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FHF
cells
SHF
cells
21
50
Gene
of FHF
(origin: lateral mesoderm)Cardiac crescent
Day 21st : SHF cells migrate to ant. & post
(CT,Atrium)., the FHF cells become tube (mainly left
ventricle) beating tube
Day 28th: looping of the heart tube & neural crest
migration to the outflow tract (form septa and aortic
arches) & ECM enlarges to produces swelling
+
Left
heart
Right
heart
heart
failure
Dyspnoea
Fatigue
Palpitation
Palpable thrill
Parasternal
heave
Pulmonary hypertension
Prolonged right
ventricle
ejection
Pressures at right heart high enough to
time
overcome left heart pressure
Reversal of shunts occur
Cyanosis
Right-to-left
shunt
Left atrium dilate
valve ring
dilate
Incomplete
closure of mitral
valve
Pathophysiology
Left
ventricle
hypertroph
Pansystoli
c murmur
Reduce Regurgitation
VSD
complianc
e
(VSD)
S3
large
heard
volume of
blood
shunted to
right
CLINICAL FEATURES
ASD
Fixed splitting
second heart
sounds (ASD)
Pathophysiology
Collapsed pulse at
periphery
Left & right shunts at ductus level (bounding)
Wide pulse
Increase pulmonary flow from aorta pressure
PDA
Clinical features
Dyspnoea
Fatigue
Palpitation
Palpable thrill
Parasternal heave
S3
Loud S2
Pansystolic
murmur
Mitral
regurgitation
Sign of congestive
heart failure
Clinical features
Dyspnoea
Fatigue
Palpitation
Palpable thrill
Parasternal heave
Fixed splitting of S2
Mild systolic murmur
Mitral regurgitation
Sign of congestive heart
failure
Turbulent
shunting
Machinery
murmur
Turbulent through
mitral valve
Mid diastolic
murmur
Increase volume
at left heart
Distention of
left heart
Vigorous nonsustained
pulsation
Hyperkinetic apex
beat
Right-to-left shunts
Decreased
diastolic BP
Increased
systolic BP
Delay Lt. ventricle
emptying
Slow closure
of aortic
valve
Reverse
splitting S2
Turbulent right
ventricle outflow
Pulmonary
systolic
ejection
Increased
pulmonary art.
pressure
Closure of
pulmonary valve too
soft + late
Single 2nd
heart sound
Central cyanosis
Hypoxia stimulate kidney & liver
Increase erythropoietin
Increased RBC
Polycythaemia
Pathophysiology
Pulmonary stenosis
Infundibular resistance
RightVSD
ventricle
volume loaded
pressure
Right ventricle
hypertrophy
Obstructive Congenital
Anomalies
Coarctation of Aorta
Narrowing or constriction of aorta
Two classic form :
infantile
adult
Clinical Features
HTN in upper extremities
Weak pulses
Hypotension in lower extremities
Radiograph notching
undersurfaces of rib
Systolic murmur
Thrill
Cardiomegaly
Pulmonary stenosis and atresia
Obstruct at the pulmonary valve
Clinical features
Right ventricular hypertrophy
Posstenotic dilatation
Aortic stenosis and atresia
Narrow and obstruct of aorta
Three major locations:
Valvular
o HYPOPLASTIC CUSPS
o THICKENED CUSPS
o ABNORMAL NUMBER OF
CUSP
o Hypoplastic- Left -Heart
Syndrome
Subvalvular
o Dense endocardial fibrous
below cusps
Supravalvular
Investigation &
Management
Atrial Septal Defect (ASD)
INVX:
ECG:
Ostium Secundum Right axis
deviation
Ostium primum Left axis deviation
Sinus venosus Invrtd P-wave
Chest X-ray
ECG:
Left atrial enlargement
X-ray:
Calcified at ductus
Aneurysm of ductus
Treatment:
Surgical closure (3-6 yr)
ASD close spontaneously upto 2 years
Prosthetic closure by pericardial graft
Treatment:
Medical :
Indomethacin 1st -7th day
(MOA: decreased PG-E level
promotes ductal closure)
Surgical :
Ligation & excision of PDA
Ideal age below 2yr
Transcatheter closure
Tetralogy of Fallot (TOF)
INVX:
ECG :
Large R wave
X-ray :
Treatment:
Medical :
Treat
cyanotic:
Squatting
Nasal O2
Morphine
Beta blockers (propanolol)
(MOA: relieve infundibular
spasms)
Sodium bicarb met. Acidosis
Surgical:
Blalock- Taussig procedure
Waterston procedure
Potts procedure