Week 2 Flashcards
1
Q
How does primitive heart start out as?
A
- straight tube
2
Q
parts of cardiac embryology and what they turn into
A
- aortic roots: blood out
- trureus arteriosus: aorta and pulmonary trunk
- bulbus crodis: smooth LV/RV -> where heart connects to other sections
- primitive ventricle: trabeculated RV/LV
- primitive atrium: trabeculated atria
- sinus venosus (blood in): smooth right atrium on left and coronary sinus on right
3
Q
Cardinal veins
- what do they form
- right and common cardinal
- posterior cardinal vein
A
- SVC and IVC
- SVC
- IVC
4
Q
Fetal circulation
- lungs
- ductusus venosus
- ductus arteriosus
- foramen ovale
A
- high pressure in lungs
- allows blood to bypass liver and go straight to the RA
- allows for blood to bypass pulm artery and go into aorta
- allows for blood to go from RA to LA
5
Q
Pressure Changes from utero to birth
- PVR
- RA
- VA
A
- PVR is high in utero because of liquid in lungs and will increase after bith because the liquid is removed and replaced by air
- RA is increased in utero and decreased after birth. It decreases after birth because the blood can now go through the lungs
- LA is decreased in utero and increased after birth because once the placenta is clamped off the pressure increases in the aorta which increases LV pressure and then increases pressure in the LA
6
Q
How do shunts cause right sided heart failure and then cyanosis?
A
when babies are born and pressures change the blood will pump from left to right side of heart -> causes eight side to over work -> causes increase in R sided pressure –> starts shunting from R to L -> causes for lungs to be missed
7
Q
VSD
- murmur
- small
- large
A
- harsh, holosystolic murmur in tricuspid area
- benign, but harsh murmur because blood is trying to flow through small hole
- surgically repaired; not loud murmur
8
Q
ASD
- effects
- pulmonic valve
- murmur
- types
A
- adds volume to R side of heart
- causes delayed closure; right sided heart pressure increases -> makes it harder for RV to pump into pulmonary artery causing delay in closure -> causing a fixed split
- systolic ejection murmur
- secundum: defect at site of foramen ovale, poor growth of secundum septum or excessive resorption of primum septum; primum: defect at ostium primum; failure of primum septum to fuse w/ endocardial cushions
9
Q
PDA
- what does it usually become?
- murmur
A
- becomes ligamentum arteriosum
- continuous, “machine like”
10
Q
Cyanotic Congenital Heart Defects
A
- Tetralogy of Fallot
- Truncus arteriosus
- Transposition of Great Vessels
- L-TGA
11
Q
Tetralogy of Fallot
- involves
- effect
- how to fix?
- murmur
- shape of heart
A
- VSD, right deviation of aortic valve, subpulm stenosis, right vent hyp
- hard to pump blood from RV to pulm artery so blood is not oxygenated
- use DA to allow blood to go back to lungs
- systolic, decrescendo-crescendo
- boot shaped
12
Q
Truncus arteriosus
- what happens?
- what happens to blood?
- cause?
A
- common arterial trunk
- mixing of blood
- by failure of neural crest cells to drive formation of aorticopulmonary septum
13
Q
Transposition of Great Vessels
- what happens?
- effect?
- how?
- commonly seen in?
A
- aorta and pulm trunk switched
- RV pumps to aorta and LV pumps to pulm trunk
- aorta form anterior and rightward of pulm artery
- gestational diabetes
14
Q
L-TGA
- what happens?
- blood flow
- effect of blood flow
A
- double switch -> aorta/ pulm artery AND LA/RA
- venous -> RA -> LV -> pulm art -> lungs -> LA -> RV -> aorta
- R- Ventricle will fail because it cannot tolerate systemic load
15
Q
Tricuspid artresia
- what is it?
- what do you need for someone to survive with this?
A
- no tricuspid valve
- need ASD -> blood to LA AND VSD or PDA to get blood into lungs
