O2 sat in chambers of fetal circulation.
Where is O2 sat highest? Lowest?
PBF ~ 7 - 15% 2nd trimester
30% 3rd trimester (lung growth so increased PBF)
20% around 38 weeks (more O2 so constricts?)
66% CO RV vs 33% LV
Left - because receiving DV blood flow (from UVC oxygenated blood) primarily without mixing in much “used” deoxygenated blood + little bit of blood from lungs
Increase ductus venosus - dilates.
Decrease HR, RR, CO
Fetus goes in hibernation mode - relies on maternal thermoregulation, decrease GI absorption, decreased RR, decrease renal tubular absorption
Preferentially sends blood to head, heart, adrenal glands (by dilating ductus venosus to increase blood to RA -> LA via FO). Abd circumference decrease in FGR fetuses (b/c less BF to those organs) and elevated MCA (diastolic flow increased as more BF to brain)
Note-tricuspid valve very sensitive to hypoxemia (therefore, babies with HIE can have TR)
UV constricts - because decrease blood flow
UA constricts - because increase O2 content
How does DCC work?
What influences ventricular wall stress?
Conceptualize Frank Starling curve
Frank starling curve - effect of increased and decreased preload
Frank starling curve - effect of increased and decreased afterload
PS, hypertelorism, downward slanting palpebral fissures, low at ears, short stature, short webbed neck, Percy’s excavation, cryotorchidism, cognitive delays, lymphedema
Noonan - most common cause of HOCM kids < 4 although most common cardiac defect with Noonan is PS
1 cyanotic congenital heart disease in infancy/childhood
ToF
1 cyanotic CHD in first week of life
TGA
describe early formation of cardiac tube
early cardiac embryology
mediator of cardiac development
mediators of septation
mediators of L-R differentiation
when does cardiac septation occur?
8 weeks
heterotaxy - what occurs
L atrial isomerism
- describe
- complications