Perfusion
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Recirculation (R), the shunting of arterial blood back into to the venous lumen, commonly occurs during veno-venous extracorporeal membrane oxygenation (VV-ECMO) and renders the monitoring of the venous line oxygen saturation no longer reflective of patient mixed venous oxygen saturation (S(V)O(2)). Previously, we failed to prove the hypothesis that, once R is known, it is possible to calculate the S(V)O(2) of a patient on VV-ECMO. We hypothesize that we can calculate S(V)O(2) during VV-ECMO if we account for and add an additional correction factor to our model for dissolved oxygen content. Therefore, the purpose of this study is to derive a more accurate model that will allow clinicians to determine S(V)O(2) during VV-ECMO when ultrasound dilution is being used to quantify R. ⋯ The original model using R and circuit saturations for the calculation of S(V)O( 2) in VV-ECMO patients is an oversimplification that fails to consider the influence of the high pO(2) of arterial blood during therapy. In the future, further improvements in this model will allow clinicians accurately to calculate S(V)O(2) in conjunction with recirculation measurements.
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The aim of this prospective, animal study was to compare brain tissue oxygen tension (PbtO(2)) with cerebral near infrared spectroscopy (NIRS) and mixed venous oxygen saturation (SVO(2)) during venoarterial extracorporeal membrane oxygenation (VA ECMO) in a porcine model. This was accomplished using twelve immature piglets with surgically implanted catheters placed in the superficial cerebral cortex to measure brain PbtO(2) and microdialysis metabolites. The NIRS sensor was placed overlying the forehead to measure cerebral regional saturation index (rSO(2)i) while SVO(2) was measured directly from the ECMO circuit. ⋯ Upon further analysis, these animals had significantly lower blood pressure (p=0.001), lower serum pH (p=0.01), and higher serum lactate (p=0.02). Additionally, in this subgroup, rSO(2)i correlated better with PbtO(2) (R(2)=0.76). These findings suggest that, in our ECMO model, rSO(2)i and SVO( 2) correlate reasonably well with each other, but not necessarily with brain PbtO(2) and that NIRS-derived rSO(2)i may more accurately reflect cerebral tissue hypoxia in sicker animals.