[Tachyphylaxis to local anesthetics].

Abstract

Tachyphylaxis to local anesthetics is defined as decrease in duration, segmental spread, or intensity of a regional block after repeated doses of equal size, i.e. to maintain a given level of effect the dose has to be increased. In contrast, time-dependent variations in pain or circadian changes in the duration of local anesthetic action only simulate the occurrence of tachyphylaxis (pseudotachyphylaxis). Tachyphylaxis appears neither to be linked to structural (ester vs amide) or pharmacological properties of the local anesthetics (short- vs long-acting) nor to technique (surface anesthesia, conduction block, spinal, caudal, or epidural anesthesia, brachial plexus block) or mode of administration (intermittent vs continuous). There is even disagreement about the clinical significance of tachyphylaxis because some authors found it in almost every patient, others less often whereas a third group did not find tachyphylaxis at all. The mechanisms underlying tachyphylaxis are open to debate. Changes in pharmacokinetics (local alterations of disposition and absorption; decrease of perineural pH) and pharmacodynamics (antagonistic effects of nucleotides or increased sodium concentration; increase in afferent input) have been implicated. None of the theoretical considerations presented are strong enough to explain tachyphylaxis. However, results from isolated nerve preparations suggest that pharmacokinetics rather than pharmacodynamics might play a role in the development of tachyphylaxis.