Late deceleration.
In some women, a maternal illness or a placental disorder can lead to a decrease in oxygen available for diffusion.
During a uterine contraction, there is a reduction in oxygen diffusion and a decrease in fetal oxygen levels.
Low fetal PO2 activates chemo receptors which are located peripherally in the Aortic arch and
in the carotid body and
centrally in the Medulla.
These receptors gradually increase peripheral vasoconstriction in which
oxygenated blood is shunted towards vital organs such as the brain,
heart, and adrenal glands. This results in Fetal hypertension.
Hypertension in the fetus activates
baroreceptors in the Aortic pressoreceptors and carotid sinus. These receptors send signals to the cardioinhibitory
center via the vagus and glossopharyngeal nerve.
Stimulation of the vagus nerve causes the fetal heart rate to gradually decrease.
This is called a late deceleration. When the contraction ends, the fetal heart rate will gradually return to the baseline.
As this is a two-step process the nadir of the deceleration appears after the peak of contraction.
Late decelerations
classify that tracing is atypical if occurring occasionally, and
abnormal if occurring in over 50% of the contractions.
