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VENTRICULAR SEPTAL DEFECT.ppt
1. VENTRICULAR
SEPTAL DEFECT
Dominic Vasco
School of Medicine & Health Sciences
Department of Clinical Medicine
Paediatrics and Child
Health III
Kabarak University Department of Clinical
Medicine
2. Learning outcomes
At the end of this lecture series the learner
should;
1. Define malnutrition and classify the
various malnutrition disorders
2. Describe the diagnosis of nutritional
disorders
3. Describe the admission criteria for
malnourished children
4. Outline the management of malnutrition
Kulimankudya Vasco Botso
3. Ventricular septal defect exists as an
opening in the ventricular septum
It allows oxygenated blood to pass from
the left ventricle through the opening in
the septum and then mix with
unoxygenated blood in the right ventricle
They are the most common type of
congenital heart defect occurring in 14 to
17% of babies born each year
Kulimankudya Vasco Botso
4. It follows failure of completion of the
partitioning process in the ventricular
septum
Kulimankudya Vasco Botso
5. Effect
Blood passes through the VSD from the
left ventricle to the right ventricle causing
the right side of the heart to handle a
larger volume of blood
The extra blood then passes through the
pulmonary artery into the lungs
This leads to pulmonary hypertension and
pulmonary congestion
Kulimankudya Vasco Botso
6. Pulmonary arteries become thickened and
obstructed due to the increased pressure
Failure to repair the defect leads to lung
disease with the pressure in the right heart
eventually exceeding the pressure in the
left creating a right to left shunt
Kulimankudya Vasco Botso
7. Due to high pressure there is tissue
damage which may occur in the right
ventricle and bacteria in the blood stream
can easily infect this area causing
bacterial endocarditis
Kulimankudya Vasco Botso
8. Clinical features
Small VSDs are asymptomatic with the
child attaining normal growth and
development
Moderate to large VSDs are associated
with delayed growth and development,
decreased exercise tolerance, recurrent
pulmonary infections and Congestive
Heart Failure during infancy
Kulimankudya Vasco Botso
9. Clinical features…
Longstanding pulmonary hypertension is
accompanied by a history of cyanosis and
decreased level of activity
Kulimankudya Vasco Botso
10. Physical Examination
Infants with small VSDs are well
developed and acyanotic
Infants with large VSDs may have poor
weight gain before 2 or 3 months of age
They may also develop CHF
Cyanosis and clubbing may be present in
patients with Eisenmenger syndrome
Kulimankudya Vasco Botso
11. A systolic thrill may be present at the
lower left sternal border with a large shunt
VSD
A precordial buldge and hyperactivity are
present with a large-shunt VSD
The S2 is loud and single in patients with
pulmonary hypertension or pulmonary
vascular obstructive disease
Kulimankudya Vasco Botso
12. A grade 2 systolic murmur is audile at the
lower left sternal border, it may be
holosystolic or early systolic
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13. Electrocardiography
ECG is normal in small VSD
Moderate VSDs cause left ventricular
hypertrophy and ocassional left atrial
hypertrophy may be seen
Large defects reveal a biventricular
hypertrophy with or without Left Atrial
Hypertrophy
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14. If pulmonary vascular disease develops
the ECG shows Right Ventricular
Hypertrophy only
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15. Chest Xray
Cardiomegally of varying degrees is
present and involves the Left atria, left
ventricle and sometimes the right ventricle
Increased pulmonary vascular markings
The degree of cardiomegaly and the
increase in pulmonary vascular markings
directly relate to the magnitude of the left
to right shunt
Kulimankudya Vasco Botso
16. Natural history
Spontaneous closure occurs in 30 to 40%
of patients with membranous VSDs and
muscular VSDs during the first 6 months
of life
CHF develops in infants with large VSDs
but usually not until 6 to 8 years of age
Pulmonary vascular obstructive disease
may begin to develop as early as 6 to 12
months of age in patients with large VSDs
but resulting right to left shunt usually
Kulimankudya Vasco Botso
18. Medical management
Treatment of CHF if it develops;
Digoxin
Diuretics
Given for 2 – 4 months
Spironolactone may be useful to
minimize potassium loss
Captopril may be given concomitantly as
an afterload reducing agent
Kulimankudya Vasco Botso
19. Frequent feeding on high calorie diet
orally or by NGT
Oral iron therapy is used to correct
anaemia
No exercise restriction is needed in the
absence of pulmonary hypertension
Maintenance of good dental hygiene and
antibiotic prophylaxis against infective
endocarditis are important
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20. Non surgical closure of selected muscular
VSDs is possible using the umbrella
device, this is still in experimental phase
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21. Surgical Management
Indications;
Small infants with large VSDs who
develop CHF and growth retardation - If
growth failure cannot be improved by
medical management the VSD should be
operated on within the first 6 months of life
If the Pulmonary artery pressure is greater
that 50% of systemic pressure, surgical
closure should be done by the end of the
first year Kulimankudya Vasco Botso
22. After 1 year of age a significant left to right
shunt should be surgically closed
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23. Surgical treatment
Palliative;
Pulmonary artery banding involves placing
a band around the pulmonary artery to
decrease the pulmonary blood flow
It increases the resistance to blood flow
through the pulmonary artery
The pressure increases in the right
ventricle and prevents excess shunting
from left to right
Kulimankudya Vasco Botso
24. Complete repair
Small defects are repaired with a purse
string approach
Large defects usually require a knitted
Dacron patch sewn over the opening
Post operative complications include
residual VSD and conduction disturbance
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25. Mortality
Surgical mortality is less than 1%
Mortality is higher for small infants
younger than 2 months of age, infants with
associated defects or infants with multiple
VSDs
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26. Post – op follow up
Activity should not be restricted unless
complications have resulted from surgery
Bacterial endocarditis prophylaxis may be
discontinued 6 months after surgery
Patients with post operative history of
transient heart block wit or without a
pacemaker requires long term follow up
Kulimankudya Vasco Botso
28. This is characterized by a connection
between the aorta and the pulmonary
artery
All babies are born with a ductus
arteriosus
As the baby takes the first breath, the
blood vessels in the lungs open up, and
blood begins to flow; the ductus arteriosus
is not needed to bypass the lungs
Most babies have a closed ductus
Kulimankudya Vasco Botso
29. In some babies, however, the ductus
arteriosus remains open (patent)
The opening between the aorta and the
pulmonary artery allows oxygenated blood
to pass back through the pulmonary artery
and mixes with the unoxygenated blood
which goes to the lungs
Kulimankudya Vasco Botso
30. This increases the blood volume in the
lungs causing congestion and pulmonary
hypertension
Kulimankudya Vasco Botso
33. In many children there is no known reason
for the ductus arteriosus remaining open
PDA is seen more often in the following;
Premature infants
Infants born to a mother who had rubella during
the first trimester of pregnancy
Kulimankudya Vasco Botso
34. Incidence
PDA occurs in 6 – 11% of all children with
Congenital Heart Disease
In many children, there is no known
reason for the ductus arteriosus remaining
open
However, PDA is seen more often
Kulimankudya Vasco Botso
35. Clinical features
History
Patients are usually asymptomatic when
the ductus is small
A large shunt PDA may cause a lower
respiratory tract infection, atelectasis and
congestive heart failure accompanied by
tachypnea, and poor weight gain
Kulimankudya Vasco Botso
36. Physical Examination
Tachycardia and tachypnea may be
present in infants with Congestive Heart
Failure
Bounding peripheral pulses with wide
pulse pressure are characteristic findings
A systolic thrill may be present at the
upper left sternal border
A grade 1 to 4 murmur continuous
machinery murmur is best heard at the left
infraclavicular area or upper left sternal
Kulimankudya Vasco Botso
37. If pulmonary vascular obstructive disease
develops, a right to left ductal shunt
results in cyanosis only in the lower half of
the body
Kulimankudya Vasco Botso
38. Electrocardiography
ECG findings are similar to those of VSD
A normal ECG or Left Ventricular
Hypertrophy is seen with small to
moderate PDA
If pulmonary vascular obstructive disease
develops, Right Ventricular Hypertrophy is
present
Kulimankudya Vasco Botso
39. Chest X ray
The findings may be normal in case of a
small shunt
Cardiomegally of varying degrees occurs
in moderate-to large-shunt PDA with
enlargement of the left atria, left ventricle
and ascending aorta
Pulmonary vascular markings are present
Kulimankudya Vasco Botso
41. Natural history
Spontaneous closure of PDA does not
usually occur in full term infants and
children
This is due to the PDA in infants being as
a result of a structural abnormality of the
ductal smooth muscle
Congestive heart failure or recurrent
pneumonia or both develop if the shunt is
large
Kulimankudya Vasco Botso
42. Pulmonary vascular obstructive disease
may develop if a large PDA with
pulmonary hypertension is left untreated
Infective endocarditis may also occur
An aneurysm of PDA may occur and
rapture later on in life
Kulimankudya Vasco Botso
43. Management
In term neonates;
Indomethacin is ineffective in term infants
with PDA and should be avoided
Anticongestive measures with Digoxin and
diuretics are indicated when CHF
develops
No exercise restriction is needed in the
absence of pulmonary hypertension
Prophylaxis for subacute bacterial
endocarditis is indicated
Kulimankudya Vasco Botso
44. Non surgical closure
Small ductus less than 4 mm in diameter are
closed by coils
Larger ones are closed by an amplatzer PDA
device
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45. Surgical closure
This is reserved for patients in whom non
surgical closure is not considered
applicable
Kulimankudya Vasco Botso
46. Management in preterm
neonates
Clinical evidence of PDA appears in 45%
of infants with birth weight of less than
1750g and about 80% of infants with birth
weight less than 1200 g
Significant PDA with CHF occurs in 15%
of premature infants with birth weight of
less than 1750 g and in 40% to 50% of
those with birth weight less than 1500 g
Kulimankudya Vasco Botso
47. Medical;
Fluid restriction to 120 mls/ day and
diuretic e.g. Furosemide 1mg/kg per day
two to three times a day may be tried for
24 to 48 hours
Pharmacologic closure of the PDA can be
achieved with indomethacin (a
prostaglandin synthetase inhibitor)
Kulimankudya Vasco Botso
48. The dose is given intravenously every 12
hours for a total of three doses
For infants less than 48 hours old 0.2
mg/kg is followed by 0.1 mg/kg two times
For those 2 to 7 days old 0.2 mg/kg times
three and for infants older than 7 days 0.2
mg/kg followed by 0.25 mg/kg times 2
Kulimankudya Vasco Botso
50. Also termed endocardial cushion defect
Accounts for about 5% of all congenital
heart diseases
They are most common in infants with
Downs syndrome
15% of infants with Downs syndrome have
ASDs
Kulimankudya Vasco Botso
51. Complete atrioventricular canal
This is a severe defect characterized by a
large communication in the septum which
separates the left and the right sides of
the heart
The hole is in the centre of the heart
where the upper and lower chambers
meet
In a child with a complete atrioventricular
canal there is one valve and it may not
close correctly Kulimankudya Vasco Botso
52. Partial atrioventricular canal
defects
The communication does not extend
between the lower chambers of the heart
and the valves are better formed
It is also called atrioventricular septal
defect
Kulimankudya Vasco Botso
55. Pathophysiology
The defect in the septum allows blood to
travel from the left side of the heart to the
right side or the other way around
There is mixture of oxygenated and
deoxygenated blood
Extra blood gets pumped into the lungs
demand an increased function of the heart
and lungs and the lungs become
congested
Kulimankudya Vasco Botso
56. Clinical features
Dyspnoea
Mild cyanosis
Newborns show signs of heart failure;
Oedema
Fatigue
Wheezing
Sweating
Irregular heartbeat
Kulimankudya Vasco Botso
57. They present with a characteristic murmur
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58. Management
Palliative pulmonary artery banding
Complete repair;
Patch closure of septal defect
Reconstruction of AV tissue
Kulimankudya Vasco Botso
60. This refers to narrowing of the aorta
It occurs anywhere but is most likely to
occur at the segment just after the aortic
arch
The narrowing restricts the amount of
blood going to the lower segment of the
body
It occurs in 8 – 11% of children with
congenital heart disease
Kulimankudya Vasco Botso
61. Effects of coarctation
The left ventricle has to work harder to
overcome the resistance and pump blood
through the narrowing in the aorta
This results in left sided heart failure
The blood pressure is higher above the
narrowing and lower below the narrowing
Kulimankudya Vasco Botso
62. Effects of coarctation…
Older children experience headaches from
too much pressure in the blood vessels in
the head or cramps in the legs or
abdomen due to too little blood in that
region
Over time the walls of the arteries may
become weakened resulting in tears and
bleeding or CVA
There is an increased risk of endocarditis
Kulimankudya Vasco Botso
65. Clinical features
History in the first 6 weeks of life;
Poor feeding
Dyspnoea
Poor weight gain
Acute circulatory shock
Kulimankudya Vasco Botso
66. Physical Examination;
Infants are pale with varying degrees of
respiratory distress
Oliguria
Anuria
General circulatory shock
Acidaemia
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67. Peripheral pulses may be weak and
thread due to congestive heart failure
The S2 is single and loud with a loud S3
gallop often being present
No heart murmur is present in 50% of
patients
A non specific ejection systolic murmur is
audible over the precordium
Kulimankudya Vasco Botso
68. Electrocardiography
A normal or rightward QRS axis and Right
Heart Failure or RBBB are present
Kulimankudya Vasco Botso
69. Chest X ray
There is marked cardiomegaly and pulmonary
oedema or pulmonary venous congestion
Kulimankudya Vasco Botso
70. Echocardiography
This demonstrates the site of the
coarctation
A suprasternal notch view reveals a thin
wedge shaped “posterior shelf” in the
posterolateral aspect of the upper
descending aorta
Kulimankudya Vasco Botso
71. Natural history
About 20% - 30% of all patients with
coarctation develop CHF by three months
of age
Undetected or untreated coarctation may
lead to early death due to CHF and renal
shut down in symptomatic patients
Kulimankudya Vasco Botso
72. Management
In symptomatic neonates, PGE1 infusion
should be started to reopen the ductus
arteriosus and establish flow to the
descending aorta and the kidneys during
the first weeks of life
Antifailure regimen with short acting
inotropic agents such as doparmine and
dobutamine, diuretics and oxygen should
be initiated
Kulimankudya Vasco Botso
73. Baloon valvuloplasty is useful in children
whom standard surgical procedure carries
a great risk
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74. Surgical management
Its indicated if CHF develops early in life
when surgery is performed as an urgent
procedure
The coarctation segment is resected and
the proximal and distal aorta are
anastomosed
Kulimankudya Vasco Botso
75. Coarctation with hypertension in the upper
extremities or with a large systolic
pressure gradient ≥ 20 mmHg between
the arms and legs indicates that an
elective surgical correction is necessary
between the ages of 4 and 6 years
Kulimankudya Vasco Botso
76. Reduction of the aorta by 50% at the level
of Coarctation is also indicative of surgery
Older children should be operated as soon
as the diagnosis is made
In asymptomatic children surgery is
performed by age 4 to 5 as delaying
surgery increases the chances of
developing essential hypertension
Kulimankudya Vasco Botso
77. In case severe hypertension, CHF or
cardiomegaly are present surgery should
be performed early
Kulimankudya Vasco Botso
78. Surgical procedures
Resection of the aortic segment and end
to end anastomosis
Occasionally a subclavian artery
aortoplasty or circular or patch grafts may
be performed
Kulimankudya Vasco Botso