Hypoxia index precisely covers the roles of FHR deceleration and bradycardia in fetal monitoring

Kazuo Maeda

doi:10.15761/jpr.1000119

Abstract

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Hypoxia index precisely covers the roles of FHR deceleration and bradycardia in fetal monitoring

Highlights

The fetal outcome was uncertain in fetal monitoring by pattern classification, because fetal outcome after 2-3 repetition of late decelerations (LD ) was favorable, while 50 min LD repetition resulted severe fetal and neonatal asphyxia, associating the loss of FHR variability and infantile brain damage, where the threshold to develop ominous outcome was unknown
As fetal bradycardia is caused by the excitation of parasympathetic center with hypoxia, while there was no bradycardia when experimental animal was anesthetized [1], and apneic bradycardia recovered to normal FHR after infusion of oxygenated blood to anencephalic neonate [2], while there was fetal brain damage followed by cerebral palsy after the loss of FHR variability, the sign of fetal brain damage is the loss of variability, but not the bradycardia or deceleration, namely, they will be only the reaction to environmental hypoxia
The sum of deceleration durations were divided by the nadir of decelerations in the hypoxia index in the evaluation of fetal outcome, in cases of the loss of variability followed by fetal brain damage or cerebral palsy

Summary

Introduction

The fetal outcome was uncertain in fetal monitoring by pattern classification, because fetal outcome after 2-3 repetition of late decelerations (LD ) was favorable, while 50 min LD repetition resulted severe fetal and neonatal asphyxia, associating the loss of FHR variability and infantile brain damage, where the threshold to develop ominous outcome was unknown. The threshold of severe variable decelerations was vague. The author thought it is necessary to create reliable evaluation of FHR decelerations

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Conclusion