By R. Miller
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Additional resources for Anesthesia [2 vols]
From a total of approximately 600,000 anesthetic administrations, the overall anesthetic-associated death rate was adjudged to be about 1:1560. In addition, many important epidemiologic data emerged. The most startling and controversial finding was a significantly higher mortality rate in patients given muscle relaxants, mainly curare, during anesthesia. Although Beecher ascribed this occurrence to an inherent drug toxicity, more likely the explanation was to be found in residual postanesthetic muscle paralysis and the associated respiratory insufficiency, which was inadequately treated or unrecognized in those days.
In the United States, crude extracts had been employed clinically to treat spasticity and to modify the convulsions induced during electroconvulsive therapy (ECT) for depression and other psychoses. C. M. Papper, of New York, had independently deemed the paralytic effects to be too much a physiologic 9 trespass to be introduced to the anesthetic regimen. No one knows what subtle influence led Griffith to inject Intocostrin during the course of a cyclopropane anesthetic without prior experimentation.
This is such a common and fundamental assumption for anesthetic pharmacokinetics that we explore the conditions that must be satisfied for this to be valid. Of course, it cannot be true that metabolism is always proportional to concentration because the metabolic capacity of the liver is not infinite. At some rate of drug flow into the liver, the metabolic capacity becomes saturated, and the pharmacokinetics ceases to behave in a linear manner. To understand the rate of metabolism quantitatively, it is necessary to start with the simple observation that the rate at which drug flows out of the liver must be the rate at which drug flows into the liver less the rate of metabolism.