Local Anesthetics

Local anesthetics are divided into two classes, esters and amides. Esters are derivatives of paraminobenzoic acid, and metabolized by plasma cholinesterase. The metabolic byproduct is paraaminobenzoic acid, a known allergen. Allergic reaction to the ester local anesthetics do, therefore, occur. In contrast, true allergic reactions to the amides are exceedingly rare. These are metabolized for the most part by the liver.

Physical and chemical properties of the local anesthetics determine potency, speed of onset, duration of action, and toxicity. The more lipid soluble agents tend to be more potent. Protein binding has an influence on duration of action, with the higher protein binding agents having a longer duration of action. Ionization of the local anesthetic has an important influence on the spped of onset. Local anesthetics cross the lipid membrane of nerve tissue in the unionized form, but the active form that binds to the Na+ channel is the ionized form. A preponderance of the unionized form will speed onset. This can be achieved by alkalinizing the local anesthetic solution, as with the addition of sodium bicarbonate.

In addition to properties of the local anesthetic itself, the differing features of nervous tissue will influence the type of blockade achieved. Nerve fiber size and myelinization are important factors on the susceptibility of fibers to local anesthetics. The smaller nerve fibers are more easily blocked. This allows for the blockade of sympathetic and sensory fibers without the blockade of motor fibers, and important feature in producing analgesia without loss of function.

Individual local anesthetics are listed in the table below. Two of the most commonly used agents are lidocaine and bupivicaine. Bupivicaine in particular is quite commonly used in nerve blocks due to its long duration of action and relative sparing of motor fibers.

Esters

Amides

Toxicity of local anesthetics can occur, particularly with accidental intraarterial injection. A spectrum of symptoms is seen, dose dependent, with the CNS and cardiovascular manifestations the most important. CNS features are seen much earlier than cardiovascular and manifest as sedation, agitation, lightheadedness, perioral numbness, tinnitus, and may progress to full seizure activity. Treatment is supportive, with airway protection and oxygenation paramount. Cardiac toxicity is manifested by decreased myocardial contractility, conduction abnormalities, arrhythmias, hypotension, and cardiovascular collapse. In particular, bupivicaine toxicity is particularly difficult to treat, as it binding affinity for cardiac tissue is approximately seventy times as great as lidocaine.

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