Umbilical cord pulsating. Theory and practice.

Dear colleagues! Allow me to share a brief observation that may explain some physiological and pathophysiological aspects of placental and umbilical cord circulation. Like everyone else, I was convinced of the arterial origin of umbilical cord pulsation. This is partially true, but not entirely true. With careful and relatively prolonged observation of umbilical cord pulsation, you can detect two stages of pulsation cessation. The first is associated with the cessation of arterial blood flow and the cessation of umbilical cord arterial pulsation. The second is manifested by the cessation of slow, weak pulse waves, resulting from the maternal blood flow pulse wave and the pulsation of the placental lacunae, and, as a result, umbilical vein pulsation. This type of placental circulation ceases with placental separation. Little attention has been paid to the second type of pulse waves in the umbilical vein. So how does venous placental blood flow to the fetus? The following factors contribute: the pumping function of the heart, the kinetic energy transferred from the pulsating umbilical arteries to the walls of the umbilical vein, and the pulsating energy of the uterine arteries and placental lacunae, which generates a pulse wave in the umbilical vein. The final waves of umbilical pulsation are like the mother's final letter, after which mother and child will be finally physically separated. Thus, these two types of pulsation are equivalent to the negative intrathoracic pressure created by inspiratory efforts.

Based on this observation, it seems to me that the mechanism for the development of distress is more obvious in the presence of a single umbilical artery or thrombosis of one of the two umbilical arteries, as one artery cannot generate sufficient kinetic energy for umbilical venous return. This is especially true in the presence of excessive umbilical vessel tortuosity, endothelial damage (for example, during meconium passage), or slowed umbilical cord blood flow (for example, when the umbilical cord is wrapped around the fetus's neck, torso, and limbs).

Previously, I was convinced that the physiologically justified time for delayed cord clamping and effective placental transfusion is the cessation of pulsation in the umbilical arteries. Cessation of arterial pulsation reflects recruitment and the establishment of sufficient blood flow in the pulmonary vessels. Now, I believe, given the right conditions, the physiologically justified time for umbilical cord clamping is separation of the placenta.

The process of evolution is very rational. An example of this is the Hyrtla anastomosis, which is characteristic of New World primates and human fetuses. The blood volume in the placenta is likely identical to the volume of pulmonary vessels, and physiologically justified, personalized, delayed cord clamping will prevent circulatory disturbances and associated complications (such as significant ductus arteriosus, intraventricular hemorrhage, and necrotizing enterocolitis) in a significant proportion of premature infants.

Thank you for your attention.

Sincerely, Alex Nouzdin