Effect of Changes in Cardiac
Output
The discussion in the previous section assumed a constant cardiac
output and examined the effect of changes in ventilation. This section considers
the reverse process. An increased cardiac output augments uptake and thereby hinders
the rise in FA/FI.
[1]
[42]
As with
a change in ventilation, a change in cardiac output scarcely affects the alveolar
concentration of a poorly soluble agent but considerably influences the alveolar
concentration of a highly soluble agent[34]
( Fig.
5-7
). The reason is similar to the reason explaining the effect of a change
in ventilation. A decrease in cardiac output can little increase the FA/FI
ratio of poorly soluble agents because the rate of rise is rapid at any cardiac output.
In contrast, nearly all of a highly soluble agent is taken up, and a halving of
blood flow through the lungs must concentrate the arterial (which equals alveolar)
anesthetic, nearly doubling its partial pressure in the case of an extremely soluble
agent.
This effect of solubility suggests that conditions that lower
cardiac output (e.g., shock) can substantially increase the alveolar anesthetic concentrations
of highly soluble agents. A higher FA/FI
ratio should be anticipated and the inspired anesthetic concentration lowered
Figure 5-7
If unopposed by a concomitant increase in ventilation,
an increase in cardiac output will decrease alveolar anesthetic concentration by
augmenting uptake. The resulting alveolar anesthetic change is greatest with the
most soluble anesthetic. FA/FI
is the alveolar concentration of anesthetic/concentration of inspired anesthetic.
(Adapted from Eger EI II: Ventilation, circulation and uptake. In
Eger EI II [ed]: Anesthetic Uptake and Action. Baltimore, Williams & Wilkins,
1974, pp 122–145.)
accordingly to avoid further depression of circulation. Shock presents a two-pronged
problem: an increase in ventilation usually accompanies a decreased cardiac output,
and both of these changes accelerate the rise in FA/FI.
Perhaps this is why such heavy reliance is placed on the use of nitrous oxide in
patients in shock. In contrast to more soluble anesthetics (e.g., halothane), the
alveolar concentration of nitrous oxide is influenced little by the associated cardiorespiratory
changes.
Anesthetics also affect circulation. Usually, they depress cardiac
output,[43]
[44]
although stimulation may occur with some agents (i.e., nitrous oxide and, transiently,
desflurane).[45]
[46]
In contrast to the negative feedback that results from respiratory depression, circulatory
depression produces a positive feedback; depression decreases uptake, and this increases
the alveolar concentration, which further decreases uptake. A potentially lethal
acceleration of the rise in FA/FI
results from the depression of cardiac output[10]
[35]
[41]
( Fig.
5-8
). The impact of this acceleration increases in importance with increasing
anesthetic solubility. High inspired concentrations of agents such as enflurane
and halothane should be administered with considerable caution, particularly if ventilation
is controlled.
Figure 5-8
Dogs given constant ventilation demonstrate different
rates of rise of the alveolar concentration of anesthetic/concentration of inspired
anesthetic (FA/FI
ratio). The rates of rise depend on the inspired halothane concentration. The two
higher concentrations accelerated the rate of rise by depressing cardiac output and
thereby decreasing uptake. (Adapted from Gibbons RT, Steffey EP, Eger EI
II: The effect of spontaneous versus controlled ventilation on the rate of rise
of alveolar halothane concentration in dogs. Anesth Analg 56:32–34, 1977.)
