| Popis: |
PvCO2 that would result from full O2Hb desaturation at a given O2-CO2 exchange ratio, in the absence of metabolic acid, may be termed maximum respiratory venous PCO2 (PvmrCO2). This theoretical condition of 100% O2 extraction, in the absence of metabolic acid, should simulate maximum aerobic PCO2 in tissue, provided that PCO2 of tissues and large veins is similar. Hence, the value of PvmrCO2 is of interest in identifying critical tissue PCO2. Analysis of the Dill nomogram indicates that PvmrCO2 is 77 torr at RQ = 1.0, PaCO2 = 40 torr in vitro, and that the PvCO2 versus SO2 relation is linear. Since the Dill nomogram is confined to the condition. [Hb] = 15 g.dL-1, [BE] = 0, the goal of the present analysis was to determine variability of PvmrCO2 with [Hb], arterial [base excess] ([BE]), and PaCO2. Venous CO2 titrations for multiple arterial conditions were simulated using published in vitro [BE] and whole blood [total CO2] formulae. In the RQ range of 0.7 to 1.0, the simulation yielded PvCO2 values that were essentially identical to those obtainable from the Dill nomogram. The simulation predicted that PvmrCO2 should decrease in direct proportion to [Hb], and increase non-linearly with decreasing arterial [BE]. The simulation further predicted that venoarterial PCO2 difference should increase linearly with increasing PaCO2. Simulated PvmrCO2-PaCO2 difference varied from 5 torr at arterial [BE] = +10 mmol/L, [Hb] = 6 g.dL-1, PaCO2 = 25 torr, RQ = 0.7 to 67 torr at [BE] = -20 mmol/L, [Hb] = 15 g.dL-1, PaCO2 = 65 torr, RQ = 1.0. It is concluded that the PvCO2 versus SO2 relation is not linear when arterial [Hb] and/or [BE] vary. An equation that predicts in vitro PvmrCO2 as a function of arterial [BE], [Hb], RQ, and PaCO2 is provided. It's accuracy in vivo should be testable. |
