European Journal of Obstetrics & Gynecology and Reproductive Biology
Original ArticleFetal heart rate in relation to its variation in normal and growth retarded fetuses
Introduction
Antenatal fetal heart rate (FHR) monitoring is widely used to assess the fetal condition. FHR variability is known to depend on several factors such as gestational age (GA), basal FHR, hypoxia, fetal behavioural states, cord compression, and the use of medication and social drugs (alcohol, smoking) [1]. Both long term (LTV) and short term (STV) FHR variation have a negative relationship with FHR. FHR variation increases with decreasing FHR and vice versa. Moreover, FHR variation increases with advancing GA [1], [2].
In intrauterine growth retarded (IUGR) fetuses, LTV is about 25% lower than in age-matched appropriately grown fetuses [3]. FHR variation gradually decreases with progressive compromise of the fetal condition [4]. This reduced FHR variation is not caused by a change in the rest-activity cycles [5]. However, it coincides with an increase in basal heart rate [4]. Usually around the same time that FHR variation falls below the norm, decelerations emerge [4], [6]. Ribbert et al. [7] found LTV in IUGR fetuses to be reduced towards the lower level of the normal range about ten days before Caesarean Section (CS) was undertaken for ‘fetal distress’. FHR variation remained fairly constant for some time before a further reduction occurred [7]. Decreased FHR variation and FHR decelerations have been found to be associated with hypoxaemia at CS and at cordocentesis [6], [8], [9], [10]. Abnormal blood flow velocity waveforms from the umbilical artery are present in the majority of fetuses long before the occurrence of fetal distress [7], [11]. The understanding of these temporal changes is important for the management of the IUGR fetus, especially with respect to the timing of delivery [12].
The negative relationship between basal heart rate and its variation in healthy fetuses, and the concomitant changes in rate (up) and variation (down) in IUGR fetuses, suggest that correction for rate may better identify those fetuses who have a reduced FHR variability irrespective of their basal heart rate. By studying FHR in relation to its variation, insight into changes in variation will improve.
The aims of the present study were: (1) to assess the relationship between FHR and FHR variation (LTV and STV) in low-risk pregnancies longitudinally from 24 weeks gestation onwards; and (2) to investigate the same relationship in the IUGR fetus.
Section snippets
Subjects and methods
FHR was monitored longitudinally in 29 singleton fetuses of healthy pregnant women, of which eleven were nulliparous. From 24 weeks GA onwards one hour recordings were made at two-weekly intervals. From 36 weeks till delivery, two hour recordings were made on a weekly basis, but only the first hour was used for the present analysis. The recordings took place at the Leicester General Hospital, Leicester, UK. All women gave their written informed consent. All pregnancies were uncomplicated, and
Results
We analysed a total of 224 recordings from the 29 fetuses of the control group, after exclusion of 14 recordings with a signal loss >30%. FHR was significantly correlated with both LTV and STV. The following models were derived; for LTV: y=−1.15x+208.7 (R=0.73; p<0.0001, n=224) and for STV: y=−0.21x+37.7 (R=0.72; p <0.0001, n=224), where y is LTV (ms) or STV (ms) and x is basal FHR (bpm)).
Multilevel analysis confirmed this strong relationship between FHR and both LTV and STV (p<0.0001) during
Comment
We have previously shown that FHR variation is negatively correlated with basal heart rate in healthy fetuses, both during ‘non-reactive’ FHR patterns (pattern A) and ‘reactive’ FHR patterns (pattern B) [20]. In the present study this was confirmed when the whole one hour recordings were considered. The relationship was strong and about 50% of the differences in FHR variation could be explained by differences in rate (R2=53% for LTV and R2=52% for STV, respectively). This implies that basal
Acknowledgments
The authors like to thank L.S.M. Ribbert, MD PhD (Department of Obstetrics and Gynaecology, St. Antonius Hospital Nieuwegein, The Netherlands), S.V. Koenen, MD and R.H. Stigter, MD (Department of Obstetrics and Gynaecology, University Hospital Utrecht, The Netherlands) for the use of their data, and P. Westers, PhD (Centre for Biostatistics, Utrecht University, The Netherlands) for his statistical advice.
This study was supported by a grant from the Commission of the European Communities
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