Cardiovascular Flashcards by Michelle Fric

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)

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Acyanotic heart lesions

VSD
ASD
PDA
coarctation

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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)

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cyanosis with left axis deviation

tricuspid atresia

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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

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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.

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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

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Trisomy 21 CHD

of all AVSDs 50% have T21

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Marfan CHD

dilated aortic root + aorta
mitral valve prolapse

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Ehlers danlos CHD

dilated aorta
mitral valve prolapse

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williams CHD

supravalvular AS/PS (normal valves but tight above valve)
PPS (small branch pulm arteries)

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Noonans CHD

PS
hypertrophic CM

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Turner CHD

bicuspid AV (the most common)
aortic stenosis
coarc aorta

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Alagille CHD

PS
PPS

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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

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maternal rubella CHD

pulmonary stenosis
PDA

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FASD CHD

VSD
PDA
ASD

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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

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difficult delivery with shoulder dystocia and meconium aspiration. baby now cyanotic. what CHD?

PPHN
R to L shunt through PDA due to pulm hypertension

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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

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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

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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