Cardiovascular Flashcards
Cyanotic heart lesions
Cyanotic heart disease (5 T’s & H)
ToF
TGA
Truncus arteriosus
TAPVR
Tricuspid atresia & Ebstein’s
Hypoplastic left heart (any LV outflow tract obstruction can result in duct dependent lesion)
Acyanotic heart lesions
VSD
ASD
PDA
coarctation
test to distinguish cyanotic from acyanotic heart lesions
hyperoxia test
If the PaO2 rises above 150 mm Hg during 100% oxygen administration, an intracardiac right-to-left shunt can usually be excluded
pre ductal ABG. (right radial)
cyanosis with left axis deviation
tricuspid atresia
Late complications fontan surgery
stenosis of the superior or inferior vena cava anastomosis
vena cava or pulmonary artery thromboembolism
protein-losing enteropathy
plastic bronchitis
immune deficiency
supraventricular arrhythmias (atrial flutter. paroxysmal atrial tachycardia)
hepatic cirrhosis (and possibly hepatic carcinoma) as a result of persistently elevated central venous pressures
Oral budesonide or sildenafil has been used with varying success to treat protein-losing enteropathy associated with the Fontan procedure. Thoracic duct ligation or embolization has been used to treat plastic bronchitis. LV dysfunction may be a late occurrence, usually not until adolescence or young adulthood. Heart transplantation is a successful treatment option for pediatric patients with “failed” Fontan circuits
Orthostatic hypotension
orthostatic hypotension (OH) is defined as a sustained DROP in the systolic BP by >20 mm Hg or diastolic BP >10 mm Hg in the 1st 3 min of upright tilt.
most common CHD in DiGeorge
ToF is most common
could also have interrupted aortic arch, truncus arteriosus, VSD, pulm atresia, vascular rings (chonal truncal outflow track anomalies!!)
if you see truncus, think digeorge
autosomal dominant
Trisomy 21 CHD
of all AVSDs 50% have T21
Marfan CHD
dilated aortic root + aorta
mitral valve prolapse
Ehlers danlos CHD
dilated aorta
mitral valve prolapse
williams CHD
supravalvular AS/PS (normal valves but tight above valve)
PPS (small branch pulm arteries)
Noonans CHD
PS
hypertrophic CM
Turner CHD
bicuspid AV (the most common)
aortic stenosis
coarc aorta
Alagille CHD
PS
PPS
Maternal diabetes CHD
HOCM
PDA
VSD
worse if the mom had diabetes at the beginning of pregnancy!
HOCM occurs if poor sugar control. can improve when baby has normal sugar
maternal rubella CHD
pulmonary stenosis
PDA
FASD CHD
VSD
PDA
ASD
maternal lupus CHD
can lead to heart block, cardiomyopathy, or valve regurgitation (monitor pregnancies if mom has lupus, monitor until 26 weeks)
neonatal lupus: cardiac, skin, liver, heme problems
if normal at birth, no ongoing screening for the child
difficult delivery with shoulder dystocia and meconium aspiration. baby now cyanotic. what CHD?
PPHN
R to L shunt through PDA due to pulm hypertension
Tetrology of Fallot 4 lesions
- VSD
- Overriding Aorta
- Right ventricular outflow tract obstruction (ex. pulmonary valve stenosis)
- RV hypertrophy
degree of stenosis depends on degree of RVOTO
CXR in ToF
Boot shaped heart
d/t RVH - turns up the apex of heart
pulmonary artery is hypoplastic so dont get a typical PA shadow
decreased pulm vascular markings
Physical exam of ToF
normal S1
Single S2
SEM at ULSB (differentiates this from TGA) - pulm stenosis murmur
ECG changes in ToF
RVH
Right axis deviation
upright T wave in V1
Tet Spells
increased shunting R–> L
toF ECG post repair
RBBB in V1
TGA
parralel circulation
needs to have mixing
- PFO
- ASD and/or PDA
- occassionally VSD
universally cyanotic (typically 70s at birth)
- degree of cyanosis depends on ability to mix
TGA murmur/exam
NO MURMUR IN TGA - no turbulence (valves are normal, normal shunts) *distinguishes from ToF
Normal S1, single loud S2 - can’t hear due to altered anatomy and pressures aren’t as varied with respirations
TGA xray
egg on a string
mediastinum is narrow because aorta/PA are overlying on top of each other so looks tall and narrow
TGA management
KEEP PDA OPEN - start prostaglandin
Needs a shunt to improve mixing
- balloon atrial septostomy if no ASD or small ASD
TGA vs. ToF
TGA
- most common immediate cyanosis at birth
- NO murmur
- CXR egg on string with normal or increased pulm markings
- usually no syndrome
ToF
- stenosis progresses over time so may not be as cyanotic at birth
- LOUD SEM murmur
- CXR decreased pulm markings and boot shapped
- most common cardiac cause of cyanosis overall (But may not be at birth)
Tricuspid atresia
think about single ventricle physiology because the RV does not form since the tricuspid is closed
all blood goes through LV
need shunts to get blood from RA to left heart
cyanotic lesion
typically has LV heave, single S2, and holosystolic murmur at LSB
Ebsteins anomaly
tricuspid valve leaflet not formed properly - think of as tricuspid regurgitation CHD
spectrum of disease
if severe, RV and RA are essentially one, RA enlarges, lots of blood can go through the ASD, less blood goes through pulmonary vessels (Cyanosis)
can get massively enlarged hearts (may not even survive fetal life because the heart prevents lungs from forming)
Ebstein’s anomaly murmur
loud, regurgitant murmur at llsb
LSB
Pericarditis: Diffuse ST Elevation and PR depression
Hyperkalemia: Tall Peaked T Waves
2nd Degree Heart Block (Wenckebach)
Pericarditis: Diffuse ST Elevation and PR depression
1st Degree HB
2nd Degree HB (Wenckebach)
Complete Heart Block
Atrial Flutter
Left Bundle Branch Block
LVH with strain
Long QT
SVT (Narrow Complex VT)
Premature Atrial Contractions
Monomorphic VT
Premature Ventricular Contractions
Right Bundle Branch Block
Torsades de Pointe
Wide Complex VT
Wide Complex VT
