Short-Term Effects of Maternal Oxygen Administration on Blood Flow Velocity Waveforms in Healthy and Growth-Retarded Fetuses

Arduini, D.; Rizzo, G.; Mancuso, Salvatore; Romaninï, Carlo

doi:10.1097/00132586-198910000-00035

Cited by 13 publications

(23 citation statements)

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“…29,30 It should be noted that several earlier Doppler studies did not observe results consistent with increased cerebral vascular resistance. [31][32][33] Further studies such as direct flow measurements of fetal cerebral blood flow under maternal hyperoxia would allow assessment of this hypothesis.…”

Section: Discussionmentioning

confidence: 99%

Absence of Po₂ change in fetal brain despite Po₂ increase in placenta in response to maternal oxygen challenge

Huen

Morris

Wright

et al. 2014

BJOG

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Objective Magnetic resonance imaging allows the noninvasive observation of PO 2 changes between air breathing and oxygen breathing through quantification of the magnetic longitudinal relaxation time T 1 . Changes in PO 2 are proportional to changes in the longitudinal relaxation rate DR 1 (where DR 1 = 1/ T 1oxygen À 1/T 1air ). Knowledge of this response could inform clinical interventions using maternal oxygen administration antenatally to treat fetal growth restriction. We present in vivo measurements of the response of the fetal-placental unit to maternal hyperoxia. Design Prospective cohort.Setting Large tertiary maternity hospital.Sample Nine women undergoing low-risk pregnancy (21-33 weeks of gestation) and five nonpregnant adults.Methods During imaging the air supply to mothers was changed from medical air (21% oxygen) to medical oxygen (100% oxygen) and T 1 was monitored over time in both the placenta and fetal brain using a periodically repeated magnetic resonance imaging sequence. To demonstrate that the method could detect a brain response, brain responses from five normal adult volunteers were measured using a similar imaging protocol.Main outcome measure Changes in T 1 following oxygen challenge.Results No significant DR 1 (P = 0.42, paired t-test) was observed in fetal brains. A significant placental DR 1 (P = 0.0002, paired t-test) of 0.02 AE 0.01/s (mean AE SD) was simultaneously observed in the same participants. In the brains of the nonpregnant adults, a significant DR 1 (P = 0.01, paired t-test) of 0.005 AE 0.002/s was observed.Conclusion Short-term maternal oxygen administration does not improve fetal brain oxygenation, in contrast to the response observed in the adult brain.

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Section: Discussionmentioning

confidence: 99%

Absence of Po₂ change in fetal brain despite Po₂ increase in placenta in response to maternal oxygen challenge

Huen

Morris

Wright

et al. 2014

BJOG

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“…Recordings were made from different fetal extra-and intracardiac districts including umbilical artery, tho racic descending aorta, renal artery, middle cerebral artery, ascending aorta, pulmonary artery and inferior vena cava. The technique followed to record velocity waveforms from these vessels has been reported else where [6.10,14], At the level of fetal middle cerebral artery, record ings were obtained before and after 15 min of oxygen administration with the mother still breathing oxygen (oxygen test), a time interval corresponding on the basis of our previous experience to the maximum fetal vascular response [15]. Oxygen was administered to the mother lying in a comfortable semirecumbent posi tion at 8 1/min through a face mask delivering 60% humidified oxygen.…”

Section: Doppler Recordingsmentioning

confidence: 99%

Analysis of Risk Factors Influencing Imminent Distress in Growth-Retarded Fetuses Undergoing Oxygen Test

et al. 1993

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We previously demonstrated a prognostic significance of maternal oxygen test in predicting imminent fetal distress. The purpose of this study was to investigate eventual other factors related to the length of the time interval elapsing between the Doppler diagnosis of brain sparing effect and abnormal fetal heart rate patterns. To this end we considered 101 growth-retarded fetuses free of structural and chromosomal abnormalities with a ratio between the pulsatility indices of umbilical and middle cerebral artery above the 95th centile in presence of a normal fetal heart rate pattern. The factors, other than the oxygen test, analyzed for a potential influence on this time interval were gestational age, presence of hypertension or preeclampsia, amniotic fluid index, severity of growth retardation (centile of the ultrasonographic estimated fetal weight) and 9 different Doppler indices calculated from extra- and intracardiac districts. Statistical actuarial methods were used to determine the effect of these prognostic factors on the duration of this time interval. The occurrence of abnormal fetal heart rate patterns (antepartum late heart rate decelerations) was used as censoring variable. The time interval between the entry in the study and delivery ranged from 1 to 39 days. Indications for delivery were fetal distress in 53 fetuses (52.4%) and different maternal or fetal complications in the remaining 48 fetuses. Multivariate analysis showed that the factors that independently affect the time interval between Doppler abnormalities and development of abnormal fetal heart rate patterns are the oxygen test (p ≤ 0.001), the percentage of reverse flow in inferior vena cava (p ≤ 0.001), gestational age (p ≤ 0.01) and the presence of hypertension (p ≤ 0.05). The knowledge of these prognostic factors may be useful in the clinical management of growth-retarded fetuses.

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“…Nicolaides et al [13] gave a direct demon stration of these findings showing a rise in fetal oxygenation at the end of a 10-min maternal oxygen treatment. In IUGR fetuses these modifications of fetal oxygenation cause changes in fetal vascular resistances at the cerebral [5] and descending aorta [5,13] levels which may affect the cardiac afterload of the left and right ventricles, respectively.…”

Section: Discussionmentioning

confidence: 99%

“…Oxygen was administered to the mother for 20 min through a face mask delivering about 60% humidified oxygen [5]. Recordings were obtained at 5-min intervals before, during (5, 10, 15 and 20 min) and after (20, 30, 35 and 40 min) maternal oxygen administration.…”

Section: Methodsmentioning

confidence: 99%

“…In IUGR fetuses, acute transmaternai oxy-gen administration induces significant changes in blood flow velocity waveforms from peripheral vessels, causing a temporary disappearance of the blood flow redistribu tion [5]. We therefore examined the effect of transmaternai oxygen administration on AV velocity waveforms in healthy and IUGR fetuses.…”

Section: Introductionmentioning

confidence: 99%

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Effects of Maternal Hyperoxygenation on Atrioventricular Velocity Waveforms in Healthy and Growth-Retarded Fetuses

Rizzo

Arduini²,

Romaninï³

et al. 1990

Neonatology

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In order to assess whether maternal hyperoxygenation induces modifications of Doppler-measured velocity waveforms across atrioventricular valves, 15 healthy and 15 growth-retarded fetuses were studied in basal conditions and during the maternal administration of 60% humidified oxygen. Recordings were performed at 5-min intervals before, during and after maternal oxygen administration. In basal conditions, growth-retarded fetuses exhibited significantly lower ratios between the velocities during early passive ventricular filling and active ventricular filling (E/A ratio) at the level of both mitral and tricuspid valves when compared to healthy fetuses. Furthermore in healthy fetuses the velocity time integral across the tricuspid valve always slightly exceeded that across the mitral valve, whilst growth-retarded fetuses showed an inversed ratio between these velocities. During oxygen administration no changes were found between the two groups of fetuses with regard to the E/A ratios. Similarly the velocity time integrals were unaffected by oxygen administration in the healthy fetuses. Besides growth-retarded fetuses exhibited significant temporary modifications during oxygen administration as expressed by an increase in the velocity time integral across the mitral valve associated with a decrease of that across the tricuspid. These changes result in an inversion of the ratio between transtricuspid and transmitral velocity time integrals reaching values similar to those of healthy fetuses. Short-term oxygen administration affects the intracardiac flow redistribution present in growth-retarded fetuses bringing it to a pattern similar to that of healthy fetuses whereas the E/A ratios were not affected by the treatment.

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Short-Term Effects of Maternal Oxygen Administration on Blood Flow Velocity Waveforms in Healthy and Growth-Retarded Fetuses

Cited by 13 publications

References 0 publications

Absence of Po₂ change in fetal brain despite Po₂ increase in placenta in response to maternal oxygen challenge

Absence of Po₂ change in fetal brain despite Po₂ increase in placenta in response to maternal oxygen challenge

Analysis of Risk Factors Influencing Imminent Distress in Growth-Retarded Fetuses Undergoing Oxygen Test

Effects of Maternal Hyperoxygenation on Atrioventricular Velocity Waveforms in Healthy and Growth-Retarded Fetuses

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Short-Term Effects of Maternal Oxygen Administration on Blood Flow Velocity Waveforms in Healthy and Growth-Retarded Fetuses

Cited by 13 publications

References 0 publications

Absence of Po2 change in fetal brain despite Po2 increase in placenta in response to maternal oxygen challenge

Absence of Po2 change in fetal brain despite Po2 increase in placenta in response to maternal oxygen challenge

Analysis of Risk Factors Influencing Imminent Distress in Growth-Retarded Fetuses Undergoing Oxygen Test

Effects of Maternal Hyperoxygenation on Atrioventricular Velocity Waveforms in Healthy and Growth-Retarded Fetuses

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Absence of Po₂ change in fetal brain despite Po₂ increase in placenta in response to maternal oxygen challenge

Absence of Po₂ change in fetal brain despite Po₂ increase in placenta in response to maternal oxygen challenge