In this article we will discuss about the changes that take place in the fetal circulation of blood at birth: 1. Primary Changes in Pulmonary and Systemic Vascular Resistance 2. Closure of the Foramen Ovale 3. Closure of the Ductus Arteriosus 4. Closure of the Ductus Venosus.
1. Primary Changes in Pulmonary and Systemic Vascular Resistance:
First, loss of the tremendous blood flow through the placenta approximately doubles the systemic vascular resistance at birth. This increases the aortic pressure as well as the pressure in the left ventricle and left atrium.
Second, the pulmonary vascular resistance greatly decreases as a result of expansion of the lungs. In the unexpanded fetal lungs, the blood vessels had been compressed because of the small volume of the lungs. Immediately on expansion, these vessels are no longer compressed and the resistance to blood flow decreases several fold.
Also in fetal life, the hypoxia of the lungs causes considerable tonic vasoconstriction of the lung blood vessels, but vasodilatation takes place when aeration of the lungs eliminates the hypoxia. All these changes together reduce the resistance to blood flow through the lungs as much as five-fold, which reduces the pulmonary arterial pressure, right ventricular and right atrial pressure.
2. Closure of the Foramen Ovale:
The low right atrial pressure and the high left atrial pressure that occur secondarily to the changes in pulmonary and systemic resistances at birth cause blood now to attempt to flow backward through the foramen ovale, i.e. from left atrium into right atrium. Consequently, the small valve that lies over the foramen ovale on the left side of the atrial septum closes over this opening, thereby preventing further flow through the foramen ovale.
In 2/3rds, the valve becomes adherent over the foramen ovale within a few months to a few years and forms a permanent closure. But even if permanent closure does not occur, the left atrial pressure throughout life remains 2-4 mm Hg more than the right atrial pressure and the back pressure keeps the valve closed.
3. Closure of the Ductus Arteriosus:
First, increased systemic resistance elevates aortic pressure; while decreased pulmonary vascular resistance reduces pulmonary arterial pressure.
As a consequence, afterbirth, blood begins to flow backward from the aorta into pulmonary artery through ductus arteriosus. However, after only a few hours the muscle wall of the ductus arteriosus constricts markedly and within 1-8 days, the constriction is usually sufficient to stop all blood flow. This is called functional closure of the ductus arteriosus. Then, during the next 1-4 months the ductus arteriosus ordinarily becomes anatomically occluded by growth of fibrous tissue into its lumen.
The cause of closure is due to increased oxygenation of the blood flowing through the ductus.
In fetal life PO2 ― 15-20 mm Hg
After birth ― 100 mm Hg
The degree of contraction of the smooth muscle in the ductus wall is highly related to the availability of O2.
Bradykinin constricts umbilical vessels and ductus arteriosus while dilating the pulmonary vascular bed. Failure of closure leads to patent ductus arteriosus.
In some instance, cause may be due to the effect of prostaglandins—vasodilatation. The treatment is Indomethacin (prostaglandin inhibitor).
4. Closure of the Ductus Venosus:
In fetal life, the portal blood from the fetus’s abdomen joins the blood from the umbilical vein, and then together passes through the ductus venosus directly into the vena cava, thus bypassing the liver. Immediately after-birth, blood flow through the umbilical vein ceases, but most of the portal blood still flows through the ductus venosus, with only a small amount passing through the channels of the liver.
However, within 1-3 hours, the muscle wall of ductus venosus contract strongly and closes this venue of flow. So, portal venous pressure rises from ‘0’ to 6-10 mm Hg, which is enough to force blood flow through the liver sinuses.
Closure of ductus arteriosus before birth causes pulmonary hypertension.