Changes in the baby's circulation at birth

2021-06-09 01:39 PM

The fundamental changes in the foetal circulation at birth are described in relation to congenital abnormalities of the ductus arteriosus and foramen ovale that persist throughout the life of a few individuals.

The fundamental changes in the foetal circulation at birth are described in relation to congenital abnormalities of the ductus arteriosus and foramen ovale that persist throughout the life of a few individuals.

The changes are briefly described in the following sections.

Decreased respiration and increased vascular resistance at birth

The major changes in the circulation at birth are, first, the loss of a lot of blood through the nahu, which is approximate twice the resistance of the vascular system at birth. The doubling of vascular resistance increases the aortic systolic pressure, as well as the pressures of the left atrium and right atrium.

Second, the resistance of the pulmonary vessels is greatly reduced when the lungs are dilated. When the foetal lungs are not dilated, blood vessels are compressed because the lungs are small in volume.

As soon as the lungs are dilated, the vessels are no longer compressed, and the vascular resistance is reduced by about 7 times. Likewise, during foetal life, hypoxemia causes a marked increase in the contractile tone of the pulmonary vessels, but vasodilation occurs when pulmonary ventilation cancels the hypoxic effect. All of these changes together reduce pulmonary blood flow resistance by as much as fivefold, reducing pulmonary artery blood pressure, right ventricular pressure, and left ventricle pressure.

Close the oval hole

The low right atrial pressure and high left atrial pressure that occur shortly after the changes in pulmonary and systemic vascular resistance at birth cause blood now to tend to flow backwards through the foramen ovale, that is, from the heart. the left atrium into the right atrium instead of going in the other direction as in the foetal stage. As a result, the small valve located on the foramen ovale on the left atrial septum closes the foramen, thereby preventing blood flow from continuing through the foramen ovale.

In two-thirds of people, the valve becomes adherent to the foramen ovale within a few months to a few years and permanently closes the foramen ovale. However, if permanent closure of the foramen ovale does not occur—a condition known as foramen ovale—for life, the left atrial pressure will normally remain 2-4 mm Hg higher than the right atrial pressure. and backpressure keeps the valve closed.

Close the ductus arteriosus

The ductus arteriosus is also closed, but for different reasons. First, increasing systemic circulatory resistance increases aortic pressure while decreasing pulmonary resistance decreases pulmonary artery pressure.

Consequently, after birth, blood flow begins to back up from the aorta into the pulmonary artery through the ductus arteriosus, instead of in the opposite direction as in the foetal stage. However, only a few hours after birth, the muscular wall of the ductus arteriosus constricts markedly, and in just 1-8 days, muscle contraction is usually sufficient to stop all blood flow. This is also known as functional closure of the ductus arteriosus. Then, during the following 1 to 4 months, the arterial pile often becomes anatomically blocked by the proliferation of fibrous tissue into its lumen.

The cause of ductus arteriosus is related to increased oxygenation of the tubular blood flow, as well as loss of the vasodilator effects of prostaglandin E2 (PGE2). During foetal life, the partial pressure of the ductus arteriosus (PO2) is only 15-20 mmHg, but it rises to about 100 mmHg within a few hours of birth. Furthermore, many experiments have shown that the smooth muscle contraction of the ductus arteriosus is strongly related to the availability of O2.

In about one in several thousand neonates, the duct is not closed, causing ductus arteriosus, the consequences of which have been described. Failure to close the ductus arteriosus is due to excessive ductal dilation caused by vasodilatory prostaglandins, especially PGE2, on the duct wall. In fact, when indomethacin is used, they block the synthesis of prostaglandins that normally lead to the closure of the ductus arteriosus.

Close the venous tube

During the foetal life portal blood from the foetal abdomen fuses with blood from the umbilical vein, and they both bypass the liver by the ductus venosus directly into the inferior vena cava just below the heart and above the liver.

Immediately after birth, blood through the umbilical vein stops, but most portal blood remains through the ductus venosus, with only a small amount passing through the hepatic channels. However, within 1-3 hours, the muscular wall of the ductus arteriosus contracts strongly and closes the ductus arteriosus. Consequently, portal pressure increases from nearly 0 to 6 to 10 mmHg, which is sufficient to push portal blood flow through the hepatic sinuses. Although the ductus arteriosus is rarely unclogged, we know very little about the causes of venous closure.