Effect of Concomitant Changes
in Ventilation and Perfusion
The preceding considerations of the effects of ventilatory and
circulatory alterations presume that only one of these variables changed while the
other remained constant, but both may change concomitantly. If both ventilation
and cardiac output increase proportionately, an intuitive expectation may be that
FA/FI would be little
altered. After all, uptake equals the product of solubility, the cardiac output,
and the alveolar-to-venous anesthetic partial pressure difference (see the earlier
anesthetic uptake equation). In the absence of other changes, doubling cardiac output
doubles uptake, and this should exactly balance the influence of doubling ventilation
on FA/FI. A doubling
of both delivery of anesthetic to the lungs and removal of anesthetic from the lungs
should produce no net change in the alveolar concentration.
However, this reasoning ignores another factor that defines uptake.
By accelerating the rate of tissue equilibration, an increase in cardiac output
accelerates the narrowing of the alveolar-to-venous partial pressure difference[47]
and thereby reduces the impact of the increase in cardiac output on uptake. A proportional
increase in ventilation and cardiac output increases the rate of rise of FA/FI.
The magnitude of the acceleration of rise in FA/FI
partly depends on distribution of the increase in cardiac output. If the increase
is distributed proportionately to all tissues (e.g., if a doubling of output doubles
flow to all tissues), the increase is fairly small[47]
[48]
( Fig.
5-9
). Conditions such as hyperthermia and thyrotoxicosis only slightly
influence the development of an anesthetizing anesthetic concentration through their
influence on FA/FI.
However, if the increase in cardiac output primarily flows to the VRG, a greater
effect is seen. Perfusion of the VRG is normally high and results in rapid equilibration.
Because blood returning from the VRG soon has the same partial pressure as it had
when it left the lungs, it cannot remove more anesthetic from the lungs. After a
few seconds or minutes, the effect of the increase in cardiac output on uptake cannot
match the added delivery of anesthetic by augmented ventilation. The result is a
considerable acceleration of the rise in FA/FI.
This effect may be seen in a comparison of the FA/FI
curves for children and adults ( Fig.
5-10
). Children (especially infants) have a relatively greater perfusion
of the VRG and consequently show a significantly faster rise in FA/FI
[6]
[49]
[50]
[51]
(see Chapter
60
). A clinical result of this accelerated rise is a more rapid development
of anesthesia in young patients. The higher perfusion of the brain further accelerates
the development of anesthesia.
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