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Correction of tissue oxygen saturations using arterial oxygen levels for cerebrovascular autoregulation analysis

机译:用动脉氧水平校正组织氧饱和性脑血管血管血管饱和分析

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Adequate perfusion of blood is fundamental to brain tissue viability, and failure to appropriately regulate cerebral blood flow is related to neurological damage. Cerebral tissue oxygenation is commonly used as a surrogate of cerebral blood flow for non-invasive measures of autoregulation, but may only be valid during periods of constant oxygen delivery. We present a new algorithm to correct for supply oxygen-induced variations in cerebral tissue oxygenation, and we validate it by measuring the improved correlation of the corrected tissue oxygenation with blood flow. The algorithm corrects tissue oxygenation by calculating its linear dependence with arterial oxygen saturation below a baseline level. A porcine model (N=8) of hypoxia is used to test the algorithm and compare the tissue oxygen correction with a blood flow reference signal. The correction provides significant improvement in the correlation between flow and tissue oxygenation (Wilcoxon signed rank, p<0.01), and for the root mean square distance between the corrected hypoxic periods and the rSO_2-flow regression line (Wilcoxon signed rank, p<0.01). This method allows the correction of tissue oxygenation levels used in the non-invasive monitoring of autoregulation.
机译:血液充分灌注是脑组织活力的基础,并且未能适当调节脑血流与神经损伤有关。脑组织氧合通常用作脑血流的替代因子,用于自侵入式自动造型,但在恒定氧递送期间只能有效。我们提出了一种校正脑组织氧合的供应氧气诱导变化的新算法,我们通过测量校正的组织氧合与血流的改善的相关性来验证。该算法通过在基线水平以下的动脉氧饱和度计算其线性依赖性来校正组织氧合。缺氧的猪模型(n = 8)用于测试算法并与血流参考信号进行比较组织氧校正。校正在流动和组织氧合(Wilcoxon签名等级,P <0.01)之间的相关性具有显着的改善,并且对于校正的缺氧时期和RSO_2流量回归线之间的根均方距离(Wilcoxon签名等级,P <0.01 )。该方法允许校正用于自动调节的非侵入性监测的组织氧合水平。

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