Long-term Fetal Heart Rate Variability Research Articles

Actocardiographic Analysis of Fetal Hypoxia Detected by the Bradycardia, Loss of Fetal Heart Rate Acceleration, and Long Term Variability

Aims: To clarify the mechanism of hypoxic Fetal Heart Rate (FHR) by the actocardio-gram. Methods: Hypoxic rabbit heart rate and PaO 2 were studied. Long Term FHR Variability (LTV) was studied in physiologic sinusoidal FHR and anencephalic fetus, the acceleration in hypoxia, and by its electronic simulation and adult heart rate. Results: Anencephalic neonatal bradycardia was caused by the excitation of remained medulla oblongata. Rabbit's bradycardia was parallel to PaO 2 bunder 50 mm Hg, which disappeared after urethane anesthesia. Human fetal bradycardia was caused by the hypoxia, because fetal PaO2 is less than 50 mm Hg. FHR acceleration was evoked in the midbrain by the large fetal movement bursts, and minor movements evoked LTV. Physiological sinusoidal FHR was a particular form of LTV. Triangular acceleration was simulated by the electronic integral circuit, and by the triangular heart rate in adult exercises. Fetal outcome was correlated to the acceleration duration. Hypoxia damaged fetal brain in nonreactive FHR, loosing acceleration, and advanced hypoxia further damaged brain a few days after the loss of acceleration, showing the loss of LTV and bradycardia. The loss of LTV which was confirmed by the frequency power spectrum was rare, but its brain damage was as severe as the apnea of anencephalic neonate, which lost cerebral respiratory center. Conclusion: Hypoxic bradycardia was evoked by the excited medulla oblongata in the decreased PaO 2 , which was lower than 50 mm Hg. The hypoxia damaged fetus in fetal bradycardia, the losses of acceleration and LTV, in relation to fetal movements.

Short-Term (0–48 h) Effects of Maternal Betamethasone Administration on Fetal Heart Rate and Its Variability

The short-term (0-48 h) effects of maternal betamethasone administration on computerized fetal heart rate (FHR) parameters were studied in 36 pregnancies at increased risk for preterm delivery. FHR was recorded for 90 min immediately before the start of betamethasone treatment and again at 6-h intervals during the next 48 h. Multiple linear regression models were used to assess the possible effects on FHR parameters of gestational age, time of day, clinical indication for treatment, and use of tocolytic drugs. Within 12 h after the start of treatment, significant increases occurred in FHR accelerations, and short- and long-term FHR variability (36%, 28%, and 22%, respectively), whereas basal FHR showed a 5% decrease. FHR variability was decreased by 10% at 42-48 h. The observed changes were more pronounced in older (29-33 wk of gestation) compared with younger fetuses (25-28 wk of gestation). Decelerations occurred only in 4 out of 11 compromised fetuses during betamethasone therapy. We conclude that there are significant changes in FHR parameters during the first 48 h after betamethasone administration. These changes are transient in normal fetuses. However, the compromised fetus may be adversely affected by betamethasone.

Fetal heart rate patterns in postasphyxiated fetal lambs with brain damage

Objective: We previously showed that in asphyxiated fetal lambs the duration of hypotension correlated well with the severity of histologic damage to the brain, whereas the duration of bradycardia did not. This study compares fetal heart rate patterns with the degree of histologic damage to the brain. Study Design: Twelve chronically instrumented near-term fetal lambs were subjected to asphyxia by umbilical cord occlusion until fetal arterial pH was <6.9 and base excess was <–20 mEq/L. An additional 4 fetuses served as sham-asphyxia controls. Fetal heart rate (from electrocardiogram), arterial blood pressure, fetal breathing movements, and electrocorticogram were continuously monitored before, during, and for 72 hours after asphyxia. Fetal brain histologic features were categorized as mild (group 1, n = 5), moderate (group 2, n = 4), and severe (group 3, n = 3). Long-term fetal heart rate variability expressed as amplitude range was assessed visually every 5 minutes from 30 minutes before asphyxia until 2 hours of recovery and at 6, 12, 24, 48, and 72 hours of recovery. Results: Long-term fetal heart rate variability amplitude decreased from 32 ± 17 beats/min (mean ± SEM) preocclusion to 4 ± 13 beats/min at the end of occlusion ( P < .001) without significant differences among the 3 groups. During 10 to 45 minutes of recovery, the long-term variability of group 1 was significantly greater than that of groups 2 and 3. At 24 to 72 hours of recovery, the long-term variability of groups 1 and 2 was significantly higher than that of group 3, which was almost 0. The “checkmark” and sinusoidal fetal heart rate patterns were observed during the recovery period in groups 2 and 3. Conclusions: Decreased long-term fetal heart rate variability and the “checkmark” and sinusoidal fetal heart rate patterns were indicators of the severity of asphyxial histologic damage in the fetal brain. (Am J Obstet Gynecol 1998;179:1329-37.)

Fetal heart rate patterns in growth-restricted fetal sheep induced by chronic fetal placental embolization

OBJECTIVE: Our purpose was to test the hypothesis that chronic placental insufficiency and intrauterine growth restriction in fetal sheep causes a decrease in the number of fetal heart rate accelerations and fetal heart rate variability. STUDY DESIGN: Chronically catheterized fetal sheep were embolized ( n = 6) daily with 15 to 50 μm latex microspheres for 21 days between 0.74 and 0.88 of gestation into the abdominal aorta, until fetal arterial oxygen content was decreased by 40% to 50% of the preembolization value. Control animals ( n = 6) received saline solution only. Signals from chest electrodes were analyzed on-line with the Sonicaid System 8000 in 2-hour epochs every 6 hours starting at 8 am over the first 48 hours of hypoxemia and for 2 hours between 8 and 10 am every other day from day 3 to day 21 of hypoxemia. Umbilical artery Doppler-derived resistance index and fetal plasma catecholamine concentrations were also measured. RESULTS: Embolized fetuses had asymmetric intrauterine growth restriction and became chronically hypoxemic ( p < 0.001) with a progressive increase in the umbilical artery resistance index ( p < 0.001). During the first 48 hours of hypoxemia the number of accelerations and decelerations and both short- and long-term fetal heart rate variability increased initially, followed by a return to control levels by 20 hours after the onset of embolization. After 21 days of hypoxemia the number of accelerations was significantly reduced by 30% compared with controls ( p < 0.05). Both short- and long-term fetal heart rate variability in control fetuses gradually increased with advancing gestational age ( p < 0.001 and p < 0.01, respectively), whereas in embolized fetuses the fetal heart rate variability remained unchanged and was 20% lower than that of controls on day 21 (both p < 0.01). CONCLUSION: Intrauterine growth restriction and long-term hypoxemia in fetal sheep are associated with a decrease in short- and long-term fetal heart rate variability, possibly because of a delay in the normal maturational changes of the autonomic control of fetal heart rate. (Am J Obstet Gynecol 1997;176:282-90.)

Neural network prediction of nonstress test results: How often should we perform nonstress tests?

OBJECTIVE: Our purpose was to predict outcomes and optimal intervals for nonstress tests of term gravid women with neural networks. STUDY DESIGN: We studied 100 normal term patients whose 30-minute nonstress tests, performed on 5 consecutive days, were computer analyzed for the following elements: fetal heart rate baseline, variability, signal loss, accelerations (>15 beats/min), and decelerations. The training set used 65 patients; the testing, 35 patients. Nonstress test data (days 1 to 4) were inputs; day 5 data were training patterns. Networks for each nonstress tet element used Brainmaker Macintosh 1.0 (California Scientific Software, Nevada City, Calif.) trained to 0.12 tolerance. Actual fetal heart rate elements and their daily differences were compared with predictions by the networks and multiple regressions. RESULTS: There was little difference between networks using daily or alternate-day inputs for predicting test performance on day 5; networks using test intervals >2 days could not be trained to tolerance. Long-term fetal heart rate variation was the nonstress test element best predicted. Daily differences networks provided better prediction of all day 5 data than did actual daily values networks or multiple regression formulas. CONCLUSIONS: Baseline long-term fetal heart rate variability seems to be the most predictable fetal heart rate element over time and should merit more consideration in overall fetal testing. Fetal heart rate elements are not easily predicted by any method for intervals longer than 2 days. Using longer test intervals might run a greater risk for unanticipated changes in nonstress test outcomes, even when fetal condition is normal.

Antenatal bleeding and fetal heart rate.

Objective of the paper was to determine the fetal heart rate (FHR) changes that occur in preterm fetuses whose mothers have suffered antepartum bleeding, versus uncomplicated controls. Over a 12-year span, 91 patients with significant antenatal bleeding (bleeding requiring inhospital observation) were examined and compared to 75 controls with uncomplicated normal pregnancies. None of the women were in labor and all were evaluated at 25-37 weeks' gestation. Excluded were: patients with any other complication (i.e., premature rupture of membranes, intrauterine growth retardation, diabetes, hypertension, collagen vascular disease, postuterine surgery, substance abuse and twins). Analysis of the FHR tracings included baseline heart rate, long-term FHR variability, and number and amplitude of FHR accelerations in 20-min segments. There was no difference in baseline heart rate in the preterm fetuses of pregnancies complicated by antepartum bleeding versus controls. However, the parameters associated with FHR reactivity (number of accelerations in 20 min, and amplitude of accelerations) were higher to a statistically significant degree in fetuses of pregnancies complicated by antenatal bleeding than in controls. Fetuses of mothers suffering antenatal bleeding exhibited significant higher rates of reactive FHR patterns at earlier gestational ages than did controls. In conclusion, there is a significant increase in FHR reactivity in pregnancies in which significant antenatal bleeding occurs, suggesting a probable acceleration in fetal central nervous system maturation in these fetuses.

7 Power spectral analysis of fetal heart rate

This chapter examines the role of power spectral analysis (PSA) in elucidation of the physiological control mechanisms of fetal heart rate and as a potential indicator of fetal well-being. The importance of fetal heart rate variability (FHRV) as an indicator of fetal oxygenation is discussed, and the limitations in the current methods of measurement of FHRV are highlighted. Evidence is presented for the paramount influence of the autonomic nervous system in the control of heart rate variability. The basic proposition underlying spectral analysis is that the two autonomic branches influence heart rate in a frequency-dependent way, and their differential effects can be determined by PSA which breaks down the heart rate trace into its component frequencies. The application of PSA to heart rate variability data is an established tool in cardiology, and the published literature related to its use in the adult, neonate and fetus is reviewed. The power spectrum is sensitive to the activity state of the fetus, particularly fetal breathing movements, which have a variable effect on short- and long-term FHRV. There are a variety of mathematical approaches to the construction of power spectra, and a particular method of data acquisition and analysis is presented together with some theoretical background. Recent experimental evidence indicates a role for PSA as an indicator of fetal activity state, and the effect of hypoxia on the spectrum of the fetus in labour is discussed. There are some problems with the technique of PSA, particularly in regard to accepted definitions and methods of analysis. It is a powerful non-invasive tool in the elucidation of fetal cardiac control, but its value in the detection of the compromised fetus has yet to be tested in a clinical trial.

Effect of Oxymorphone Hydrochloride on Ovine Fetal Heart Rate Variability

In order to determine the effect of the narcotic analgesic oxymorphone hydrochloride (Numorphan, DuPont) on fetal heart rate (FHR) variability, mathematical indices of short-term and long-term FHR variability were determined continuously from R–R intervals of the electrocardiogram in eight chronically instrumented ovine fetuses for 60 min before and after a maternal intravenous bolus of 0.04 mg/kg oxymorphone. The index of short-term variability decreased from 12.7 ± 2.0 during control to 9.7 ± 1.7 during the period from 10 to 30 min after oxymorphone administration during periods of low-voltage, high-frequency electrocortical activity (LVHF ECoG) (P < 0.05). Mean FHR was decreased from 169 ± 8 beats per minute (bpm) during control to 155 ± 7 bpm 30 to 50 min after oxymorphone (P < 0.05). Fetal electrocortical activity was also determined and the decrease in FHR short-term variability occurred despite an increase in the percent time spent in LVHF electrocortical activity from 53 ± 4% during the control pe...

Human fetal behavioral states after vibratory stimulation

A total of 14 healthy pregnant women between 37 and 41 weeks' gestational age were studied to determine the effects of a 5-second external vibratory stimulus (100 Hz, square wave) on human fetal behavioral states. Fetal behavioral state observations were made with simultaneous recordings of fetal heart rate, gross fetal body movements, and fetal eye movement between 8:30 am and 4:00 pm . During the first episode of behavioral state 1 F (quiet sleep state) ≥ 10 minutes duration on two consecutive half days, the vibratory stimulus was placed on the surface of the maternal abdomen over the fetal head. Each fetus received one 5-second vibratory stimulus during either the first or second half day of observation. The time at which the instrument was applied but no vibratory stimulus was administered was considered as the control period. All women were then observed for 2 hours after the control period and after stimulation. A transition period from a quiet sleep state to a stable active sleep state (state 2F, rapid eye movement sleep) averaged ≤ 53 minutes after stimulation, as compared with 23 minutes after the control period. These changes in fetal behavioral states persisted for 20 minutes after vibratory stimulation. There also was an immediate and sustained increase in long-term fetal heart rate variability, the number of fetal heart rate accelerations and gross fetal body movement during the first 20 minutes after stimulus, without changes in basal fetal heart rate. We hypothesize that changes in fetal behavior seen after application of low frequency vibratory stimulus are more physiologic than the profound changes in fetal heart rate and gross fetal body movement previously described after vibratory acoustic stimulation with an electronic artificial larynx.

Human fetal behavioral states after vibratory stimulation

A total of 14 healthy pregnant women between 37 and 41 weeks' gestational age were studied to determine the effects of a 5-second external vibratory stimulus (100 Hz, square wave) on human fetal behavioral states. Fetal behavioral state observations were made with simultaneous recordings of fetal heart rate, gross fetal body movements, and fetal eye movement between 8:30 AM and 4:00 PM. During the first episode of behavioral state 1F (quiet sleep state) greater than or equal to 10 minutes duration on two consecutive half days, the vibratory stimulus was placed on the surface of the maternal abdomen over the fetal head. Each fetus received one 5-second vibratory stimulus during either the first or second half day of observation. The time at which the instrument was applied but no vibratory stimulus was administered was considered as the control period. All women were then observed for 2 hours after the control period and after stimulation. A transition period from a quiet sleep state to a stable active sleep state (state 2F, rapid eye movement sleep) averaged less than or equal to 3 minutes after stimulation, as compared with 23 minutes after the control period. These changes in fetal behavioral states persisted for 20 minutes after vibratory stimulation. There also was an immediate and sustained increase in long-term fetal heart rate variability, the number of fetal heart rate accelerations and gross fetal body movement during the first 20 minutes after stimulus, without changes in basal fetal heart rate. We hypothesize that changes in fetal behavior seen after application of low frequency vibratory stimulus are more physiologic than the profound changes in fetal heart rate and gross fetal body movement previously described after vibratory acoustic stimulation with an electronic artificial larynx.

Vibratory acoustic stimulation in 26- to 32-week, small-for-gestational-age fetus

Seven pregnant women with early-onset (less than 32 weeks' gestation) intrauterine growth retardation were studied to examine fetal heart rate and fetal activity patterns after vibratory acoustic stimulation. All studies were done between 26 and 32 weeks' gestation. All fetuses but one were not acidotic at birth. There was a reduced time during which accelerations (50% less), long-term fetal heart rate variability (25% less), and body movements (60% less) occurred in small-for-gestational-age fetuses compared with these times in age-matched normally grown fetuses. Fetal heart rate and fetal activity patterns were not significantly altered after stimulation with the electronic artificial larynx. We hypothesized that severe, early-onset (less than 32 weeks' gestation), chronic nutritional deprivation of human fetuses is associated with a delay in the functional maturation of fetal sensory receptors.

Fetal heart rate and activity patterns in growth-retarded fetuses: Changes after vibratory acoustic stimulation

Seventeen pregnant women who subsequently were delivered of infants with birth weights less than the third percentile were studied for examination of fetal heart rate and fetal activity patterns before and after a 5-second external vibratory acoustic stimulation. None of the fetuses was acidotic at birth. A reduced time was noted during which accelerations in heart rate occurred (50% less) and long-term fetal heart rate variability (25% less) in small for gestational age fetuses compared with age-matched, normally grown fetuses. The incidence of gross fetal body movements was significantly lower (40% less) in small for gestational age fetuses than in those who were appropriate for gestational age. Fetal heart rate and fetal activity patterns after stimulation with the electronic artificial larynx in small for gestational age fetuses were similar to those of appropriate for gestational age fetuses.

Fetal heart rate and fetal activity patterns after vibratory acoustic stimulation at thirty to thirty-two weeks' gestational age

Twenty pregnant women between 30 and 32 weeks' gestational age were studied to examine the effects of a 5-second external vibratory acoustic stimulus on the fetal heart rate, fetal heart rate variability, and fetal activity patterns. There was an immediate significant increase in the basal fetal heart rate for 10 minutes compared with controls. There was also a significant increase in the mean duration of fetal heart rate accelerations without any change in the number of fetal heart rate accelerations. There were no changes in long-term fetal heart rate variability, fetal breathing, and gross fetal body movements.

Patterns of human fetal heart rate accelerations from 26 weeks to term

Computerized analysis of the distribution of 2598 fetal heart rate accelerations in 83 healthy fetuses at 26 to 40 weeks' gestation demonstrated that the currently used definition of an acceleration as greater than or equal to 15 beats/min for greater than or equal to 15 seconds is applicable only after 30 weeks' gestational age in fetuses with a basal fetal heart rate of less than or equal to 128 beats/min. A significant negative correlation was found between the mean hourly basal fetal heart rate and the mean amplitude of fetal heart rate accelerations from 30 weeks to term. There was also a significant maturational process in the pattern of fetal heart rate and fetal heart rate accelerations that occurred between 26 and 28 and between 30 and 32 weeks; this was characterized by a decrease in basal fetal heart rate, an increase in the amplitude of fetal heart rate accelerations, and an increase in long-term fetal heart rate variability.

The change in fetal activity periods in diabetic and nondiabetic pregnancies

Fetal active and quiet periods of behavioral activity were determined at 28 to 32 weeks' and 36 to 40 weeks' gestational age in insulin-dependent diabetic pregnancies and in normal pregnancies resulting in infants with weights appropriate for gestational age. Fetal active and quiet periods were based on observations of fetal movements and long-term fetal heart rate variability. The number of fetal active-quiet periods, the average duration of fetal quiet periods, and the average duration of fetal active periods were the three parameters evaluated. In the normal pregnancy groups, with increasing fetal gestational age from 28 to 32 weeks to 36 to 40 weeks there was an increase in the length of the active and quiet periods with fewer active-quiet cycles per hour. The fetuses of the diabetic women had findings similar to those of the normal group at 28 to 32 weeks; these findings were essentially unchanged at 36 to 40 weeks. These findings suggest delayed development of the active-quiet cycles in these diabetic pregnancies.

Effect of acute hypoxemia and respiratory acidosis on the fetal heart rate in monkeys

The fetal heart rate (FHR) response to acute nonacidemic hypoxemia and to acute respiratory acidosis was studied in unanesthetized pregnant monkeys by means of chronically implanted catheters and electrodes. Average FHR and short- and long-term FHR variability were analyzed separately. The FHR response to either hypoxemia or hypercapnia consisted of slowing and increased variability. The slowing was more consistent with hypercapnia than with hypoxemia. Long-term FHR variability increased with both test stresses. The increase in short-term FHR variability was much greater in response to hypoxemia than to hypercapnia. Both the FHR slowing and the increases in variability in response to the test stresses were reduced by prior administration of atropine to the fetus.

Studies of antepartum behavioral state in the human fetus at term

This prospective study describes intrauterine behavioral states in the human fetus. The variables used are fetal movement and two expressions of fetal heart rate (FHR): long-term variability and baseline rate. Fetal movement was recorded with the use of two strain gauges. FHR was measured with a transabdominal fetal electrocardiographic processor. Sixteen fetuses of normal pregnant patients were studied near term. One-minute periods called “epochs” were classified as quiet, active, and intermediate, based on the presence or absence of fetal movement (longer in duration than one second), increased or decreased long-term FHR variability, and the baseline of the FHR. Complete agreement in epoch classification was noted in 79.3 per cent of the 2,054 epochs analyzed. Quiet and active one-minute epochs were clustered into longer time periods representing quiet and active fetal behavior states similar to those seen in the neonate. The overall visual evaluation of the tracings based on the above noted criteria demonstrated the presence of quiet, active, and transitional states in the fetus. Mean duration of a complete cycle, including the quiet, active, and transitional states, was 62.3 minutes. The mean duration in the quiet state was 22.8 minutes and the mean duration in the nonquiet states (active and transitional) was 39.5 minutes. The significance of these intrauterine behavioral states is stressed.