Báo cáo y học: "Venous oxygen saturation as a physiologic transfusion trigger"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: Venous oxygen saturation as a physiologic transfusion trigger. | Vallet et al. Critical Care 2010 14 213 http content 14 2 213 CRITICAL CARE REVIEW L_ Venous oxygen saturation as a physiologic transfusion trigger Benoit Vallet Emmanuel Robin and Gilles Lebuffe This article is one of ten reviews selected from the Yearbook of Intensive Care and Emergency Medicine 2010 Springer Verlag and co-published as a series in Critical Care. Other articles in the series can be found online at http ccforum series yearbook. Further information about the Yearbook of Intensive Care and Emergency Medicine is available from http series 2855. Introduction Venous oxygen saturation is a clinical tool which integrates the whole body oxygen uptake-to-delivery VO2-DO2 relationship. In the clinical setting in the absence of pulmonary artery catheter PAC -derived mixed venous oxygen saturation SvO2 the central venous oxygen saturation ScvO2 is increasingly being used as a reasonably accurate surrogate 1 . Central venous catheters CVCs are simpler to insert and generally safer and cheaper than PACs. The CVC allows sampling of blood for measurement of ScvO2 or even continuous monitoring if an oximetry catheter is being used. The normal range for SvO2 is 68 to 77 and ScvO2 is considered to be 5 above these values 2 . A decrease in hemoglobin Hb g dl is likely to be associated with a decrease in DO2 when cardiac output CO remains unchanged since DO2 CO x CaO2 where CaO2 is arterial oxygen content and is Hb X SaO2 x where SaO2 is the arterial oxygen saturation in and is the oxygen-carrying capacity of Hb in mlO2 g Hb when one ignores the negligible oxygen not bound to Hb 1 . A decrease in Hb is one of the four determinants responsible for a decrease in SvO2 or ScvO2 alone or in combination with hypoxemia decrease in SaO2 an increase in VO2 without a concomitant increase in DO2 or a fall in cardiac output. When DO2 decreases VO2 is maintained at least initially by an increase in oxygen extraction O2ER since O2ER vO2 .

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