The mechanism of action of LAs is to decrease the rate and degree of depolarization and repolarization, decrease conduction velocity, and prolong the refractory period of the neural action potential. LAs bind to receptor sites on the voltage-gated sodium channels (a four-subunit transmembrane protein) in the neuronal membrane and impair or block sodium influx, thereby blocking or slowing nerve conduction. Potency is related to lipid solubility and p Ka; the higher the lipid solubility and the lower the p Ka, the more un-ionized drug present at tissue pH. The un-ionized form traverses lipid layers to the axoplasm. However, the drug must return to the cationic state to bind to the channel receptors. Buffering, by the addition of sodium bicarbonate (NaHCO 3), increases the amount of uncharged drug available and decreases pain of infiltration. Duration of action is related to protein binding: the longer the LA binds to the sodium channel, the longer the duration of the blockade.
Addition of epinephrine (usually 1:200,000 or 5 pg/mL) provides a longer duration of anesthesia, provides wound hemostasis, and slows systemic absorption, thereby decreasing the potential for toxicity and allowing a greater volume of agent to be used for extensive laceration repair. Epinephrine may actually increase the pain of infiltration because it lowers the overall pH of the solution. Epinephrine should never be used in an end-arterial field, e.g., digits, pinna, nose, penis. Inadvertent intraarterial injection of LA with epinephrine or infiltration into an end-arteriole region can cause prolonged vasospasm and ischemia. This may be reversed with local or intravascular injection of 1.5 to 5 mg phentolamine. Phentolamine, 2 mg, has been used successfully as a "digital block" for digital ischemia. Use of 10 mg has been reported for local infiltration in the extremities. The side effect of phentolamine, hypotension, is less likely in this setting.
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