Effects of Anesthetic-depressed Ventilation and Cardiac Output on Anesthetic Uptake: A Computer Nonlinear Simulation


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Abstract

A nonlinear mathematical model of anesthetic uptake and distribution has been used to account for changes in ventilation and perfusion induced by progressive increase in anesthetic depth. The results show greater differences in anesthetic uptake than have been predicted from models that have not considered the effects of anesthetics on these physiologic variables. During spontaneous ventilation with halothane or isoflurane, the higher the inspired concentration, the slower the rate of alveolar anesthetic increase. Progressively increasing ventilatory depression, and eventually apnea, limit delivery of anesthetic to the lung and prevent alveolar concentration from rising above 3 per cent, regardless of the inspired concentration. During controlled ventilation with halothane, alveolar concentration increases as cardiac output diminishes. As cardiac arrest occurs, the alveolar curves become unstable and rapidly rise to the inspired concentration. The use of such nonlinear models may allow prediction of limits to which anesthetic drugs and techniques can be used safely.

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