Includes all good things for topic

1. CONGENITAL HEART
DEFECTS / DEFECTS OF
CARDIO VASCULAR
SYSTEM
PRESENTED BY – KUMARI MANU
NURSING TUTOR
KNPI

2. DEFINITION
Heart defects are one of the most common
congenital anomalies that may involve
chambers, valves and great vessels arising
from the heart in most of the cases causes
unknown.

3. ETIOLOGY
• The exact causes are unknown in 90% of
cases.
• Factors associated with congenital heart
defects include
Fetal or maternal infections like rubella
during first trimester of pregnancy.
 Chromosomal abnormalities such as trisomy
13, 18 and 21.
Maternal insulin dependent diabetes
Teratogenic effect of drugs and alcohols.

4. TYPES
OF CHD
CYANOTIC ACYANOTIC

5. CYANOTIC DEFECTS
DECREASED
PULMONARY
BLOOD FLOW
MIXED BLOOD FLOW
Tetralogy of fallot Transportation of great
arteries
Tricuspid atresia Total anomalous pulmonary
venous connection
Truncus arteriosus
Hypoplastic left heart
syndrome

6. ACYANOTIC DEFECTS
INCREASE PULMONARY
BLOOD FLOW
OBSTRUCTION TO
BLOOD FLOW
ASD Coarctation of aorta
VSD Aortic stenosis
PDA Pulmonic stenosis
Partial anomalous
pulmonary venous return
Congenital mitral stenosis

7. ACYANOTIC HEART
DEFECTS
It is a congenital (present at birth) structural
heart problems where blood with enough
oxygen flows abnormally, usually from the
heart's left side to the right, without
immediately causing a blue tint (cyanosis).

8. VENTRICULAR SEPTAL
DEFECT (VSD)

9. DEFINITION
• Is an abnormal opening in the septum
between right & left ventricles.
• It is the most common acyanotic
congenital heart disease with left to
right shunt. It is found approximately
25% of all CHD.
• The size of the defect can be large or
small.

10. TYPES OF VSD
Large VSDS
 Restrictive
 Non restrictive
Types of VSD by
location
 Peri-membranous
 Muscular

11. RESTRICTIVE VSD
• Defect size is small or partially restricted by
septal tissue.
• Limits blood flow from left ventricle to right
ventricle.
• Produces a large pressure gradient across
the defect.
• Less pulmonary overcirculation; symptoms are
mild.

12. NON-RESTRICTIVE VSD
• Defect is large with no resistance to blood
flow.
• Equalization of left and right ventricular
pressures.
• Large left-to-right shunt increased
→
pulmonary blood flow.
• Leads to heart failure and pulmonary
hypertension if untreated.

13. PERIMEMBRANOUS VSD
• Most common type. Located in the membranous
part of the interventricular septum, near the
tricuspid and aortic valves. May be associated
with aortic valve prolapse and regurgitation.
MUSCULAR VSD
• Located in the muscular part of the
interventricular septum. Can be single or
multiple (“swiss cheese” septum). Often close
spontaneously, especially small defects.

14. PATHOPHYSIOLOGY
A defect in the interventricular septum
allows blood to flow from the left ventricle
(high pressure) to the right ventricle (low
pressure)
This left-to-right shunt increases pulmonary
arterial blood flow
Excess pulmonary circulation causes
pulmonary congestion and edema

15. Increased blood returns to the left atrium
and left ventricle, leading to volume
overload
Left ventricular dilation and hypertrophy
develop to compensate
Persistent increased pulmonary flow
causes pulmonary hypertension.

16. Pulmonary vascular resistance gradually
rises, reducing the shunt
Eventually shunt may reverse to right-to-
left (Eisenmenger syndrome)
Clinical manifestation

17. CLINICAL
MANIFESTATIONS
• Small VSD are asymptomatic
• In large defects symptoms develop within one to
two months
Failure to thrive & Congestive heart failure
• Medium sized defects produce symptoms such as
dyspnea, tachypnea, slow physical development,
feeding difficulties and frequent pulmonary
infection

18. • Pale delicate looking
• Tachycardia
• Excessive sweating associated with feeding
• Poor weight gain
• Biventricular hypertrophy
• Pansystolic murmur heard maximal down the
left sternal border accompanied by the
thrill (“Whoooosh” (continuous, no gap)
or “lub–whoooosh–dub”)

19. DIAGNOSTIC EVALUATION
• History of illness
• Physical examination (harsh systolic murmur
& pulmonary second sound)
• Chest x-ray
• ECG reveals biventricular hypertrophy
• Echocardiograph

20. MANAGEMENT
• 75 to 80% of small ventricular septal
defects and five to 10 percent of large
VSDs will spontaneously close usually during
the first two years of life.
• Infants with small ventricular septal defects
require no surgery except antibiotics to
prevent endocarditis.

21. • Infants with moderate to large ventricular
septal defects were symptomatic showing
signs of congestive heart failure and failing
to grow are usually medically managed by
the combination of digoxin (inc. contractions)
and diuretics (dec. fluid in circulation),
bisoprolol (regular heart beat).

22. SURGICAL
MANAGEMENT
• Surgery is done as one stage or two stage
operation.
• One stage operation with patch closure of
VSD by open heart method
can be performed.
• Second stage include cardio
pulmonary bypass surgery

23. • Moderate to small sized ventricular septal
defects are closed by PURSE STRING
SUTURES.
• Large defect a synthetic DACRON PATCH is
used to close the defect
• The cardiac tissue covers the patch
completely within 6 months of surgery

24. PURSE
STRING
SUTURES

25. DACRON
PATCH

26. COMPLICATIONS
• Residual VSDs
• Recurrent respiratory tract infections
• Infective endocarditis
• Eisenmenger’s syndrome
• Pulmonary stenosis
• Failure to thrive

27. ATRIAL SEPTAL DEFECT

28. DEFINITION
• Is an abnormal opening between right and
left atria resulting left to right shunting of
blood
• It accounts for 9% of
all CHDs

29. TYPES OF ASDS
OSTIUM
SECUNDU
M
OSTIUM
PRIMUM
SINUS
VENOSUS

31. OSTIUM SECUNDUM ASD
• It is the most common type of ASDs. An
abnormal opening in the middle of the atrial
septum presents due to abnormal development
of the septum secundum.
OSTIUM PRIMUM ASD
• It is also known as partial atrioventricular canal
defect. It presents an abnormal opening at the
bottom of the atrial septum due to improper
development of the septum primum.

32. SINUS VENOSUS ASD
• It is an abnormal opening at the top of the
atrial septum. There may be increased
association with anomalous connection of
the right pulmonary vein to the right atrium
or right SVC.

33. PATHOPHYSIOLOGY
A defect in the atrial septum allows blood to flow
from the left atrium (higher pressure) to the right
atrium (lower pressure)
This produces a left-to-right shunt at the atrial level
Increased blood volume enters the right atrium and
right ventricle

34. Leads to right atrial and right ventricular dilation
Excess blood flows to the pulmonary circulation, causing
pulmonary over-circulation
Over time, this may lead to pulmonary hypertension
Increased pulmonary vascular resistance may reverse the shunt
(Eisenmenger syndrome)

35. CLINICAL
MANIFESTATIONS
• Ostium secundum and sinus venosus ASDs
are usually asymptomatic
• Child may have recurrent chest infections
• Dyspnea on exertion
• Easy fatigability
• Bulging of the chest
• Poor weight gain
• Cardiac enlargement

36. DIAGNOSTIC EVALUATION
• History collection
• Physical examination
Ascultation of heart sound
• In ostium secundum ASD soft systolic murmur
heard best at the left upper sternal border.
• In ostium primum asd systolic murmur heard
best at the lower left sternal border
because of mitral regurgitation.

37. • Chest x-ray shows right atrial and
ventricular dilation and increased
pulmonary marking
• ECG demonstrates right ventricular
hypertrophy and right axis deviation.
• Two dimensional echocardiogram with
doppler study

38. MANAGEMENT
• Small, asymptomatic ASDs:
• Often, no immediate treatment is needed, just
regular checkups (watchful waiting).
• Symptom control:
• Medications manage issues arising from the
defect, such as:
• Diuretics (e.G., Furosemide): reduce fluid
buildup in lungs/body (heart failure).

39. • Beta-blockers: control
irregular heartbeats
(arrhythmias).
• Antiarrhythmics: manage
palpitations or fainting.
• Blood thinners
(anticoagulants): lower clot
risk, especially after a
repair.

40. SURGICAL
MANAGEMENT
• The surgical repair is most often done
through a median sternotomy and requires
cardio pulmonary bypass
• If the defect is small purse string closure is
done by the stretching around the opening
and pulling it closed
• If the defect is large a knitted Dacron patch
is sewn over the defect

41. COMPLICATIONS
• Cardiac enlargement
• Dysrhythmias
• Ineffective endocarditis
• Pulmonary arterial hypertension
• Growth retardation

43. PATENT DUCTUS
ARTERIOSUS

44. DEFINITION
It is the persistent vascular
connection between the
pulmonary artery and the
aorta. When ductus
arteriosus remains patent
and open after birth, the
blood flows in the ductus
from the aorta to the
pulmonary artery due to
higher pressure in the

45. PATHOPHYSIOLOGY
Ductus arteriosus remains open after
birth
Aortic pressure > Pulmonary artery
pressure
Blood flows from aorta pulmonary
→
artery (left-to-right shunt)

46. ↑ Pulmonary blood flow
↑ Blood returns to left atrium and left
ventricle
Volume overload of left heart
Leads to Pulmonary congestion
Left ventricular hypertrophy
Congestive heart failure

47. CLINICAL
MANIFESTATION
• A small and moderate size PDA are usually
asymptomatic
• Congestive heart failure
• Failure to thrive
• Dyspnea on feeding
• Recurrent respiratory infections
• Irritability and fatigue

48. • Continuous machinery murmur (best heard at left
infraclavicular area)
• Bounding pulse
• Wide pulse pressure
• Pulmonary congestion
• Crepitations on auscultation
• Signs of pulmonary edema (in large PDA)

49. DIAGNOSTIC EVALUATION
• History of illness
• Physical examination- Auscultation of
heart sounds reveals continuous
murmur (machinery murmur) heard at 2
left intercoastal space or below the right
clavicle.
• Chest x-ray shows cardiomegaly
• 2D echocardiogram with doppler study
• ECG reveals left arterial dilation and left
ventricular hypertrophy.

50. MANAGEMENT
Medical management
• In symptomatic patient with
PDA, indomethacin 0.1- 0.25
mg/kg/dose/IV- TDS very
slowly is administered ever 12
to 24 hours for 3 doses. For
pharmacological closure of
ductus arteriosus WHICH should
be administer before the age of
10 days.

51. NURSING
MANAGEMENT
• Supportive care is provided with rest
• Adequate intake of calorie for weight gain
• Promotion of normal growth and
development with routine care.
• Emotional support for the parents.

52. SURGICAL
MANAGEMENT
• Transection or ligation of patent
ductus arteriosus via a lateral
thoracotomy, a closed heart
intervention is performed.
• It is done preferably between 3 and
10 years of age in asymptomatic
patients.

54. CPARCTATION OF
AORTA

55. DEFINITION
“Coarctation of the aorta is a congenital
narrowing of a segment of the aorta (aortic
arch), most commonly just distal to the origin of
the left subclavian artery near the ductus
arteriosus, resulting in obstruction to blood flow”.

57. TYPES

58. CONT…
PRE-DUCTAL (INFANTILE
TYPE)
• Narrowing proximal to the ductus arteriosus
• Seen in newborns and infants
• Ductus arteriosus is usually patent
• Severe symptoms after ductal closure
• Causes early heart failure and shock

59. CONT…
POST-DUCTAL (ADULT TYPE)
• Narrowing distal to the ductus arteriosus
• Seen in children and adults
• Ductus arteriosus usually closed
• Presents with hypertension and weak femoral
pulses

60. CONT…
JUXTA-DUCTAL TYPE
• Narrowing at the level of ductus arteriosus
• Features overlap infantile and adult types
• Commonly associated with PDA

61. CONT…
OTHER CLASSIFICATION
• Discrete coarctation – short, localized
narrowing
• Long-segment coarctation – extended
narrowing of the aorta

62. PATHOPHYSIOLOGY
Narrowing of the aorta causes
increased resistance to blood flow
Proximal to the narrowing (head
& upper limbs): Blood pressure,
↑
Left ventricular hypertrophy due to
pressure overload

63. Distal to the narrowing (lower
limbs): Blood flow and perfusion,
↓
Collateral circulation develops
In infants, closure of the ductus
arteriosus may precipitate acute
heart failure and shock

64. CLINICAL
MANIFESTATIONS
• Increased BP in the upper part of the body
resulting in headache dizziness fainting
Nosebleed.
• In Lowell extremities the BP is relatively low
resulting in absent or diminished femoral &
pedal pulse.
• Weakness or pain in their legs on exercise.
Their legs may be cooler than arms

65. • Infants usually present with congestive
heart failure and failure to thrive
symptoms include respiratory distress,
poor weight gain, feeding problems,
irritability and tachycardia.
• Mottling is often seen in lower
extremities, infant with coarctation and
PDA may have adequate blood flow to
the lower extremities good pedal pulse
and no difference in blood pressure in
upper and lower extremities once PDA
closes symptoms develop.

66. DIAGNOSTIC EVALUATION
• Blood pressure measurement: upper limb BP
higher than lower limb
• Pulse examination: radio-femoral delay
• Chest x-ray: Rib notching (due to collateral
circulation), Figure-of-3 sign
• EEG, Echocardiography:
confirms diagnosis & severity
• CT angiography/MRI

67. MANAGEMENT
MEDICAL MANAGEMENT
• Prostaglandin E (in neonates) to keep ductus
₁
arteriosus open
• Antihypertensive drugs ( -
β blockers, ACE inhibitors)
• Management of heart failure if present
SURGICAL MANAGEMENT
• Resection with end-to-end anastomosis
• Subclavian flap aortoplasty
• Patch aortoplasty
• Ballon aortaplasty

70. COMPLICATIONS
• Severe hypertension
• Aortic rupture
• Heart failure
• Stroke
• Infective endocarditis