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Part 4. Managing Anesthesia Care
Section C. Anesthesia Drugs and Drug Delivery Systems
Chapter 44. Pharmacology of Local Anesthetics
James E. Heavner, DVM, PhD
1. PharmacodynamicsLocal anesthetics stop the propagation of action potentials in nerve axons by preventing the influx of sodium through voltage-gated sodium channels in the axon membrane. Other actions of local anesthetics, for example, effects on other voltage-gated ion channels and ligand-gated ion channels, may be important for their analgesic action and/or for undesired side effects.
2. ChemistryLocal anesthetics are weak bases with three structural parts: a hydrophilic end and a lipophilic end linked by an amino ester or an amino amide bond. The bond is the basis for classifying local anesthetics into 2 groups: the amino esters and the amino amides. Optical isomers of local anesthetics with an asymmetric carbon atom usually differ in potency, duration of action, and toxicity.
3. Expression of local anesthetic actionIn vitro, there generally is a positive correlation between molecular weight of local anesthetic molecules and lipophilicity, protein binding, duration of action, potency, and toxicity; there is an inverse relation with speed of onset. In vivo expression of local anesthetic action is dependent on other factors as well, such as injection site, dose, intrinsic vasoactivity, and formulation. The manifestation of sensory versus motor block varies and is dependent on many factors, including the agent and type of block technique.
4. PharmacokineticsLocal anesthetics usually are injected near the target site instead of..."
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