- The significance of maternal and fetal autonomic neural control changes in preeclamptic women
The significance of maternal and fetal autonomic neural control changes in preeclamptic women
PERINATOLOGY AND PEDIATRIC. UKRAINE. 2017.3(71):32-38; doi 10.15574/PP.2017.71.32
Grishchenko O. V., Lakhno I. V., Demchenko O. B., Storchak A. V., Bobritskaya V. V., Dudko V. L.
Kharkiv Medical Academy of Postgraduate Education, Ukraine
Preeclampsia is one of the most important problems of modern obstetrics. Preeclampsia complicates from 5.0% to 16.0% of pregnancies, 5 times increases the risk of perinatal losses and accounts more than 50 000 cases of maternal deaths in the world annually.
Objective — to investigate the state of maternal and fetal autonomic nervous regulation in healthy pregnancy and in preeclampsia.
Material and methods. 292 pregnant women were examined, 154 of them were preeclamptic. The variables of sympathovagal balance, central maternal hemodynamics and spectral analysis of the blood flow velocity curves in the cord vein were studied.
Results. Preeclampsia develops on a background of sympathetic overactivity, a suppression of total autonomic tone and parasympathetic branch of regulation. This helps to provide a hyperkinetic type of central maternal hemodynamics, which compensatory supports a sufficient level of perfusion of end-organs in women with mild and moderate preeclampsia. The lack of vagal tone, the further decrease in autonomic nervous regulation coupled with the peripheral vascular resistance increase and cardiac index decrease play the important roles in the development of hypokinetic type of central maternal hemodynamics in patients with severe preeclampsia. The latter leads to the dissociation of maternal and fetal regulatory mechanisms.
Conclusions. Hemodynamic isolation of the fetus leads to its sympathetic overactivity, a decrease in the total level of autonomic nervous regulation, centralization of hemodynamics and fetal distress.
Key words: preeclampsia, autonomic nervous regulation, hemodynamics, umbilical vein, vagal repercussions theory.
References
1. Theilen LH, Fraser A, Hollingshaus MS et al. (2016). All-Cause and Cause-Specific Mortality After Hypertensive Disease of Pregnancy. Obstet Gynecol. 128; 2: 238—244. https://doi.org/10.1097/AOG.0000000000001534; PMid:27400006 PMCid:PMC4961555
2. Malberg H, Bauernschmitt R, Voss A et al. (2007). Analysis of cardiovascular oscillations: a new approach to the early prediction of pre-eclampsia. Chaos. 17; 1: 015113.
3. Anthony J, Damasceno A, Ojjii D. (2016). Hypertensive disorders of pregnancy: what the physician needs to know. Cardiovasc J Afr. 27; 2: 104—110. https://doi.org/10.5830/CVJA-2016-051; PMid:27213858 PMCid:PMC4928160
4. Weel IC, Baergen RN, Romao-Veiga M et al. (2016). Association between placental lesions, cytokines and angiogenic factors in pregnant women with preeclampsia. PLoS One. 11; 6: e0157584.
5. Berhan Y. (2016). No Hypertensive disorder of pregnancy; no preeclampsia-eclampsia; no gestational hypertension; no hellp syndrome. Vascular disorder of pregnancy speaks for all. Ethiop J Health Sci. 26; 2: 177—186. https://doi.org/10.4314/ejhs.v26i2.12; PMid:27222631 PMCid:PMC4864347
6. Andreas M, Kuessel L, Kastl SP et al. (2016). Bioimpedance cardiography in pregnancy: a longitudinal cohort study on hemodynamic pattern and outcome. BMC Pregnancy Childbirth. 16; 1: 128.
7. Brown CA, Lee CT, Hains SM, Kisilevsky BS. (2008). Maternal heart rate variability and fetal behavior in hypertensive and normotensive pregnancies. Biol Res Nurs. 10; 2: 134—144. https://doi.org/10.1177/1099800408322942; PMid:18829597
8. Lee SW, Khaw KS, Ngan Kee WD et al. (2012). Haemodynamic effects from aortocaval compression at different angles of lateral tilt in non-labouring term pregnant women. Br J Anaesth. 109; 6: 950—956. https://doi.org/10.1093/bja/aes349; PMid:23059960
9. Van Leeuwen P, Geue D, Thiel M et al. (2009). Influence of paced maternal breathing on fetal-maternal heart rate coordination. PNAS. 106; 33: 13661-13666. https://doi.org/10.1073/pnas.0901049106; PMid:19597150 PMCid:PMC2728950
10. Lakhno I. (2017). The autonomic repercussions of fetal and maternal interaction in pre-eclampsia. Serbian Journal of Experimental and Clinical Research. 18; 2: 125—131. https://doi.org/10.1515/sjecr-2017-0018
11. Lakhno I. (2016). Maternal respiratory sinus arrhythmia captures the severity of pre-eclampsia. Archives of Perinatal Medicine. 22; 2: 14—17.
12. Scholten RR, Lotgering FK, Hopman MT et al. (2015). Low plasma volume in normotensive formerly preeclamptic women predisposes to hypertension. Hypertension. 66; 5: 1066—1072. https://doi.org/10.1161/HYPERTENSIONAHA.115.05934; PMid:26370891
13. Maeda K. (2014). Preeclampsia is caused by continuous sympathetic center excitation due to an enlarged pregnant uterus. J Perinat Med. 42; 2: 233—237. https://doi.org/10.1515/jpm-2013-0096; PMid:23846133
14. Kao CK, Morton JS, Quon AL et al. (2016). Mechanism of vascular dysfunction due to circulating factors in women with pre-eclampsia. Clin Sci (Lond). 130; 7: 539—549. https://doi.org/10.1042/CS20150678; PMid:26733722
15. Uzan J, Carbonnel M, Piconne O et al. (2011). Pre-eclampsia: pathophysiology, diagnosis, and management. Vasc Health Risk Manag. 7: 467—474. PMid:21822394 PMCid:PMC3148420
16. Riedl M, Suhrbier A, Stepan H et al. (2010). Short-term couplings of the cardiovascular system in pregnant women suffering from pre-eclampsia. Philos Trans A Math Phys Eng Sci. 368; Is 1918: 2237—2250.
17. Sugerman HJ. (2011). Hypothesis: preeclampsia is a venous disease secondary to an increased intra-abdominal pressure. Med Hypotheses. 77; 5: 841—849. https://doi.org/10.1016/j.mehy.2011.07.051; PMid:21862236