Cardiac Pathophysiology in Pediatrics
Fetal Circulation
Placental Oxygenation
We get O2 from the placenta, it comes up through the umbilical vein, thru the
inferior vena cava and into the right atrium then thru the
...
Cardiac Pathophysiology in Pediatrics
Fetal Circulation
Placental Oxygenation
We get O2 from the placenta, it comes up through the umbilical vein, thru the
inferior vena cava and into the right atrium then thru the foramen ovale into
the left atrium, left ventricle, and out to the body
Thru the superior vena cava, where there’s deoxygenated blood returning
from the upper part of the body it travels into the right atrium and gets mixed
with oxygenated blood that came from the placenta via the inferior vena cava.
After entering the right atria some of the blood will leave the right atria
through the tricuspid valve into the RV and some of it can go to the
pulmonary artery (but blood will try to avoid the lungs because in infants the
pressure is very high in the lungs). It avoids the lungs thru use of the ductus
arteriosis shunt, which shunts blood away from high pressured lungs and
instead to the aorta (this blood is oxygenated bc it mixes with the oxygenated
blood that comes from the umbilical vein thru the inferior vena cava into the
right atrium) and to the rest of the body.
(SN: the blood that travels thru the inferior cava can mix with the blood in the
right atria…there is no vessel? It goes thru the foramen ovale (shunts that
diverts blood away from the lung)
Everyone post neonatally- the lungs have low pressure, huge amount of
space, easy to go to.
In fetuses the lung vasculature is very high pressure bc there is no O2 in the
lungs, filled with amniotic fluid. This causes that hypoxic vasoconstriction
response in the lungs- the blood doesn’t want to go to the lungs. It gets
diverted from the lungs ex.
Some blood goes to the lungs. Enough to main perfusion, delivery of O2
Placental oxygenation
o Inferior vena cava, RA, FO, LA, LV, AO
Low arterial oxygenation
o There is mixing of oxygenated and deoxygenated blood which is why
fetal O2 stats are low
o Fetal pO2 30-35 mmHg
o Fetal O2 saturation 60-70%
o Thats why when babies are born, they don’t have a brightly colored
look.
Tissue oxygenation maintained with high cardiac output (the hrtbeat is really
fast. They increase delivery)
o Tachynea and tachycardia are their main methods of compensations
o High cardiac output= tachycardia
o That’s why in infants- slow HR is a very bad things bc it decreases
tissue oxygenation bc they are totally relying on that fast HR for tissue
oxygenation
o There is a left shift of the O2 curve (as well)
One of the biggest factors of O2 transport and delivery is
cardiac output . Ex. HR is the biggest determinant of cardiac
output (refer to figure13- 13 p. 266)
As an adult we don’t have:
Ductus venosus – connection of the umbilical vein with the inferior vena cava
Shunts:
Foramen ovale
Dustus arteriosis
They all close at a certain point
The ductus arteriosus closes at:
A. 12-15 weeks gestation
B. 28-32 weeks gestation
C. Within 12 hours of delivery
D. 24 -72 hours of life
E. Is dependent on the type of delivery
Transitional circulation
Involves the closing of some of these shunts and duct.
SN: Resistance- opposition to passage
Pulmonary vascular resistance (drops dramatically
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