Uterine contraction
→ compression of the fetal head, especially during descent
→ transient rise in intracranial pressure and alteration in cerebral blood flow
→ stimulation of medullary vagal centers, similar to a Cushing-type reflex
→ increased vagal outflow to the fetal heart
→ gradual fetal bradycardia (early deceleration).

Because head compression increases and resolves in step with the contraction, the FHR tracing is a smooth, symmetrical mirror image:

It is usually a physiological, benign vagal reflex and is not ordinarily due to fetal hypoxemia or acidosis. This is described in Creasy & Resnik’s Maternal-Fetal Medicine as an autonomic response to intracranial pressure/cerebral blood-flow changes from head compression (p. corresponding section on Periodic Heart Rate Patterns). The NCBI review of early decelerations gives the same mechanism.

Umbilical cord compression occurs, often during a contraction
→ umbilical vein is compressed first because it is thin-walled
→ reduced venous return from placenta to fetus
→ transient fetal hypovolemia
→ sympathetic activation and peripheral vasoconstriction
→ rise in fetal blood pressure.

With more sustained compression:
→ umbilical arteries are compressed
→ fetal systemic vascular resistance and blood pressure rise further
→ baroreceptors in the carotid sinus/aortic arch are stimulated
→ vagal activation
→ abrupt fall in FHR: variable deceleration.

When the compression releases:
→ blood pressure falls and the FHR recovers, sometimes with a brief overshoot or “shoulder” acceleration.

Variable decelerations vary in timing, depth, and shape because cord compression may occur at different points relative to a contraction. They are often transient and tolerable, but recurrent deep/prolonged variable decelerations can indicate significant cord compression and risk hypoxemia if prolonged. Miller’s Anesthesia, 10e describes early decelerations as vagal responses associated with head compression and variable decelerations as associated with umbilical cord compression.