Fetal heart rate variability reflects the interplay between the sympathetic and parasympathetic nervous systems, with moderate variability (6 to 25 bpm fluctuation) indicating adequate oxygenation and intact central nervous system function. Late decelerations result from uteroplacental insufficiency causing transient fetal hypoxemia during contractions, triggering a chemoreceptor-mediated vagal response that slows the heart rate after the peak of the contraction. Postpartum hemorrhage pathophysiology centers on failure of the myometrium to contract adequately after placental separation, leaving spiral arteries at the placental site open and bleeding; this accounts for approximately 80 percent of cases attributed to uterine atony. Eclamptic seizures arise from cerebral vasospasm and endothelial dysfunction in the setting of severe preeclampsia, with magnesium sulfate acting as a central nervous system depressant and vasodilator to raise the seizure threshold.