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Modern medicine can trace the use of local anesthetics back to the year 1884 when the Austrian Physician Karl Koller first used topical cocaine to assist with an ophthalmologic operation.1 The premier Surgeon William Halstead first used injected cocaine to generate the intentional blockade of nerve transmission the following year.2 Halsted’s experiments with cocaine soon led to a concurrent dependency.3 The emerging illicit market for this compound soon prompted the search for a less toxic agent.3 Procaine, more commonly known by its trade name Novocain, was the first synthetic local anesthetic. It is a benzoic acid ester derivative developed by the German chemist Alfred Einhorn in 1904. Procaine had fewer drawbacks than its cocaine predecessor but was far from the ideal agent. Lidocaine was the first amide local anesthetic agent and was initially produced in 1945. The market for more effective agents continued to blossom. No less than 20 additional agents were developed for use as local anesthetics, each possessing unique pharmacokinetic properties to tailor its utility to specific clinical applications. They are all synthetic derivatives of cocaine.

The clinical utilization of these agents has become widespread throughout all medical specialties parallel to the proliferation in pharmacologic development. The daily practice of Emergency Medicine presents multiple scenarios that necessitate their use. The Emergency Physician must maintain a familiarity with the local anesthetic agents available and their individual characteristics, have an expertise in their delivery, be well-informed of the potential side effects, and know how to avoid and treat adverse reactions to ensure the safest and most optimal pain relief.


Neuronal function and signal conduction are dependent upon a negative resting intracellular electrical potential (approximately –70 mV) as compared to the surrounding extracellular environment at a cellular level. This polarity results from the abundance of sodium (Na+) cations found within the extracellular space. Membrane-based sodium-potassium (Na+/K+) pumps establish this sodium gradient. Adjacent voltage-gated sodium channels maintain the gradient by inhibiting the concentration of mediated and electrically driven sodium influx that would invariably result. A small intracellular sodium influx ensues upon the stimulation of an idle neuron. This sodium influx results in a slight depolarization of the resting membrane potential. The voltage-gated sodium channels reflexively open when a critical threshold of sodium influx is met. This results in a massive sodium ion influx and widespread membrane depolarization.4-6 Impulse transmission proceeds as this membrane depolarization is propagated down the entire length of the nerve fiber.7

Local anesthetic agents function by reversibly binding to membrane-based sodium channels and inhibiting the initial sodium influx that results upon the stimulation of an idle neuron.4-9 If a significant number of these channels are blocked, the critical threshold of sodium influx required for the voltage-gated sodium channel opening cannot be met, widespread membrane depolarization cannot occur, and nerve impulses will not ...

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