Lidocaine is one of the most widely used local anesthetics in medicine, employed to temporarily numb a specific area of the body for minor procedures, dental work, or to manage localized pain. Despite its intended purpose to block the sensation of pain, patients frequently report a sharp, temporary sting or burn immediately upon injection. This paradoxical discomfort can be significant. Understanding why this common anesthetic causes a brief but intense burning sensation requires a look into its mechanism of action and the chemical formulation necessary for its stability. The science behind this phenomenon reveals a conflict between the drug’s chemical requirements and the body’s natural physiology.
How Lidocaine Blocks Pain Signals
Lidocaine’s primary function is to interrupt the transmission of pain signals before they can reach the brain, creating a temporary, localized communication blackout. It achieves this by acting directly on nerve cells, or neurons, responsible for carrying these electrical messages. The drug works by stabilizing the neuronal membrane, preventing the nerve from initiating and conducting electrical impulses known as action potentials.
The mechanism centers on tiny structures embedded in the nerve cell membrane called voltage-gated sodium channels. These channels must open to allow sodium ions (Na+) to rush into the nerve cell, which creates the electrical signal. Lidocaine molecules enter the nerve cell and physically block these sodium channels from the inside.
By binding to and inactivating the sodium channels, lidocaine prevents the necessary influx of positive ions. This inhibition stabilizes the nerve cell, meaning it cannot depolarize or fire an action potential. With the nerve impulse effectively halted, the pain signal cannot travel along the nerve fiber to the central nervous system. This blockage results in the desired loss of sensation and localized numbness. The anesthetic effect is rapid in onset, typically beginning within minutes of administration, and lasts until the drug molecules diffuse away from the sodium channels.
The Chemistry Behind the Burning Sensation
The momentary burning sensation experienced during a lidocaine injection is a direct consequence of its chemical formulation necessary for long-term stability. Commercial injectable lidocaine solutions are highly acidic, often having a pH that ranges between 3.5 and 5.5. This low pH is achieved through the addition of an acid, typically hydrochloric acid, which keeps the lidocaine molecule in a water-soluble, ionized form and prevents the degradation of the solution, especially when it contains a preservative like epinephrine.
When this acidic solution is injected into body tissues, the sudden, sharp difference in acidity irritates the local pain receptors. Human tissues naturally maintain a near-neutral physiological pH of about 7.4. Injecting a solution that is significantly more acidic creates a chemical shock to the sensory nerves.
This acidic environment directly stimulates nociceptors, which are specialized pain-sensing neurons. Among these are acid-sensing ion channels (ASICs) located on the free nerve endings, which are sensitive to drops in pH. The sudden rush of hydrogen ions (the chemical marker of acidity) from the anesthetic solution activates these channels, causing them to fire a pain signal. The brain interprets this signal as a sharp, burning sensation. This discomfort is a response to the chemical irritation of the acidic solution, not the anesthetic molecule itself.
Strategies for Reducing Injection Discomfort
Medical professionals employ several techniques to counteract the acidity of the lidocaine solution and improve patient comfort during injection. The most common and effective strategy is buffering, which involves adding a neutralizing agent to the anesthetic just before administration.
Buffering the Solution
Sodium bicarbonate, or “bicarb,” is the agent of choice, as it is a weak base that raises the pH of the acidic lidocaine solution. By buffering the solution, the pH is adjusted closer to the body’s natural physiological pH of 7.4, often reaching a range between 7.3 and 7.6. This neutralization drastically reduces the chemical irritation of the nociceptors, minimizing the burning sting experienced by the patient. A typical ratio involves mixing one part of 8.4% sodium bicarbonate solution with ten parts of the lidocaine solution.
The buffering process also has the secondary benefit of accelerating the onset of the anesthetic effect. Lidocaine is more effective when it is in its non-ionized, lipid-soluble form, which allows it to pass easily through the nerve cell membrane to reach the sodium channels. Raising the pH increases the proportion of the non-ionized form of the drug, allowing it to penetrate the nerve cell membrane more quickly and start blocking pain faster.
Physical Techniques
Beyond chemical adjustments, physical techniques further reduce discomfort. Warming the lidocaine solution to approximately body temperature (around 40°C) prior to injection minimizes the thermal shock to the tissue, which also contributes to the painful sensation.
A careful, slow injection technique is routinely used. Injecting the solution too quickly can cause rapid tissue distension and pressure, which activates pain receptors independently of the chemical irritation.