Fetal oxygenation

Research Article

Abstract

This review focuses on the role of oxygen and the changes in oxygen levels in pregnancy in the human placenta. In the first trimester, the physiological conversion of the spiral arteries restricts maternal blood flow into the intervillous space creating a low oxygen environment for the trophoblast and the embryo. In the second trimester, progressive conversion of the spiral arteries allows unhindered entrance of maternal blood into the intervillous space. In early pregnancy, pathology of spiral artery conversion may promote premature flow of maternal blood resulting in miscarriage. In more advanced pregnancy, incomplete conversion of spiral arteries impairs maternal blood flow to the placenta, causing chronic hypoxia and growth restriction of the fetus. Chronically reduced maternal supply of oxygen to the placental-fetal unit may be partially balanced by metabolic reprogramming of the placenta. Acute impairment of oxygenation in the perinatal period and its effect on the placental-fetal unit will also be discussed. Uterine contractions in labor result in a 60% reduction in uteroplacental perfusion, causing transient fetal and placental hypoxia. A healthy term fetus with a normally developed placenta is able to accommodate this transient hypoxia by activation of the peripheral chemoreflex, resulting in a reduction in oxygen consumption and a centralization of oxygenated blood to critical organs, namely the heart, brain, and adrenals. Providing there is adequate time for placental and fetal reperfusion between contractions, these fetuses will be able to withstand prolonged periods of intermittent hypoxia and avoid severe hypoxic injury. However, there exists a cohort of fetuses in whom abnormal placental development in the first half of pregnancy results in failure of endovascular invasion of the spiral arteries by the cytotrophoblastic cells and inadequate placental angiogenesis. This produces a high-resistance, low-flow circulation predisposing to hypoperfusion, hypoxia, reperfusion injury, and oxidative stress within the placenta. Furthermore, this renders the placenta susceptible to fluctuations and reduction in uteroplacental perfusion in response to external compression and stimuli (as occurs in labor), further reducing fetal capillary perfusion, placing the fetus at risk of inadequate gas/nutrient exchange. This placental dysfunction predisposes the fetus to intrapartum fetal compromise. In the absence of a rare catastrophic event, intrapartum fetal compromise occurs as a gradual process when there is an inability of the fetal heart to respond to the peripheral chemoreflex to maintain cardiac output. This may arise because of placental dysfunction reducing pre-labor myocardial glycogen stores necessary for anaerobic metabolism or due to an inadequate placental perfusion between contractions to restore fetal oxygen and nutrient exchange. If the hypoxic insult is severe enough and long enough, profound multiorgan injury and even death may occur. This review provides a detailed synopsis of the events that can result in placental dysfunction, how this may predispose to intrapartum fetal hypoxia, and what protective mechanisms are in place to avoid hypoxic injury.