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Congenital Heart Defects - Coggle Diagram
Congenital Heart Defects
ASD
auscultation: left upper sternal boarder murmur associated with pulmonic valve overload, fixed S2 as pressure equallized through ASD
multiple cardiac outputs flow to lung
indicated for closure if pulmonic flow is too high, elevated pulm arterial pressure, or cyanosis (Eisenmanger syndrome)
path: 4 types
most common: secundum (failure of septum primum to close foramen ovale), ostium, sinus, unroofed coronary
Normal physiology: after birth, pulm resistance drops as lungs expand and replace fluid with air, right heart pressure drops, and septum primum is pushed against secundum, closing PFO
ECG: may see p wave peak with large R wave from right side hypertrophy
VSD
Diagnosis: no murmur in the delivery room and then murmur several days later
In delivery room, high pulm art pressure -> high RV pressure -> no shunt, no murmur
holosystolic Murmur at LLSB, obliterate S1
Later in life can see Left heart dialation as increased cardiac output return to left side
Feared sequella: congenital congestive heart failure with overloaded lungs
Types
Anatomical types
Can close
muscular and membranous
never close: inlet and outlet
Clinical Categories
Pressure Restrictive (small VSD)
Non- Pressure Restrictive
large hole, low pressure gradient between LV and RV, lots of flow through VSD, lots of flow to lungs, left heart dialation
Tetrology of Fallot
path: anterior rotation of the infindibular septum creates overriding aorta, pulmonary stenosis, VSD, and resulting RV hypertrophy.
tet spell is an infindibular muscle spasm (likely brought on by crying)
child squats to increase SVR by kinking femoral arteries
increase SVR, increase LV pressure
reverse R to L Shunting, normalize with L to R shunt, which resolves cyanosis
Diagnosis
likely congenital dx
see boot on CXR, show RV hypertrophy
Murmur: LLSB VSD, LUSB PS
Surgical Repair at 3-6 months
close VSD, prevent future RV hypertrophy
genetic risk: 22q11, T21
Transposition of Great Arteries
Path: aorta connected to RV, pulm art connect to LV
Babies are dependent on at least 2 levels of shunting to facilitate oxgenation of blood
Need to deliver at Cardiac surgery hospital, emergency management is PG, oxygen with intubation (glandins cause resp depression), umbilical cath (with possible baloon septostopy), fluids, ECG, Xray, echo, and transfer
Appearance: baby is blue as a squid
Labs and imaging: CMP, lactate, CBC, cap gas, blood cultures,
Cyanotic Heart Disease
Neonatal Management
Prostaglandin E to keep ductus Patent (ductal dependent lesion)
Consider atrial septal catheter dialation if rely upon that shunt
Childhood ED Management
Diagnosis
Differential
Key Primary Care Screening Questions
Trouble breathing or fast breathing
Poor feeding: type, quantity, frequency, tiring
trouble growing
Rational for Failure to Thrive in CHD
If not pressure restricted, VSD or ASD allows multiple cardiac outputs to enter RV
multiple CO go to lungs
engorged pulm arteries
increased pulm blood flow causes tachypnea
feeding increases metabolic demand to use muscles
tachypnea requires shorter, more frequent feeds and tire with feeding
need more calories to pump multiple cardiac outputs
end: less caloric intake and more demand lead to FTT, see on growth chart as baby falling off curve
Pulmonary stenosis
auscultation: LUSB systolic murmur with radiation to the posterior lung fields (following pulmonary arteries)
3 locations: supervalvular, valvular, and subvalvular
ECG: possible RV hypertrophy (large R wave in V1)
In neonatal period, significant PS can cause cyanosis because increases RA pressure, which pushes open the foramen ovale and require R to L shunt
