PvCO(2) that would result from full O(2)Hb desaturation at a given O-2
-CO2 exchange ratio, in the absence of metabolic acid, may be termed m
aximum respiratory venous PCO2 (PvmrCO(2)). This theoretical condition
of 100% O-2 extraction, in the absence of metabolic acid, should simu
late maximum aerobic PCO2 in tissue, provided that PCO2 of tissues and
large veins is similar. Hence, the value of PvmrCO(2) is of interest
in identifying critical tissue PCO2. Analysis of the Dill nomogram ind
icates that PvmrCO(2) is 77 torr at RQ = 1.0, PaCO2 = 40 torr in vitro
, and that the PvCO(2) versus SO2 relation is linear. Since the Dill n
omogram is confined to the condition, [Hb] = 15 g . dL(-1), [BE] = 0,
the goal of the present analysis was to determine variability of PvmrC
O(2) with [Hb], arterial [base excess] ([BE]), and PaCO2. Venous CO2 t
itrations for multiple arterial conditions were simulated using publis
hed in vitro [BE] and whole blood [total CO2] formulae. In the RQ rang
e of 0.7 to 1.0, the simulation yielded PvCO(2) values that were essen
tially identical to those obtainable from the Dill nomogram. The simul
ation predicted that PvmrCO(2) should decrease in direct proportion to
[Hb], and increase non-linearly with decreasing arterial [BE]. The si
mulation further predicted that venoarterial PCO2 difference should in
crease linearly with increasing PaCO2. Simulated PvmrCO(2) - PaCO2 dif
ference varied from 5 ton at arterial [BE] = +10 mmol/L, [Hb]= 6 g . d
L(-1), PaCO2 = 25 torr, RQ = 0.7 to 67 ton. at [BE] = -20 mmol/L, [Hb]
= 15 g . dL(-1), PaCO2 = 65 ton, RQ = 1.0. It is concluded that the P
vCO(2) versus SO2 relation is not linear when arterial [Hb] and/or [BE
] vary. An equation that predicts in vitro PvmrCO(2) as a function of
arterial [BE], [Hb], RQ, and PaCO2 is provided, It's accuracy in vivo
should be testable.