Background Optimal oxygen levels in pregnant mothers undergoing mechanical ventilation are not known. This study examined the effects of four maternal oxygenation ranges on fetal hemodynamics and oxygenation in late-preterm lambs. Methods Thirty-seven ewes were intubated, sedated, and surgically catheterized, while exposed to varying FiO2 concentrations (0.1–1.0). Fetal lambs were partially exteriorized via hysterotomy for serial carotid blood gas and flow measurements. Maternal oxygenation was categorized as hyperoxia (PaO₂ > 150 mmHg), normal (81–150 mmHg), ARDSnet target (55–80 mmHg), and hypoxemia (<55 mmHg). Results Fetal carotid oxygen content was comparable between hyperoxia and normal oxygenation with stable cerebral oxygen delivery (DO₂: 2.0 ± 1.2 vs. 2.1 ± 1.7 mL/kg/min). In contrast, PaO₂ 55–80 mmHg and <55 mmHg were associated with significantly reduced fetal oxygen content (5.2 ± 3.7 and 4.0 ± 3.1 mL/dL, respectively) versus >150 mmHg, though only <55 mmHg differed significantly from 81–150 mmHg. Cerebral DO₂ trended lower in hypoxemic groups (1.6 ± 1.6 and 1.1 ± 1.1 mL/kg/min) but did not reach significance. Conclusions Maternal hyperoxia exposure is buffered by the fetoplacental circulation minimizing fetal cerebral risk. When maternal PaO₂ < 80 mmHg, particularly < 55 mmHg, fetal carotid oxygen content declines, potentially compromising cerebral oxygen delivery. Impact <UnorderedList Mark="Bullet"> <ItemContent> Pregnant women are highly susceptible to severe respiratory illness and ARDS, yet guidance on optimal maternal oxygen targets is limited. </ItemContent> <ItemContent> We investigated how varying maternal PaO₂ levels affect fetoplacental circulation and in-utero oxygenation. </ItemContent> <ItemContent> Using a large mammalian model of acute maternal hypoxia, we assessed whether maternal ARDSnet oxygenation targets (PaO₂ 55–80 mmHg, SpO₂ 88–95%) can be safely applied in pregnancy. Fetal carotid oxygen content decreased at maternal ARDSnet targets and when below PaO₂ 55 mmHg, with a non-significant trend toward reduced fetal cerebral oxygen delivery. Application of a maternal ARDSnet strategy may lead to suboptimal fetal oxygenation. </ItemContent> </UnorderedList>

Impact of varying range of maternal oxygenation targets on fetal oxygenation and fetoplacental circulation in an ovine model of pregnancy

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2026年3月18日

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Nithi Fernandes,
Satyan Lakshminrusimha,
Praveen Chandrasekharan,
Munmun Rawat,
Sylvia Gugino,
Justin Helman,
Michelle J. Lim

摘要

Background

Optimal oxygen levels in pregnant mothers undergoing mechanical ventilation are not known. This study examined the effects of four maternal oxygenation ranges on fetal hemodynamics and oxygenation in late-preterm lambs.

Methods

Thirty-seven ewes were intubated, sedated, and surgically catheterized, while exposed to varying FiO₂ concentrations (0.1–1.0). Fetal lambs were partially exteriorized via hysterotomy for serial carotid blood gas and flow measurements. Maternal oxygenation was categorized as hyperoxia (PaO₂ > 150 mmHg), normal (81–150 mmHg), ARDSnet target (55–80 mmHg), and hypoxemia (<55 mmHg).

Results

Fetal carotid oxygen content was comparable between hyperoxia and normal oxygenation with stable cerebral oxygen delivery (DO₂: 2.0 ± 1.2 vs. 2.1 ± 1.7 mL/kg/min). In contrast, PaO₂ 55–80 mmHg and <55 mmHg were associated with significantly reduced fetal oxygen content (5.2 ± 3.7 and 4.0 ± 3.1 mL/dL, respectively) versus >150 mmHg, though only <55 mmHg differed significantly from 81–150 mmHg. Cerebral DO₂ trended lower in hypoxemic groups (1.6 ± 1.6 and 1.1 ± 1.1 mL/kg/min) but did not reach significance.

Conclusions

Maternal hyperoxia exposure is buffered by the fetoplacental circulation minimizing fetal cerebral risk. When maternal PaO₂ < 80 mmHg, particularly < 55 mmHg, fetal carotid oxygen content declines, potentially compromising cerebral oxygen delivery.

Impact

Pregnant women are highly susceptible to severe respiratory illness and ARDS, yet guidance on optimal maternal oxygen targets is limited.

We investigated how varying maternal PaO₂ levels affect fetoplacental circulation and in-utero oxygenation.

Using a large mammalian model of acute maternal hypoxia, we assessed whether maternal ARDSnet oxygenation targets (PaO₂ 55–80 mmHg, SpO₂ 88–95%) can be safely applied in pregnancy. Fetal carotid oxygen content decreased at maternal ARDSnet targets and when below PaO₂ 55 mmHg, with a non-significant trend toward reduced fetal cerebral oxygen delivery. Application of a maternal ARDSnet strategy may lead to suboptimal fetal oxygenation.