Is the placenta efficient or inefficient compared to the lung at gas exchange?
inefficient
fetal blood distribution max’s what?
02 delivery to vital tissues (heart, brain)
what % of cardiac output do cardiac lungs receive? why?
5-8%. because of high pulm vascular resistance.
in the fetus, the umbilical vein is ox or deox?
ox from placenta
regulation of pulm vascular resistance: what causes vasoconstriction?
generally: mechanical means, 02, hormones from arachodonic acid.
- low 02 and low pH (remember this is pulm so it is backwards in terms of pH)
- leukotrienes
- thromboxane A2
regulation of pulm vascular resistance: what causes vasodilation?
mostly endothelial-derived.
what structures does the ductus arteriosus connect?
connects pulm artery and aorta. allows oxygenated blood from the placenta to pass directly into systemic circ.
what keeps the ductus open?
prostaglandin E2 keeeeeeeps the ductus open!
what makes the ductus close? think about where it is produced.
the absence of PGE2 allows the ductus to close… PGE2 is made in the placenta, cleared by the fetal lung
what is ET1? what does it do?
endothelin 1, major constrictor of the ductus arteriosus.
for term infants, how does the ductus close?
functional closure with smooth muscle vasoconstriction within hours of birth. local action.
anatomic occlusion over days with intimal thickening and loss of smooth muscle cells from inner muscle media
what are the molecules responsible for closing the ductus?
02 appears to be ultimately responsible.
incr in P02 increases for formation of ET-1.
ET-1 promotes constriction, overcomes the dilating effects of PGE2/NO
also, removal of the placenta decreases the concentration of PGE2
what are some physiological changes that cause changes in pulmonary vasc at birth?
fetal circulation pattern turns into what? which turns into what?
fetal –> transitional –> neonatal
what are characteristics of the transition from fetal to transitional circ?
what forces characterize the transition from transitional to neonatal circulation?
what are 2 categories of failure to transition?
persistence of fetal circulation, and a patent ductus arteriosus
what can cause a delay in the decrease in pulm vascular resistance?
definition of asphyxia?
failure of gas exchange: low Pa02, high PaC02
what happens during perinatal asphyxia (leading to persistence of fetal circ?)?
clinical presentation of a neonate with hypoxia due to a decr in pulm blood flow?
cyanosis, low 02 sat, incomplete correction in Pa02 when breathing 100% 02. (basically due to a shunt)
describe the hyperoxia test
allows you to tell is a problem in pa02 is due to a shunt (persistence of fetal circ) or due to a problem with gas exchange in the lung.
if due to PFC, giving 100% 02 won’t help. if due to a problem of incomplete gas exchange in the lung, it will raise Pa02.
why might a pulm vasc bed not develop properly?
congenital pulm hypoplasia, secondary pulm hypoplasia (diaphragmatic hernia, neuro causes of decr fetal breathing)
why might there be functional obstruction to neonate lungs?
polycythemia with incr viscosity decr pulm blood flow.
polycythemia is high levels of RBCs in blood, seen w mothers with gestational diabetes