1. The document discusses various acyanotic heart diseases seen in pediatrics including ventricular septal defect (VSD), atrial septal defect (ASD), patent ductus arteriosus (PDA), coarctation of the aorta, aortic stenosis, and pulmonary stenosis. Clinical features, diagnosis using tools like echocardiography, and treatment approaches are described for each condition. 2. Complications of untreated defects include heart failure, infections, pulmonary hypertension, and Eisenmenger's syndrome. Critical cases may present in the neonatal period with shock, while milder cases cause symptoms like fatigue later in childhood. 3

1. DONE BY: MOHAMMED ABDULBAST
SUPERVISED BY: DR. NOORJAN
Acyanotic Heart
Disease

3. CARDIAC EVALUATION AND INTRODUCTION
TO CONGENITAL HEART LESIONS
1- History
− Children do not present with the typical features of congestive
heart failure as seen in adults.
− Age is very important when assessing child.
* Infants:
Feeding difficulties
Easily fatigued
Sweating while feeding
Rapid respirations
*Older children:
Shortness of breath
Dyspnea on exertion
Note
Orthopnea and nocturnal dyspnea are rare findings in children.

4. CARDIAC EVALUATION AND INTRODUCTION TO
CONGENITAL HEART LESIONS
2-Physical examination
− Need to refer to normal heart and respiratory rates
for ages to determine tachycardia and tachypnea.
− Height and weight should be assessed to
determine proper growth.
− Always get upper and lower extremity blood
pressures and pulses.
− Hepatosplenomegaly suggests right-sided heart
failure.
− Rales on auscultation may indicate pulmonary
edema and left-sided heart failure.
− Cyanosis and clubbing result from hypoxia.

5. CARDIAC EVALUATION AND INTRODUCTION TO
CONGENITAL HEART LESIONS

6. CARDIAC EVALUATION AND INTRODUCTION TO
CONGENITAL HEART LESIONS
3-Diagnostic tests
1-chest radiograph - Evaluate:
° Heart size
° Lung fields
° Ribs for notching
° Position of great vessels
2− Electrocardiogram
3− Echocardiography—definitive diagnosis
4− Other—MRI, cardiac catheterization, angiography,
exercise testing
Note
Echocardiography is the best test for diagnosing all
cardiac congenital defects.

7. CARDIAC EVALUATION AND INTRODUCTION TO CONGENITAL
HEART LESIONS
Embryology—knowledge of cardiac embryology is helpful for
understanding congenital cardiac lesions, their presentations,
symptoms, and treatment

8. Acyanotic heart disease
1- volume load most common , and the most common of
these are left-to-right shunt lesions.
includes :
- Ventricular septal defect [VSD]
- Atrial septal defect [ASD]
- Patent ductus arteriosus [PDA]
2- increase in pressure load, most commonly secondary
to ventricular outflow obstruction (PS, AS) or narrowing
of one of the great vessels .
Include:
- Aortic stenosis
- Coarctation of aorta
- Pulmonary stenosis

9. Ventricular septal defect (VSD)
Def:- Abnormal communication in septum dividing
RV and LV, most common CHD (25 %).
- may occur in any portion of the septum, mostly
membranous type 75%.
-VSDs in the midportion or apical region of
- the ventricular septum are muscular in type and
may be single or multiple(Swiss cheese septum)
@They associated with several genetic conditions
e.g., trisomy 21.

10. Ventricular septal defect (VSD)

11. Symptoms :
-After birth size of the LT-to-RT shunt initially limited.As pulmonary
vascular resistance continues to fall in the 1st few weeks after birth
left-to-right shunt develops, and clinical symptoms become apparent
- Small asymptomatic
Restrictive <0.5 cm2
- Large dyspnea
poor feeding
poor growth
recurrent pulmonary infection
heart failure profuse perspiration
Norestrictive >1cm2

12. Signs :
- Small harsh loud holosystolic murmur over
LLSB
- Large prominence of left precordium
palpable parasternal lift
displaced apex beat (lt. side in
hypertrophy)
less harsh pansystolic murmur at
LLSB
mid-diastolic murmur at apex at
mitral valve

13. Imaging tests :
- ECG LF atrial and ventricular enlargement
and hypertrophy BUT in LVSD Rt. V is also
hypertrophy
- CXR cardiomegaly
enlargement of the LF ventricle
increase pulmonary vascularity
increased pulmonary blood flow
- Echo size and site of the VSD

15. Treatment :
Small most of them close spontaneously with first
2 years
- Large less likely to resolve sponatously
diuretics (± digoxin)
after-load reduction
Control of HF & prevent development of sever
pulomnary diseas
Surgery poor growth
pulmonary hypertension despite
treatment

16.  Complications of VSD
− Large defects lead to heart failure,
- failure to thrive
− Endocarditis
− Pulmonary hypertension

17. Eisenmenger Syndrome
 Eisenmenger Syndrome Transformation of any untreated left-
to-right shunt into a bidirectional or right-to-left shunt
When the ratio of p:S resistance 1 : 1, the shunt , the signs of
heart failure abate, and the patient
Characterized by :
dyspnea, fatigue, palpitations,
cyanosis, hypoxemia, clubbing,
High jugular venous preasure
• Results from high pulmonary blood flow, causing medial
hypertrophy of pulmonary vessels and increased pulmonary
vascular resistance.
typically by a ventricular septal defect, atrial septal defect, or
less commonly, patent ductus arteriosus

18. Atrial Septal Defect (ASD) ostium secondum
Def: abnormal communication in septum dividing
RA and LA.
@defect in the region of the fossa ovalis is the
most common form.
- structurally normal (AV) valves.
- openings ≥2 cm in diameter are common in
symptomatic older children.
- In early life the are asymptomatic the defect of
slow flow
Females outnumber males 3 : 1

19.  The degree of LT to-RT shunting is dependent on
1-the size of the defect.
2 -compliance of the right and left ventricles.
3- vascular resistance in the pulmonary and
systemic circulations.
@@ large defects, the ratio of pulmonary to
systemic blood flow is usually 2 : 1 - 4 : 1.

20. Clinical manifestations :-
- Symptoms mostly asymptomatic
FTT
exercise intolerance in old
childreen
- Signs mild left precordial bulge
palpable RT ventricular impulse at LLSB
systolic ejection murmur in the region
the left middle and upper sternal border.
A loud S1, the S2 is characteristically
fixed widely split .
mid-diastolic murmur at the LLSB
tricuspid

21. Imaging :
- ECG RT axis deviation
RT ventricular enlargement
- CXR cardiomegaly
RT atrial % ventricle enlargement
prominent pulmonary artery
- Echo size and site of defect
catheterized before surgical closure

22. Treatment :
Medical management rarely indicated
Closure Surgical or by trans catheter device
In all symptomatic patients
-asymptomatic patients with a Qp : Qs ratio of at
least 2 : 1.
@@The timing for elective closure is usually after
the 1st yr and before entry into school.
Complications of ASD
− Dysrhythmia

23. Atrioventricular Septal Defects (Ostium
Primum and Atrioventricular Canal or
Endocardial Cushion Defects
 When both ASDs and VSDs occur, which are
contiguous, and the atrioventricular valves are
abnormal ,Patients with trisomy 21 are at a higher risk
for endocardial cushion defects.
 Left-to-right shunt at both atrial and ventricular levels;
some right-to-left shunting with desaturation (mild,
intermittent cyanosis)

24. Clinical manifestations :-
Symptoms early heart failure
infections,
hepatomegaly
failure to thrive
minimal cyanosis
Signs Cardiac enlargement.
A precordial bulge and lift,
S1 is normal or accentuated.
The S2 is widely split if the pulmonary flow is massive
A low-pitched, mid-diastolic rumbling murmur
at the lower left sternal border.
pulmonary systolic ejection murmur .
Is produced by the large pulmonary flow.
The harsh apical holosystolic murmur of
mitral insufficiency radiate to axilla.
;

25. Diagnosis:-
-CXR moderate-severe cardiac enlargement
caused by the prominence of both ventricles and atria.
The pulmonary artery is large.
pulmonary vascularity is increased
-ECG signs of biventricular hypertrophy,
right atrial enlargement
superior QRS axis
− Echocardiogram (gold standard)

26. Treatment:-
-surgery more difficult with heart failure and
pulmonary hypertension
(due increased pulmonary artery pressure by
6−12 months of age) operation must be performed
in infancy
Complications
− Without surgery—death from heart failure
− With surgery—arrhythmias, congenital heart
block

27. Patent Ductus Arteriosus (PDA)
The ductus arteriosus allows blood to flow from the
pulmonary artery to the aorta during fetal life.
Failure of the normal closure of this vessel results in blood
flow from the aorta to the pulmonary artery
RISK FACTOR
− More common in girls by 2:1
− Associated with maternal rubella infection
− Common in premature infants (developmental, not
heart disease)
note:- a PDA persists beyond the first week of life, it is
unlikely to close spontaneously.

29. clinical manifestation :
- Symptoms asymptomatic in small
symptoms of heart failure in large
- Singns widened pulse pressure
bounding arterial pulses
thrill may be palpable
continuous, machine-like murmur can
be heard at the left infraclavicular area, radiating along the
pulmonary arteries and often well heard over the left side of
the back.
@@ mid-diastolic murmur at the apex

30. Imaging tests :
- ECG Normal in small PDA
LF ventricular hypertrophy
RT ventricular hypertrophy with
pulmonary hypertension
- CXR normal in small PDA
increased pulmonary vascularity
full pulmonary artery silhouette
- Echocardiography is gold stander

31. Treatment :
Spontaneous closure in term infant is
uncommon
Elective closure of small, hemodynamically
insignificant PDAs is controversial
Moderate and large PDAs managed initially with
diuretics, but eventually require closure
• Complications
− Congestive heart failure
− Infective endocarditis

32. Coarctation of the Aorta
 Defi—narrowing at any point from transverse arch to iliac
bifurcation; 90% just below origin of left subclavian artery
at origin of ductus arteriosus (juxtaductal coarctation).

Coarctation of the aorta has a high association with
Turner syndrome
@@@Tubular hypoplasia (preductal, infantile type)
Pathophysiology
 1. Increased afterload on heart causes LVH
 2. Upper body hypertensive, whereas lower body/Gl tract
hypoxic or ischemic
##Among aortic coarctation patients, 50% have another
defect, many have a bicuspid aortic valve, and 5% have
berry aneurysms in the circle of Willis.

35. clinical manifestation :
Clinical presentation: age of presentation depends
on severity/collaterals
1. Critical coarctation: neonatal presentation, blood
flow to lower body dependent on ductus arteriosus
~ heart failure/shock with decreased femoral pulses
2. Mild coarctation: may present at any age, even in
adulthood
a. Fatigue, poor growth
b. Systolic murmur, decreased femoral pulses,
hypertension

36. Diagnosis
1.C-XRAY :Severe (infantile)—increased heart size
and pulmonary congestion
2. Echo: primary imaging test but can be limited
3. Cardiac magnetic resonance imaging
(MRI)/computed tomography (CT): best
test to determine full anatomy of arch

37. Treatment
 1. Critical coarctation in neonates: start PGE1
immediately for ductal patency
 2. Surgical repair
@@Prognosis is good if discovered early, although re-
coarctetion is a risk.

Complications
 − Associated cerebrovascular disease
 − Systemic hypertension
 − Endocarditis
 − Aortic aneurysms

38. Aortic Stenosis
Definitions:-Left-sided obstruction due to aortic
abnormality
a. Valve abnormality most common (bicuspid,
unicuspid/dysplastic)
b. Subaortic stenosis
c. Supravalvar stenosis
Cause/pathophysiology
 1. limited flow across LV outflow tract causes
diminished cardiac output
 2. Can lead to LVH and LV dysfunction
 3. Abnormal valve can also have insufficiency

40. Clinical presentation
1. Critical AS: presents in neonatal period with poor LV function, poor
cardiac output, acidosis, shock
2. Less severe forms present with progressive fatigue and heart failure
3. Cardiac exam findings
a. Systolic ejection click
b. Systolic ejection murmur along right upper sternal border
c. If aortic insufficiency, may have early high-frequency diastolic
murmur
4. Rarely patients may have syncope or sudden cardiac death
Testing
1. CXR: may have cardiomegaly, dilated aortic root
2. Echo: quantify gradient and assess valve morphology
Therapy
1. Balloon valvuloplasty or surgical valvotomy
2. Eventually may need valve replacement

41. Pulmonary stenosis
Definitions: Right-sided obstructive lesion
a. Valvar stenosis most common ( 90%)
b. Subvalvar: associated with TOF and double-
outlet RV
c. Supravalvar: pulmonary artery narrowing
Pathophysiology
 1. Limited flow across RV outflow tract limits
blood flow to lungs ~ RV hyperttophy and
dysfunction, decreased cardiac output
 2. Abnormal valve can also have insufficiency

42. Clinical presentation
1. Critical PS: presents in newborns with cyanosis and RV dysfunction
2. Less severe forms present with fatigue and exercise intolerance
3. Cardiac exam: systolic ejection click, systolic ejection murmur at left
upper
sternal border, prominent RV impulse, fixed widely split S2
Testing
Echo to evaluate pulmonary valve morphology and gradient, RVH
Therapy
1. Critical PS: may require PGE1 infusion on to provide systemic blood
flaw
2. If asymptomatic and mild, can be followed; usually not progressive
3. Moderate to severe: usually progressive, requiring balloon
valvuloplasty (preferred), surgical valvotomy, or valve replacement

43. .

44. Quiz ^_^
 Q1 )A 3-month-old child presents with poor feeding,
poor weight gain, and tachypnea.
 Physical examination reveals a harsh, pansystolic 3/6
murmur at the left lower sternal border, and
hepatomegaly
1- diagnosis ?
2- investigation to send ?
3- treatment ?
4- complication?
Q2)A PDA may be life preserving in which CHD (give 2
condition) and how you kept it open?
Q3) what CHD cause early neonatal shock? Give 2
condition