ANATOMY AND PHYSIOLOGY OF MATERNAL FETAL CIRCULATION

ANATOMY AND PHYSIOLOGY OF MATERNAL FETAL CIRCULATION

          Pregnancy is a high-flow, low resistance state of cardiovascular hemostasis associated with remarkable hemodynamic changes. A progressive fall of vascular resistance in the uterine, placental and umbilical arteries is evident with increasing gestational age, producing high end-diastolic flow (Kurjak et al., 1991).

Uteroplacental Circulation:

          The main uterine artery is a branch of the internal iliac artery. At the level of the internal os of cervix, it bifurcates into the descending (cervical) and ascending (corporal) branches. At the uterine tubal jundion, the ascending branch anastomoses with the ovarian artery to form an arterial arcade. The tortuous ascending uterine artery gives off approximately eight branches of arcuate arteries, which then traverses the outer one-third of the myometrium.

          The impedance to blood flow in both uterine arteries decreases gradually from early pregnancy until the end of second trimester. More dramatic changes occur in the second trimester, when the uterus begins to grow rapidly, thereby uncoiling the main uterine and spiral arteries. Between 26 and 28 weeks of gestation, uterine arteries reach their maximal dilatation and minimal resistance (Thaler et al.1990).

          The uroplacental flow increases throughout pregnancy from approximately 50 mI/mm during early pregnancy up to 450-600ml/mm near term. During normal pregnancy, the trophobiastic cells enter the lumen of the spiral arteries, partially replacing the endothelium and progressing down up to the level of the endometrium. By 16-22 weeks gestation, trophoblasts migrates along the entire length (intramyometrial portion) of the spiral arteries and strips it of its muscular elastic coat (Brosens et al.,1983)

          This transformation leads to formation of a low resistance vascular system, progressing from the radial artery into the intervillous spaces, the pressure falls about 70 to 80 mm Hg in the former to 10 mm Hg in the latter.

Fetoplacental Circulation:

          During fetal life oxygenation is carried out in placenta. The tortuous umbilical cord is the lifeline of fetus. It has two umbilical arteries and one umbilical vein. A considerable amount of oxygenated blood returning from the placenta through the umbilical vein is directed through the ductus venosus to the inferior vena cava into the right atrium, through the foramen ovale, this oxygenated blood is directed to the left atrium and then to the left ventricle.

          Blood from the right ventricle is ejected either into the pulmonary circulation or through the ductus arteriosus into the descending aorta. About 50% of the blood flow through the aorta passes back to the placenta via the umbilical arteries (Campbell et aL,1995) Elk Nes et al, 1980).

          Blood flow through the fetal heart is “parallel” rather than “serial” because of the presence of ductus arteriosus between the pulmonary trunk and the aorta. Both the ventricles eject blood into the aorta simultaneously rather than blood moving first through the right ventricle, then the pulmonary circulation, and finally the left ventricle as in the adult.

          The blood returns to the fetus by the umbilical vein, emptying into the portal sinus. Then the major portion of the blood passes through ductus venosus to inferior vena cava, just before it enters into the right atrium.

          About 50% of inferior vena caval blood passes directly through the foramen ovate into the left atrium to mix up with pulmonary blood and then enters the left ventricle. Well oxygenated blood from the left ventrkie is directed through the ascending aorta to supply the coronary arteries and the upper body organs, thus preferentially perfusing the brain. This blood enters pulmonary artery, which is in direct continuity with descending aorta via ductus arteriosus and perfuses the lower body and placenta.

The increase of how is attributed to:

1. Increase in intravascular bed in the fetal villi in mid pregnancy, reduction in the thickness of tissue layer between the fetal capillaries and maternal intervillous spaces.
2. To a rise in the fetal arterial pressure in late pregnancy.

          A diastolic component in the umbilical artery flow velocity waveform appears during the early second trimester and the resistance continues to decline until term (Schulman et al 1984).

Fetal Cerebral Circulation:

          The fetal cerebral blood flow is of a high impedance, low flow circulation. )t is a more sensitive parameter of fetal oxygenation status than umbilical blood flow. The increase in the diastolic component as the pregnancy progresses is interpreted as decrease in cerebral resistance due to brain development. This increase in diastolic component begins later in the cerebral arteries (at approximately 25 weeks) than in umbilical arteries (approximately 15 weeks).