Oxygen metabolism and oxygenation of the newborn

Andresen, Jannicke H; Saugstad, Ola Didrik

doi:10.1016/j.siny.2020.101078

Cited by 18 publications

(11 citation statements)

References 75 publications

(82 reference statements)

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“…We found that the increase in oxygen delivery for lambs resuscitated in 100% FiO 2 was not matched by an increase in oxygen consumption following ROSC to compensate for an accumulated oxygen deficit. In contrast to normal conditions where oxygen delivery in a newborn is approximately 3 times higher than consumption, as corroborated at the fetal and post-hyperaemic time points, we found oxygen delivery to be up to 8 times higher than consumption in the 15 min after ROSC 33 . Our findings are consistent with those of neonatal calf and lamb studies that were performed days after birth, well after the transitional period had occurred 34,35 .…”

Section: Discussionsupporting

confidence: 70%

Excess cerebral oxygen delivery follows return of spontaneous circulation in near-term asphyxiated lambs

Badurdeen

Gill

Kluckow

et al. 2020

Sci Rep

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Hypoxic-ischaemia renders the neonatal brain susceptible to early secondary injury from oxidative stress and impaired autoregulation. We aimed to describe cerebral oxygen kinetics and haemodynamics immediately following return of spontaneous circulation (ROSC) and evaluate non-invasive parameters to facilitate bedside monitoring. Near-term sheep fetuses [139 ± 2 (SD) days gestation, n = 16] were instrumented to measure carotid artery (CA) flow, pressure, right brachial arterial and jugular venous saturation (SaO2 and SvO2, respectively). Cerebral oxygenation (crSO2) was measured using near-infrared spectroscopy (NIRS). Following induction of severe asphyxia, lambs received cardiopulmonary resuscitation using 100% oxygen until ROSC, with oxygen subsequently weaned according to saturation nomograms as per current guidelines. We found that oxygen consumption did not rise following ROSC, but oxygen delivery was markedly elevated until 15 min after ROSC. CrSO2 and heart rate each correlated with oxygen delivery. SaO2 remained > 90% and was less useful for identifying trends in oxygen delivery. CrSO2 correlated inversely with cerebral fractional oxygen extraction. In conclusion, ROSC from perinatal asphyxia is characterised by excess oxygen delivery that is driven by rapid increases in cerebrovascular pressure, flow, and oxygen saturation, and may be monitored non-invasively. Further work to describe and limit injury mediated by oxygen toxicity following ROSC is warranted.

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Section: Discussionsupporting

confidence: 70%

Excess cerebral oxygen delivery follows return of spontaneous circulation in near-term asphyxiated lambs

Badurdeen

Gill

Kluckow

et al. 2020

Sci Rep

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“…Antioxidative capacity is constituted by superoxide dismutases, catalases, heme oxygenases, flavin-containing enzymes, glutathione, and thioredoxin, which are the most prominent and best-studied candidates. This makes preterm infants especially vulnerable to ROS-induced injury [ 47 ]. The most relevant features of ROS tissue injury, following their accumulation, are ascribed to oxidative damage to proteins, lipids, and DNA [ 48 ].…”

Section: Ros-induced Injury To the Immature Lung As A Key Driver Of Bpdmentioning

confidence: 99%

Oxygen Toxicity to the Immature Lung—Part II: The Unmet Clinical Need for Causal Therapy

Behnke

Dippel

Choi

et al. 2021

IJMS

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Oxygen toxicity continues to be one of the inevitable injuries to the immature lung. Reactive oxygen species (ROS) production is the initial step leading to lung injury and, subsequently, the development of bronchopulmonary dysplasia (BPD). Today, BPD remains the most important disease burden following preterm delivery and results in life-long restrictions in lung function and further important health sequelae. Despite the tremendous progress in the pathomechanistic understanding derived from preclinical models, the clinical needs for preventive or curative therapies remain unmet. This review summarizes the clinical progress on guiding oxygen delivery to the preterm infant and elaborates future directions of research that need to take into account both hyperoxia and hypoxia as ROS sources and BPD drivers. Many strategies have been tested within clinical trials based on the mechanistic understanding of ROS actions, but most have failed to prove efficacy. The majority of these studies were tested in an era before the latest modes of non-invasive respiratory support and surfactant application were introduced or were not appropriately powered. A comprehensive re-evaluation of enzymatic, antioxidant, and anti-inflammatory therapies to prevent ROS injury is therefore indispensable. Strategies will only succeed if they are applied in a timely and vigorous manner and with the appropriate outcome measures.

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“…In this review, we summarize recent findings with respect to the association between hyperoxemia and outcomes in critically ill pediatric patients. For an in-depth review of oxygen physiology in premature infants and in the delivery room, the reader is directed elsewhere (8)(9)(10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

Hyperoxemia Is Associated With Mortality in Critically Ill Children

2021

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Multiple studies among adults have suggested a non-linear relationship between arterial partial pressure of oxygen (PaO2) and clinical outcomes. Meta-analyses in this population suggest that high levels of supplemental oxygen resulting in hyperoxia are associated with mortality. This mini-review focuses on the non-neonatal pediatric literature examining the relationship between PaO2 and mortality. While only one pilot pediatric randomized-controlled trials exists, over the past decade, there have been at least eleven observational studies examining the relationship between PaO2 values and mortality in critically ill children. These analyses of mixed-case pediatric ICU populations have generally reported a parabolic (“u-shaped”) relationship between PaO2 and mortality, similar to that seen in the adult literature. However, the estimates of the point at which hyperoxemia becomes deleterious have varied widely (300–550 mmHg). Where attempted, this effect has been robust to analyses restricted to the first PaO2 value obtained, those obtained within 24 h of admission, anytime during admission, and the number of hyperoxemic blood gases over time. These findings have also been noted when using various methods of risk-adjustment (accounting for severity of illness scores or complex chronic conditions). Similar relationships were found in the majority of studies restricted to patients undergoing care after cardiac arrest. Taken together, the majority of the literature suggests that there is a robust parabolic relationship between PaO2 and risk-adjusted pediatric ICU mortality, but that the exact threshold at which hyperoxemia becomes deleterious is unclear, and likely beyond the typical target value for most clinical indications. Findings suggest that clinicians should remain judicious and thoughtful in the use of supplemental oxygen therapy in critically ill children.

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Oxygen metabolism and oxygenation of the newborn

Cited by 18 publications

References 75 publications

Excess cerebral oxygen delivery follows return of spontaneous circulation in near-term asphyxiated lambs

Excess cerebral oxygen delivery follows return of spontaneous circulation in near-term asphyxiated lambs

Oxygen Toxicity to the Immature Lung—Part II: The Unmet Clinical Need for Causal Therapy

Hyperoxemia Is Associated With Mortality in Critically Ill Children

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