Baseline Fetal Heart Rate Variability Research Articles

Fetal Cardiovascular Decompensation During Labor Predicted From the Individual Heart Rate Tracing: A Machine Learning Approach in Near-Term Fetal Sheep Model.

Background: When exposed to repetitive umbilical cord occlusions (UCO) with worsening acidemia, fetuses eventually develop cardiovascular decompensation manifesting as pathological hypotensive arterial blood pressure (ABP) responses to fetal heart rate (FHR) decelerations. Failure to maintain cardiac output during labor is a key event leading up to brain injury. We reported that the timing of the event when a fetus begins to exhibit this cardiovascular phenotype is highly individual and was impossible to predict.Objective: We hypothesized that this phenotype would be reflected in the individual behavior of heart rate variability (HRV) as measured by root mean square of successive differences of R-R intervals (RMSSD), a measure of vagal modulation of HRV, which is known to increase with worsening acidemia. This is clinically relevant because HRV can be computed in real-time intrapartum. Consequently, we aimed to predict the individual timing of the event when a hypotensive ABP pattern would emerge in a fetus from a series of continuous RMSSD data.Study Design: Fourteen near-term fetal sheep were chronically instrumented with vascular catheters to record fetal arterial blood pressure, umbilical cord occluder to mimic uterine contractions occurring during human labor and ECG electrodes to compute the ECG-derived HRV measure RMSSD. All animals were studied over a ~6 h period. After a 1–2 h baseline control period, the animals underwent mild, moderate, and severe series of repetitive UCO. We applied the recently developed machine learning algorithm to detect physiologically meaningful changes in RMSSD dynamics with worsening acidemia and hypotensive responses to FHR decelerations. To mimic clinical scenarios using an ultrasound-based 4 Hz FHR sampling rate, we recomputed RMSSD from FHR sampled at 4 Hz and compared the performance of our algorithm under both conditions (1,000 Hz vs. 4 Hz).Results: The RMSSD values were highly non-stationary, with four different regimes and three regime changes, corresponding to a baseline period followed by mild, moderate, and severe UCO series. Each time series was characterized by seemingly randomly occurring (in terms of timing of the individual onset) increase in RMSSD values at different time points during the moderate UCO series and at the start of the severe UCO series. This event manifested as an increasing trend in RMSSD values, which counter-intuitively emerged as a period of relative stationarity for the time series. Our algorithm identified these change points as the individual time points of cardiovascular decompensation with 92% sensitivity, 86% accuracy and 92% precision which corresponded to 14 ± 21 min before the visual identification. In the 4 Hz RMSSD time series, the algorithm detected the event with 3 times earlier detection times than at 1,000 Hz, i.e., producing false positive alarms with 50% sensitivity, 21% accuracy, and 27% precision. We identified the overestimation of baseline FHR variability by RMSSD at a 4 Hz sampling rate to be the cause of this phenomenon.Conclusions: The key finding is demonstration of FHR monitoring to detect fetal cardiovascular decompensation during labor. This validates the hypothesis that our HRV-based algorithm identifies individual time points of ABP responses to UCO with worsening acidemia by extracting change point information from the physiologically related fluctuations in the RMSSD signal. This performance depends on the acquisition accuracy of beat to beat fluctuations achieved in trans-abdominal ECG devices and fails at the sampling rate used clinically in ultrasound-based systems. This has implications for implementing such an approach in clinical practice.

0853 Fetal Heart Rate Variability Increases During Maternal Sleep Apnea Events

Abstract Introduction While studies have established that SDB during pregnancy increases the risk of adverse maternal outcomes, fetal effects are less well studied. Evidence suggests that fetal heart rate decelerations, an indicator of fetal distress, may be elicited by SDB. We examined the relationship between maternal SDB events and fetal heart rate (FHR) and fetal heart rate variability (FHRV). Methods Obese (BMI≥30kg/m2) non-smoking women carrying singleton fetuses underwent overnight polysomnography (34-37 weeks gestational age), with simultaneous fetal heart rate monitoring. Standard methods were used to score sleep, SDB events (apneas/hypopneas) and to analyze fetal heart rate parameters. Using linear mixed effect models, we examined changes in mean FHR and FHR variability (expressed by FHR SD) between the 10-second period immediately before individual SDB events, during events to the end of the associated oxygen desaturation period, and the 10-second period immediately following the SDB event. Results Valid PSG and FHR data were obtained from 85 third trimester maternal-fetal dyads. Across all participants, there were 2779 maternal SDB events (apneas or hypopneas). Mean AHI for individual subjects was 9.04 (SD 13.75). 39 women had OSA (AHI≥5), which was mostly mild. Mean FHR did not change significantly during and after episodes of SDB episodes compared to pre-event FHR, and did not change afterwards compared to during events, in unadjusted or adjusted (sleep stage, apnea type, degree of desaturation, age) analyses. In unadjusted analyses, FHRV significantly increased during SDB episodes compared to pre-SDB FHRV. After SDB events, FHRV was significantly lower than during SDB events. In fully adjusted models, these findings remained highly significant. FHRV was not significantly different after SDB events compared to pre-SDB event FHRV in unadjusted or adjusted models. Conclusion We observed consistent changes in FHR variability during and after maternal SDB events. Mean FHRV significantly increased during maternal SDB episodes compared to baseline FHRV, and decreased after SDB episodes. In contrast, mean FHR did not change significantly before, during and after SDB episodes. These data demonstrate that the fetus reacts to maternal SDB events, and raise questions about persistent effects of maternal SDB on the developing fetus. Support NIH HD079411

Does the saltatory pattern on cardiotocograph (CTG) trace really exist? The ZigZag pattern as an alternative definition and its correlation with perinatal outcomes

Background The saltatory pattern (SP) has been defined by guidelines as a uniformly increased bandwidth of >25 beats per min lasting for 30 min. However, previous research suggest that it is very unusual to observe such a “uniform” increase in the bandwidth persisting for >30 min. Baseline fetal heart rate variability (FHRV) on cardiotocography reflects the integrity of the central nervous system. During labor, in the presence of a gradually-evolving hypoxia associated with the onset of metabolic acidosis, FHRV may be reduced. However, if a fetus is exposed to rapidly-evolving hypoxia, it may not have sufficient time to release catecholamines and the perfusion of central organs can be impaired. In such cases, simultaneous increased activity of the sympathetic nervous system to obtain more oxygen as well as enhanced parasympathetic activity to reduce the myocardial workload can lead to autonomic instability. This exaggerated autonomic response can be seen frequently on the cardiotocograph as a rapid, irregular, abrupt “up and down” fluctuation across the baseline (amplitude >25 beats per min). The authors have termed this pattern as “ZigZag” when apparent for a minimum of 1 min. It differs from the SP in terms of duration and uniformity of the bandwidth. Objective To determine the incidence of the SP during labor as well as a shorter and less uniform version of the SP newly called “ZigZag pattern” (ZZP). The intention was to correlate them with perinatal outcomes, taking into account the duration of the ZZP. Study design A retrospective analysis of 500 consecutive cardiotocograph traces was performed to identify saltatory patterns and ZigZag patterns of 1 and 2 min of duration. Apgar scores, umbilical cord pH values and admission to the Neonatal Unit were evaluated and correlated with the cardiotocograph findings. Results Not a single case of the SP was observed. A ZZP of 1 min of duration (ZZP1) was identified in 30.1% of the CTG during the last hour prior to delivery; ZZP lasting for 2 min (ZZP2) were identified in 8.9% of cases during the same period. Apgar scores at 1 min of ≤7 were significantly more frequent in newborns where the ZZP was observed (36.7% in ZZP1 and 54.5% in ZZP2 versus 9.5% in fetuses without); similarly, the Apgar scores at 5 min of ≤7 were also more frequent when ZZP was observed (6.7% in ZZP1 and 13.6% in ZZP2 versus 1.1% in controls). Moderate acidosis (pH 7.0–7.10) was more common in fetuses with the ZZP (14.3% in ZZP1 and 15% in ZZP2) compared to those without (4.6 and 7.2%, respectively). Similarly, mild acidosis (pH 7.1–7.2) was more common with the ZZP (40.3% in ZZP1 and 35% in ZZP2 versus 27.6 and 31.7%, respectively without ZZP). The neonatal admission rate was significantly higher in fetuses with the ZZP (8.7% in ZZP1 and 11.4% in ZZP2 versus 1.1% in controls). Conclusions In line with previous research, our study suggest that SP is an almost nonexistent phenomenon. Alternatively, the ZigZag pattern (ZZP) has been defined as an exaggerated, irregular, “up and down” fluctuation of the baseline variability with an amplitude of >25 beats per min, lasting for 1 min or longer. It represents autonomic instability during human labor and it differs from the SP in terms of uniformity and length. Newborns with a ZZP during active maternal pushing were found to have statistically-significant lower Apgar scores at the 1st and 5th min, moderate and mild acidosis in the umbilical artery and an 8.7–11.4-fold higher neonatal admission rate. Clinicians should stop oxytocin infusion and/or active maternal pushing to improve fetal oxygenation if the ZZP is observed.

Physiological CTG interpretation: the significance of baseline fetal heart rate changes after the onset of decelerations and associated perinatal outcomes

Objective To determine the perinatal outcomes in fetuses with baseline fetal heart rate changes with preceding decelerations on the cardiotocography (CTG) trace, and to interpret CTG traces from the aspect of fetal physiology. Materials and methods A retrospective analysis of 500 consecutive CTG traces was carried out. The presence of repetitive variable and late decelerations followed by the changes in the baseline including baseline tachycardia and abnormal baseline variability were determined. Perinatal outcomes including Apgar scores and umbilical arterial pH at birth, NNU admission, and meconium-stained amniotic fluid were analyzed. We interpreted the changes in CTG based on fetal physiology. Results When repetitive variable and late decelerations were present without tachycardia (n = 81), none of the fetuses had an Apgar score <7 at 5 minutes or an umbilical cord pH <7. After the onset of fetal tachycardia (n = 262), fetuses showed decreased Apgar scores and umbilical arterial pH(p < .01), however, there was no significant difference in the rate of abnormal 5 min Apgar score, abnormal PH and NNU admission, if the baseline variability remained normal. However, if the baseline variability was abnormal (n = 44), (either increased or reduced) after tachycardia, there was a statistically significant increase in poor perinatal outcomes. Fetuses with abnormal versus normal variability had lower Apgar scores ≤7 at 5 min (29.6 versus 0.9%, p = .000); umbilical cord arterial pH <7 at birth (29.5 versus 0%, p = .000); increased admission to the NNU (27.3 versus 3.7%, p = .000) and increased incidence of meconium-stained amniotic fluid (38.6 versus 22.5%, p = .024). These serial changes in CTG could be interpreted and predicted by the application of fetal physiology. Conclusions There were significant differences in perinatal outcomes when fetuses were exposed to evolving intrapartum hypoxic stress culminating in an abnormal baseline fetal heart rate variability, which was preceded by repetitive decelerations, followed by an increase in the baseline heart rate. However, despite ongoing decelerations, if the baseline variability remained normal, none of the fetuses had a pH of <7. Therefore, the knowledge of fetal physiological response to evolving hypoxic stress can be reliably used to determine fetal compensation.

Correlation between Nonreassuring Patterns in Fetal Cardiotocography and Birth Asphyxia

Objectives: Cardiotocography (CTG) is a tool for assessing the fetus during labor and identifying the risk of asphyxia. Abnormal CTG can lead to stress in the physician and mother and result in their decision in terminating the pregnancy and the complications of an emergency cesarean section. The purpose of this study was the evaluation of the correlation between nonreassuring patterns in fetal CTG and birth asphyxia. Materials and Methods: In a cross-sectional analytic study, 324 term pregnant women were included. The association between nonreassuring patterns in CTG (fetal tachycardia, fetal bradycardia, absent or minimal baseline variability, and absence of acceleration and periodic or episodic deceleration) and birth asphyxia were assessed. Results: Birth asphyxia existed in 10 newborns; in all cases mild hypoxic ischemic encephalopathy (HIE) was observed. Within the nonreassuring CTG patterns, baseline fetal heart variability and periodic or episodic deceleration had a significant relationship with birth asphyxia. Most asphyxia cases had occurred in absent and minimal baseline fetal heart rate (FHR) variability (R = 0.49, P < .001). In periodic or episodic decelerations, most asphyxia cases occurred in recurrent late decelerations with normal baseline variability and variable decelerations with shoulders or overshoots (R = 0.42, P = .014). Conclusion: With regard to the findings of the present study we can use nonreassuring cardiotocographic patterns, especially absent and minimal baseline FHR variability and periodic or episodic decelerations in prediction of birth asphyxia. It seems however that most birth asphyxias occur in normal cardiotocographs.

Electronic fetal heart rate monitoring in five fetuses with Ebstein's anomaly

It is not clear whether fetuses with Ebstein's anomaly are likely to show abnormalities on electronic fetal heart rate (FHR) monitoring during labor. We performed retrospective analysis of FHR monitoring results obtained between 2.5 and 0.5 h prior to delivery in all of five fetuses prenatally diagnosed as having Ebstein's anomaly and born at our institution during the period between March 2005 and July 2011. All five mothers attempted to give birth vaginally. The results of FHR monitoring in 100 consecutive women with otherwise healthy singletons who attempted vaginal delivery were included as controls. The absence of FHR acceleration (4/5 [80%]), decreased baseline FHR variability (3/5 [60%]) and late deceleration (4/5 [80%]) were seen significantly more often in the five fetuses with Ebstein's anomaly than the 100 fetuses born to control women (6.0%, 6.0%, and 10%, respectively). Fetuses with Ebstein's anomaly during labor were likely to exhibit absent acceleration, decreased baseline FHR variability and late deceleration compared to infants without cardiac structural anomalies.

Near-term fetal response to maternal spoken voice

Knowledge about prenatal learning has been largely predicated on the observation that newborns appear to recognize the maternal voice. Few studies have examined the process underlying this phenomenon; that is, whether and how the fetus responds to maternal voice in situ. Fetal heart rate and motor activity were recorded at 36 weeks gestation (n=69) while pregnant women read aloud from a neutral passage. Compared to a baseline period, fetuses responded with a decrease in motor activity in the 10s following onset of maternal speech and a trend level decelerative heart rate response, consistent with an orienting response. Subsequent analyses revealed that the fetal response was modified by both maternal and fetal factors. Fetuses of women who were previously awake and talking (n=40) showed an orienting response to onset of maternal reading aloud, while fetuses of mothers who had previously been resting and silent (n=29) responded with elevated heart rate and increased movement. The magnitude of the fetal response was further dependent on baseline fetal heart rate variability such that largest response was demonstrated by fetuses with low variability of mothers who were previously resting and silent. Results indicate that fetal responsivity is affected by both maternal and fetal state and have implications for understanding fetal learning of the maternal voice under naturalistic conditions.

Fetal acidemia and electronic fetal heart rate patterns: Is there evidence of an association?

Objective. Despite the ubiquity of electronic fetal monitoring, the validity of the relationship between various fetal heart rate (FHR) patterns and fetal acidemia has not yet been established in a large unselected series of consecutive pregnancies. The aim of this study was to examine the published literature for evidence of such a relationship.Methods. Four hypotheses based on assumptions in common clinical use were examined. The literature was searched for relationships between certain aspects of FHR patterns (e.g., degree of FHR variability, depth of decelerations), and fetal acidemia, or fetal vigor (5-minute Apgar score ≥7). We also attempted to relate duration of these patterns to the degree of acidemia. Using standardized FHR nomenclature we defined patterns based on baseline FHR variability, baseline rate, decelerations, and accelerations.Results. The following relationships were observed: (1) Moderate FHR variability was strongly associated (98%) with an umbilical pH >7.15 or newborn vigor (5-minute Apgar score ≥7). (2) Undetectable or minimal FHR variability in the presence of late or variable decelerations was the most consistent predictor of newborn acidemia, though the association was only 23%. (3) There was a positive relationship between the degree of acidemia and the depth of decelerations or bradycardia. (4) Except for sudden profound bradycardia, newborn acidemia with decreasing FHR variability in combination with decelerations develops over a period of time approximating one hour. Most studies identified were observational and uncontrolled (grade III evidence of US Preventive Services Task Force); however, there was general agreement amongst the various studies, strengthening the validity of the observations.Conclusions. The validity of the relationship between certain FHR patterns and fetal acidemia and/or vigor, is supported by observations from the literature. In addition four assumptions commonly used in clinical management are supported. These conclusions need to be confirmed by a prospective examination of a large number of consecutive, unselected FHR patterns, and their relationship to newborn acidemia. Pending the completion of such studies, these observations can be used to justify certain aspects of current clinical management, and may assist in standardizing the diversity of opinions regarding FHR pattern management.

Intrapartum fetal heart rate monitoring in cases of cytomegalovirus infection

ObjectiveSeveral studies have shown that abnormal intrapartum fetal heart rate patterns are the results from pre-existing fetal brain damage. We evaluated intrapartum fetal heart rate pattern of cytomegalovirus-infected fetuses and correlated the patterns with neurologic outcomes. Study designBetween 1991 and 2001, there were 20 cytomegalovirus-infected fetuses. We selected 40 fetuses as control subjects that were matched for gestational age and birth weight. Fetal heart rate was interpreted according to the guidelines of the National Institute for Child and Human Development. The incidence of abnormal fetal heart rate pattern and umbilical blood gases were compared between both groups. We also investigated the factors that contributed to abnormal fetal heart rate pattern in the cytomegalovirus group. ResultsNonreassuring fetal heart rate patterns (prolonged deceleration and recurrent late deceleration) were observed in 8 of 20 fetuses (prolonged deceleration, 7 fetuses; recurrent late deceleration, 1 fetus) in the cytomegalovirus group and in 3 of 41 fetuses (prolonged deceleration, 1 fetus; recurrent late deceleration, 2 fetuses) in the control group (P<.05, Fisher test). Baseline fetal heart rate variability was minimal in 4 of the 7 prolonged deceleration cases in the cytomegalovirus group. Umbilical pH <7.1 was found for 1 fetus in the cytomegalovirus group. The average umbilical arterial pH values were similar in both the groups. In the cytomegalovirus group, there were no differences in the incidence of contributing factors between 8 fetuses with abnormal fetal heart rate pattern (prolonged deceleration and recurrent late deceleration) and 8 fetuses with no change. There were 3 fetuses with cerebral palsy: 2 fetuses in the no change group and 1 fetus in the prolonged deceleration group. Antigenemia was positive exclusively in 4 cases with abnormal fetal heart rate pattern (P<.05). ConclusionCytomegalovirus-infected fetuses are more likely to show abnormal intrapartum fetal heart rate patterns than low-risk control fetuses, which suggests that the perinatal detection of cytomegalovirus is necessary to distinguish hypoxic-ischemic encephalopathy.

Late Second-Trimester Nonstress Test Characteristics in Preterm Delivery before 32 Weeks of Gestation

Objective: To clarify electronic fetal heart rate (FHR) monitoring characteristics in pregnancies with preterm delivery before 32 weeks of gestation, using the late second-trimester nonstress test. Methods: Among 953 children born from 1993 to 1996, we identified 100 singleton infants born before 32 weeks of gestation in whom second-trimester (24–27 weeks of gestation) electronic fetal monitoring (EFM) records were obtained. Individual components of the FHR patterns [baseline rate, baseline FHR variability, presence of acceleration (at least 10 beats/min for at least 10 s) and periodic or episodic deceleration (at least 25 beats/min for at least 15 s)] and birth characteristics were compared between pregnancy with or without second-trimester decelerations. Results: Among 100 infants, 65 had and 35 did not have second-trimester decelerations. There were no significant differences in gestational age at birth, birth weight, cord arterial blood pH, Apgar score and meconium staining between pregnancies with second-trimester decelerations and those without second-trimester decelerations. There were no significant differences in baseline rate and baseline variability between pregnancies with or without second-trimester decelerations. The number of accelerations in pregnancies with second-trimester decelerations was significantly more frequent than that in pregnancies without second-trimester decelerations (p < 0.001). There was a significant increase in the occurrence of premature rupture of the membranes (PROM; 60.0%) in pregnancies with second-trimester decelerations, when compared with events (37.1%) related to pregnancies without second-trimester decelerations (p < 0.05). There were no significant differences in the onset of breech presentation, cervical incompetency, preeclampsia and abnormal FHR pattern at birth between pregnancies with second-trimester decelerations and those without second-trimester decelerations. Pregnancies with PROM after second-trimester EFM were significantly more likely to have second-trimester decelerations than those without PROM (75.0 vs. 54.2%, p < 0.05). Conclusion: Periodic or episodic decelerations during late second-trimester EFM were associated with an increased risk of the occurrence of PROM in pregnancies with preterm delivery before 32 weeks of gestation.

INTRAPARTUM FETAL SURVEILLANCE: Is It Worthwhile?

Potentially significant intrapartum fetal asphyxia occurs in approximately 20 per 1000 births. Moderate and severe fetal asphyxia exposure with newborn morbidity occurs in 3 to 4 1000 births, with brain damage and subsequent disability in at least 1 per 1000 births. Although the prevalence of moderate and severe asphyxia is modest, prevention is important because of the serious implications of this complication to the child, family, and society. Because of the limited predictive value of clinical risk factors, the interpretation of patterns in a fetal heart rate record has become the primary screening test for intrapartum fetal asphyxia. Despite extensive clinic experience and numerous clinical trials, the benefits of EFM as a screening test have not been established, and harm may occur owing to unnecessary intervention. This observation raises serious ethical issues. When an intervention is initiated by the clinician rather than the patient, the clinician under greater obligation to ensure that the benefits outweigh the harm. Several factors complicate the demonstration of benefits of EFM as a screening test. There is no consensus regarding a protocol of fetal surveillance for low-risk patient who account for approximately 25% of intrapartum fetal asphyxia. Moderate and severe asphyxia cannot be prevented when asphyxial exposure has occurred before labor or before the onset of fetal surveillance. Prediction of intrapartum fetal asphyxia cannot occur when the quality of the record does not permit interpretation. Interpretation of predictive fetal heart rate patterns cannot occur unless the record is consistently and carefully scored. Prediction of most cases of intrapartum fetal asphyxia on the basis of fetal heart rate patterns is possible but difficult. Because the goal of intrapartum fetal surveillance is the prevention of moderate and severe fetal asphyxia, prediction must be achieved before fetal decompensation. Prediction must occur before absent baseline fetal heart rate variability evident in the record, which is uniformly associated with cerebral dysfunction and, in some cases, brain damage. The possibility of fetal asphyxia must be considered when, within a 1-hour window of recording, there are two or more cycles of minimal baseline fetal heart rate variability and two or more cycles of late or prolonged decelerations or both. Because approximately 9 of 10 predictive fetal heart rate patterns are false-positive, supplementary tests to confirm the diagnosis and to identify false-positives to prevent unnecessary intervention are essential. Until such time as additional fetal assessment tests are validated, blood gas and acid-base assessment of fetal blood can provide a definitive diagnosis and identify false-positive predictions.

Comparison of late–second-trimester nonstress test characteristics between small for gestational age and appropriate for gestational age infants

Objective: To compare electronic fetal heart rate (FHR) monitoring characteristics between appropriate for gestational age (AGA) fetuses and small for gestational age (SGA) fetuses and to determine whether SGA fetuses have specific abnormalities at second-trimester electronic fetal monitoring (EFM), using nonstress test. Methods: Among 953 children born from 1993–1996, we identified 500 singleton infants born after 36 weeks’ gestation of uncomplicated pregnancies in whom second-trimester (24–27 weeks’ gestation) EFM records were obtained. Individual components of FHR patterns (baseline rate, baseline FHR variability, presence of acceleration [at least 10 beats per minute for at least 10 seconds], and periodic or episodic deceleration [at least 25 beats per minute for at least 15 seconds]) and birth characteristics were compared between AGA and SGA infants, or between pregnancies with or without second-trimester decelerations. Results: Among 500 infants, 443 were AGA and 57 SGA; 105 had and 395 did not have second-trimester decelerations. Baseline FHR variability (12.9 ± 3.2 beats per minute) in SGA fetuses was significantly higher than variability (10.3 ± 3.4 beats per minute) in AGA fetuses ( P < .001). Small for gestational age fetuses were significantly more likely to have second-trimester decelerations than AGA fetuses (33.3% vs 19.4%, P < .05). There were no significant differences in baseline rate and accelerations between AGA and SGA infants. Small for gestational age infants were more frequent in pregnancies with second-trimester decelerations, compared with those without second-trimester decelerations (18.1% vs 9.6%, P < .05). Baseline FHR variability in pregnancies with second-trimester decelerations was significantly higher than in pregnancies without second-trimester decelerations (12.2 ± 3.7 vs 10.0 ± 3.1 beats per minute, P < .001). Conclusion: Periodic or episodic decelerations and increased FHR variability during late second-trimester EFMwere associated with an increased risk of SGA birth weight.

Prophylactic intrapartum amnioinfusion: A randomized clinical trial

Amnioinfusion was performed in a prospective, randomized trial of 60 women in the latent phase of labor with oligohydramnios, as defined by an amniotic fluid index ≤5.0 cm. All fetuses were at least 37 weeks' gestational age, had normal baseline fetal heart rate variability, and no clinically significant fetal heart rate decelerations at the outset. Subjects in the amnioinfusion group ( n = 30) were titrated to and maintained at an amniotic fluid index level ≥8.0 cm throughout labor. In the group receiving amnioinfusion, significantly lower rates of meconium passage ( p = 0.04), severe variable decelerations ( p = 0.04), end-stage bradycardia ( p = 0.05), and operative delivery for fetal distress ( p = 0.002) occurred. Significantly higher umbilical arterial blood pH values were also noted in the infusion group ( p = 0.02). We conclude that prophylactic intrapartum amnioinfusion is an important technique for the reduction of intrapartum morbidity.

Prophylactic intrapartum amnioinfusion: A randomized clinical trial

Amnioinfusion was performed in a prospective, randomized trial of 60 women in the latent phase of labor with oligohydramnios, as defined by an amniotic fluid index less than or equal to 5.0 cm. All fetuses were at least 37 weeks' gestational age, had normal baseline fetal heart rate variability, and no clinically significant fetal heart rate decelerations at the outset. Subjects in the amnioinfusion group (n = 30) were titrated to and maintained at an amniotic fluid index level greater than or equal to 8.0 cm throughout labor. In the group receiving amnioinfusion, significantly lower rates of meconium passage (p = 0.04), severe variable decelerations (p = 0.04), end-stage bradycardia (p = 0.05), and operative delivery for fetal distress (p = 0.002) occurred. Significantly higher umbilical arterial blood pH values were also noted in the infusion group (p = 0.02). We conclude that prophylactic intrapartum amnioinfusion is an important technique for the reduction of intrapartum morbidity.

Maternal and fetal effects of low-dosage bupivacaine paracervical block.

Vasoconstriction of the uterine arteries, hypertonus of the uterus, and the direct toxic effects of a local anesthetic on the fetus or a combination of the above have been presented as etiological factors of fetal bradycardia following paracervical block. The reduce fetal side-effects a superficial and lowdosage technique of PCB have been advocated. We have studied the effects of 25 mg of bupivacaine PCB using the above technique on fetal heart rate pattern (FHR), fetal acid-base balance, uterine activity, placental blood flow and maternal and fetal plasma levels of bupivacaine in 38 patients. The analgesic effect of a single 25 mg of bupivacaine PCB was good in 76%, moderate in 12% and poor in 12% of the cases. No changes in maternal heart rate or in blood pressure were noted. Fetal bradycardia defined as a decrease of mean fetal heart rate of at least 20 bpm or an absolute rate less than 100 bpm and a duration greater than two minutes occurred in 12% of the cases. The mean amplitude of the baseline fetal heart rate variability decreased significantly after PCB and a silent pattern (an amplitude less than 5 bpm) was observed in 20% of the cases. The most frequent (27%) pathological finding in our study was the disappearance of FHR accelerations after PCB. Similarly early and late decelerations of FHR occurred more often after PCB than during the control period before the block. The fetal pH from scalp blood samples did not, on average, decrease after PCB, but did so in cases with fetal bradycardia. Intervillous blood flow as measured by the 133Xe washout method did not change when measured before and after PCB. In addition in three cases with fetal bradycardia the changes in the intervillous blood flow were minimal. No significant changes in the mean uterine tone, amplitude and frequency of contractions were observed after PCB. However, an obvious uterine hypertonus was observed after PCB was observed in three cases of fetal bradycardia but not in two other cases of bradycardia or in the 8 cases of silent FHR pattern. Mean maternal bupivacaine concentration 20 minutes after PCB was 0.14 +/- 0.06 microgram/ml and 0.07 +/- 0.04 microgram/ml at birth. Simultaneous fetal and umbilical venous and arterial concentrations were correspondingly 0.04 +/- 0.02 microgram/ml, 0.03 +/- 0.01 microgram/ml and 0.03 +/- 0.01 microgram/ml, and they were significantly lower than respective maternal concentrations.(ABSTRACT TRUNCATED AT 400 WORDS)

Fetal baseline heart rate variability estimation: I. Comparison of clinical and stochastic quantification techniques

Baseline fetal heart rate variability is an important parameter in the evaluation of fetal status during the intrapartum period. Prior descriptions of variability have largely been either visual-subjective or stochastic in nature. Unfortunately, correlation between the two has not been substantiated. Sample heart rate tracings were evaluated for variability by a panel of nine experts. Interobserver agreement in the evaluation of variability was high; correlation between visual subjective and stochastic methods was low. The implications are discussed.

The effect of lumbar epidural anesthesia on fetal heart rate baseline variability.

Baseline fetal heart rate (FHR) variability has become an important parameter in the diagnosis of fetal distress when electronically monitoring the fetus. Loss of the baseline variability has been noted to be associated with fetal distress, and in association with late deceleration or severe variable deceleration patterns has been shown to be ominous. Baseline FHR variability, however, has been modified not only by fetal distress but also by prematurity and the administration of certain drugs to the mother. Because FHR is often monitored during labor in parturients given lumbar anesthesia, the question of the effect of this procedure on FHR variability arose. Fifteen such patients with no antepartum or intrapartum complications were studied in active labor. All were monitored by electrocardiography on a continuous basis, FHR being studied before and after epidural anesthesia with lidocaine, with and without epinephrine. Of the 15 patients, tracings in 8 (53 percent) revealed a minimal or moderate change in baseline variability within several minutes of drug injection. This change in variability was recorded from 4 to 18 minutes, after which time the pre-epidural FHR variability was reestablished. Although the mechanism for this result was not definitively determined, such variability in FHR does not in itself seem significant of fetal distress but suggests supportive measures for the patient.