Maternal stress and the fetal heart rate

Something goes bump in the night and suddenly your heart is racing. The link between stress and heart rate has been well established. Catecholamines are released from the adrenal medulla and the sympathetic nervous system is activated. These have a fairly short duration of effect. Cortisol is released from the adrenal cortex and has a longer duration of effect, and is therefore easier to measure. Cortisol has been well established as a measure of stress in physiological research.

What is less well known is the impact of maternal stress on the fetal heart rate and the consequences of this. When that thing goes bump in the night and stresses the woman, what happens to the fetal heart rate? It’s an important question. If maternal stress is associated with changes in fetal heart rate patterns, then we should take stress levels into consideration when interpreting fetal heart rate patterns seen with CTG monitoring. If there is an association with abnormal patterns, then considering the psychological impact of care processes on women’s stress levels is also important.

The impact of CTG use on maternal emotional state

There has been a small amount of research examining the relationship between CTG use and maternal anxiety or stress. This is something I have written about before. In 1985, a team of researchers based in Israel measured serum cortisol, along with other stress hormones before, during, and after a period of CTG monitoring (Shalev, et al., 1985). All women were at least 38 weeks pregnant, some women were not in labour and others were in early labour. Among women who were not in labour, those exposed to CTG monitoring had a sharp rise in cortisol levels immediately after monitoring was commenced, with levels remaining higher up to 30 minutes after CTG monitoring was complete (they didn’t measure beyond this point in time). Among women who were in labour, cortisol levels were more than double those who were not in labour, with no significant difference between those with and those without CTG monitoring.

In 2008 Manusco, et al. documented an increase in women’s anxiety levels after antenatal CTG monitoring. There has been little further exploration in this area until this year. Researchers have flipped the question on its head, and are now asking whether maternal emotional states and elevated cortisol levels have an impact on fetal heart rate patterns.

The impact of emotions on fetal heart rate

A German research team recently published findings regarding the link between fetal heart rate variability (the amount of wiggle up and down around the baseline heart rate) and maternal emotional state as measured by a bank of validated psychological questionnaires (Semeia, et al., 2023). They used a magnetocardiograph, rather than a Doppler based cardiotocograph, to gather fetal heart rate data from women who were 32 – 38 weeks pregnant. The measures of fetal heart rate variability they studied were those used in physiology research examining the potential for heart rate variability monitoring in adults to be used as a biomarker for emotional state (see for example Zhu, et al., 2019) rather than those used clinically in maternity care provision.

Women with overall high stress levels had fetuses with lower levels of LF heart rate variability (this measures both sympathetic and parasympathetic activity). When the researchers separated women according to whether the source of stress related to depressive or anxious symptoms, there was a difference in the type of fetal heart rate variability impacted. For depression LF was lower, while for anxiety NN10 and HF (both measures of parasympathetic activity) were lower. The difference did not persist into postnatal life for women with high depression scores, but infants born to women with higher anxiety continued to have reduce HF variability in the postnatal period.

Another team of researchers (Singh, et al., 2023) recently explored the relationship between women’s anxiety level, stress hormones, and fetal heart rate. 40 women completed the State-Trait Anxiety Inventory and then had a period of CTG monitoring at 30 weeks of pregnancy. During this period of monitoring, vibroacoustic stimulation was applied and the fetal response to this was noted. The “normal” response to this is for the fetus to have a period of fetal heart rate acceleration soon after the stimulus.

They found women with high trait anxiety scores (indicating a long term predisposition to anxious responses) had high levels of corticotropin releasing hormone (this stimulates cortisol production), a trend towards higher cortisol levels (but not statistically significant), and their fetuses were much less likely to respond to vibroacoustic stimulation with an accelerative pattern (18% vs 83%, p = 0.002).

The impact of maternal cortisol levels on fetal heart rate

Researchers based in Turkey recently published their work looking at the relationship between maternal cortisol levels and fetal heart rate patterns in the third trimester (Turan, et al., 2023). They identified two groups of women on the basis of either normal (203 women) or elevated (197 women) salivary cortisol levels. Fetal heart rate patterns were recorded by CTG. All women were in the third trimester (the mean gestational age was 36 weeks) and were not in labour. Women with decelerations on the CTG were excluded.

There was a significant difference in the number of women with a “reactive” fetal heart rate pattern, with 97% of women with normal cortisol achieving this and only 51% of women with elevated levels of cortisol. The baseline fetal heart rate was higher in women with elevated cortisol (but both rates were well within what is considered normal – mean of 142 bpm vs 138 bpm, p=0.027). After correcting for other factors that might impact on baseline fetal heart rate, elevated cortisol levels continued to exert a statistically significant impact.

The differences were subtle and unlikely to make a large impact on clinical decision making. In hindsight, it would have been useful to include women with CTGs showing decelerations. Knowing whether decelerations were more common in women with high cortisol levels or not would be clinically useful information.

How do we make sense of this information?

Maternal stress alters autonomic nervous system tone and the endocrine system via the stress response – this is well established. The interrelationships between maternal stress and emotions, fetal heart rate, and the physiological mechanisms that regulate those relationships are not (yet) well mapped out. But there is evidence to suggest something is going on here, and further research is worth pursuing. There are two possibilities I can think of (and probably others I haven’t considered):

High levels of maternal stress, with higher sympathetic tone cause vasoconstriction in the placental bed, reduce placental blood flow, and therefore fetal oxygenation. The fetus compensates for this and changes in the heart rate are a sign of this compensation. In a vulnerable fetus, with prolonged high levels of maternal stress, it might be possible the threshold for compensation is exceeded and hypoxia becomes a problem.
Maternal and fetal neuroendocrine environments might be co-regulated. That is, changes in fetal heart rate and stress hormone levels might simply mirror the physiological changes in the woman, without any change in fetal oxygenation. While this means there is no risk for hypoxic damage, there might still be long term consequences on nervous system development, mediated by epigenetic mechanisms for example.

What does this mean for clinical practice?

There are many good reasons why maternity professionals should identify maternal stress and distress and provide support and assistance to mitigate this, not just related to the potential impact on fetal heart rate patterns. For example, there is robust evidence that depression, anxiety, and high levels of perceived stress are associated with higher rates of spontaneous preterm labour (Staneva, et al., 2015). Therapeutic relationships developed in continuity of care models are likely to be effective in reducing women’s distress and this might explain why lower rates of preterm birth have been documented for women in midwifery continuity of care (Sandall, et al., 2016). Ensuring all women can access continuity of care and build a supportive relationship with their midwife (and/or other maternity professionals) is an important starting point.

We should also pay attention to birth room environment, both in terms of the physical space and also the psychosocial environment. Women who had negative birth experiences have described how the birth environment generated fear (Nilsson, 2014). Constant surveillance by an unseen observer outside the room (as central fetal monitoring was in use) and unequal distributions of power generated anxiety. One woman described the resultant disconnection with her birth:

It was as if somebody else controlled the delivery. As if it was something else, you know, you could see it on the monitors . . . how the contractions were and how the baby was. It felt as if I was not at one with my body. I was sort of not in my own body or part of it.
p. 201

Fahy, Foureur, and Hastie provide useful and practical advice about how to generate birth environments that feel safe and reduce women’s stress in their book Birth Territory and Midwifery Guardianship (2008). I recommend it to any maternity professional seeking to improve care in this area – and particularly those involved in the physical (re)design of birthing spaces in healthcare settings. It is well past time we also ask some serious questions about the impact of central fetal monitoring on women’s emotional state in labour and on birth outcomes. And I’m mindful that while the potential for better birth environments to improve perinatal outcome is a motivator for investment and change, making the experience of care better for women is an important end point on its own.

References

Fahy, K., Fouler, M., & Hastie, C. (2008). Birth Territory and Midwifery Guardianship. Elsevier.

Mancuso, A., De Vivo, A., Fanara, G., Denaro, A., Laganà, D., & Maria Accardo, F. (2008). Effects of antepartum electronic fetal monitoring on maternal emotional state. Acta Obstetricia et Gynecologica Scandinavica, 87(2), 184-189. https://doi.org/10.1080/00016340701823892

Nilsson, C. (2014). The delivery room: is it a safe place? A hermeneutic analysis of women’s negative birth experiences. Sexual & Reproductive Healthcare, 5(4), 199-204. https://doi.org/10.1016/j.srhc.2014.09.010

Sandall, J., Soltani, H., Gates, S., Shennan, A., & Devane, D. (2016). Midwife-led continuity models versus other models of care for childbearing women. Cochrane Database of Systematic Reviews, 4(11), CD004667. https://doi.org/10.1002/14651858.CD004667.pub5

Semeia, L., Bauer, I., Sippel, K., Hartkopf, J., Schaal, N. K., & Preissl, H. (2023). Impact of maternal emotional state during pregnancy on fetal heart rate variability. Comprehensive Psychoneuroendocrinology, 14. https://doi.org/10.1016/j.cpnec.2023.100181

Shalev, E., Eran, A., Harpaz-kerpel, S., & Zuckerman, H. (1985). Psychogenic stress in women during fetal monitoring (hormonal profile). Acta Obstetricia et Gynecologica Scandinavica, 64(5), 417-420. https://doi.org/10.3109/00016348509155159

Singh, P., Sheikher, C., & Sharma, A. (2023). To study the effect of an acute mother stress reaction and anxiousness on the heart rate of the foetus. International Journal of Life Sciences, Biotechnology & Pharma Research, 12, 1-6.

Staneva, A., Bogossian, F., Pritchard, M., & Wittkowski, A. (2015). The effects of maternal depression, anxiety, and perceived stress during pregnancy on preterm birth: A systematic review. Women & Birth, 28(3), 179-193. https://doi.org/10.1016/j.wombi.2015.02.003

Turan, A., & Kaya, C. (2023). Effect of maternal cortisol levels on fetal heart rate patterns in primiparous pregnant women in the third trimester. Revista da Associação Médica Brasileira, 69(5), e20221610. https://doi.org/10.1590/1806-9282.20221610

Zhu, J., Ji, L., & Liu, C. (2019). Heart rate variability monitoring for emotion and disorders of emotion. Physiological Measurement, 40(6), 064004. https://doi.org/10.1088/13616579/ab1887