51. Fetal acid–base balance after betamethasone administration: relation to fetal heart rate variability
- Author
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Simon Shenhav, Michael Volodarsky, Ofer Gemer, and Eyal Y. Anteby
- Subjects
Adult ,medicine.medical_specialty ,Fetal Heart Rate Variability ,Acid–base homeostasis ,Betamethasone ,Fetus ,Pregnancy ,Internal medicine ,Heart rate ,medicine ,Humans ,skin and connective tissue diseases ,Retrospective Studies ,Acid-Base Equilibrium ,business.industry ,Infant, Newborn ,Obstetrics and Gynecology ,General Medicine ,Heart Rate, Fetal ,medicine.disease ,Tocolytic Agents ,Endocrinology ,embryonic structures ,Premature Birth ,Female ,sense organs ,business ,medicine.drug - Abstract
To explore whether the known decrease in fetal heart rate variability, which follows antenatal betamethasone administration is related to fetal acid-base changes.A retrospective study of 42 women with premature delivery following a single course of betamethasone. The study group consisted of 21 women who delivered within 48 h following first injection of betamethasone. The 21 women who delivered later than 48 h formed the control group. Fetal heart rate variability measurements and cord acid-base values were compared.The mean fetal heart rate variability (beats per minute) before the administration of betamethasone was significantly higher than at 24 h [8.05 (SD 3.15) vs. 5.32 (SD 2.27); p0.001]. This was evident in both the groups, with no significant difference between them. In the control group, the mean variability before betamethasone administration and the variability prior to delivery were not significantly different [8.48 (SD 3.46) vs. 7.26 (SD 3.03); p=0.36]. There were no significant differences between study and control groups regarding the arterial cord acid-base values at delivery [pH 7.29 (SD 0.15) vs. 7.31 (SD 0.1); p=0.38].Assuming that the fetal heart rate and the acid-base status prior to delivery would be a reflection of the effects of betamethasone as evident by reduced fetal heart rate variability, our data does not support acid-base changes as a pathophysiological mechanism.
- Published
- 2008