Prework 3: Fetal Circulation and Congenital Heart Defects Flashcards
describe the general fetal circulation
blood is oxygenated in the placenta and delivered to the embryo via the umbilical vein
most blood passes through the ductus venosus within the liver and returns to the RA via the IVC
blood returns to the placenta via 2 umbilical arteries
what is the right to left fetal shunt?
blood shunted from RA to LA via foramen ovale
shunted from pulm outflow to aortic arch via ductus arteriosus
lung bypasses
what happens with the first breaths at birth
bradykinin is released from lungs
vascular resistance is decreased in lungs
increased O2 levels cause smooth muscle to contract, increasing blood flow to lungs
what is the result of increasing blood flow to the lungs?
increased blood returning from lungs into the LA
significant increase in LA pressure
why does the pressure in the RA decrease after birth?
blood flow to the RA decreased because blood flow from placenta is lost when cord is cut
result of LA pressure > RA pressure
septum primum is pushed against septum secundum closing the foramen ovale
anatomically closes within 1 year
normal closure of ductus arteriosus
functionally closes within 36 h of birth due to loss of prostaglandin E
anatomically closes within 3 months forming ligamentum arteriosum
symptoms of patent DA
rapid breathing increase in the work of breathing rapid HR more frequent respiratory infections tiring more easily poor eating/growth
what population is prone to PDA and what is a treatment?
premature infants are slower in closing the DA
indomethican, a prostaglandin inhibitor can be given to speed closure
epidemiology of congenital heart defects
heart and vascular abnormalities make up largest category of birth defects
1% of liveborn infants
incidence 10x higher in stillborns
inherited defects that affect heart development
genes that encode transcription factors
cause partial loss of function
autosomal dominant
6-10% of babies with CHDs have chromosomal abnormalities (associated with genetic syndromes)
environmental stresses and CHDs
during 1st trimester, these stresses can alter the same genes and conceivably lead to acquired defects that mimic those produced by heritable mutations
maternal diseases linked to heart defects
insulin dependent diabetes
hypertension
shunt
abnormal communication between chambers or blood vessels
allows blood to flow down pressure gradients
obstruction
abnormal narrowing of chambers, valves, or blood vessels
atresia
complete obstruction of chambers, valves blood vessels
hypertrophy
increase in muscle mass of cardiac chamber (increased size of cells)
hypoplasia
decrease in muscle mass of cardiac chamber (fewer cells) BEFORE birth
atrophy
decrease in volume and muscle mass of cardiac chamber (degeneration of cells) AFTER birth
left to right shunt examples
systemic to pulmonary
ASD
VSD
PDA
right to left shunt examples
TOF
transposition of great arteries
persistent truncus arteriosus (common arterial trunk)
obstruction examples
coarctation of the aorta
valvular stenosis or atresia
effects of left to right shunt
increased pulm blood flow
not initially associated with cyanosis
chronically elevates both V and P in pulm circulation, leading to medial hypertrophy of pulmonary arteries and vasoconstriction
RVH results
end stage of left to right shunt
Eisenmenger syndrome
pulmonary resistance approaches systemic levels
left to right shunt becomes a right to left shunt
effects of right to left shunt
pulmonary circulation is bypassed, thus decreasing pulmonary blood flow
poorly oxygenated venous blood enters the systemic arterial system
hypoxia and cyanosis results
paradoxical embolism
emboli from venous circulation bypass the lungs and enter the systemic circulation
happen in right to left shunts
