Maternal Hyperoxygenation Research Articles

Acute maternal hyperoxygenation protocol: consensus opinion from the Fetal Heart Society.

Acute maternal hyperoxygenation protocol: consensus opinion from the Fetal Heart Society.

Pulmonary vascular reactivity in growth restricted fetuses using computational modelling and machine learning analysis of fetal Doppler waveforms

The aim of this study was to investigate the pulmonary vasculature in baseline conditions and after maternal hyperoxygenation in growth restricted fetuses (FGR). A prospective cohort study of singleton pregnancies including 97 FGR and 111 normally grown fetuses was carried out. Ultrasound Doppler of the pulmonary vessels was obtained at 24–37 weeks of gestation and data were acquired before and after oxygen administration. After, Machine Learning (ML) and a computational model were used on the Doppler waveforms to classify individuals and estimate pulmonary vascular resistance (PVR). Our results showed lower mean velocity time integral (VTI) in the main pulmonary and intrapulmonary arteries in baseline conditions in FGR individuals. Delta changes of the main pulmonary artery VTI and intrapulmonary artery pulsatility index before and after hyperoxygenation were significantly greater in FGR when compared with controls. Also, ML identified two clusters: A (including 66% controls and 34% FGR) with similar Doppler traces over time and B (including 33% controls and 67% FGR) with changes after hyperoxygenation. The computational model estimated the ratio of PVR before and after maternal hyperoxygenation which was closer to 1 in cluster A (cluster A 0.98 ± 0.33 vs cluster B 0.78 ± 0.28, p = 0.0156). Doppler ultrasound allows the detection of significant changes in pulmonary vasculature in most FGR at baseline, and distinct responses to hyperoxygenation. Future studies are warranted to assess its potential applicability in the clinical management of FGR.

Abstract 14220: Establishing Dosing Parameters for the Use of Maternal Hyperoxygenation to Affect Fetal Cardiovascular Physiology

Introduction: Maternal hyperoxygenation (MH) has been used to aid in the prognosis of fetal abnormalities. No data exist on the dose-response relationship or washout time of short-term MH administration related to fetal cardiovascular effects. Hypothesis: There may be a dose-response to MH with effect on pulmonary vascular resistance as measured by pulmonary artery pulsatility index (PAPI) and combined cardiac output (CCO). Aims: The aims of this study were: to determine the appropriate MH dose to obtain a physiologic response (i.e. decrease in PAPI), to evaluate the change in CCO, and to identify the washout period. Methods: Expectant mothers with normal fetal echocardiograms were prospectively recruited from 3/2019 to 6/2023. A research echocardiogram with MH was performed after 31 weeks gestation. Fetal cardiac abnormalities and other comorbidities were excluded. Patients were randomly assigned to either; 2 liters (L) nasal cannula (NC), 4L NC or 8L facemask, all at 100% Fi0 2 . Measurements of PAPI and CCO were performed at baseline, at 1 minute (min) and at 5 min intervals to 20 mins. The same time points were repeated off oxygen. Differences in PAPI were compared between doses and between time points using a mixed effects model. Results: We recruited 29 patients at a mean gestational age of 32.9 (± 0.9 weeks). On oxygen, there was a statistically significant decrease in the PAPI at 8L (-0.18 per min, 95% CI -0.32, -0.05), with the largest decrease occurring between baseline and 5 mins, and PAPI stabilizing after 10 mins (figure). During the washout period, starting at 1 min off oxygen, PAPI values normalized, with no statistically significant changes with 2L, 4L or 8L compared to baseline. No effect on CCO was seen from MH administration. Conclusions: An oxygen dose of 8L is needed for an appropriate PAPI response, with the largest effect occurring before 10 mins. After oxygen is removed, PAPI values normalize by one min. Changes in CCO were not seen with MH in this normal population.

Abstract 17366: Effects of Acute Maternal Supplemental Oxygen on the Fetal Circulation in Transposition of the Great Arteries

Introduction: The presence of a restrictive atrial septum in the setting of transposition of the great arteries (TGA) is associated with a high risk of hypoxic ischemic injury upon transition to postnatal circulation. Fetal cardiovascular magnetic resonance (CMR) measures of vessel flow and oxygen saturation provide a unique opportunity to study fetal TGA hemodynamics at baseline and during acute maternal hyperoxygenation. Methods: Thirty-one pregnant mothers with fetuses diagnosed with TGA and an intact ventricular septum (n=23) or small ventricular septal defect (n=8) were recruited and underwent fetal CMR in room air and during administration of 10L/min of oxygen by face mask for up to 45 minutes. Blood flow and oxygen saturations were measured in the major fetal vessels using cine phase contrast MRI and MR relaxometry at baseline and during hyperoxygenation. Results: Two patients exhibited severe restriction at the atrial septum, one undergoing fetal atrial septostomy at 37 weeks and one requiring cannulation onto ECMO shortly after birth. Both revealed reversal of the usual relationship of oxygen saturation between the aorta and the main pulmonary artery at baseline and during hyperoxygenation, i.e. in TGA with restrictive atrial septum the saturations are higher in the aorta than pulmonary. Acute maternal supplemental oxygen was associated with increased pulmonary blood flow (p=0.008) and reduced foramen ovale (p=0.01) and ductus arteriosus shunting (p=0.01). There were no significant changes in umbilical vein, descending aorta and superior vena cava flow. Fetal oxygen saturations increased throughout fetal circulation (p<0.0001) with an associated increase in fetal oxygen delivery (p=0.007), but no increase in fetal cerebral oxygen delivery (p=0.58). Conclusions: This study characterized the effects of acute maternal supplemental oxygen on the fetal circulation in patients with TGA and confirmed the redistribution of flow toward the fetal pulmonary circulation. We observed higher oxygen saturations in the aorta than main pulmonary artery in fetuses with TGA with an intact or highly restrictive atrial septal communication. This finding could be helpful in selecting patients for prenatal or emergency neonatal balloon atrial septostomy.

Effect of maternal hyperoxygenation on neonatal outcomes among women in labour with pathological cardiotocography: an open-label randomized controlled trial

Hyperoxygenation has shown promise in improving suspicious fetal heart patterns in women in labor. However, the effect of hyperoxygenation on neonatal outcomes in women in labor with pathologic fetal heart rate tracing has not been studied. This study aimed to evaluate the effect of fractional inspiration of oxygen of 80% compared with fractional inspiration of oxygen of 40% on neonatal outcomes in women with pathologic fetal heart rate tracing. This randomized, open-label, parallel arm, outcome assessor-blinded clinical trial was conducted in a large tertiary care university hospital. Singleton parturients aged ≥18 years at term gestation in active labor (cervical dilatation of ≥6 cm) with pathologic fetal heart rate tracing were recruited in the study. Pathologic fetal heart rate tracing was defined according to the International Federation of Gynecology and Obstetrics 2015 guidelines. The International Federation of Gynecology and Obstetrics classifies fetal heart rate tracings into 3 categories (normal, suspicious, and pathologic) based on rate, variability, and deceleration. Women in the intervention arm received oxygen at 10 L/min via a nonrebreathing mask, and those in the usual care arm received oxygen at 6 L/min with a simple face mask. Oxygen supplementation was continued until cord clamping. The primary outcome measure was a 5-minute Apgar score. The secondary outcome measures were the proportion of neonatal intensive care unit admission, umbilical cord blood gas variables, level of methyl malondialdehyde in the cord blood, and mode of delivery. Overall, 148 women (74 women in the high fractional inspiration of oxygen arm and 74 in the low fractional inspiration of oxygen arm) with pathologic fetal heart rate tracing were analyzed. The demographic data, obstetrical profiles, and comorbidities were comparable. The median 5-minute Apgar scores were 9 (interquartile range, 8-10) in the hyperoxygenation arm and 9 (interquartile range, 8-10) in the usual care arm (P=.12). Furthermore, the rate of neonatal intensive care unit admission (9.5% vs 12.2%; P=.6) and the requirement of positive pressure ventilation (6.8% vs 8.1%; P=.75) were comparable. Concerning cord blood gas parameters, the hyperoxygenation arm had a significantly higher base deficit in the umbilical vein and lactate level in the umbilical artery. The cesarean delivery rate was significantly lower in women who received hyperoxygenation (4.1% [3/74]) than in women who received normal oxygen supplementation (25.7% [19/74]) (P=.00). In addition, umbilical vein malondialdehyde level in the umbilical vein was lower in the hyperoxygenation group (8.28±4.65 μmol/L) than in the normal oxygen supplementation group (13.44±8.34 μmol/L) (P=.00). Hyperoxygenation did not improve the neonatal Apgar score in women with pathologic fetal heart rate tracing. In addition, neonatal intensive care unit admission rate and blood gas parameters remained comparable. Therefore, the results of this trial suggest that a high fractional inspiration of oxygen supplementation confers no benefit on neonatal outcomes in women with pathologic fetal heart rate tracings and normal oxygen saturation.

A short session of maternal hyperoxygenation ameliorates the cerebral oxygenation difference between fetuses with and without congenital heart defects

ObjectivesTo assess if a 10 min session of maternal hyperoxygenation increases cerebral tissue oxygenation as measured by magnetic resonance imaging (MRI) T2* in fetuses with and without congenital heart defects (CHDs). Study designAt mean gestational ages of 32 (early) and 37 (late), we measured fetal cerebral T2* before and during the last minutes of a 10 min maternal hyperoxygenation (oxygen 10 l/min, Hudson non-rebreathing mask) in 22 fetuses without CHDs and 11 fetuses with CHDs using a 1.5 Tesla Philips scanner with a breath-hold, multi-echo, gradient-echo sequence. ResultsDuring maternal hyperoxygenation equilibrium, the mean fetal cerebral T2* values in CHD fetuses seemingly normalized and were comparable to those in fetuses without CHD breathing ambient air. Hyperoxygenation T2* was 160 ms (CI 149–170) early and 123 ms (CI 112–134) late in fetuses with CHD and ambient air T2* was 158 ms (CI 152 to 164) early and 126 ms (CI 120–131) late in fetuses without CHD, (p=0.97). Lower ambient air cerebral T2* z-score at the late-stage scan was correlated with lower head circumference z-scores at birth. ConclusionOur findings suggest that fetal cerebral oxygenation in CHD fetuses can reach normal values during a short session of maternal hyperoxygenation. This supports the hypothesis that tissue hypoxia can influence brain development in fetuses with CHD. However, since side effects of fetal hyperoxygenation have been described, it remains to be determined if chronic maternal hyperoxygenation has a positive impact on the fetal brain in CHDs.

Evaluation of fetoplacental oxygenation in a rat model of gestational diabetes mellitus using BOLD-MRI at 7.0-T

Objective: To compare the differences in blood oxygen level-dependent (BOLD) parameters following maternal hyperoxia between normal pregnancy and pregnancy in the rat model of gestational diabetes mellitus (GDM). Methods: GDM was induced by high-fat and sucrose diet (HFS) combined with an intraperitoneal injection of streptozotocin (STZ). On embryonic day 19 (E19), the two groups of pregnant rats were imaged using a 7.0-T animal MRI scanner. TurboRARE was initially used to localize the fetoplacental units (FPUs). Next, multiple gradient echo BOLD was performed during the air and oxygen inhalation periods. T2* map was then generated, and the baseline T2* and absolute changes in T2* value (ΔT2*, difference between T2*oxy and T2*air) were calculated. Following the MRI scan, the placentas and fetuses were aseptically stripped, weighed, and immunostained. Results: Nine rats were used in this study. After maternal oxygen inhalation, T2* increased significantly in all subjects in both groups. The ΔT2* for the placenta (5.97 vs. 7.81 msec; P = 0.007) and fetal brain (2.23 vs. 3.97 msec; P = 0.005) differed significantly between the GDM and control groups. Histochemical detection of placental glycogen content and inflammatory cytokines (IL-6 and TNF-α) showed significantly higher levels in the GDM than in the normal placenta. Conclusions: BOLD-MRI revealed abnormalities in the fetoplacental response to maternal hyperoxygenation in rats with GDM. We believe that this approach can potentially be used to evaluate placental dysfunction and assess the state of the fetus during pregnancy with GDM.

Maternal hyperoxygenation during pregnancy as a tool in fetal disease diagnosis and treatment

Maternal hyperoxygenation (MHO) consists of giving pregnant women (60% to 100%) oxygen through a facemask and using ultrasound assess or monitor the influence on fetal cardiovascular circulation. This review discusses the findings and the utility of acute and chronic MHO in various fetal diseases.

Advances in Maternal–Fetal Imaging

Advances in Maternal–Fetal Imaging

Utility of Fetal Echocardiography with Acute Maternal Hyperoxygenation Testing in Assessment of Complex Congenital Heart Defects.

Fetal echocardiography is an excellent tool for accurately assessing the anatomy and physiology of most congenital heart defects (CHDs). Knowledge gathered from a thorough initial fetal echocardiogram and serial assessment assists with appropriate perinatal care planning, resulting in improved postnatal outcomes. However, fetal echocardiography alone provides limited information about the status of the pulmonary vasculature, which can be abnormal in certain complex CHDs with obstructed pulmonary venous flow (hypoplastic left heart syndrome with restrictive atrial septum) or excessive pulmonary artery flow (d-transposition of the great arteries, usually with a restrictive ductus arteriosus). Fetuses with these CHDs are at high risk of developing severe hemodynamic instability with the immediate transition from prenatal to postnatal circulatory physiology at the time of birth. Adjunctive use of acute maternal hyperoxygenation (MH) testing in such cases can help determine pulmonary vascular reactivity in prenatal life and better predict the likelihood of postnatal compromise and the need for emergent intervention. This comprehensive review discusses the findings of studies describing acute MH testing in a diverse spectrum of CHDs and congenital diagnoses with pulmonary hypoplasia. We review historical perspectives, safety profile, commonly used clinical protocols, limitations, and future directions of acute MH testing. We also provide practical tips on setting up MH testing in a fetal echocardiography laboratory.

Does maternal hyperoxygenation have any effect on the fetal circulatory system in normal growth and late-onset IUGR fetuses?

Abstract Objective: maternal hyperoxygenation (MHO) has been recommended as an alternative treatment for fetuses with IUGR. We wanted to evaluate the effect of MHO treatment on ductus venosus (DV) and pulmonary vein (PV) doppler flow measurements in fetuses with late-onset IUGR. Materials and Methods: A total of 63 pregnant women were enrolled in the study (32 pregnant women diagnosed with IUGR and 31 women with normal growth). The control group comprised 31 randomly selected age-matched and gestational-age-matched healthy pregnant women who presented to the antenatal clinic on the exact dates as the women in the study group. Results: In the IUGR group, MHO significantly increased the PI value of DV (0.50 (0.40, 0.58) to 0.62 (0.60, 0.65). p<.001). The DV-S, DV-D, and S/a values of the DV increase significantly for the IUGR group. DV- a value of DV decreased significantly from 52.00 (49.25, 52.75) to 41.50 (38.50, 42.75) p<.001. Comparison of Doppler findings in healthy fetuses before and after oxygen inhalation did not change significantly. Also, The PI value in the PV did not change significantly following maternal hyper oxygenation in the In the IUGR group (pre-O2: 0.80 (0.73, 0.88) and post-O2: 0.80 (0.70, 0.90)). Conclusion: We detected a statistically significant increase in both DV and PV blood flow during MHO administration in late-onset IUGR fetuses. Since increased DV and PV blood flow is associated with increased cardiac output, we think that it will reduce foetal hypoxia in fetuses with IUGR.

Hypoplastic Left Heart Syndrome: Is There a Role for Fetal Therapy?

During fetal life some cardiac defects may lead to diminished left heart growth and to the evolution of a form of hypoplastic left heart syndrome (HLHS). In fetuses with an established HLHS, severe restriction or premature closure of the atrial septum leads to left atrial hypertension and remodeling of the pulmonary vasculature, severely worsening an already poor prognosis. Fetal therapy, including invasive fetal cardiac interventions and non-invasive maternal hyperoxygenation, have been introduced to prevent a possible progression of left heart hypoplasia, improve postnatal outcome, or secure fetal survival. The aim of this review is to cover patient selection and possible hemodynamic effects of fetal cardiac procedures and maternal hyperoxygenation in fetuses with an evolving or established hypoplastic left heart syndrome.

Fetal growth of left-sided structures and postnatal surgical outcome in borderline left heart varies by cardiac phenotype.

There are two borderline left-heart phenotypes in the fetus: (1) severe aortic stenosis (AS), which is associated with a 'short, fat', globular left ventricle (LV), LV systolic dysfunction and LV growth arrest; and (2) severe left-heart hypoplasia (LHH), which is associated with a 'long, skinny' LV, laminar flow across hypoplastic mitral and aortic valves and arch hypoplasia. Both phenotypes may be counseled for possible single-ventricle palliation. We aimed to compare the rates of left-sided cardiac structure growth and Z-score change over gestation and to describe the postnatal outcomes associated with these two phenotypes. We hypothesized that the left-sided structures would grow faster in fetuses with LHH compared to those with AS, and that those with LHH would be more likely to achieve biventricular circulation. This was a retrospective cohort study using data collected in an institutional cardiology database between April 2001 and April 2018. We included fetuses with severe AS or severe LHH, and with at least two fetal echocardiograms. Inclusion criteria for the AS group included: aortic-annulus Z-score < -2.0, severe AS, depressed LV function, retrograde systolic flow in the aortic arch and endocardial fibroelastosis. Inclusion criteria for the LHH group included: aortic-annulus Z-score < -2.0, hypoplastic but apex-forming LV, normal LV function and retrograde systolic flow in the aortic arch. Exclusion criteria were: abnormal cardiac connections, other forms of structural congenital heart disease, cardiomyopathy, history of fetal aortic valvuloplasty and participation in a maternal hyperoxygenation study. Measurements and respective Z-scores for the aortic-valve annulus, mitral-valve annulus, LV long- and short-axis dimensions, along with aortic-arch measurements, were collected longitudinally for each fetus and plotted over time for both cohorts. Mean slopes of change in dimension and Z-scores over gestation were calculated and compared between the two groups using mixed generalized linear regression accounting for repeated measures. A subanalysis was performed, matching six fetuses from each group for initial aortic-annulus Z-score and gestational age, due to the significant differences in these two variables between the original cohorts. In total, 53 fetuses with 158 echocardiograms were included. In the AS cohort, there were 20 (38%) fetuses with 65 echocardiograms, and in the LHH cohort there were 33 (62%) fetuses with 93 echocardiograms. On the first echocardiogram, LHH fetuses had a later gestational age and a larger aortic-annulus diameter. The rate of aortic-annulus growth was greater in the LHH group compared with the AS group (mean ± SD, 0.15 ± 0.01 mm/week for LHH vs 0.07 ± 0.01 mm/week for AS (P < 0.001)). While the LHH group had a decrease in aortic-annulus Z-score over time, this was at a slower rate than the decrease in the AS group (mean ± SD, -0.04 ± 0.02/week for LHH vs -0.13 ± 0.02/week for AS (P < 0.001)). A similar pattern was seen for the mitral-valve and LV short-axis-dimension Z-scores. Subanalysis of six fetuses from each group matched for initial aortic-annulus Z-score and gestational age demonstrated similar findings, with the LHH group Z-scores decreasing at a slower rate than those in the AS group. Fifty-two of the 53 fetuses were liveborn, one LHH fetus dying in utero. Of the 20 liveborn in the AS cohort, 15 (75%) infants underwent single-ventricle palliation, two (10%) underwent biventricular repair and three (15%) died prior to intervention. Of the 32 liveborn in the LHH cohort, three (9.4%) underwent single-ventricle palliation, 28 (87.5%) achieved biventricular circulation, of which six required no surgery, and one (3.1%) died prior to intervention. The left-sided cardiac structures grow at a faster rate in fetuses with severe LHH than they do in fetuses with severe AS, and the Z-scores decrease at a slower rate in fetuses with severe LHH than they do in those with severe AS. The majority of infants in the LHH group did not undergo single-ventricle palliation. This information can be useful in counseling families on the expected growth potential of the fetus's aortic valve, mitral valve and LV, depending on the cardiac phenotype. © 2022 International Society of Ultrasound in Obstetrics and Gynecology.

Impact of Maternal Hyperoxygenation on Myocardial Deformation and Loading Conditions in Fetuses with and without Left Heart Hypoplasia

Maternal hyperoxygenation (MHO) is used in a variety of clinical applications, but its impact on fetal cardiovascular physiology is poorly understood. Our aims were to describe the effects of MHO on myocardial deformation parameters and on ultrasound-based metrics of preload and afterload and to assess the differential effect of MHO on fetuses with left heart hypoplasia (LHH). We hypothesized that the effects of MHO would be modulated by loading conditions and that fetuses with LHH would be more sensitive to changes in preload and afterload induced by MHO. We performed a post hoc analysis of 36 fetal echocardiograms performed as part of a pilot study of MHO in LHH (n=9) and control (n=9) fetuses. Oxygen was administered via 8L face mask for 10minutes. Right ventricular (RV) and left ventricular (LV) longitudinal strain and strain rate, estimated aortic and pulmonary cardiac output, pulmonary vein velocity-time integral (VTI) and pulsatility indices (PI) of the middle cerebral artery (MCA), pulmonary arteries (PA), and umbilical artery (UA) were measured at three time points: baseline, during MHO, and 10minutes after removal of MHO. Maternal hyperoxygenation induced decreases in LV strain and strain rate and increases in RV strain and strain rate. Pulmonary artery PI decreased and pulmonary vein VTI increased, suggesting decreased pulmonary vascular resistance and increased pulmonary venous return. Most findings did not return to baseline after removal of MHO. We found no significant effect of MHO on MCA or UA PI. Left heart hypoplasia cases demonstrated similar effects of MHO in control cases, with larger changes in pulmonary vein VTI and LV strain rate. The effects ofMHOon LV and RV mechanics suggest that changes in deformation indices may be explained by increases in LV preload and decreases in RV afterload. The time period for recovery of fetal hemodynamics from MHO is ill-defined.

Can Erythropoietin Reduce Hypoxemic Neurological Damages in Neonates With Congenital Heart Defects?

Congenital heart defects (CHD), the most common cause of birth defects with increasing birth prevalence, affect nearly 1% of live births worldwide. Cyanotic CHD are characterized by hypoxemia, with subsequent reduced oxygen delivery to the brain, especially critical during brain development, beginning in the fetus and continuing through the neonatal period. Therefore, neonates with CHD carry a high risk for neurological comorbidities, even more frequently when there are associated underlying genetic disorders. We review the currently available knowledge on potential prevention strategies to reduce brain damage induced by hypoxemia during fetal development and immediately after birth, and the role of erythropoietin (EPO) as a potential adjunctive treatment. Maternal hyper-oxygenation had been studied as a potential therapeutic to improve fetal oxygenation. Despite demonstrating some effectiveness, maternal hyper-oxygenation has proven to be impractical for extensive clinical application, thus prompting the investigation of specific pathways for pharmacological intervention. Among those, the role of antioxidant pathways and Hypoxia Inducible Factors (HIF) have been studied for their involvement in the protective response to hypoxic injury. One of the proteins induced by HIF, EPO, has properties of being anti-apoptotic, antioxidant, and protective for neurons, astrocytes, and oligodendrocytes. In human trials, EPO administration in neonates with hypoxic ischemic encephalopathy (HIE) significantly reduced the neurological hypoxemic damages in several reported studies. Currently, it is unknown if the mechanisms of pathophysiology of cyanotic CHD are like HIE. Neonates with cyanotic CHD are exposed to both chronic hypoxemia and episodes of acute ischemia-reperfusion injury when undergo cardiopulmonary bypass surgery requiring aortic cross-clamp and general anesthesia. Our review supports future trials to evaluate the potential efficiency of EPO in reducing the hypoxemic neurologic damages in neonates with CHD. Furthermore, it suggests the need to identify early biomarkers of hypoxia-induced neurological damage, which must be sensitive to the neuroprotective effects of EPO.

The Influence of Hyperoxygenation on Fetal Brain Vascularity Measured Using 3D Power Doppler Ultrasound and the Index “Fractional Moving Blood Volume”

Introduction: Maternal hyperoxygenation effects on fetal cerebral hemodynamics are largely unknown. This study aimed to determine efficacy and reliability of a validated power Doppler ultrasound (US) index, fractional moving blood volume (FMBV), at measuring fetal cerebral vasculature changes during maternal hyperoxia. Methods: The fetal cerebral effects of 10 min of hyperoxygenation at 2 flow rates (52%/60% FiO₂) were evaluated in women in their third trimester of pregnancy. 2D-US and 3D-US in a transverse plane were performed before, during, and following maternal hyperoxygenation with FMBV estimation performed offline. Results: Forty-five cases provided data for analysis. Mean intraobserver ICCs were 0.89 (3D-FMBV) and 0.84 (2D-FMBV). A significant difference in vascularity before and during and before and after 60% hyperoxia was observed (p < 0.05), whereas no significant differences were found at 52% hyperoxia (p > 0.05). Significant differences in vascularity were found between 2D-FMBV and 3D-FMBV (p < 0.01). Conclusion: Measurement of fetal cerebral vascularity by 3D-FMBV and 2D-FMBV was highly reproducible. The differing cerebral vascular changes seen with 60% but not 52% FiO₂ suggest a possible “threshold effect” that may have influenced prior studies. Further studies are needed to assess cerebral effects of maternal hyperoxygenation on compromised fetuses.

Maternal Hyperoxygenation Testing in Fetuses with Hypoplastic Left-Heart Syndrome: Association with Postnatal Atrial Septal Restriction

Introduction: In fetuses with hypoplastic left-heart syndrome (HLHS), maternal hyperoxygenation (MHO) may aid risk stratification. We hypothesized that pulmonary vein (Pvein) velocity time integral (VTI) change with MHO would more reliably identify neonates who undergo emergent atrial septoplasty (EAS) than changes in pulmonary arterial pulsatility index (PA PI). Methods: Fetuses with HLHS who underwent MHO testing at our institution between 2014 and 2019 were identified. Data were reviewed in a blinded, retrospective manner. Pvein VTI ratio (prograde:retrograde) was calculated. The primary outcome was neonatal EAS. Results: Twenty-seven HLHS fetuses underwent MHO, and 5 (19%) underwent EAS. Without MHO, a Pvein VTI ratio <3 conferred 60% sensitivity and 100% specificity for EAS. With MHO, a Pvein VTI ratio <6.5 conferred 100% sensitivity and specificity. For an intermediate group of fetuses with a baseline Pvein VTI ratio 3–7, the ratio decrease with MHO conferred 100% sensitivity and specificity. Compared to the Pvein VTI ratio, PA PI was less accurate in identifying EAS neonates. Discussion/Conclusion: Addition of MHO appears to improve the diagnostic ability of the Pvein VTI ratio to identify HLHS fetuses who undergo EAS. The Pvein VTI ratio change may more accurately identify fetuses who undergo EAS than change in PA PI and has less interobserver variability.

OC11.04: Effect of maternal hyperoxygenation on pulmonary circulation in growth‐restricted fetuses: a machine learning analysis of Doppler

OC11.04: Effect of maternal hyperoxygenation on pulmonary circulation in growth‐restricted fetuses: a machine learning analysis of Doppler

Maternal hyperoxygenation in congenital heart disease.

The importance of prenatal diagnosis and fetal intervention has been increasing as a preventative strategy for improving the morbidity and mortality in congenital heart disease (CHD). The advancements in medical imaging technology have greatly enhanced our understanding of disease progression, assessment, and impact in those with CHD. In particular, there has been a growing focus on improving the morbidity and mortality of fetuses diagnosed with left-sided lesions. The disruption of fetal hemodynamics resulting from poor structural developmental of the left outflow tract during cardiogenesis is considered a major factor in the progressive lethal underdevelopment of the left ventricle (LV). This positive feedback cycle of inadequate flow and underdevelopment of the LV leads to a disrupted fetal circulation, which has been described to impact fetal brain growth where systemic outflow is poor and, in some cases, the fetal lungs in the setting of a restrictive interatrial communication. For the past decade, maternal hyperoxygenation (MH) has been investigated as a diagnostic tool to assess the pulmonary vasculature and a therapeutic agent to improve the development of the heart and brain in fetuses with CHD with a focus on left-sided cardiac defects. This review discusses the findings of these studies as well as the utility of acute and chronic administration of MH in CHD.

Nifedipine disturbs fetal cardiac function during hypoxemia in a chronic sheep model at near term gestation

Nifedipine is a widely used drug in pregnancies complicated by maternal hypertensive disorders that can be associated with placental insufficiency and fetal hypoxemia. The evidence regarding fetal myocardial responses to nifedipine in hypoxemia is limited. We hypothesized that nifedipine would not impair fetal sheep cardiac function under hypoxemic environment. In particular, we investigated the effects of nifedipine on fetal ventricular functional parameters and cardiac output. A total of 21 chronically instrumented fetal sheep at 122 to 134 gestational days (term, 145 days) were included in this study. Fetal cardiac function was evaluated by measuring global longitudinal strain, indices describing ventricular systolic and diastolic function, and cardiac outputs using two-dimensional speckle tracking and tissue and spectral pulsed-wave Doppler echocardiography. Fetal carotid artery blood pressure and blood gas values were invasively monitored. After baseline data collection, fetal hypoxemia was induced by maternal hyperoxygenation. After hypoxemia phase data collection, 9 fetuses received nifedipine infusion, and 12 fetuses received saline infusion. Data were collected 30 and 120 minutes after the infusion was started. After 120 minutes of data collection, maternal and fetal oxygenation were normalized, and normoxemia phase data were collected, while infusion was continued. Hypoxemia decreased fetal carotid artery mean arterial pressure from 40 (8) mm Hg to 35 (8) mm Hg (P<.007), and left ventricular global longitudinal strain showed less deformation than at baseline (P=.001). Under hypoxemia, nifedipine caused a reduction in right ventricular global longitudinal strain (P<.05), a decrease in right ventricular isovolumic relaxation velocity and its deceleration (P<.01) indicating diastolic dysfunction, and a drop in right ventricular cardiac output (P<.05). Nifedipine did not alter fetal left ventricular functional parameters or cardiac output. When normoxemia was restored, fetal right ventricular functional parameters and cardiac output returned to baseline level. In hypoxemic fetus, nifedipine impaired right ventricular function and reduced its cardiac output. The detrimental effects of nifedipine on fetal right ventricular function were abolished, when normoxemia was restored. Our findings suggest that in a hypoxemic environment nifedipine triggers detrimental effects on fetal right ventricular function.