By M.R. Pinsky, L. Brochard, J. Mancebo
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Extra info for Applied Physiology in Intensive Care Medicine
1) . Since the PO2 and PCO2 in each alveolus is determined by ˙ ratio, a line through all PO2–PCO2 value pairs the V˙A/Q can be drawn connecting two endpoints of mixed venous blood and inspired gas composition. Each point on this ˙ values from 0 (representing perline represents V˙A/Q fused but not ventilated alveoli, thus corresponding to shunt areas) to ∞ (representing ventilated but not perfused alveoli, thus corresponding to dead space). Theoretically, the most efficient gas exchange should be expected in a perfectly homogeneous lung, with an overall ˙ value near unity.
CaO2 ¼ ðHb Â 1:36 Â SaO2 Þ þ ðPaO2 Â 0:0031Þ ð2Þ Oxygen demand can be summarized in the whole-body oxygen consumption (VO2), which is expressed mathematically by the Fick principle as the product of CO and arteriovenous O2 content difference (CaO2CvO2): VO2 ¼ CO Â ðCaO2 À CvO2 Þ ð3Þ where mixed venous O2 content (CvO2) is: CvO2 ¼ ðHb Â 1:36 Â SvO2 Þ þ ðPvO2 Â 0:0031Þ ð4Þ Equation 3 may be transposed to: VO2 CvO2 ¼ CaO2 À ð5Þ CO As physically dissolved oxygen can be neglected, Eq. 5 may be written as: VO2 Hb Â 1:36 Â SvO2 % ðHb Â 1:36 Â SaO2 Þ À CO VO2 ð6Þ , SvO2 $ CO Equation 6 also demonstrates that SvO2 is directly proportional to the ratio of VO2 to CO.
0. 0 while the modest levels of intrapulmonary shunt remain unchanged, a response that strongly suggests HPV release. Both responses to pure O2 breathing are accompanied with increases in PaO2, which are much more prominent in patients with COPD. The increase in intrapulmonary shunt in ALI/ARDS is likely due to RA. If cardiac output increases as part of the sympathetic response to arterial hypoxemia, one may also see a parallel increase in mixed venous PO2 owing to increased O2 delivery. This can offset the increased shunt fraction minimizing the decrease in PaO2.