https://www.selleckchem.com/products/cc-92480.html
001), as was arterial oxyhaemoglobin saturation (81 ± 9 versus 98 ± 5%, p less then 0.001). Cerebral venous oxyhaemoglobin saturation correlated poorly with superior caval pressure in both groups. When estimated by linear mixed effects model, arterial oxyhaemoglobin saturation was the primary determinant of central venous oxyhaemoglobin saturation in both groups (β = 0.79, p = 3 × 10-14); for every 1% point increase in arterial oxyhaemoglobin saturation, there was a 0.79% point increase in venous oxyhaemoglobin saturation. In this mode
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