FETAL CIRCULATION
One thing that is usually not made clear when talking about
fetal circulation is why it is specifically set up the way it is. We know that
the placenta, interfacing with mom’s circulation, is acting as a substitute for
the lungs (gas exchange), and the kidneys and intestines (nutrient and waste
exchange). The lungs are full of fluid and consequently have high vascular resistance, so they receive very little of the total amount of
blood pumped out by the heart, while the placenta has low vascular resistance to encourage more blood to flow through it. Fetal hemoglobin also plays a part,
as it has a greater affinity for oxygen, allowing it to load oxygen from the
placenta at the same low O2 saturation that in mom’s adult hemoglobin causes
the unloading of oxygen.
Theoretically, the placenta could perform molecule exchange much like a dialysis machine does, by simply taking
blood from a blood vessel, performing the exchange, and
then delivering the blood back to the systemic circulation via the same or a different vessel. The rest of the
circulation would not need to be any different from an adult’s. But it is.
Because what’s left out of most discussions is that in addition to gas and
nutrient exchange, the fetal circulation is responsible for the preferential
delivery of oxygenated blood to the most important organs; the brain, heart
and liver. Fetal circulation first drops off a significant portion of oxygenated
blood straight to the liver, and then shunts the remainder of oxygenated blood
directly to the brain and heart, while it shunts deoxygenated blood past
these organs. And this requires three modifications:
1. Ductus venosus (connects umbilical vein directly to the
IVC)
2. Foramen ovale (an opening between the shared wall of the
left and right atria)
3. Ductus arteriosus (connecting the pulmonary artery to the
descending aorta)
Fresh, oxygenated, nutrient-rich blood coming from the
placenta via the umbilical vein is divided up between the developing liver and the ductus
venosus, which connects to the IVC. This blood from the IVC streams across the
right atrium, and is shunted straight through the foramen ovale to the left
atrium, where it ends being pumped by the left ventricle to the aortic arch,
directly perfusing the brain and heart.
At the same time, the deoxygenated blood from the rest of
the body sluggishly enters the right atrium, via the SVC and the IVC distal to
the ductus venosus. This blood ends up getting pumped by the right ventricle
into the pulmonary artery. Most of it bypasses the lungs and the aortic arch
via the ductus arteriosus, and then mixes with the highly oxygenated blood from
the aortic arch at the descending aorta, to perfuse the rest of the body.
To recap, despite the fact that highly oxygenated blood from
the placenta enters the the right atrium via the IVC, the same place where the
rest of the systemic circulation ALSO enters via the SVC and IVC, the anatomy actually
encourages ‘preferential streaming’ of the highly oxygenated blood through the
foramen ovale into the left atrium and consequently to the brain and
myocardium. The deoxygenated blood from the systemic circulation bypasses the
aortic arch, therefore never reaching the brain. They only come together at the
descending aorta after the brain and heart have received the most oxygen-rich
blood, perfusing the rest of the body and flowing via the umbilical arteries
back to the placenta, where CO2 and waste products are removed, and O2 and
nutrients are picked up.
DUCTAL DEPENDENT LESIONS
After birth, fluid in the lungs is cleared and placental
circulation is clamped off. Pulmonary vascular resistance decreases, and blood
starts flowing into the pulmonary artery, causing a decrease in RA pressure.
Blood from the lungs returns to the LA via the pulmonary vein, increasing
pressure there. As RA pressures decrease and LA pressures increase, the right to left flow across the foramen ovale and ductus arteriosus decreases, and they both close off soon after
birth. The right side of the heart pumps blood to the lungs, the left side to the rest of the body, and congenital heart lesions (structural/anatomic defects of the heart and major blood
vessels) involve problems with how these two parts of the circulatory system, driven by different sides of the heart, connect. These lesions can be broken down into three functional categories:
1. circulation bypasses the lungs
(pulmonary
stenosis, pulmonary atresia, tricuspid atresia, tetralogy of fallot)
2. circulation bypasses the body
(aortic stenosis, aortic coarct,
hypoplastic left heart syndrome)
3. circulation between the lungs and the body is completely
disconnected
(transposition
of the great arteries)
Lesions in all three of these categories can cause parts of
the body to not receive any oxygenated blood, evident as cyanosis, and some of these
lesions are termed ‘ductal dependent’. This means that the effects of the lesion (poor or no mixing of the two parts of the circulatory system) are
mitigated while the ductus arteriosus remains open, (maintaining some mixing
of the pulmonary and systemic circulation).*
If a neonate develops cyanosis or dyspnea that is not
responsive to supplemental oxygen, then the differential includes problems with
oxygen delivery (i.e. lung issue) or problems with circulation itself. This is
when it becomes important to assess whether the infant has a ductal dependent
heart lesion. Aside from getting an echocardiogram to evaluate the lesion, this
is done by monitoring preductal and postductal oxygen saturations, i.e. pulse
oximetry of a preductal extremity (one that is supplied by the aorta proximal
to where the ductus arteriosus inserts, classically the right arm but also the
left) and a postductal extremity (one of the lower legs). A difference of
>10% O2 saturation between the two extremities indicates that they are
likely getting blood from different parts of the circulation, and the ductus
arteriosus is still patent. If there is cyanosia AND the test is positive (i.e. there is an actual difference in oxygen saturations between the extremities),
there is a high chance that they have a ductal-dependent cardiac lesion. This means that any worsening cyanosis signifies relative hypoxia of those parts of the
body that will soon be getting only deoxygenated blood if the ductus arteriosus
closes off completely.
Identifying a ductal dependent lesion is important because
we can do something about it: we can medically prevent the ductus from closing
using a continuous IV infusion of Prostaglandin E, which relaxes the smooth
muscle in the walls of the vasculature. Consequently one of the major side
effects of PGE is hypotension, and the infant has to be observed closely while
on the drip, with resuscitative fluids and inotropes available. Usually they
will require intubation and ventilation as the other major side effect is
apnea. (NSAIDS inhibit the COX enzymes that make prostaglandins, so they are absolutely contraindicated.)
*Note that just as lesions are ductal dependent, many lesions are only compatible with life due to additional shunts between the right/pulmonary and left/systemic circulation, e.g. atrial and ventricular septal defects.
