Professional Documents
Culture Documents
Acyanotic Congenital Heart Diseases
Acyanotic Congenital Heart Diseases
By Meilleurs Amis
Remember: INCREASED VOLUME LOAD- ASD, VSD, PDA, AVSD Lonelybitter
ATRIAL SEPTAL ATRIOVENTRICULAR VENTRICULAR SEPTAL PATENT DUCTUS
DEFECT SECUNDUM SEPTAL DEFECT DEFECT ARTERIOSUS
Descriptio Present at the site of Also called Endocardial MOST COMMON cardiac Abnormal persistence
n fossa ovalis cushion defect malformation 25% of of a normal fetal
Consists of contiguous atrial CHD vascular channel
and ventricular septal most common are the between the
defects with markedly MEMBRANOUS TYPE(in pulmonary artery
abnormal AV valves the posteroinferior and aorta
Component of heart defects position, anterior to the
in asplenia and septal leaflet of the TV)
polysplenia syndrome
Pathophys Despite the large In Ostium primum SMALL lesion <5mm The higher aortic
iology pulmonary blood defects L-R shunt across VSD is pressure pressure postnatally,
flow(PBF), pulmonary the atrial defect and MV restrictive RVP is blood shunts left to
arterial pressure (PAP) ( occ. TV) insufficiency The normal right through the
is usually normal shunt is usually moderate LARGE DEFECT >10mm ductus, from the
because of the to large, PAP is normal or RV and LV pressures aorta to the
absence of a high only mildly increased are equalized pulmonary artery
pressure In Complete AVSD- the L-R Qp:Qs ratio-described the
communication occurs at both the atrial magnitude of the
between the and ventricular levels intracardiac shunts
pulmonary and Additional shunting from
systemic circulations the LV to RA because of
absence of the AV septum
Shunting Size of defect Level of PVR (Pulmonary Size of the defect Resistance offered
depends Relative compliance vascular resistance) Level of pulmonary by the ductus
on: of the RV and LV vascular resistance Level of PVR
Relative PVR and
SVR
History ASYPTOMATIC Failure to thrive Small VSDs- Small PDA-
Large defect rarely Repeated respiratory tract asymptomatic asymptomatic
produce clinical HF in infections Moderate to large Large PDA- result in
childhood Exercise intolerance VSDs- delayed growth heart failure,
May have subtle failure Easy fatigability and development, retardation of
to thrive and Signs of CHF dyspnea, feeding physical growth and
exercise intolerance difficulties, profuse frequent lower
perspiration, decreased respiratory tract
exercise tolerance, infections and
repeated pulmonary atelectasis
infections, CHF are
common during infancy
Physical RV systolic lift at the Hyperdynamic precordium Small shunts- loud, Small shunt- (+)
Examinati LPSB S1 normal or accentuated harsh or blowing HSM classical
on S2 widely split and S2 wide, fixed splitting LPSB continuous
fixed in all phases of Pulmonary systolic Large shunts- less harsh machinery
respiration ejection murmur but more blowing murmur LUSB and
SYSTOLIC EJECTION preceded by a click holosystolic murmur normal peripheral
MURMUR (SEM) AT Low pitched mid diastolic (HSM) at the left pulses
THE LEFT rumble at the LLSB parasternal border Large shunts-
MIDSTERNAL Harsh apical holosytolic (LPSB) tachycardia, apical
BORDER murmur of mitral Mid-diastolic ,low pitched diastolic rumble,
(LMSB)/LEFT UPPER regurgitation rumble at the apex due bounding peripheral
STERNAL BORDER to incrased blodd flow arterial pulses and a
(LUSB) caused by across the MV and wide pulse pressure
increased flow indicates Qp:Qs >/= 2:1 PVOD- accentuated
across the right P2, right-to-left
ventricular outflow shunt results in
tract(RVOT) into differential cyanosis
the pulmonary (cyanosis of lower
artery half of the body
only)
ATRIAL SEPTAL ATRIOVENTRICULAR VENTRICULAR SEPTAL PATENT DUCTUS
DEFECT SECUNDUM SEPTAL DEFECT DEFECT ARTERIOSUS
ECG RAD (Right axis Superior/Extreme QRS Small VSDs- normal Small PDA normal
deviation) axis Moderate VSDs- LAE, Moderate PDA LAE,
RVE LVH LV
rsR pattern on R Large VSDs- LAE, Large PDA LAE, left
precordial leads combined ventricular ventricular or
hypertrophy biventricular
hypertrophy
Chest X- Xray- RIGHT side will Cardiomegaly Small defect- Normal Small PDA normal
ray be enlarged! (RAE Increased pulmonary size heart, normal PVM size heart and
and RVE) and vascular markings Large defect- normal PVM
pulmonary Prominent MPA Cardiomegaly of varying Large PDA
vascualrity is degrees: LAE, LVE, BVE; cardiomegaly ,
INCREASED Increased PVM, prominent
prominent MPA pulmonary artery
with increased
pulmonary vascular
markings
Treatment Surgical or MEDICAL: MEDICAL: Requires surgical or
transcatheter device Management of CHF Treatment of CHF: catheter closure
closure for all SBE prophylaxis diuretics, digitalis Small PDA
symptomatic patients High calorie formulas -rationale for closure
and also for SURGICAL: Correct anemia is prevention of
Asymptomatic Early surgical repair(3-8 SBE prophylaxis: bacterial
patients with a Qp:Qs months): early maintenance of good endarteritis.
ratio of at least 2:1or PVOD (pulmonary vascular dental hygiene and -closed with
those with RVE occlusive disease antibiotic intravascular coils
Timing of elective Non-surgical Large PDA
pulmonary HPN)
closure:umbrella - closure is
surgery: after the 1st
device accomplished to
year and before
treat heart failure.
school entry
-closed with an
PERCUTANEOUS INDICATIOSN FOR
umbrella-like
CATHETER DEVICE SURGERY:
device
CLOSURE procedure Any age with large defects
of choice in whom clinical sxs and
Surgical treatment -
failure to thrive cannot
less than 1%
be controlled medically
Closure of the ductus
Between 6 and 12 months
is indicated in
old with large defects
asymptomatic
associated with
patients -1 yr. of
pulmonary hypertension
age
even if symptoms are
controlled medically
Older than 24 months with SURGICAL CLOSURE:
Indications:
a Qp:QS ratio greater
than 2:1 PDA regardless of size
Those WITH is an indication for
SUPRACRISTAL VSD of surgery
any size because of the Timing: anytime
HIGH RISK FOR AV between 6 months
REGURGITATION and 2 years when
diagnosis is made
PROCEDURE: ligation
and division
through left
posterolateral
thoracotomy
without CP bypass
Natural NO CHANCE OF Membranous and Spontaneous
History SPONTANEOUS muscular small VSDs: closure does not
CLOSURE spontaneous closure in usually occur in
Heart failure occurs 1 2 30-50% of during the 1st full term infants
months of life 2 years of life, may (structural
Recurrent pneumonia decrease in size with age abnormality)
Without intervention: Inlet and CHF or recurrent
most die by 2-3 years of infundibulardefects:d pneumonia, PVOD
age o not become smaller or Infective endocarditis
PVOD close spontaneously Aneurysm of PDA: rare