Dentaltown July 2017 - 106

Fig. 2: How local anesthetics work
Soduim channel

Na+

Action potential
Na+
Na+
Interior of cell becomes positive,
Pain message sent to brain Na+
Na+
Na+ action potential is generated

Peripheral
pain

Dr
Na

Drug

Soduim channel

No action potential
No message of pain sent

Drug

-H+
+H+

Drug

+H+
-H+

Drug

Peripheral
pain

Friel CJ, et al: Local anesthetic use in perioperative areas, Perioperative Nurs Clin 5:203-214, 2010

Fig. 3: The Anutra system

Fig. 4: The Gow-Gates injection technique

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JULY 2017 // dentaltown.com

for 2 percent lidocaine with 1:100K epinephrine was 8.7 minutes,
with a standard deviation of 3.1 minutes.
Another issue with local anesthetics has always been the discomfort
during injection and the unpredictability of the onset of profound
pulpal anesthesia. A weakly basic amide, lidocaine is unstable at
its pH of 7.9 and therefore is prepared in acidic formulations to
increase its stability and shelf life. The resultant pH is typically 4.7.
For comparison, the human body has a neutral pH of approximately 7.4; that of lemon juice is a 2.0. The literature showed that
lidocaine with epinephrine was approximately 1,000 times more
acidic than subcutaneous tissue.

Buffering
So, how does buffering enhance the onset of local anesthesia?
To understand buffering, we must first look at the physiology and
mechanics of how local anesthetic works.
Local anesthetics produce anesthesia by inhibiting excitation of
nerve endings or by blocking conduction in peripheral nerves. This
is achieved by anesthetics reversibly binding to and inactivating
sodium channels (Fig. 2). Sodium influx through these channels
is necessary for the depolarization of nerve cell membranes and
subsequent propagation of impulses along the course of the nerve.
When a nerve loses depolarization and capacity to propagate an
impulse, the individual loses sensation in the area supplied by the
nerve. They get numb.
All local anesthetics except for cocaine are vasodilators; most
anesthetics we use have epinephrine added to counteract this
vasodilation. Without it, the duration of our blocks or infiltrates
would be too short for most dental procedures. This adds another
reason why the anesthetic solution must be acidic to maximize
stability in solution and shelf-life.
In review, the reasons include:
* Local anesthetic solutions are aqueous solutions. If provided
at a pH close to 7.4, the lipid-soluble uncharged form could
precipitate out because of its lower water solubility.
* The uncharged base form is more unstable at physiological
pH, so degradation is minimized at a low pH, where the
drug is predominantly in the charged form.
* The adrenaline added to some local anesthetic solutions is
unstable at the physiological pH and more stable at an acidic
pH.
Buffering the anesthetic solutions before injections immediately
increases the active form of the drug, facilitating more-rapid diffusion
of the anesthetic through interstitial tissues and decreasing common
latency periods associated with the patient's own physiology,
anatomy, and kinetics toward the anesthetic solution. In addition,

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