In humans, EIAH severity correlates most consistently
and inversely with A-aDO2. Interindividual differences
in PaCO2 or the ventilatory equivalent for V˙ O2 (or
V˙ CO2) are also commonly found to correlate signifi-
cantly with EIAH; however, there are many exceptions,
especially in mild EIAH, and thus the degree of hyperventilation
accounts for less of the variance in PaO2 in
most studies. Those men and women, in both young and
old age groups, who experience severe EIAH have
almost equal contributions from the absence of hyperventilation
and widened A-aDO2 to their hypoxemia,
compared with nonhypoxemic subjects at comparable
V˙ O2max. For combined human and animal group mean
data (Table 1), variations in O2 saturation at maximum
exercise are best predicted from a multiple linearregression
model (r 5 0.93)2, where ventilation (as
reflected by PaCO2
) explains ,60% of the variance in
SaO2
, V˙ O2max accounts for 25% of it, and A-aDO2 for the
remainder.
Why Inadequate Hyperventilatory Compensation?