The maternal syndrome of preeclampsia is mediated by placental syncytiotrophoblast (STB), when this is stressed by uteroplacental malperfusion or other pathology. As part of a highly coordinated stress response it releases pro-inflammatory and dysangiogenic signals to the preeclamptic mother, which to stimulate a stronger vascular inflammatory response than normal, with an antiangiogenic bias. Two broad subtypes of pre-eclampsia are recognised of early and late onset, best defined by the time of delivery (<34 weeks (early), > 37 weeks (late), with 34-37 weeks as a transitional zone with attributes of both). Placentally derived angiogenic factors are used as preeclampsia biomarkers. They are least effective for prediction and diagnosis of late onset disease. However, as markers of STB stress, their physiological changes at term demonstrate that STB stress develops in all pregnancies. The biomarkers reveal that the duration of pregnancies is restricted by placental capacity, such that there is increasing placental dysfunction, at and beyond term. This could capacity include limitations imposed by the size of the uterus, the capacity of the uteroplacental circulation and, possibly, the supply of villous progenitor trophoblast cells. Limited placental capacity explains the increasing risks of post-maturity, including preeclampsia. Early-onset preeclampsia is predictable because there is early pregnancy pathology, namely poor placentation, and early STB stress. Prediction of preeclampsia at term is not effective because there is no early STB pathology. Moreover, biomarkers cannot accurately diagnose term preeclampsia against a background of universal STB dysfunction, which may or may not be clinically revealed before spontaneous or induced delivery. In this sense, post-term pregnancy is, at best, a pseudo normal state. However, the markers may prove useful in screening for women with more severe problems of post maturity.