The rate of absorption of a local anesthetic into the bloodstream is affected by the dose administered, the vascularity at the site of injection, and the specific physicochemical properties of the drug itself. Local anesthetics gain entrance into the bloodstream by absorption from the injection site, direct intravenous injection, or absorption across the mucous membranes after topical application. Direct intravascular injection occurs accidentally when the needle used for infiltration of the local anesthetic lies within a blood vessel, or it occurs intentionally when lidocaine is used for the control of cardiac arrhythmias.
All tissues will be exposed to local anesthetics after absorption, but concentrations will vary among the organs. Although the highest concentrations appear to occur in the more highly perfused organs (i.e., brain, kidney, and lung), factors such as degree of protein binding and lipid solubility also affect drug distribution. The lung can absorb as much as 90% of a local anesthetic during the first pass. Consequently, the lungs can act as a buffer to prevent higher and therefore more toxic concentrations.
Placental transfer of local anesthetics is known to occur rapidly, fetal blood concentrations generally reflecting those found in the mother. However, the quantity of drug crossing to the fetus is also related to the time of exposure, that is, from the time of injection to delivery. Subtle neurobehavioral changes in the neonate are detectable for as long as 8 hours after mepivacaine administration to the mother but are absent following the use of bupivacaine, lidocaine, and chloroprocaine. In general, minimal amounts of chloroprocaine reach the fetus because of its rapid hydrolysis by serum cholinesterase; this feature is its principal advantage in obstetrics.
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