Effect of Hyperoxia on Cerebral Blood Flow Velocity and Regional Oxygen Saturation in Patients Operated on for Severe Traumatic Brain Injury–The Influence of Cerebral Blood Flow Autoregulation

Sahoo, Sarasa Kumar; Sheshadri, Veena; Sriganesh, Kamath; Reddy, K.R. Madhsudana; Radhakrishnan, M.; Gs, Rao

doi:10.1016/j.wneu.2016.10.116

Cited by 11 publications

(12 citation statements)

References 26 publications

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“…Indeed, Nortje et al (195) noted that in brain regions where the baseline (i.e., posttrauma) cerebral metabolic rate of oxygen (CMRO 2 ) was reduced below 37 mol•100 ml Ϫ1 •min Ϫ1 , hyperoxia increased CMRO 2 from 23 to 30 mol•100 ml Ϫ1 • min Ϫ1 , whereas no changes in global CBF or O 2 extraction fraction were observed, therefore suggesting that hyperoxia essentially affects at-risk tissues. Sahoo et al (239) recently confirmed this site-specific response, observing that cerebral oxygen saturation was not only solely improved in the operated cerebral hemisphere (following severe TBI) but also that this increase was linked with impaired cerebral autoregulation. It was postulated that the ability of the cerebrovasculature to vasoconstrict in response to hyperoxia is impaired following TBI, in turn allowing oxygenation to increase.…”

Section: Traumatic Brain Injurymentioning

confidence: 79%

Highs and lows of hyperoxia: physiological, performance, and clinical aspects

Brugniaux

Coombs

Barak

et al. 2018

American Journal of Physiology-Regulatory, Integrative and Comp

100

108

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Molecular oxygen (O) is a vital element in human survival and plays a major role in a diverse range of biological and physiological processes. Although normobaric hyperoxia can increase arterial oxygen content ([Formula: see text]), it also causes vasoconstriction and hence reduces O delivery in various vascular beds, including the heart, skeletal muscle, and brain. Thus, a seemingly paradoxical situation exists in which the administration of oxygen may place tissues at increased risk of hypoxic stress. Nevertheless, with various degrees of effectiveness, and not without consequences, supplemental oxygen is used clinically in an attempt to correct tissue hypoxia (e.g., brain ischemia, traumatic brain injury, carbon monoxide poisoning, etc.) and chronic hypoxemia (e.g., severe COPD, etc.) and to help with wound healing, necrosis, or reperfusion injuries (e.g., compromised grafts). Hyperoxia has also been used liberally by athletes in a belief that it offers performance-enhancing benefits; such benefits also extend to hypoxemic patients both at rest and during rehabilitation. This review aims to provide a comprehensive overview of the effects of hyperoxia in humans from the "bench to bedside." The first section will focus on the basic physiological principles of partial pressure of arterial O, [Formula: see text], and barometric pressure and how these changes lead to variation in regional O delivery. This review provides an overview of the evidence for and against the use of hyperoxia as an aid to enhance physical performance. The final section addresses pathophysiological concepts, clinical studies, and implications for therapy. The potential of O toxicity and future research directions are also considered.

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Section: Traumatic Brain Injurymentioning

confidence: 79%

Highs and lows of hyperoxia: physiological, performance, and clinical aspects

Brugniaux

Coombs

Barak

et al. 2018

American Journal of Physiology-Regulatory, Integrative and Comp

100

108

View full text Add to dashboard Cite

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“…Again, this might be due to impaired autoregulation on the injured side. In a study on head injury patients, it was shown that increasing FIO 2 increased rSO 2 values only on the injured side of the brain, with documented impaired autoregulation using transcranial Doppler (Sahoo et al, ). In head injuries, even though an operable lesion is seen on one side, the injury is quite heterogenous.…”

Section: Discussionmentioning

confidence: 99%

Regional cerebral tissue oxygen saturation changes following blood transfusion in neuro‐intensive care unit patients – a pilot observational study

Radhakrishnan

Shaikh

Surve

et al. 2018

Transfusion Medicine

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“…The lactate MR spectroscopy demonstrates that in ischemic core and contralateral striatum, the lactate levels are not affected by NH, whereas, in the region of mismatch, lactate levels changed with changes in O 2 delivery ( 47 ). The T2*-weighted MRI studies showed positive CBF changes to O 2 challenge in the mismatch region, in contrast to negative CBF changes in normal tissue due to O 2 -induced vasoconstriction ( 16 , 48 ). Indeed, the increase in BBC through augmentation of rCBF in the VO 2 buffer supply dependent phase (i.e., in mismatch region) improves local acidosis, unlock the mitochondrial suppression, and decrease the lactate levels.…”

Section: Clinical Interpretationmentioning

confidence: 92%

“…NH induces a negligible increase in the amount of arterial O 2 content and DO 2 , whereas it is associated with an important augmentation of PtiO 2 , without significant change in cerebral metabolic rate of O 2 consumption (CMRO 2 ) ( 11 – 14 ). Furthermore, studies using positron emission tomography, magnetic resonance imaging (MRI), and near-infrared spectroscopy showed an active O 2 extraction fraction (OEF) in the non-necrotic tissue during NH ( 9 , 15 – 18 ) with negligible increase of regional SO 2 (rSO 2 ) at 2.8 ± 1.82% ( 9 ) or without changes in rSO 2 in tissue with intact autoregulation ( 16 ). The data of OEF at 0.56 ± 0.06 in reversible tissue, which although reduced from viable tissue to infarction ( 19 ), discards the possibility of a luxury perfusión in these cases.…”

mentioning

confidence: 99%