Fetal compromise usually develops when oxygen delivery is reduced, oxygen demand is increased, or fetal compensatory mechanisms fail. Early in compromise, the fetus redistributes blood flow toward vital organs such as the brain, heart, and adrenal glands. This compensation may preserve oxygenation temporarily, but it is not unlimited. During contractions, uterine blood flow normally decreases transiently. A healthy fetus tolerates this because placental reserve and fetal oxygen stores are adequate. When placental reserve is limited, repeated contractions can lead to progressive hypoxemia. Hypoxemia means reduced oxygen in the blood. If hypoxemia persists, anaerobic metabolism increases, lactic acid accumulates, and fetal metabolic acidosis develops. Acidemia is clinically important because it increases the risk of neonatal encephalopathy, low Apgar scores, need for resuscitation, and long-term neurologic injury. Different fetal heart rate patterns reflect different mechanisms. Early decelerations usually occur with fetal head compression and are generally benign when variability is normal. Variable decelerations usually reflect umbilical cord compression. Late decelerations reflect uteroplacental insufficiency because the fetal heart rate decreases after the peak of the contraction, when fetal oxygenation is most stressed. Prolonged...