Fetal Cardiovascular System Research Articles

The Autonomic Repercussions of Fetal and Maternal Interaction in Pre-eclampsia

Abstract Pre-eclampsia (PE) is one of the severe complications of pregnancy that leads to fetal deterioration. The aim of the investigation was to determine the role of maternal respiratory sinus arrhythmia (RSA) in regulation of fetal circulatory system in case of healthy pregnancy and in PE. The investigation of maternal and fetal HRV and umbilical venous blood flow velocity spectral analysis in 106 patients at 34-40 weeks of gestation was performed. 30 of them had healthy pregnancy and were involved in the Group I. In Group II 44 pregnant women with mild-moderate PE were observed. 32 patients with severe PE were monitored in Group III. The maternal sympathetic overactivity modulated HRV in PE. The suppression of RSA was explored in preeclamptic patients. The Doppler spectrograms of the umbilical veinous blod flow had the oscillatory peak with a frequency about 0.5 Hz. The above peak characterized the participation of the maternal RSA in fetal hemodynamics. Strong relationship between maternal RMSSD and amplitude of RSA associated peak, maternal and fetal RMSSDs was found in healthy pregnancy. No considerable relationship was revealed between the maternal RMSSD and the amplitude of 0.5 Hz frequency peak, the maternal and fetal RMSSDs in the patients with severe PE. The maternal RSA propagated its influence on the fetal umbilical venous blood flow and the fetal autonomic nervous regulation in normal gestation. The control of fetal hemodynamics diminished in the mild-moderate PE and even disappeared in severe PE.

Foetal premature atrial contractions during the second and third trimester are not associated with foetal breathing

Foetal premature atrial contractions (PACs) are the most commonly encountered and also the most benign foetal arrhythmia. A retrospective cohort study was conducted with the objective to assess whether the presence of foetal breathing was associated with the presence of foetal PACs. A further objective was to evaluate whether this association would affect neonatal outcomes at a high volume referral centre. The diagnosis of PACs was based on the observation of a premature atrial contraction followed by a ventricular contraction on ultrasound myocardial M-mode. Trained ultrasonographers documented in the ultrasound report whether or not foetal breathing was present with PACs. 91 exams were identified, which included 75 individual pregnancies. Six women were identified who had foetal PACs associated with foetal breathing on ultrasound evaluation. Foetuses with PACs did not differ between the associated breathing and no-associated breathing groups with respect to maternal age, parity, mode of delivery, gestational age at delivery or birthweight. This study reaffirms that isolated PACs are a benign finding. Furthermore, it adds to the pool of literature on foetal PACs in that it is not associated with abnormal pregnancy outcomes regardless of the presence or absence of foetal breathing.Impact statement• What is already known on this subjectSince foetal breathing can effect Doppler ultrasound assessment of the foetal cardiovascular system, it is reasonable to consider that it may impact conditions such as foetal arrhythmias.• What the results of this study addFoetal breathing does not impact on the presence of premature atrial contractions.• What the implications are of these findings for clinical practice and/or further researchFoetal breathing is not associated with the finding of foetal premature atrial contractions.

The effect of maternal hyperoxygenation on fetal circulatory system in normal growth and IUGR fetuses. What we can learn from this impact

Purpose: The objectives of study were to assess and compare the effects of maternal hyperoxygenation on fetal circulation, in fetuses with intrauterine growth retardation and normal fetal growth.Methods: Twelve singleton pregnant women with normal fetal growth and 12 singleton pregnant women with intrauterine growth restriction were recruited. Mean gestational age of 35.2 ± 3.5 and 34.7 ± 3.9 weeks, respectively. Doppler blood flow velocity waveforms were obtained from the middle cerebral artery, umbilical, main and proximal right pulmonary arteries. Pulsatility indices were calculated for all the vessels. Peak systolic velocity was determined for the middle cerebral artery. Following baseline measurements; each woman received 70% humidified oxygen for 10 min. Doppler measurements were then repeated.Results: The pulsatility index in the middle cerebral artery increased significantly from 1.5 ± 0.27 to 1.88 ± 0.48, respectively (p = .006) in the high-risk group. However, it did not change significantly in the low-risk group. Hyperoxygenation caused a significant decrease in pulsatility indices in the pulmonary arteries for both groups.Conclusions: Hyperoxygenation interrupts the relative brain-sparing effect in the intrauterine growth retardation group, but it did not significantly change the pulsatility index of the middle cerebral artery in fetuses with adequate weight. The pulsatility index in the pulmonary arteries decreased significantly following hyperoxygenation.

Autonomic imbalance captures maternal and fetal circulatory response to pre-eclampsia

BackgroundPre-eclampsia (PE) is a gestational disease featured by hypertension, arterial systemic vasculopathy, multiple organ failure and fetal compromise.The aim of the investigation was to determine the role of maternal respiratory sinus arrhythmia (RSA) in regulation of the fetal circulatory system in case of healthy pregnancy and in PE.MethodsThe investigation of maternal and fetal HRV and fetal CTG variables in 106 patients at 34–40 weeks of gestation was performed. 30 of them had healthy pregnancy and were involved in the Group I. In Group II 44 pregnant women with mild-moderate PE were observed. 32 patients with severe PE were monitored in Group III.ResultThe maternal sympathetic overactivity modulated HRV in PE by suppressing total power (TP) and parasympathetic tone. The lack of RSA was explored in preeclamptic patients. The centralization of hemodynamics was a result of the hypersympatheticotonia in severe PE. Fetal circulatory response to PE featured by an increased sympathetic tone. The modulated fetal CTG variables captured the suppression of fetal biophysical activity and the development of fetal distress in severe PE.Strong relationship between maternal and fetal TPs, maternal and fetal RMSSDs was found in healthy pregnancy. The correlations between the maternal and fetal TPs, the maternal and fetal RMSSDs in the patients with severe PE were disturbed.ConclusionThe maternal RSA propagated its influence on the fetal autonomic nervous regulation in normal gestation. The maternal and fetal hemodynamic coupling was reduced in PE.

The hemodynamic repercussions of the autonomic modulations in growth-restricted fetuses

ObjectivesIdiopathic fetal growth restriction is considered to be associated with hemodynamic abnormalities.The study was aimed to the investigation of the relationship between fetal and maternal autonomic balance, arterial and venous hemodynamic Doppler indices and CTG variables in case of normal fetal development and fetal growth restriction. Methods106 patients at 32–40weeks of gestation were enrolled in the study. 30 of them had healthy pregnancy and were involved in Group I. In Group II, 44 pregnant women with fetal growth restriction and normal umbilical hemodynamic Doppler indices were observed. 32 patients with fetal growth restriction and an absent or reversed end-diastolic umbilical flow were monitored in Group III. The curves of maximum blood flow velocity were isolated and their spectral components were determined from the umbilical Doppler spectrograms. The maternal and fetal heart rate variability, conventional CTG patterns were obtained from RR-interval time series registered from maternal abdominal wall electrocardiographically. ResultsThe increased adrenergic regulation has modulated parasympathetic impact on fetal cardiovascular system. The decreased reactivity was mirrored in low LTV, lack of accelerations and an increased score of decelerations.The CTG findings were also featured by the revealed correlations demonstrated an obvious relationship between fetal and maternal hemodynamics in healthy pregnancy. It was possible to speculate that a controlling signal of 0.5Hzhas played a significant role in the umbilical venous blood flow. The decreased fetal autonomic tone and the fetal and maternal hemodynamic decoupling were found in growth-retarded fetuses. ConclusionFetal heart rate pattern was influenced by maternal and fetal autonomic tone. Maternal cardiovascular oscillations were reflected in the umbilical circulation in healthy pregnancy Fetal distress was featured by sympathetic overactivity and the reduction of vagal tone. Such autonomic modulations was manifested by the decelerative pattern of CTG and deteriorated umbilical hemodynamics.

IMPACT OF CHRONIC ARTERIAL HYPERTENSION ON CLINICAL AND METABOLIC NEONATAL ADAPTATION

Aim. To assess the impact of chronic arterial hyper-tension on clinical and metabolic adaptation of fullterm newborns. Methods. 65 full-term neonates born to women with chronic arterial hypertension were included in the study. 42 neonates born to women with arterial hypertension stage I were enrolled into Group 1, and 23 neonates born to mothers with arterial hypertension stage II were included in Group 2. Levels of renin, angiotensin II, aldosterone, natriuretic peptides, endothelin-1 in umbilical cord blood and peripheral blood were measured with the ELISA. Stable nitric oxide metabolites levels were measured using the Griess assay. Results. Chronic high blood pressure during pregnancy has been found to affect fetal central nervous system and cardiovascular system. Early neonatal period in infants of women with chronic arterial hypertension is associated with a high incidence of perinatal CNS injury, continuing with little change during the first three months of life. The features of the cardiovascular system in neonates of women with arterial hypertension stage II include hypertension and tachycardia at birth, violation of atrioventricular conduction on the first three days of life, open patent foramen ovale up to the first three months of life, whereas neonates born to women with arterial hyper-tension stage I have hypotension on the first day of life. Elevated levels of angiotensin II in neonates born to women with chronic arterial hypertension at birth and reduced levels of endogenous nitrite in the first three months of life suggest the activation of the renin-angiotensin-aldosterone system in the antenatal period, which may cause endothelial dysfunction in early infancy. Conclusions. 1. Chronic high blood pressure in pregnancy is as-sociated with perinatal CNS damage in the newborn, continued during the first three months of life. 2. Stage 1 of hypertension in pregnancy associated with hypotension in newborns on the first day of life; and stage 2 of hypertension in pregnancy associated with hypertension and tachycardia newborn at birth, a violation of his atrioventricular conduction on the 3rd day of life and preservation until the age of three open oval window. 3. Chronic high blood pressure in pregnancy is as-sociated with an increase in cord blood levels of angiotensin II decrease in peripheral blood concentration of endogenous nitrite in the age of three months.

Sildenafil therapy for fetal cardiovascular dysfunction during hypoxic development: studies in the chick embryo.

Common complications of pregnancy, such as chronic fetal hypoxia, trigger a fetal origin of cardiovascular dysfunction and programme cardiovascular disease in later life. Sildenafil treatment protects placental perfusion and fetal growth, but whether the effects of sildenafil transcend the placenta to affect the fetus is unknown. Using the chick embryo model, here we show that sildenafil treatment directly protects the fetal cardiovascular system in hypoxic development, and that the mechanisms of sildenafil protection include reduced oxidative stress and increased nitric oxide bioavailability; Sildenafil does not protect against fetal growth restriction in the chick embryo, supporting the idea that the protective effect of sildenafil on fetal growth reported in mammalian studies, including humans, is secondary to improved placental perfusion. Therefore, sildenafil may be a good candidate for human translational antioxidant therapy to protect the chronically hypoxic fetus in adverse pregnancy. There is a need for developing clinically translatable therapy for preventing fetal origins of cardiovascular disease in pregnancy complicated by chronic fetal hypoxia. Evidence shows that sildenafil protects placental perfusion and fetal growth. However, whether beneficial effects of sildenafil transcend onto the fetal heart and circulation in complicated development is unknown. We isolated the direct effects of sildenafil on the fetus using the chick embryo and hypothesised that sildenafil also protects fetal cardiovascular function in hypoxic development. Chick embryos (n=11 per group) were incubated in normoxia or hypoxia (14% O2 ) from day 1 and treated with sildenafil (4mgkg-1 day-1 ) from day 13 of the 21-day incubation. Hypoxic incubation increased oxidative stress (4-hydroxynonenal, 141.1±17.6% of normoxic control), reduced superoxide dismutase (60.7±6.3%), increased phosphodiesterase type 5 expression (167±13.7%) and decreased nitric oxide bioavailability (54.7±6.1%) in the fetal heart, and promoted peripheral endothelial dysfunction (70.9±5.6% AUC of normoxic control; all P<0.05). Sildenafil treatment after onset of chronic hypoxia prevented the increase in phosphodiesterase expression (72.5±22.4%), protected against oxidative stress (94.7±6.2%) and normalised nitric oxide bioavailability (115.6±22.3%) in the fetal heart, and restored endothelial function in the peripheral circulation (89.8±2.9%). Sildenafil protects the fetal heart and circulation directly in hypoxic development via mechanisms including decreased oxidative stress and enhanced nitric oxide bioavailability. Sildenafil may be a good translational candidate for human antioxidant therapy to prevent fetal origins of cardiovascular dysfunction in adverse pregnancy.

Inactivation of maternal Hif-1α at mid-pregnancy causes placental defects and deficits in oxygen delivery to the fetal organs under hypoxic stress

A critical transition occurs near mid-gestation of mammalian pregnancy. Prior to this transition, low concentrations of oxygen (hypoxia) signaling through Hypoxia Inducible Factor (HIF) functions as a morphogen for the placenta and fetal organs. Subsequently, functional coupling of the placenta and fetal cardiovascular system for oxygen (O2) transport is required to support the continued growth and development of the fetus. Here we tested the hypothesis that Hif-1α is required in maternal cells for placental morphogenesis and function. We used Tamoxifen-inducible Cre-Lox to inactivate Hif-1α in maternal tissues at E8.5 (MATcKO), and used ODD-Luciferase as a reporter of hypoxia in placenta and fetal tissues. MATcKO of Hif-1α reduced the number of uterine natural killer (uNK) cells and Tpbpa-positve trophoblast cells in the maternal decidua at E13.5 -15.5. There were dynamic changes in all three layers of E13.5-15.5 MATcKO placenta. Of note was the under-development of the labyrinth at E15.5 associated with reduced Ki67 and increased TUNEL staining consistent with reduced cell proliferation and increased apoptosis. Labyrinth defects were particularly evident in placentas connected to effectively HIF-1α heterozygous null embryos. MATcKO had no effect on basal ODD-Luciferase activity in fetal organs (heart, liver, brain) at any stage, but at E13.5-15.5 resulted in enhanced induction of the ODD-Luciferase hypoxia reporter when the dam’s inspired O2 was reduced to 8% for 4 hours. MATcKO also slowed the growth after E13.5 of fetuses that were effectively heterozygous for Hif-1α, with most being non-viable at E15.5. The hearts of these E15.5 fetuses were abnormal with reduction in size, thickened epicardium and mesenchymal septum. We conclude that maternal HIF-1α is required for placentation including recruitment of uNK and trophoblast cells into the maternal decidua and other trophoblast cell behaviors. The placental defects render the fetus vulnerable to O2 deprivation after mid-gestation.

Effect of maternal zinc supplementation on the cardiometabolic profile of Peruvian children: results from a randomized clinical trial.

Zinc is an essential micronutrient for the development of the fetal renal, cardiovascular and metabolic systems; however, there is limited evidence of its effects on the postnatal cardiometabolic function. In this study, we evaluated the effect of maternal zinc supplementation during pregnancy on the cardiometabolic profile of the offspring in childhood. A total of 242 pregnant women were randomly assigned to receive a daily supplement containing iron+folic acid with or without zinc. A follow-up study was conducted when children of participating mothers were 4.5 years of age to evaluate their cardiometabolic profile, including anthropometric measures of body size and composition, blood pressure, lipid profile and insulin resistance. No difference in measures of child cardiometabolic risk depending on whether mothers received supplemental zinc during pregnancy. Our results do not support the hypothesis that maternal zinc supplementation reduces the risk of offspring cardiometabolic disease.

Effect of uterine contractions on fetal heart rate in pregnancy: a prospective observational study.

The new Holter monitoring technology enables long-term electrocardiographic recording of the fetal heart rate without discomfort for the mother. The aim of the study was to assess the feasibility of a fetal Holter monitor. This technology was further used to study fetal heart rate outside the hospital setting during normal daily activities and to test the hypothesis that uterine activity during pregnancy influences fetal heart rate. Prospective observational study including 12 healthy pregnant women at 20-40weeks of gestation. Data were collected using the Monica AN24 system. Outcome measures were fetal heart rate, maternal heart rate, and uterine activity categorized according to the strength of the electrohysterographic signal. The recordings had a median length of 18.8h, and fetal heart rate and maternal heart rate were obtained with success rates of 73.1 and 99.9%, respectively. Uterine activity was found to affect fetal heart rate in all participants. Compared with the basal tone and mild levels of uterine activity, moderate and strong levels of uterine activity were associated with increases in fetal heart rate of 4.0 and 5.7beats/min, respectively. At night, the corresponding increases were 4.9 and 7.6beats/min. Linear correlations were found between maternal heart rate and fetal heart rate in 11 of the 12 cases, with a mean coefficient beta of 0.189. Both maternal heart rate and fetal heart rate exhibitedadiurnal pattern, with lower heart rates being recorded at night. Uterine activity during pregnancy is associated with a graded response in fetal heart rate and may represent a physiological challenge for the development and adaptation of the fetal cardiovascular system.

Pregnancy-driven cardiovascular maternal miR-29 plasticity in obesity.

Obesity in pregnancy (MO) is a risk factor for maternal and/or fetal cardiovascular system disorders. This study evaluated maternal CVS expression of microRNA-29 family and its target molecules in MO to test the hypotheses: CVS miR-29 concentrations are increased in pregnancy and decreased in MO. Non-pregnant (n=4), pregnant obese (POb, n=4), and pregnant non-obese (PnOb, n=4) baboons (Papio spp.) were studied. Maternal left ventricle (LV), left atrium (LA), and aortic arch (AA) were collected at the end of gestation. Expression of MiR-29 and elastin (ELN) mRNA were quantified. LA miR-29 (a, c) expression was highest in PnOb. In the LV, miR-29b expression trended lower (P=.059) for PnOb animals. ELN mRNA expression correlated positively with miR-29b expression in AA (r=.76, P=.03). Maternal obesity diminishes miR-29 adaptation to pregnancy. Pharmacologic, tissue-specific targeting of miRNA-29 may represent a strategy for prevention and treatment of MO complications.

Fetal echocardiography for early detection of congenital heart diseases.

Fetal echocardiography is a complete two-dimensional and Doppler ultrasound evaluation of the human fetal cardiovascular system. It is completely noninvasive, harmless, and also serves as the fetal electrocardiogram. To analyze the fetal echocardiographic cases referred to a tertiary cardiac center. A total of 478 cases of fetal echocardiograms performed over a period of 5.5years were compiled and analyzed. Details regarding gestational age, maternal, family history, exposure to teratogens, and reason for referral were recorded. The average gestational age at referral was 24.8±4.6weeks and maternal age was 24.7±4.3years. Indications for referrals were abnormal fetal cardiac scan in 128 (26.8%), previous sibling with congenital heart disease (CHD) in 99 (20.7%), maternal indications in 87 (18.2%), echogenic intracardiac focus (EIF) in 87 (18.2%), high risk in 50 (10.5%), rhythm problems in 21 (4.4%), and others (extracardiac malformations) in 6 (1.2%). In the 87 CHD cases diagnosed, nearly 70% had complex CHD and 66.7% were referred only after 22weeks of gestation. A further 103 cases had EIF, 17 cases had fetal arrhythmia, 3 cases had cardiac masses, and the remaining 268 cases had normal fetal echocardiograms. Fetal echocardiography can effectively identify abnormal hearts and has enhanced prenatal detection of CHD. The concern in the Indian scenario is the late referrals, lack of follow-up, and financial difficulties, all of which conspire against the chance of the fetus with heart disease getting appropriate treatment.

The Tree(s) of Life: The Human Placenta and My Journey to Learn More about It.

The Tree(s) of Life: The Human Placenta and My Journey to Learn More about It.

Cardiovascular cast model fabrication and casting effectiveness evaluation in fetus with severe congenital heart disease or normal heart.

To investigate the application and effectiveness of vascular corrosion technique in preparing fetal cardiovascular cast models, 10 normal fetal heart specimens with other congenital disease (control group) and 18 specimens with severe congenital heart disease (case group) from induced abortions were enrolled in this study from March 2013 to June 2015 in our hospital. Cast models were prepared by injecting casting material into vascular lumen to demonstrate real geometries of fetal cardiovascular system. Casting effectiveness was analyzed in terms of local anatomic structures and different anatomical levels (including overall level, atrioventricular and great vascular system, left-sided and right-sided heart), as well as different trimesters of pregnancy. In our study, all specimens were successfully casted. Casting effectiveness analysis of local anatomic structures showed a mean score from 1.90±1.45 to 3.60±0.52, without significant differences between case and control groups in most local anatomic structures except left ventricle, which had a higher score in control group (P=0.027). Inter-group comparison of casting effectiveness in different anatomical levels showed no significant differences between the two groups. Intra-group comparison also revealed undifferentiated casting effectiveness between atrioventricular and great vascular system, or left-sided and right-sided heart in corresponding group. Third-trimester group had a significantly higher perfusion score in great vascular system than second-trimester group (P=0.046), while the other anatomical levels displayed no such difference. Vascular corrosion technique can be successfully used in fabrication of fetal cardiovascular cast model. It is also a reliable method to demonstrate three-dimensional anatomy of severe congenital heart disease and normal heart in fetus.

Nitric Oxide is a Central Common Metabolite in Vascular Dysfunction Associated with Diseases of Human Pregnancy.

Preeclampsia (PE), gestational diabetes mellitus (GDM), and maternal supraphysiological hypercholesterolaemia (MSPH) are pregnancy-related conditions that cause metabolic disruptions leading to alterations of the mother, fetus and neonate health. These syndromes result in fetoplacental vascular dysfunction, where nitric oxide (NO) plays a crucial role. PE characterizes by abnormal increase in the placental blood pressure and a negative correlation between NO level and fetal weight, suggesting that increased NO level and oxidative stress could be involved. GDM courses with macrosomia along with altered function of the fetal cardiovascular system and fetoplacental vasculature. Even when NO synthesis in the fetoplacental vasculature is increased, NO bioavailability is reduced due to the higher oxidative stress seen in this disease. In MSPH, there is an early development of atherosclerotic lesions in fetal and newborn arteries, altered function of the fetoplacental vasculature, and higher markers of oxidative stress in fetal blood and placenta, thus, vascular alterations related with NO metabolism occur as a consequence of this syndrome. Potential mechanisms of altered NO synthesis and bioavailability result from transcriptional and post-translational NO synthases (NOS) modulation, including phosphorylation/dephosphorylation cycles, coupling/uncoupling of NOS, tetrahydrobiopterin bioavailability, calcium/calmodulin-NOS and caveolin-1-NOS interaction. Additionally, oxidative stress also plays a role in the reduced NO bioavailability. This review summarizes the available information regarding lower NO bioavailability in these pregnancy pathologies. A common NO-dependent mechanism in PE, GDM and MSPH contributing to fetoplacental endothelial dysfunction is described.

Fetal in vivo continuous cardiovascular function during chronic hypoxia.

Key points The in vivo fetal cardiovascular defence to chronic hypoxia has remained by and large an enigma because no technology has been available to induce significant and prolonged fetal hypoxia whilst recording longitudinal changes in fetal regional blood flow as the hypoxic pregnancy is developing.We introduce a new technique able to maintain chronically instrumented maternal and fetal sheep preparations under isobaric chronic hypoxia for most of gestation, beyond levels that can be achieved by high altitude and of relevance in magnitude to the human intrauterine growth‐restricted fetus.This technology permits wireless recording in free‐moving animals of longitudinal maternal and fetal cardiovascular function, including beat‐to‐beat alterations in pressure and blood flow signals in regional circulations.The relevance and utility of the technique is presented by testing the hypotheses that the fetal circulatory brain sparing response persists during chronic fetal hypoxia and that an increase in reactive oxygen species in the fetal circulation is an involved mechanism. Although the fetal cardiovascular defence to acute hypoxia and the physiology underlying it have been established for decades, how the fetal cardiovascular system responds to chronic hypoxia has been comparatively understudied. We designed and created isobaric hypoxic chambers able to maintain pregnant sheep for prolonged periods of gestation under controlled significant (10% O2) hypoxia, yielding fetal mean PaO2 levels (11.5 ± 0.6 mmHg) similar to those measured in human fetuses of hypoxic pregnancy. We also created a wireless data acquisition system able to record fetal blood flow signals in addition to fetal blood pressure and heart rate from free moving ewes as the hypoxic pregnancy is developing. We determined in vivo longitudinal changes in fetal cardiovascular function including parallel measurement of fetal carotid and femoral blood flow and oxygen and glucose delivery during the last third of gestation. The ratio of oxygen (from 2.7 ± 0.2 to 3.8 ± 0.8; P < 0.05) and of glucose (from 2.3 ± 0.1 to 3.3 ± 0.6; P < 0.05) delivery to the fetal carotid, relative to the fetal femoral circulation, increased during and shortly after the period of chronic hypoxia. In contrast, oxygen and glucose delivery remained unchanged from baseline in normoxic fetuses. Fetal plasma urate concentration increased significantly during chronic hypoxia but not during normoxia (Δ: 4.8 ± 1.6 vs. 0.5 ± 1.4 μmol l−1, P<0.05). The data support the hypotheses tested and show persisting redistribution of substrate delivery away from peripheral and towards essential circulations in the chronically hypoxic fetus, associated with increases in xanthine oxidase‐derived reactive oxygen species.

The fetal brain sparing response to hypoxia: physiological mechanisms.

How the fetus withstands an environment of reduced oxygenation during life in the womb has been a vibrant area of research since this field was introduced by Joseph Barcroft, a century ago. Studies spanning five decades have since used the chronically instrumented fetal sheep preparation to investigate the fetal compensatory responses to hypoxia. This defence is contingent on the fetal cardiovascular system, which in late gestation adopts strategies to decrease oxygen consumption and redistribute the cardiac output away from peripheral vascular beds and towards essential circulations, such as those perfusing the brain. The introduction of simultaneous measurement of blood flow in the fetal carotid and femoral circulations by ultrasonic transducers has permitted investigation of the dynamics of the fetal brain sparing response for the first time. Now we know that major components of fetal brain sparing during acute hypoxia are triggered exclusively by a carotid chemoreflex and that they are modified by endocrine agents and the recently discovered vascular oxidant tone. The latter is determined by the interaction between nitric oxide and reactive oxygen species. The fetal brain sparing response matures as the fetus approaches term, in association with the prepartum increase in fetal plasma cortisol, and treatment of the preterm fetus with clinically relevant doses of synthetic steroids mimics this maturation. Despite intense interest into how the fetal brain sparing response may be affected by adverse intrauterine conditions, this area of research has been comparatively scant, but it is likely to take centre stage in the near future.

A Mobile Full-Time Daily System for Fetal Monitoring

The article describes a mobile hardware and software system designed for daily monitoring of the state of fetal and maternal cardiovascular systems. The assessment is carried out by means of recording and further online analysis of acoustic data, obtained from the abdominal surface of a pregnant woman’s body. The components and operating principles of the hardware and software system designed are described. The results of experimental studies aimed at assessing the applicability of a method of acoustic data analysis implemented in the system developed are shown. The results obtained have been compared with the results obtained using cardiotocography.

Cardiovascular Transition of the Extremely Premature Infant and Challenges to Maintain Hemodynamic Stability.

The intricate fetal circulatory blood flow undergoes abrupt changes and restructuring at birth, allowing transition to extrauterine life and survival. In the extremely low-birth-weight newborn infant (birth weight <1000 g), these changes are affected by the immaturity of the fetal cardiovascular and pulmonary systems. The immature physiology associated with the inability to transition properly can lead to a poor prognosis and create problematic issues for the clinical management of these infants. Potentially problematic issues and complications include immature myocardium, adrenal insufficiency, patent ductus arteriosus, hypotension, and anemia. Understanding the unique transition to extrauterine life for these infants, problems that arise from immaturity and incomplete transition, and current approaches to management will help nurses and physicians caring for ELBW infants to improve the care they give and minimize mortality and morbidity in this vulnerable population. This article will review transitional physiology for term and preterm newborns, potential problems and complications, and current management approaches.

Adaptive responses of cardiac function to fetal postural change as gestational age increases.

ObjectiveThe cardiovascular system maintains homeostasis through a series of adaptive responses to physiological requirements. However, little is known about the adaptation of fetal cardiac function to gravity, according to gestational age. In the present study, we aimed to evaluate the adaptive responses of cardiac function to postural changes, using Tei index measurements.MethodsFetal echocardiography and Doppler examination were performed on 114 women with vertex singleton pregnancies at 19 to 40 weeks' gestation. Participants were placed in an upright seated position, and the Tei index for fetal left ventricular cardiac function was measured. The women were then moved into a supine position and the Tei index was re-measured.ResultsThe mean Tei index when measured in an upright seated position was significantly lower than that measured in a supine positioning for all fetuses (0.528±0.103 vs. 0.555±0.106, P=0.014, respectively). This difference was also noted in fetuses with a gestational age of 28–40 weeks (0.539±0.107 vs. 0.574±0.102, P=0.011, respectively). However, there was no difference in the Tei index between an upright seated and a supine position among fetuses with a gestational age of <28 weeks (0.505±0.091 vs. 0.516±0.103, P=0.571, respectively).ConclusionPostural changes from an upright seated to a supine position result in an increased Tei index after a gestational age of 28 weeks. This appears to reflect maturation in the adaptive responses of the fetal cardiovascular system to postural changes.