of the PR
interval is probably due to the enlargement of the
atria that is common in ASDs and the increased
distance due to the defect itself.

20. 3 Cardiac catheterization. In
this test, a thin, flexible tube
(catheter) is inserted into a
subclavian vein or femoral vein.
Catheterization measures how
well heart is pumping and check
the function of heart valves.
Using catheterization, the blood
pressure in lungs also can be
measured.

21. 4 Magnetic resonance
imaging (MRI). MRI is a
technique that uses a magnetic
field and radio waves to create
3-D images of heart and other
organs and tissues within body.
doctor may request an MRI if
echocardiography can't
definitively diagnose an atrial
septal defect.

22. 5 Pulse oximetry. This
painless test measures how well
oxygen is reaching to tissues. It
helps detect whether oxygenated
blood is mixing with
deoxygenated blood, which can
help diagnose the type of heart
defect present. A small clip on
fingertip measures the amount of
oxygen in blood.

23. Treatment
• Small deffect may close spontaneously
• Recommended age for surgery is 2-4 years of
age
• Median sternotomy and Cardio pulmonary
bypass
• Purse string closure
• Defect is large then Dacron patchsewn over
the defect.

24. Medications may include those to:
• Diuretic-These agents are used to relieve
volume overload and pulmonary congestion
in patients with CHF. Injectable solution-
10mg/mL,Oralsolution-
10mg/mL,40mg/5mL,Tablets:20mg,40mg,
80mg
TREATMENTS

25. • Angiotensin-converting enzyme inhibitors-The
primary indication for ACE inhibition for CHF
and/or significant mitral regurgitation is to
decrease afterload. These drugs cause a
decrease in blood pressure Neonates: 0.05-0.1
mg/kg/dose q8-24hr, titrate dose up to 0.5
mg/kg/dose q6-24hr
– Infants: 0.15-0.3 mg/kg/dose; titrate dose upward
to maximum 6 mg/kg/day in 1-4 divided doses;
2.5-6 mg/kg/day usually required

26. – Children: 0.3-0.5 mg/kg/dose; titrate to maximum
6 mg/kg/day divided BID/QID
– Older children: 6.25-12.5 mg/dose q12-24hr;
titrate to no more than 6 mg/kg/day divided
BID/QID
– Adolescents: 12.5-25 mg/dose q8-12hr; may
increase by 25 mg/dose q1-2Weeks to maximum
450 mg/day.

27. VENTRICULAR SEPTAL DEFECT

28. “A hole in the wall between the two lower
chambers is called a ventricular septal defect.”
DEFINITION

29. VSDs are the most common congenital cardiac
anomalies. They are found in 30-60% of all
newborns with a congenital heart defect, or
about 2-6 per 1000 births. During heart
formation, when the heart begins life as a
hollow tube, it begins to partition, forming a
septa. If this does not occur properly it can
lead to an opening being left within the
ventricular septum.
INCIDENCE

30. • Down syndrome
following conditions during pregnancy can
increase risk of having a newborn with a heart
defect.
• Rubella infection.
Becoming infected with rubella (German
measles) while pregnant can increase the risk
of fetal heart defects. The rubella virus crosses
the placenta and spreads through the fetus'
circulatory system damaging blood vessels and
organs, including the heart.
RISK FACTORS

31. • Poorly controlled diabetes.
Uncontrolled diabetes in the mother in turn affects the
fetus' blood sugar, causing various damaging effects
to the developing fetus.
• Drug or alcohol use or exposure to certain
substances.
Use of certain medications, alcohol or drugs or
exposure to chemicals or radiation during pregnancy
can harm the developing fetus.

32. CLASSIFICATION
May be classified according to location:
membranous (accounting for 80%) or
muscular. May vary in size from a small
pinhole to absence of the septum, which results
in a common ventricle.

33. CLINICAL MANIFESTATION
• Signs and symptoms of serious heart defects
often appear during the first few days, weeks
and months of a life.
• Signs and symptoms of a large ventricular
septal defect may include:
• A bluish tint to the skin, lips and fingernails
(cyanosis)
• Poor eating, failure to thrive.
• Fast breathing or breathlessness.

34. • Easy tiring
• Swelling of legs, feet or abdomen
• Rapid heart rate
• Sometimes a ventricular septal defect isn't
detected until a person reaches adulthood and
develops signs or symptoms of heart failure,
such as shortness of breath.

35. Ventricular septal defects often cause a heart
murmur that doctor can hear using a
stethoscope. If doctor hears a heart murmur or
finds other signs or symptoms of a heart
defect, he or she may request one or more of
these tests:
• Chest X-ray
• Electrocardiogram (ECG)
• Echocardiogram
• Cardiac catheterization
TESTS AND DIAGNOSIS

36. TREATMENT
• Spontaneously close
• Antibiotics
• Digoxin and Diurretics
• Surgery

37. PATENT DUCTUS ARTERIOSUS
(PDA)

38. DEFINITION
patent ductus arteriosus (PDA) the vessel does
not close and remains "patent" resulting in
irregular transmission of blood between two of
the most important arteries close to the heart,
the aorta and the pulmonary artery.”

39. INCIDENCE
Patent ductus arteriosus is a common finding
in premature infants, occurring in as many as
80% of infants born before 28 wk gestation.
There is a progressive decrease in frequency of
persistence of the ductus with increasing
gestational age. Persistent patency of the
ductus in term infants occurs in about 1 in
2000 live births.

40. CLINICAL MANIFESTATION
PDA is usually diagnosed after age 6 to 8 wk on the basis of a
continuous murmur at the upper left sternal border. The
peripheral pulses are full, with a widened pulse pressure.
While some cases of PDA are asymptomatic, common
symptoms include:
• tachycardia
• shortness of breath
• Cardiomegaly
• Left subclavicular thrill
• Bounding pulse
• Widened pulse pressure

41. • Patients typically present in good health, with normal
respirations and heart rate. If the ductus is moderate
or large, widened pulse pressure and bounding
peripheral pulses are frequently present, reflecting
increased left ventricular stroke volume and diastolic
runoff of blood into the initially lower-resistant
pulmonary vascular bed. Prominent suprasternal and
carotid pulsations may be noted secondary to
increased left ventricular stroke volume.
• Poor growth
• Differential cyanosis, i.e. cyanosis of the lower
extremities but not of the upper body.

42. TREATMENTS
• Medical management
Administration of
indomethacin(prostaglandin inhibitor) has
proved successful in closing a PDA in
preterm infants and some newborns
before the age of 10 days.
Orally dose 0.2mg /kg tds at an interwal of 12 to
24 hours.

43. Surgery
• Surgical closure can be done at any age.
• Lateral Thoracotomy

44. COARCTATION OF THE AORTA
DEFINITION
“Coarctation of the aorta or aortic
coarctation is defined by narrowing
of the aorta, the large blood vessel
that branches off heart and delivers
oxygen-rich blood to body. When this
occurs, heart must pump harder to
force blood through the narrow part of
aorta."

45. • Idiopathic cause
• genetic conditions, such as Turner syndrome. .
Women and girls with this syndrome have 45
chromosomes, with one missing or incomplete X
chromosome, instead of 46. About 10 percent of
women and girls with Turner syndrome have aortic
coarctation.
• Coarctation of the aorta usually occurs beyond the
blood vessels that branch off to upper body and
before the blood vessels that lead to lower body. This
often means high blood pressure in arms, but low
blood pressure in legs and ankles.
CAUSES

46. The effect of a narrowing within the aorta
is increased pressure proximal to the
defect (upper extremities) and decreased
pressure distal to it (lower extremities).
PATHOPHYSIOLOGY

47. • The patient may have high blood pressure and
bounding pulses in the arms, weak or absent
femoral pulses, and cool lower extremities
with lower blood pressure, There are signs of
congestive heart failure (CHF) in infants. In
infants with critical coarctation, the
hemodynamic condition may deteriorate
rapidly with severe acidosis and hypotension.
• Pale skin
• Irritability
CLINICALMANIFESTATION

48. • Profuse sweating
• High blood pressure
• Shortness of breath, especially during exercise
• Headache
• Muscle weakness
• Leg cramps or cold feet
• Nosebleeds
• Left untreated, aortic coarctation in babies may
lead to heart failure and death.

49. • Rupture of the aorta
• Premature coronary artery disease narrowing
of the blood vessels that supply the heart
• Weakened or bulging artery in the brain
(cerebral aneurysm)
In addition, if the coarctation of the aorta is
severe, heart may not be able to pump
adequate blood to the organs of body, resulting
in the failure of organs such as kidneys or
liver.
COMPLICATIONS

50. TESTS AND DIAGNOSIS
The age at which people with coarctation of
the aorta are diagnosed depends on the severity
of the condition. If the aortic coarctation is
severe, it's usually diagnosed during infancy.
Adults and older children tend to have milder
cases and usually appear healthy until a doctor
detects:
• High blood pressure in the arms

51. • A blood pressure difference between arms and
legs
• A weak or delayed pulse in the legs
• A heart murmur — an abnormal whooshing
sound caused by turbulent blood flow

52. Diagnostic tests
Tests to confirm a diagnosis of coarctation of
the aorta include:
• Chest X-ray.
• Echocardiogram.
• Electrocardiogram (ECG). If the coarctation
of the aorta is severe, the ECG will show that
might have a thickened heart muscle
(ventricular hypertrophy).

53. • Magnetic resonance imaging (MRI). An
MRI of chest will reveal the location of the
coarctation of the aorta and determine whether
it affects other blood vessels in body.
• Cardiac catheterization

54. TREATMENTS
Treatment options for coarctation of the aorta
depend on age of child. when diagnosed and
how narrowed aorta is. Other heart defects
may be repaired at the same time as aortic
coarctation. Treatment approaches usually
consist of surgery or a procedure called
balloon angioplasty.

55. MEDICATION
• Medication isn't used to repair coarctation of
the aorta, but it may be used to control blood
pressure before surgery. Although repairing
aortic coarctation improves blood pressure,
many people will still need to take medication,
even after a successful surgery.

56. • Child with severe coarctation of the aorta may
receive a drug called prostaglandin E. This
drug helps keep the ductus arteriosis open,
providing a bypass for blood flow around the
constriction, until the coarctation is repaired.

57. SURGICAL TREATMENT
• Surgical repair is the treatment of choice for
infants younger than 6 months of age and for
patients with long-segment stenosis or
complex anatomy; it may be performed for all
patients with coarctation. Repair is by
resection of the coarcted portion with an end-
to-end anastomosis of the aorta or enlargement
of the constricted section using a graft of
prosthetic material or a portion of the left
subclavian artery.

58. Because this defect is outside the heart and
pericardium, cardiopulmonary bypass is not
required, and a thoracotomy incision is used.
Postoperative hypertension is treated with
intravenous sodium nitroprusside, esmolol, or
milrinone followed by oral medications, such
as angiotensin-converting enzyme inhibitors or
beta blockers. Residual permanent
hypertension after repair of coarctation of the
aorta (COA) seems to be related to age and
time of repair.

59. To prevent both hypertension at rest and
exercise-provoked systemic hypertension after
repair, elective surgery for COA is advised
within the first 2 years of life. There is a 15%
to 30% risk of recurrence in patients who
underwent surgical repair as infants.
Percutaneous balloon angioplasty techniques
have proved to be effective in relieving
residual postoperative coarctation gradients.

60. • Nonsurgical treatment—Balloon angioplasty
is being performed as a primary intervention
for COA in older infants and children. In
adolescents, stents may be placed in the aorta
to maintain patency. Recent studies have
demonstrated that balloon angioplasty is
effective in children and that aneurysm
formation is rare. The high restenosis rate in
young infants limits its application in this
group.

61. • Prognosis—Mortality is less than 5% in
patients with isolated coarctation; risk is
increased in infants with other complex cardiac
defects.

62. PREVENTION
Coarctation of the aorta can't be prevented,
because it's usually present at birth. However,
if child has a condition that increases the risk
of aortic coarctation, such as Turner syndrome,
another heart defect or a family history of
congenital heart disease, early detection can
help. Discuss the risk of aortic coarctation with
doctor.

63. PULMONARY VALVE STENOSIS

64. AORTIC STENOSIS

65. ATRIOVENTRICULAR CANAL DEFECT

66. Treatment
• Baloon valvuloplasty
• PG1 administration
• Resection of hypertrophied muscle
• For supravascular stenosis the area of
obstruction is incised and a patch graft is
inserted,

67. Thank you.