Use Bicarbonate as A Buffer to Local Anesthetics, Especially for Skin Infiltration
Hooman Rastegar Fassaei MD
Steven L. Orebaugh MD
Local anesthetics reversibly block impulse conduction along nerve axons and other excitable membranes that utilize sodium channels as the primary means of action potential generation. The local anesthetics used clinically consist of a lipid-soluble, substituted benzene ring linked to an amine group via an alkyl chain containing either an amide or an ester linkage.
Local anesthetics are weak bases (pKa 7.6 to 9). These agents are poorly soluble in water and therefore are usually marketed in acidic hydrochloride salt solutions (pH 3 to 6). In this form, the local anesthetic rapidly becomes reduced to a cationic form. This process is readily reversible, and the relative proportions of neutral base and ionized form will equilibrate as described by the Henderson-Hasselbach equation:
Log (cationic form/uncharged form) = pKa − pH
The proportions of the drug that exist in each form depend on the pH of the solution and the pKa, or dissociation constant, of the particular drug. This dissociation constant (pKa) denotes the pH at which the ionized and neutral forms of the molecule are present in equal amounts. Since the pKa of most local anesthetics is in the range of 7.6 to 9.0, the larger fraction in the body fluids at physiologic pH will be the charged, cationic form.
Local anesthetics reversibly block conduction of action potentials by interacting with the intracellular portion of the voltage-gated sodium channels. It is the charged form of the local anesthetic molecule that appears to interact with this portion of the channel. The local anesthetic must first penetrate the lipid-rich neural cell membrane as the uncharged, lipid-soluble form.
BUFFERING LOCAL ANESTHETICS TO DECREASE ONSET TIME
Local anesthetics are administered in an acidic solution, so most of the agent is in the ionized form, which is lipophobic. Therefore, the drug must first be converted to the nonionized form in sufficient quantity to enter the nerve cell. This depends on the pKa of the local anesthetic and the pH of the tissue. Once inside the nerve cell, the lower pH converts the drug back into the ionized form, which is then able to block the sodium channels.
Increasing the pH of the carrier solution of local anesthetics with sodium bicarbonate will favor the formation of a more neutral base form of the drug. This uncharged molecule is more capable of diffusing through the cell membrane and will theoretically result in more rapid nerve blockade.
The addition of sodium bicarbonate to local anesthetic solutions has been reported to decrease the time of onset of conduction blockade. Alkalinization of solutions of bupivacaine or lidocaine accelerates the onset of brachial plexus and epidural blockade in some studies but not others. In addition, a recent animal study suggests that alkalinization of lidocaine decreases the duration of peripheral nerve blocks if the solution does not also contain epinephrine.
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