Umbilical cord prolapse constitutes an acute interruption of the fetal lifeline. The umbilical vein (carrying oxygenated blood at PaO2 ~30 mmHg) is the sole source of fetal oxygenation. Complete occlusion produces fetal bradycardia within seconds via vagal reflex, followed by metabolic acidosis (pH drop of 0.04/min of total occlusion). At 10 minutes of complete occlusion, fetal pH approaches 7.0 with base excess exceeding -12 mEq/L, producing irreversible hypoxic-ischemic encephalopathy. Partial intermittent compression during contractions produces variable decelerations that worsen progressively. The clinician must recognize risk factors preemptively, order controlled amniotomy when indicated, manage the acute emergency pharmacologically, and determine delivery timing and method based on clinical urgency and fetal status.