Cardiorespiratory effects of delayed cord clamping

While umbilical cord clamping (UCC) at birth is considered to be an innocuous act, whether or not it is depends upon when it occurs during the infant’s transition to newborn life. Before birth, the placenta receives a large proportion of cardiac output and is the site of fetal gas exchange. As such, umbilical venous return provides highly oxygenated blood for the fetus and is a major source of preload for cardiac output, particularly for the left ventricle. This is because fetal pulmonary blood flow (PBF) is low so the left ventricle depends upon umbilical venous return to sustain its output, which flows via the foramen ovale into the left atrium. At birth, aeration of the lungs not only allows the lungs to take over the role of gas exchange, but by stimulating a large increase in PBF, it also allows pulmonary venous return to replace umbilical venous return as the main source of left ventricular preload. Consequently, UCC before lung aeration not only separates the infant from its gas exchange organ, but also deprives the left ventricle of preload. This understanding provides the rationale for delaying UCC until after the infant has initiated air-breathing and explains much of the beneficial cardiovascular effects of delayed UCC. However, the debate about the timing of UCC has almost entirely focused on the concept of a time-dependent placental transfusion after birth; a process that is complex and difficult to explain physiologically. As it is possible that in some circumstances the infant may lose blood to the placenta, it is important to understand the underlying factors determining the distribution of blood between the infant and placenta during delayed UCC to avoid this situation. Whatever the mechanisms, we now know that labor and vaginal birth are major determinants of this distribution. As such, it is possible that “placental transfusion” is the act of rebalancing the blood volume distribution between infant and placenta during following vaginal birth.