Umbilical cord clamping at birth has a major impact on an infant s cardiovascular system that varies in significance depending upon whether the infant has commenced breathing. As umbilical venous return is a major source of preload for the left ventricle during fetal life, recent experimental evidence has shown that clamping the umbilical cord severely limits cardiac venous return in the absence of pulmonary ventilation. As a result, cardiac output greatly reduces and remains low until breathing commences. Once the infant begins breathing, aeration of the lung triggers a large increase in pulmonary blood flow, which replaces umbilical venous return as the source of preload for the left ventricle. As a result, cardiac output markedly increases, as indicated by an increase in heart rate immediately after birth. Thus, infants born apnoeic and hypoxic and have their cords immediately clamped, are likely to have a restricted cardiac output combined with hypoxia. As increased cardiac output is a major physiological defence mechanism that counteracts the effects of hypoxaemia, limiting the increase in cardiac output exposes the infant to ischaemia along with hypoxia. However, if the infant commences breathing, aerates its lungs and increases pulmonary blood flow before the umbilical cord is clamped, then pulmonary venous return can immediately take over the supply of left ventricular preload upon cord clamping. As a result, there is no intervening period of reduced preload and cardiac output and the large swings in arterial pressures and flows are reduced leading to a more stable circulatory transition.
|Pages (from-to)||355 - 360|
|Number of pages||6|
|Journal||Archives of Disease in Childhood: Fetal and Neonatal Edition|
|Publication status||Published - 2015|