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Effects of maternal breathing rate, psychiatric status, and cortisol on fetal heart rate.

ABSTRACT: Women's experiences during pregnancy are predictive of variation in neurobehavioral profiles in their children. Few studies have assessed these relationships during the prenatal period. In 113 women in the 36(th) -38(th) gestational week (mean age 26.3 ± 5.4 years), electrocardiogram, blood pressure, respiration, salivary cortisol, and fetal heart rate (HR) were measured during baseline, a psychological challenge (Stroop color-word matching task), and a standardized paced breathing protocol. Subjects underwent the Structured Clinical Interview for DSM-IV prior to testing and were grouped as: depressed, co-morbid for depression and anxiety, anxiety disorder only, and control. There was a significant main effect of maternal diagnostic group on fetal HR only during the Stroop task: fetuses of women in the co-morbid group had a greater HR increase compared to controls (p < .05). Overall, fetuses showed robust increases in HR during paced breathing (p < .0001), and there was no significant difference by maternal diagnosis. For both tasks, changes in fetal HR were independent of women's concurrent cardiorespiratory activity. Finally, although cortisol was higher in the co-morbid group (p < .05), across all participants, there was a trend for maternal baseline cortisol to be positively associated with average fetal HR (p = .06). These findings indicate that variation in fetal HR reactivity-an index of emerging regulatory capacities-is likely influenced by multiple acute and chronic factors associated with women's psychobiology.

SUBMITTER: Monk C

PROVIDER: S-EPMC3747960 | biostudies-literature | 2011 Apr

REPOSITORIES: biostudies-literature

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Effects of maternal breathing rate, psychiatric status, and cortisol on fetal heart rate.

Monk Catherine C Fifer William P WP Myers Michael M MM Bagiella Emilia E Duong Jimmy K JK Chen Ivy S IS Leotti Lauren L Altincatal Arman A

Developmental psychobiology 20101117 3

Women's experiences during pregnancy are predictive of variation in neurobehavioral profiles in their children. Few studies have assessed these relationships during the prenatal period. In 113 women in the 36(th) -38(th) gestational week (mean age 26.3 ± 5.4 years), electrocardiogram, blood pressure, respiration, salivary cortisol, and fetal heart rate (HR) were measured during baseline, a psychological challenge (Stroop color-word matching task), and a standardized paced breathing protocol. Sub ...[more]

PMID: 21400485

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Project description:BackgroundMaternal sleep-disordered breathing is associated with adverse pregnancy outcomes and is considered to be deleterious to the developing fetus. Maternal obesity potentiates sleep-disordered breathing, which, in turn, may contribute to the effect of maternal obesity on adverse fetal outcomes. However, only a few empirical studies have evaluated the contemporaneous effects of maternal sleep-disordered breathing events on fetal well-being. These events include apnea and hypopnea with accompanying desaturations in oxyhemoglobin.ObjectiveThis study aimed to reconcile contradictory findings on the associations between maternal apnea or hypopnea events and clinical indicators of fetal compromise. It also sought to broaden the knowledge base by examining the fetal heart rate and heart rate variability before, during, and after episodes of maternal apnea or hypopnea. To accomplish this, we employed overnight polysomnography, the gold standard for ascertaining maternal sleep-disordered breathing, and synchronized it with continuous fetal electrocardiography.Study designA total of 84 pregnant women with obesity (body mass index >30 kg/m2) participated in laboratory-based polysomnography with digitized fetal electrocardiography recordings during or near 36 weeks of gestation. Sleep was recorded, on average, for 7 hours. Decelerations in fetal heart rate were identified. Fetal heart rate and heart rate variability were quantified before, during, and after each apnea or hypopnea event. Event-level intensity (desaturation magnitude, duration, and nadir O2 saturation level) and person-level characteristics based on the full overnight recording (apnea-hypopnea index, mean O2 saturation, and O2 saturation variability) were analyzed as potential moderators using linear mixed effects models.ResultsA total of 2936 sleep-disordered breathing events were identified, distributed among all but 2 participants. On average, participants exhibited 8.7 episodes of apnea or hypopnea per hour (mean desaturation duration, 19.1 seconds; mean O2 saturation nadir, 86.6% per episode); nearly half (n=39) of the participants met the criteria for obstructive sleep apnea. Only 45 of 2936 apnea or hypopnea events were followed by decelerations (1.5%). Conversely, most (n=333, 88%) of the 378 observed decelerations, including the prolonged ones, did not follow an apnea or a hypopnea event. Maternal sleep-disordered breathing burden, body mass index, and fetal sex were unrelated to the number of decelerations. Fetal heart rate variability increased during events of maternal apnea or hypopnea but returned to initial levels soon thereafter. There was a dose-response association between the size of the increase in fetal heart rate variability and the maternal apnea-hypopnea index, event duration, and desaturation depth. Longer desaturations were associated with a decreased likelihood of the variability returning to baseline levels after the event. The mean fetal heart rate did not change during episodes of maternal apnea or hypopnea.ConclusionEpisodes of maternal sleep apnea and hypopnea did not evoke decelerations in the fetal heart rate despite the predisposing risk factors that accompany maternal obesity. The significance of the modest transitory increase in fetal heart rate variability in response to apnea and hypopnea episodes is not clear but may reflect compensatory, delimited autonomic responses to momentarily adverse conditions. This study found no evidence that episodes of maternal sleep-disordered breathing pose an immediate threat, as reflected in fetal heart rate responses, to the near-term fetus.

Project description:ObjectiveThis study aimed to determine whether maternal cortisol levels affect fetal heart rate patterns in primiparous pregnant women in the third trimester.MethodsThis cross-sectional descriptive study included 400 primiparous pregnant women with uncomplicated pregnancies between November and December 2022. The study included primiparous pregnant women over 18 years old in the third trimester who had not exercised for at least 2 h before the fetal heart rate monitoring and had a healthy pregnancy without consuming any food or drink. Fetuses with decelerating heartbeats and pregnant women who showed uterine contraction and cervical dilation during the fetal heart rate monitoring were excluded from the study. Research data were collected with the data collection form. The fetal heart rate data were collected using a cardiotocograph. At least two accelerations during the 20-min nonstress test period were the basis for diagnosing a reactive nonstress test. About 5 mL of maternal saliva for cortisol measurements was collected before fetal heart rate monitoring. Research data were analyzed with IBM SPSS Statistics for Macintosh, Version 28.0. A p-value of <0.05 was considered significant.ResultsThere were no significant differences in the comparison of the groups in terms of education and income status, family type, fetal gender, pregnancy planning status, BMI and age averages, or gestational week averages (p>0.05). The number of at least two accelerations required for the diagnosis of reactive NST was also higher in Group 1 (maternal salivary cortisol level ≤24.20). A moderately positive relationship between fetal heart rate and maternal salivary cortisol was observed (r=0.448, p=0.000). In total, 11.9% of the total change in fetal heart rate level is explained by maternal cortisol (R2=0.119). Maternal cortisol increases fetal heart rate level (ß=0.349).ConclusionThese findings suggest that stress in primiparous pregnant women with high cortisol levels may influence fetal heart rate patterns. It was revealed that the increase in cortisol level, considered a stress hormone, may be a harbinger of fetal tachycardia.

Project description:Background: Prenatal exposure to serotonin reuptake inhibitor (SRI) antidepressants increases risk for adverse neurodevelopmental outcomes, yet little is known about whether effects are present before birth. In relation to maternal SRI pharmacokinetics, this study investigated chronic and acute effects of prenatal SRI exposure on third-trimester fetal heart rate variability (HRV), while evaluating confounding effects of maternal depressed mood. Methods: At 36-weeks' gestation, cardiotocograph measures of fetal HR and HRV were obtained from 148 pregnant women [four groups: SRI-Depressed (n = 31), SRI-Non-Depressed (n = 18), Depressed (unmedicated; n = 42), and Control (n = 57)] before, and ~5-h after, typical SRI dose. Maternal plasma drug concentrations were quantified at baseline (pre-dose) and four time-points post-dose. Mixed effects modeling investigated group differences between baseline/pre-dose and post-dose fetal HR outcomes. Post hoc analyses investigated sex differences and dose-dependent SRI effects. Results: Maternal SRI plasma concentrations were lowest during the baseline/pre-dose fetal assessment (trough) and increased to a peak at the post-dose assessment; concentration-time curves varied widely between individuals. No group differences in fetal HR or HRV were observed at baseline/pre-dose; however, following maternal SRI dose, short-term HRV decreased in both SRI-exposed fetal groups. In the SRI-Depressed group, these post-dose decreases were displayed by male fetuses, but not females. Further, episodes of high HRV decreased post-dose relative to baseline, but only among SRI-Non-Depressed group fetuses. Higher maternal SRI doses also predicted a greater number of fetal HR decelerations. Fetuses exposed to unmedicated maternal depressed mood did not differ from Controls. Conclusions: Prenatal SRI exposure had acute post-dose effects on fetal HRV in late gestation, which differed depending on maternal mood response to SRI pharmacotherapy. Importantly, fetal SRI effects were sex-specific among mothers with persistent depressive symptoms, as only male fetuses displayed acute HRV decreases. At trough (pre-dose), chronic fetal SRI effects were not identified; however, concurrent changes in maternal SRI plasma levels suggest that fetal drug exposure is inconsistent. Acute SRI-related changes in fetal HRV may reflect a pharmacologic mechanism, a transient impairment in autonomic functioning, or an early adaption to altered serotonergic signaling, which may differ between males and females. Replication is needed to determine significance with postnatal development.

Dataset Information

Effects of maternal breathing rate, psychiatric status, and cortisol on fetal heart rate.

Publications

Effects of maternal breathing rate, psychiatric status, and cortisol on fetal heart rate.

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