The oxygen flux test

It has been suggested that if an increase in Do2 results in an increase in Vo2, this is evidence of covert tissue hypoxia. This is highly controversial. Concerns have been expressed about complications of increasing cardiac output above normal and the production of toxic O 2 free radicals at the peripheries. Also, some authors have attributed the increase in Vo2 to a statistical artifact due to mathematical coupling of errors in cardiac output determination by thermodilution and have claimed that this phenomenon is not seen when Vo2 is calculated independently of cardiac output by indirect calorimetry.

An alternative approach of plotting the OER against CI and ignoring the Vo2 as a therapeutic goal has been suggested by Silance §tM (1994). Indeed, Vo2 may change independently of tissue hypoxia owing to pain, agitation, or use of sedation and analgesia. It would seem reasonable to try, wherever possible, to achieve an OER as close to normal as possible, and in some situations such as septic shock, acute respiratory distress syndrome, and trauma to aim at a value of 20 per cent provided that underlying cardiac disease has been excluded. ■

Estimation of V02 from respiratory gases

In theory, the volume of oxygen consumed can be calculated by subtracting the expired volume of oxygen ( VeO2) from the inspired volume (ViO2). FiO2 and FeO2 must be measured, and expired volume is routinely and easily measured. Because the respiratory ratio is rarely 1.0 there is a difference between inspired and expired gas volumes. Therefore inspired volume is commonly calculated from measurements of N2 concentrations. As FiO2 increases above 0.6, errors in measuring N2

concentrations increase expotentially.

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