Fetal Circulation

Fetal Circulation: Overview Fetal circulation flows as follows: Venous blood from the fetus leaves the fetus and enters the placenta in the umbilical ARTERIES (yes, arteries!). The placenta is where gas exchange takes place between maternal and fetal blood. There are two key differences between gas exchange in the placenta versus the lung. First, diffusion of O2 in the placenta is DIFFUSION limited. This means that the limiting factor in O2 extraction for the fetus IS NOT the volume of blood that arrives at the placenta for gas exchange. In other words, more “fresh” blood to the placenta from the mother will NOT really impact how much O2 the fetus can actually acquire via gas exchange. This brings us to the second difference between lung and placental gas exchange. In order to COMPENSATE for this diffusion-limitation in the placenta, the fetus is equipped with a special fetal hemoglobin molecule that is “left-shifted” with respect to adult hemoglobin. This means that fetal hemoglobin can “soak up” more O2 than adult hemoglobin at any given O2 partial pressure. Now, as far as flow is concerned, “fresh” blood from placenta leaves exits the placenta via the umbilical vein en route to the liver. Upon arriving at the liver, this blood is actually shunted away from liver circulation straight to the inferior vena cava where it can then enter the right heart. Some blood remains in the right heart, while some continues through the FORAMEN OVALE and into the LEFT HEART at which point it will be ejected into systemic circulation via the aorta. Now, we should look at the portion of blood that remains in the right heart (as opposed to flowing through the foramen ovale). This blood enters the right heart, and is pumped into pulmonary circulation by way of the PULMONARY ARTERY. However, instead of going to the lungs, most of this blood traveling in the pulmonary artery “RE-ENTERS” systemic circulation. It is able to do this because the wall of the pulmonary artery has a HOLE in it called the DUCTUS ARTERIOSUS through which blood can bypass the lungs and flow directly into the aortic arch and the systemic circulation thereafter. The cycle repeats itself once blood perfuses the tissues and the venous blood again arrives to the placenta via the umbilical arteries!

Fetal Circulation: Parturition Uterine contractions squeeze head and body thereby expelling fluid from fetal lung. Subsequent contractions deliver the placenta thereby severing connection between fetal and maternal blood supply. During birthing process, placental capillaries are crushed, and thus the fetal systemic circuit’s resistance goes up almost 2 fold. (remember: placental circ. WAS about HALF of TOTAL fetal circ., thus removing this parallel circuit would DOUBLE resistance)

Fetal Circulation: Parturition Contd. Assuming that CO remains the same, doubling resistance should also double the pressure within fetal circulation (by P=QR) Also, another effect of increasing R is that this briefly DECREASES movement of blood into the IVC, which results in a decrease in RIGHT ATRIAL PRESSURE! Now, pressure in LEFT atrium is higher than right, and so flow of blood through foramen ovale stops! (See pic to visualize this)

Fetal Circulation: Parturition Contd. Flap of tissue in Left Heart covers up the Foramen Ovale. Now even LEFT to RIGHT blood flow (due to reversal of relative atrial pressure) cannot take place. As a result, RV output can ONLY enter the pulmonary artery.

Fetal Circulation: First Breath Post-birth, pO2 goes down while pCO2 goes up (this is new to the baby); this is sensed by chemorecs and initiates first breath. Also, breathing may be influenced by gasps due to “startle reflex”. (baby is startled upon seeing new things etc…and so gasps, which helps with first breath too) The loss of “immersion reflex” may influence breathing. (immersion reflex = if underwater, as in utero, drive to breathe goes down. Post birth, this inhibition is removed, thus baby tries to breathe)

Fetal Circulation: First Breath Contd. Need to generate 80cm of water worth of pressure to establish alveolar liquid-air interface upon first breath. Need to therefore decrease INTRATHORAIC (IT) pressure by a lot via contraction of diaphragm and external intercostals. This decrease in IT pressure not only allows enough of a pressure gradient to breathe, but also elicits MAJOR changes in circulation.

Fetal Circulation: First Breath Contd. When IT pressure is decreased, the pressure in lungs goes down too, SO…there is less pressure surrounding the pulmonary vessels as well (think about this…) Because of this, there is now a greater difference in pressure between right ventricle (we didn’t do much to P here) and pulmonary vessels (P went down here). This difference now allows for more blood to flow through these vessels since they are now more dilated

Fetal Circulation: First Breath Contd. Now, vessels exhibit HIGH FLOW and LOW RESISTANCE properties characteristic of adult pulmonary circulation. Also, since you are now oxygenating the alveoli, you release the hypoxia-induced vasoconstrictive tendencies which were predominant during fetal circulation.

Fetal Circulation: First Breath Contd. As breathing continues, a greater % of blood from the RV enters the pulmonary circulation. This increases FLOW to the LEFT ATRIUM, which causes an increase in LA pressure. (this increase in LA pressure also prevents movement of blood from RA to LA via a patent foramen ovale…critical because it prevents venous blood from mixing with arterial blood!!!)

Fetal Circulation: Ductus Arteriosus (DA) Since blood flow through lung increases after birth, so does return of blood to the LA and, by extension, to the LV!!! Increase in blood flow to LV, via STARLING FORCES, increases LV contractility. This increases aortic systolic pressure. Increase in aortic pressure prevents blood moving from RIGHT to LEFT into the DA (see pic!!!).

Fetal Circulation: Ductus Arteriosus (DA) DA acts like other systemic vessels; that is, when introduced to high O2 environments, they CONSTRICT. Thus, when pulmonary circulation improves after birth, P02 increases as well. Thus, the DA constricts!!! Prostacyclins prevent the constriction of the DA. One way to treat patent DA is to administer a prostacyclin synthesis inhibitor such as INDOMETHICIN.

Fetal Circulation: Ductus Arteriosus (DA) LAST NOTE: During fetal circ, RV pressure is higher than LV pressure because of reasons already discussed (hypoxic vasoconstriction, we haven’t decreased IT pressure yet, fluid surrounding the lungs in utero etc…) After birth, this all reverses such that LV pressure is greater than RV pressure. You will therefore see a switch from a thick RV wall during fetal life to a thick LV wall during adult life. (ie. Wall thickness reflects pressure levels…since muscle grows in response to work…and work = PRESSURE * Volume)