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Referat

First Recognizition of Acyanotic


Congenital Heart Disease
DIETER ALYONA, Sked
0961050054

Background
Various congenital abnormalities (congenital anomaly).
Congenital Heart Disease (CHD) is the most common abnormality.
In the United States, the prevalence of congenital heart disease
around 8-10 of 1,000 live births, with a third of them manifest in
critical condition in the first year of life and 50% of the gravity of the
first month of life ends with death.
In Indonesia, with a population of 200 million inhabitants and a live
birth rate of 2%, it is estimated there are about 30,000 patients with
CHD.

Etiology and Epidemiology


Acyanotic congenital heart disease is a disease with
structural abnormalities and cardiac or circulatory function
due to interruption or failure of development of cardiac
structures in the early phase of fetal development, without
symptoms of cyanosis.
Acyanotic congenital heart disease are 75% of the
prevalence of congenital heart defects. Consists of the effects
of structural heart defects, with or without gout from left to
right (Left to Right Shunt = ltrs).

A-CHD
- Increased pulmonary blood flow
Ventricular Septal Defect (VSD)
Atrial Septal Defect (ASD)
Patent Ductus Arteriosus (PDA)
Endocardial cushion defects (ECD)
- Normal pulmonary blood flow
Pulmonary Stenosis (PS)
Aortic Stenosis (AS)
Coarctatio Aorta (CoA)

Increased pulmonary blood flow


The increase in pulmonary blood volume will
decrease the flower (compliance) lung and
improve breathing effort. Leakage of fluid into
the interstitial space and alveoli, may cause
pulmonary edema.
Cardiac remodeling can occur, with cardiac
dilatation and hypertrophy of the heart muscle in
mild scale. If the condition remains untreated,
the pulmonary resistance will continue to rise,
and at a time of gout will turn from right to left
(Right-to-left
shunt)
or
also
called
Eisenmenger's syndrome.

Ventricular Septal Defect (VSD)


A defect in the form of one or more holes that are on the wall that separates the
left and right ventricles.
(25-30%)

Ventricular Septal Defect (VSD)


Anamnesis

Physical Examination

Dyspnoe

Heart sounds : normal

Impaired growth

Thrill palpable and noisy


pansystolic

Lung Infection (sindrom


eisenmenger)

In Eisenmenger: cyanotic (rightleft shunt), the child fails to grow,


heart sounds II hardened

More to VSD
Thorax: cardiomegaly, increased pulmonary vascularity, hilar blood vessels
thicken
ECG: an increase in the activity of the left ventricle, mitral P (enlargement
of the left atrium), when pulmonary hypertension right ventricular
hypertrophy
Echocardiography: the direction of the shunt, the pressure a.pulmonalis
Cardiac catheterization and angiography: to prove the increase in oxygen
saturation in the right ventricle. Angiography shows the magnitude and
direction of the shunt, and detecting aortic regurgitation

Atrial Septal Defect (ASD)


Congenital heart disease form holes (defects)
in the interatrial septum (septum between the
porch) that occurs due to failure of fusion of the
fetus - the interatrial septum.

Atrial Septal Defect (ASD)

Primum ASD
There is a gap at the bottom of the atrial
septum, namely the atrial septum primum.

Atrial Septal Defect (ASD)


ASD secundum
There are holes in place fossa ovalis
pathological. Defects can be small to very
large so that it covers most of the septum.
The result is a shunt from the right atrium to
the left atrium, with a load volume in the
atrium and right ventricle

Atrial Septal Defect (ASD)

Clinical features:
Dyspnoe and recurrent respiratory tract infections
Physical examination:
There noisy "systolic ejection" on the left second
intercostal space

Atrial Septal Defect (ASD)


Supporting investigation
Torax Photo: AP chest radiograph
showed right atrial prominent, and with
prominent pulmonary conus, right atrial
and ventricular enlargement. Dilated
pulmonary arteries, and increased
pulmonary vascularity
ECG obtained right axis deviation,
normal
atrial
complex,
normal
conduction,
and
left
ventricular
hypertrophy. Primum defect showed left
axis deviation (left axis deviation) firstdegree AV block (PR interval extenders)

Patent Ductus Arteriosus (PDA)

The ductus arteriosus open after


birth (5-10%)
Due to higher aortic pressure,
blood flow around 5-10 mm distal to
the left subclavian artery through
the duct runs from the aorta to the
pulmonary artery generally funnelshaped with a smaller orifices that
lead to pulmonary artery.

Patent Ductus Arteriosus (PDA)


Mild
Anamnesis

Physical examination

Radiology

Medium

Heavy

asimptomatik

feeding difficulties, recurrent


respiratory tract infections

Difficulty eating and stunted


growth

Palpable vibration
noise in the second
intercostal left sternal

-Palpableof Noisy vibrations in the


second intercostal space left
sternal
-- On auscultation: continuous
noisy II-III intercostal left sternal

-Wide pulse pressure


-Palpable vibration noise in
the second -intercostal
space left sternal noisy
systolic
-Middiastolik noisy at apex

Normal EKG and


Ekokardiografi

- Photo thorax: cardiomegaly,


increased pulmonary vascularity,
enlarged hilar vessels
ECG: left ventricular hypertrophy
Echocardiography: left atrial
dilation and a.pulmonalis

Endocardial cushion defects (ECD)

Endocardial cushion defects (ECD) or AVSD In this disorder does not


happen the separation between the mitral valve ring and tricuspid valve
so that there is a big hole atrioventricular valve ring connecting the two
atria and two ventricles simultaneously, complete Form consists of the
posterior inlet VSD, ostium primum ASD that may progress to ventricular
defect, and the anterior portion of the mitral valve.

Endocardial cushion defects (ECD)


On history, ECD can occur without symptoms.
In extreme cases, patients may indicate poor feeding,
chronic of upper respiratory tract infections, pneumonia, and
growth failure.
Might also be obtained information from mothers of
children who often cry, often stops when eating, and their
nostril breathing. In older children, the manifestation of ECD
is more toward a state of congestive heart failure, with
reduced activity and play, fatigue, spasms, and edema.

Increasing Pressure Load


Babies can experience a critical situation a few
hours after birth. Severe pulmonary stenosis in
the newborn period will show symptoms of right
heart failure (hepatomegaly, peripheral edema)
and can occur right-to-left shunt through a
patent foramen ovale were not closed, so
cyanosis may occur later.
Severe aortic stenosis in the newborn period will
show symptoms of left heart failure (pulmonary
edema, poor perfusion), and may be
accompanied by progressive total circulatory
collapse.

Pulmonary Stenosis (PS)


The presence of an obstruction in the road or a right
ventricular outflow tract. Pulmonary and branches. Narrowing
of the pulmonary stenosis can occur under the valve, which is
in the infundibulum (Subvalvular or infundibular stenosis), the
valve alone (valvular).

Pulmonary Stenosis (PS)


Pulmonary valvular stenosis
One such disorder is a bicuspid pulmonary valve (only
consists of two cusps), or thick and each valve attached to
the end that causes pulmonary valvular stenosis.
Infundibular pulmonary stenosis
Tissue resorption disruption bulb cardiac hypertrophy occurs
during development infundibulum which will cause the
infundibular pulmonary stenosis

Pulmonary Stenosis (PS)


Physical Examination:
On palpation of the chest, ribs palpable vibration noisy II interrupted
the left edge of the sternum
The first heart sound normal ejection followed click
Split second heart sound heard widening with increased severity of
obstruction, due to increased right ventricular ejection duration
Noisy systolic pulmonary stenosis always sounded on, rough nature,
punctum maximum in the second intercostal space left parasternal
and spread along the left sternal line and apex
Supporting Investigation:
X-ray: dilatation pascastenosis on a.pulmonalis, heart size is normal
but who have experienced heart failure
ECG: QRS axis deviation to the right with the right ventikel
hypertrophy, which is indicated by the high R wave in the conduction
of the right chest with deep S waves in V5 and V6

Aortic Stenosis (AS)

Narrowing of the aorta which


can occur at the level of
Subvalvular,
valvular,
or
supravalvular
SA valvular:
Most of the aortic valve has 2
pieces valve (bicuspid) which
will usually cause mild or
moderate aortic stenosis.

Aortic Stenosis (AS)


SA Subvalvular:
Subaortic
stenosis,
similar
membrane below the aortic valve

in

SA SUPRAVALVULAR:
From the outside of the aorta
appeared normal, but the walls are
very thick, which is composed of
fibrous tissue. Aortic lumen becomes
smaller, can be up to 1/3 the normal
lumen. Ventricular hypertrophy is
often found.

Aortic Stenosis (AS)


Anamnesis

Physical examination

Substernal pain

With increasing degree of obstruction,


pulse intensity will be reduced, enlarged
heart, and the apex will be pushed to
the left

Dyspnoe
Dizziness or syncope during
the activity

In aortic valvular stenosis is mild to


moderate tone will sound "early systolic
ejection", the most audible at the apex
and left sternal line.
Systolic noisy vibrations are in the crook
suprasternal
or
in
a.karotis.
on
auscultation
mild aortic stenosis split second heart
sounds were normal in the second
degree heart sounds heard are single
In severe aortic stenosis will sound
paradoxical split second heart sound.

Aortic Stenosis (AS)


Supporting investigation
ECG: may show left ventricular hypertrophy due to left
ventricular pressure load
ECHO: clearly indicate the type of stenosis (Subvalvular,
valvular, supravalvular) and aortic valve biskuspid. With
Doppler can determine the degree of stenosis

Coarctatio Aorta (CoA)


Localized narrowing of the
aorta which generally occurs
at the ductus arteriosus
(juxtaductal coarctation).

Coarctatio Aorta (CoA)


Clinical manifestations

Physical examination

shortness of breath,
hepatomegaly, with a small
pulse, oliguria or anuria

Palpable of brachial pulse


that normal or strong, while
the femoral and dorsalis
pedis
pulse
was
not
palpable or impalpable small

headache, pain in the legs


and feet, or occur epistaxis
(in older children)

On auscultation of the heart


I and II are generally normal,
and to be found in the area
noisy
subtle
systolic
pulmonary

Coarctatio Aorta (CoA)


Supporting investigation
X-ray:
left
ventricular
hypertrophy, rib notcing,
picture 3 reverse
ECG:
look
right
ventricular hypertrophy.
In older children there are
descriptions
of
left
ventricular
hypertrophy
with an inverted T at V3
and V6

General handling

- ASI / High calories of formula milk.


- NGT / OGT (with heart failure - low water and salt)
- Profilactic antibiotic of any dental prosedure.

Conservative - MM
The objective medical therapy also to avoid the development of
pulmonary vascular obstructive disease or the development of
congestive heart failure. If it turns out heart failure and
circumstances related to lung problems still occur, diuretics and
digoxin is the indication.
Diuretics can be given is furosemide (Neonates is 0.5-1 mg/kg/day in
1-3 a day). In infants and children, the dose given was 0.5-2
mg/kg/day, in 2-4 feedings.

Digitalis in children is 0.25 mg/kg/day given in 4 doses every 6


hours. In premature infants, the maximum dose is 20
mg/kg/day orally. In children, the recommended maintenance
dose is 8-12 mg/kg/day divided into two doses.

Conservative - MM

ACE Inhibitor such as captopril. Dose for neonates is 0.05-0.1


mg/kg/dose given 1-4 times per day. For infants, the
recommended dose is 0.15-0.3 mg/kg/dose every 6-24 hours.
For older children, the dose of captopril is 0.3-0.5 mg/kg/dose
in 1-4 feedings.
PDA - Indomethacin, at a dose of 0.1 mg/kg IV every 12 hours in 3
doses for infants < 48 hours. In infants aged 2-7 days the dose of 0.2
mg/kg iv / 12 hours divided into 3 doses. For infants > 7 days is
given a dose of 0.25 mg/kg iv / 12 hours in 3 doses.
CoA - prostaglandin-E : 0.05-0.15 mcg/kg/min IV, then the dose is
gradually lowered to 0.02-0.05 mcg/kg/min.

Surgical therapy

Conclusion

Congenital heart disease (CHD) is a common heart defect that is


caused by the progress of CV (cardiovascular) system during
embryo.
Generally caused by two factors: endogenous factors (heredity)
and exogenous factors (environmental). Hereditary disorder can
be caused by abberasi chromosome and gene mutations,
whereas the environmental causes mainly due to viruses or other
rubella in the mother during pregnancy, drugs such as
thalidomide and other can be caused by radiation.

Thank You!!!