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Approach for Acyanotic heart

diseases
ASD
VSD
PDA
History - ASD
F > M Osteum Secundum ASD
Asymptomatic mostly
Incidental detection of murmer
Symptoms depend on 1)Size 2)difference in
gradient b/w two atria
Time or presentation of large shunts in ASD

Infants : 6-8weeks
Older ages
Dec PVR.
LV stiff (age/ischemia)
Rt ventricle more compliant
Shunt increases
Pressure gradient
Present in 4th 5th decade
Shunt
CCF Common
CCF uncommon
Fatigue, dyspnea, edema etc
Atrial arrhythmias Palpitations
Thrombogenic
Systemic embolization
Paradoxical embolization
Cyanosis in ASD

Direction of deoxygenated blood


Increased PVR from IVC through prominant
Eustachian valve/Thebesian valve
Usually in older age To Left Atrium
< 1 Year Spontaneous closure
Death uncommon < 0.1%
10 - 20 Years Usually asymptomatic
- 13% have Pulmonary Hypertension
- 9% have Eisenmengers
30 Years 80 - 86 % asymptomatic
4% may have Rheumatic disease of Mitral valve
> 40 Years Pulmonary Hypertension 6 14%
Arrhythmias
Eisenmengers
CCF
Examination
Holt-Oram syndrome
Hypoplastic thumb, absent radius,
humerus (Upper limb skeletal abn
+ ASD)

Downs Primum + Secundum ASD

Noonans Secundum ASD + PS


Downs
Noonans
Loud S1
Wide fixed split second heart sound
Soft cresendo-Decresendo Ejection systolic
murmer Left upper sternal border
Inc flow across Tricuspid Mid diastolic
murmer Left lower sternal border
Cyanosis
Associations
Secundum ASD Functional Mitral valve
prolapse
Primum ASD Endocardial cushion defects
Sinus venosus ASD PAPVC
Coronary sinus ASD Left SVC
Chest Xray
Pulmonary plethora
Enlarged Right
atrium and Right
ventricle
Cardiomegaly
ECG

NSR/AF
Rt axis deviation
Rt sided volume overload
Left axis deviation Septum primum ASD

Negative P wave in Sinus venosus ASD


2D ECHO
Confirmation of Location (Type of ASD)
Size of ASD
Anatomical land marks
Associated lesions
Hemodynamics (Shunts)
Chamber enlargement
Subcostal view Best for
PFO, Secundum ASD
Sagittal view Look for
superior and inferior rims
Insertion of RUPV, SVC
(sinus venosus, Coronary
sinus ASD)
4 chamber view Only
looked for Chamber
enlargement. Not
diagnosis of ASD (High
false dropouts)
4 chamber view
(See mainly
chamber enlargement)
Adults High parasternal short axis view (Alt
to subcostal view)
Avoid closure in
patients with PVR > 8 woods
Or PA pressure >2/3rd systemic pressure
Net R L Shunt
No response to pulm vasodilator therapy
Failed occlusion test
When to intervene
Patient with Large defects (>8mm)
Large shunts with Qp/Qs > 1.5-2:1
RV volume overload with/without symptoms
Small VSDs and PFO if risk of paradoxical
embolus (pregnancy, scuba divers, previous
stroke)
Transcatheter ASD closure
Ostium secondum ASD
L R Shunt (Qp:Qs 1.5 or more)
RV volume overload
Normal pulmonary venous drainage
Max ASD diameter <30mm
Distance of >5mm from margins of defect to
AV valve, SVC, RUL pulmonary vein, IVC
Surgery/ Not for device closure
Sinus venosus, Coronary sinus type, Primum
type
Secundum and PFO if defect >38mm diameter
or defect with insufficient rims (<5mm)
VSD
Determinants of hemodynamics
Size of VSD
PVR
SVR
Associated defects ASD, PDA, RVOT/Arch
obstruction
Location of VSD is irrelevant
Small VSD <1/3rd size of aortic root
Restrictive
Qp/Qs <1.4:1, Less LV volume overload
Doesnt develop Inc PVR
AR, Bacterial endocarditis is common
Moderate 1/3 2/3rd size of aortic root
Qp/Qs 1.4-2.2:1, Moderate LV volume overload
Hypertrophy
Low PVR. Rarely progresses to PH
Large(Nonrestrictive) >2/3rd size
Qp/Qs >2.2:1
LA, LV RV hypertrophy
Inc Pulm venous and art pressure
As PVR >SVR R-L shunt, Cyanosis
History
F>M
Large VSDs Tachypnea, chest retractions, feeding
difficulties, suck rest suck cycles, sweating on forehead,
repeated resp tract infections, failure to thrive
Moderate parents observe pulsations on precordium,
mild tachypnea, cough during feeding, fatigue, Frequent
Resp tract infections
Small VSD Murmer on routine examination,
asymptomatic
Large VSD, high PVR exertional dyspnea, cyanosis,
syncope, hemoptysis
Pulse : Small normal
Moderate brisk(vigorous LV ejection)
Large & CHF Low volume pulse
Eisenmenger Normal (Systemic stroke volume
maintained)
JVP: Normal. If raised rules out VSD
Precordial movements:
Mod to large VSDs visible precordial pulsations, LV
type apex, hyperdynamic
Small to moderate precordial thrill in 3rd and 4th
ICS left sternal border
Large VSD + high PVR Parasternal heave, palpable
P2 in left ICS
S1 Normal
S2 normal with normal split
Pulm component is loud in Large VSDs.
murmur in small VSDs is grade 4/6, harsh long systolic,crescendo-
decrescendo best heard along the lower LSB.
In very small apical or muscular defects the murmur is soft, grade 2/6 as
the defect closes during systole
The murmur in moderately large defects are long, low pitched
decrescendo murmur best heard in LSB.
The systolic mumurs in outle defects are heard in the second ICS and
may radiate upwardsto the left into the suprasternal notch and into the
left side ofneck. In outlet defects, the holosystolic murmur is crescendo
orcresendo-decresendo. W
hen the shunt is large (Qp/Qs > 2:1),
a short mid-diastolic murmur is heard at the apex due to the increased
flow across the mitral valve. The soft blowing early diastolic
decrescendo murmur in the left second and third ICS could be due to
associated AR and peripheral signs are present if the AR is significant
In patients with large VSDs with high PVR, the LV
precordial impulse is replaced by the RV impulse.
There is a very short soft decrescendo murmur or
rarely no murmur in balanced shunts. The ejection click
may be heard due to the flow in the dilated
hypertensive pulmonary trunk.
Second sound is quite loud, palpable with narrow
splitting.
The third sound of RV origin may be present along the
LSB. There is no diastolic rumble at apex
1. Spontaneous diminution in size or closure.
2. Development of right ventricular outflow tract
obstruction
(Gasuls effect).
3. Development of AR.
4. Development of left ventricular outflow tract
obstruction.
5. Development of pulmonary vascular obstructive
disease.
6. Infective endocarditis.
Spontaneous closure:
Muscular > perimembranous
Restrictive >> Non restrictive

Mechanisms: Septal leaflet of tricuspid


NCC/RCC of Aortic valve
Fibrous tissue ingrowth septal ameurysm
Growth and hypertrophy of muscles
Vegetations of IE
RVOT Obstruction
Hypertrophied crista supraventricularis
Infundibular stenosis
(More with perimembranous)
dec in symptoms of cardiac failure in infanr.
Cyanosis
Aortic Regurgitation
73% in outlet VSDs
Perimembranous 14%
Subaortic stenosis
Pulm vasc obstruction
IE (vegetation on septal leaflet of tricuspid)
Gerbode defect large shunt Biventricular volume
overload.
VSD (LV)
ASD (RV)
Small defect silent
Large similar to vsd
ECG
Mirror to physiology
size of the VSD, degree of volume overload and
PVR
Small VSD Normal ECG
Moderate LAD, LVH
Large unrestrictive Biventricular hypertrophy,
RAD
Gerbode defect Biventricular enlargement, Rt
atrial P waves + LVH
Chest Xray
2d echo
Apical 4 chamber view Inlet VSD, Mid muscular, Apical
muscular
PLAX perimembranous
PSAX (semilunar valve level) defect in Outlet septum
1o clock
Defect in subaortic septum 11 12 o clock
PSAX(mitral valve) ant defects of trabecular septum
12-1 O clock
Mid muscular defects 9-12 O clock
Inlet defects 7-9 O clock