Local anesthetics create a chemical roadblock between the source of pain and the brain by interfering with the ability of a nerve to transmit electrical signals or action potentials. The local anesthetic blocks the operation of a specialized gate called the sodium potential. When the sodium channel of a nerve is blocked, the nerve signals cannot be transmitted. The only location at which the local anesthetic molecules have access to the nerve membrane is at the nodes of Ranvier, where there is an abundance of sodium channels. The interruption of a nerve signal in a myelinated nerve (such as a dental nerve) occurs when nerve depolarization (the nerve signal) is blocked at three consecutive nodes of Ranvier.
Local anesthetics are vasodilators and are eventually absorbed into the circulation. They have systemic effects that are directly related to their blood plasma level. Overdose with local anesthetics can result in CNS depression, convulsions, elevated heart rate, and blood pressure.
Vasoconstrictors (epinephrine and levonordefrin) are added to local anesthetics to counteract the vasodilatory action, slowing the removal of the anesthetic from the area of the nerve and thus prolonging its action. Different anesthetics have different rates of onset of symptoms and duration of action. The more acidic a local anesthetic solution is the slower the onset of action. The more closely the equilibrium pH for a given anesthetic approximates physiologic pH, the more rapid the onset of anesthetic action. The better the local anesthetic molecule binds to the protein in the nerve’s sodium channel, the longer the duration of anesthesia.