Fetal compromise develops when fetal oxygen supply is reduced, fetal oxygen demand increases, or fetal compensatory mechanisms fail. The pathophysiology depends on timing and mechanism. In chronic placental insufficiency, the placenta cannot deliver adequate oxygen and nutrients over time. This may occur with hypertensive disorders, pre-existing diabetes with vascular disease, fetal growth restriction, renal disease, autoimmune disease, smoking, substance use, or abnormal placentation. The fetus may adapt by reducing growth velocity, decreasing movement, conserving energy, and redistributing blood flow. Ultrasound may show fetal growth restriction, oligohydramnios, abnormal Doppler studies, or reduced biophysical activity. In acute uteroplacental insufficiency, oxygen transfer suddenly drops. Examples include placental abruption, uterine rupture, severe maternal hypotension, maternal hypoxemia, cord prolapse, sustained uterine tachysystole, or a catastrophic maternal event such as seizure, trauma, hemorrhage, or cardiac arrest. Acute compromise may present with sudden fetal bradycardia, recurrent late decelerations, absent variability, maternal abdominal pain, vaginal bleeding, shock, or a change in contraction pattern. In cord-related compromise, the issue is intermittent or sustained obstruction of fetal blood flow through the umbilical cord. Variable decelerations are classically associated with cord...