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Ventilation, solubility, and distribution of blood flow have a combined impact on the increase in the alveolar anesthetic partial pressure (i.e., the rise in the FA/FI ratio). For all agents, FA/FI initially increases rapidly, regardless of agent solubility[11] [12] ( Fig. 5-2 ) because of the absence of an alveolar-to-venous anesthetic partial pressure difference (i.e., there is no anesthetic in the lung to create a gradient) and the absence of uptake in the first moment of induction. The capacity of ventilation to increase FA/FI is unopposed. Delivery of anesthetic to the alveoli by ventilation increases the alveolar-to-venous partial pressure difference. The resulting increase in uptake increasingly opposes the effect of ventilation to drive the
Figure 5-2
The rise in alveolar (FA)
anesthetic concentration toward the inspired (FI)
concentration is most rapid with the least soluble anesthetics, nitrous oxide and
desflurane, and slowest with the most soluble anesthetic, halothane. All data are
from human studies. (Data from Yasuda N, Lockhart SH, Eger EI II, et al:
Kinetics of desflurane, isoflurane, and halothane in humans. Anesthesiology 74:489–498,
1991, and from Yasuda N, Lockhart SH, Eger EI II, et al: Comparison of kinetics
of sevoflurane and isoflurane in humans. Anesth Analg 72:316–324, 1991.)
The balance struck between ventilation and uptake does not remain constant. FA/FI continues to rise, but at a slower rate than in the first minute. This secondary rise results from the progressive decrease in uptake by the VRG, a decrease to an inconsequential amount after 8 minutes. By about 8 minutes, three fourths of the cardiac output returning to the lungs (i.e., the blood from the VRG) contains nearly as much anesthetic as it had when it left the lungs. The consequent rise in venous anesthetic partial pressure decreases the alveolar-to-venous partial pressure difference and therefore the uptake, allowing ventilation to drive the alveolar concentration upward to a second knee at roughly 8 minutes.
After 8 minutes, the MG and FG become the principal determinants of tissue uptake. The slow decrease in the anesthetic partial pressure difference between arterial
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