Increase In Fetal Heart Rate Variability Research Articles

Quality of fetal heart rate monitoring with transabdominal fetal ECG during maternal movement in labor: A prospective study.

Transabdominal electrocardiographic (TAfECG) acquisition of fetal heart rate (FHR) signals has recently been introduced into leading commercial cardiotocographic (CTG) monitors. Continuous wireless transmission of signals has raised the possibility of the technology being used during maternal mobilization in labor. This study aims to evaluate signal quality and accuracy of TAfECG acquisition of FHR signals during static and active maternal positions in labor when compared with Doppler signals and with the gold-standard method of fetal scalp electrode (FSE). A total of 76 women with singleton term pregnancies in the active first stage of labor had simultaneously acquired FHR with TAfECG, Doppler, and FSE. Participants were asked to complete a supervised mobilization scheme, comprising five sequential 10-min periods of lying down, standing, sitting, walking, and rocking on the birthing ball. The three FHR signals were compared, defining signal loss as the percentage of signals under 20 bpm or exceeding 250 bpm and accuracy as the difference with FSE values. Computer analysis was used to quantify variability, accelerations, and decelerations. Static labor positions (lying down, standing, and sitting) were compared with active labor positions (walking and rocking on the birthing ball). Average signal loss was 5.3% with TAfECG (3.2% in static and 7.4% in active positions) and 15.5% with Doppler (8.3% in static and 30.7% in active positions). Average accuracy was 3.5bpm with TAfECG (1.9bpm in static and 5.04 bpm in active positions) and 13.9bpm with Doppler (3.2bpm in static and 24.7bpm in active positions). Average variability was similar with TAfECG and FSE in static positions but significantly higher with TAfECG in active positions (23.6 vs. 13.5 bpm, p < 0.001). In static labor positions, TAfECG provides a low signal loss, similar to that obtained with FSE, and a good signal accuracy, so the technique can be considered reliable when the mother is lying down, standing, or sitting. During maternal movement, TAfECG causes an artificial increase in FHR variability, which can cause false reassurance regarding fetal oxygenation. Doppler signals are unreliable during maternal movements.

Sympathetic neural activation does not mediate heart rate variability during repeated brief umbilical cord occlusions in near-term fetal sheep.

Changes in fetal heart rate variability (FHRV) and ST segment elevation (measured as the T/QRS ratio) are used to evaluate fetal adaptation to labour. The sympathetic nervous system (SNS) is an important contributor to FHRV under healthy normoxic conditions, and is critical for rapid support of blood pressure during brief labour-like asphyxia. However, although it has been assumed that SNS activity contributes to FHRV during labour; this has never been tested, and it is unclear whether the SNS contributes to the rapid increase in T/QRS ratio during brief asphyxia. Thirteen chronically instrumented fetal sheep at 0.85 of gestation received either chemical sympathectomy with 6-hydroxydopamine (6-OHDA; n = 6) or sham treatment (control; n = 7), followed 4-5 days later by 2 min episodes of complete umbilical cord occlusion repeated every 5 min for up to 4 h, or until mean arterial blood pressure fell to <20 mmHg for two successive occlusions. FHRV was decreased before occlusions in the 6-OHDA group (P < 0.05) and 2-4.5 h during recovery after occlusions (P < 0.05) compared to the control group. During each occlusion there was a rapid increase in T/QRS ratio. Between successive occlusions the T/QRS ratio rapidly returned to baseline, and FHRV increased above baseline in both groups (P < 0.05), with no significant effect of sympathectomy on FHRV or T/QRS ratio. In conclusion, these data show that SNS activity does not mediate the increase in FHRV between repeated episodes of brief umbilical cord occlusion or the transient increase in T/QRS ratio during occlusions.

Biphasic changes in fetal heart rate variability in preterm fetal sheep developing hypotension after acute on chronic lipopolysaccharide exposure.

Perinatal exposure to infection is highly associated with adverse outcomes. Experimentally, acute, severe exposure to gram-negative bacterial lipopolysaccharide (LPS) is associated with increased fetal heart rate variability (FHRV). It is unknown whether FHRV is affected by subclinical infection with or without acute exacerbations. We therefore tested the hypothesis that FHRV would be associated with hypotension after acute on chronic exposure to LPS. Chronically instrumented fetal sheep at 0.7 gestation were exposed to a continuous low-dose LPS infusion (n = 12, 100 ng/kg over 24 h, followed by 250 ng·kg(-1)·24 h(-1) for a further 96 h) or the same volume of saline (n = 10). Boluses of either 1 μg LPS or saline were given at 48, 72, and 96 h. Low-dose infusion was not associated with hemodynamic or FHRV changes. The first LPS bolus was associated with tachycardia and suppression of nuchal electromyographic activity in all fetuses. Seven of twelve fetuses developed hypotension (a fall in mean arterial blood pressure ≥5 mmHg). FHRV was transiently increased only at the onset of hypotension, in association with increased cytokine induction and electroencephalogram suppression. FHRV then fell before the nadir of hypotension, with transient suppression of short-term FHRV. After the second LPS bolus, the hypotension group showed a biphasic pattern of a transient increase in FHRV followed by more prolonged suppression. These findings suggest that infection-related hypotension in the preterm fetus mediates the transient increase in FHRV and that repeated exposure to LPS leads to progressive loss of FHRV.

ECG and Heart Rate Variability Changes in Preterm and Near-Term Fetal Lamb Following LPS Exposure

The aim of this study is to evaluate the myocardial response in the preterm and near-term fetal lamb with infection. Chronically instrumented fetal lambs were exposed to lipopolysaccharide (LPS), and the fetal electrocardiogram (FECG) ST waveform was examined using STAN. Fetal heart rate variability (FHRV) was automatically analyzed by adapting a polynomial function to the RR sequence in the FECG. Preterm fetuses exposed to >90 ng/kg LPS died within 8 hours of LPS administration, a response not seen in near-term fetuses. In both surviving and nonsurviving preterm fetuses, cardiovascular responses were characterized by decreased arterial pressure, negative T waves, and tachycardia accompanied by an increase in FHRV. Similar changes were not observed in the near-term fetuses after LPS. The study shows that preterm lambs are more sensitive to LPS in terms of myocardial/cardiovascular response than the more mature fetuses are. High FHRV and negative ST waveform seem to characterize the LPS-induced stress response in preterm fetuses.

Influence of sympathetic tone on heart rate during vagal stimulation and nitroprusside induced hypotension in ovine fetus

Objective To characterize effects of sympathetic tone on fetal heart rate (FHR) reflex responses and FHR variability in late gestation. Design/Methods Changes in FHR and autonomic tones were studied (i) after electrical vagal stimulation and (ii) during nitroprusside-induced hypotension, in seven late gestation ovine fetus in control condition (ctrl), after dobutamine (β1-activation) and atenolol (β1-blockade). Results are expressed as mean ± SEM. Results (i) Minimal FHR after vagal stimulation was not influenced by atenolol or dobutamine but dobutamine accelerated FHR normalization. (ii) During nitroprusside induced hypotension atenolol inhibited the initial increases in FHR and FHR variability (measured by SD and LFnu) but not the bradycardia occurring below a mean arterial pressure of 38 ± 2 mmHg. Dobutamine did not abolish the depressor reflex. During hypotension the positive chronotropic effect of sympathetic tone increased from 15 ± 2 to 42 ± 7 bpm then decreased at a rate of − 7.6 ± 1.5 bpm mmHg − 1 , vagal negative chronotropic influence steadily increased at a rate of 1.9 ± 0.4 bpm mmHg − 1 . Changes in FHR variability were not correlated with vagal or sympathetic chronotropic effects. Conclusions β1-stimulation does not affect sinus-node response to vagal stimulation but improves the speed of FHR normalization. FHR response to hypotension depends on an initial increase in both sympathetic and parasympathetic chronotropic effects that is associated with a sympathetic dependent increase in FHR variability and is followed by a withdrawal of sympathetic tone.

Fetal heart rate variability and brain stem injury after asphyxia in preterm fetal sheep.

This study was undertaken to determine the mechanisms mediating changes in fetal heart rate variability (FHRV) during and after exposure to asphyxia in the premature fetus. Preterm fetal sheep at 0.6 of gestation (91 +/- 1 days, term is 147 days) were exposed to either sham occlusion (n = 10) or to complete umbilical cord occlusion for either 20 (n = 7) or 30 min (n = 10). Cord occlusion led to a transient increase in FHRV with abrupt body movements that resolved after 5 min. In the 30 min group there was a marked increase in FHRV in the final 10 min of occlusion related to abnormal atrial activity. After reperfusion, FHRV in both study groups was initially suppressed and progressively increased to baseline levels over the first 4 h of recovery. In the 20 min group this improvement was associated with return of normal EEG activity and movements. In contrast, in the 30 min group the EEG was abnormal with epileptiform activity superimposed on a suppressed background, which was associated with abnormal fetal movements. As the epileptiform activity resolved, FHRV fell and became suppressed for the remainder of the study. Histological assessment after 72 h demonstrated severe brain stem injury in the 30 min group but not in the 20 min group. In conclusion, during early recovery from asphyxia, epileptiform activity and associated abnormal fetal movements related to evolving neural injury can cause a confounding transient increase in FHRV, which mimics the normal pattern of recovery. However, chronic suppression of FHRV was a strong predictor of severe brain stem injury.