Local Anaesthetics: Blocking the Nerve Signal
A dentist numbs your tooth and you feel nothing — but numb an infected abscess the same way and the injection barely works. Why does the very same drug fail exactly where pain is worst? The answer is a piece of chemistry you already met in absorption, now playing out at the tip of a needle. Local anaesthetics are elegant, everyday, and — injected into the wrong place — quietly dangerous.
A patient comes to the emergency department with a deep cut that needs stitches. The doctor injects lidocaine around the wound, waits a minute, and sews it up painlessly. But in the next bay, a patient with a throbbing dental abscess gets the same lidocaine — and yelps at the needle: the anaesthetic just won't take hold in the inflamed, infected tissue. Same drug, same dose, opposite result. The reason is the pH of the tissue, and it's the same acid-base logic from the absorption articles, now deciding whether a nerve goes numb.
How they work: blocking the sodium channel
Local anaesthetics block voltage-gated sodium channels on nerves. A nerve carries a pain signal by firing an action potential, which depends on sodium rushing in through voltage-gated sodium channels. Local anaesthetics plug those channels, so the nerve can't fire and the pain signal never travels — numbness. The catch is HOW the drug reaches the channel: it must cross the nerve's fatty membrane in its uncharged (unionized) form, then become charged (ionized) inside to block the channel from within. This is the pH-partition idea from absorption. In infected, acidic tissue, more of the drug is stuck in its charged form outside the nerve and can't cross — which is exactly why lidocaine fails in an abscess.
Esters vs amides
Local anaesthetics come in two chemical families. The esters (procaine, benzocaine, tetracaine) are broken down by enzymes in the plasma and more often cause allergic reactions. The amides (lidocaine, bupivacaine, ropivacaine) are metabolized by the liver and rarely cause allergy — the more commonly used group. A simple way to tell them apart: amide names contain two 'i's (lidocaine, bupivacaine). A useful clinical point on speed and duration: bupivacaine is long-acting (good for prolonged pain relief) but also the most cardiotoxic; lidocaine is a fast, medium-duration all-rounder.
Anaesthetists often mix adrenaline into the local anaesthetic — and it's the alpha-1 vasoconstriction from the adrenergic articles at work. Constricting the local vessels keeps the anaesthetic at the site longer (prolonging numbness), reduces bleeding in the field, and slows the drug's absorption into the bloodstream (lowering the risk of systemic toxicity). One classic caution: avoid adrenaline in areas supplied by end-arteries — fingers, toes, nose, ears — where cutting off blood flow could cause tissue death.
- Local anaesthetics block voltage-gated sodium channels → the nerve can't fire → numbness.
- They cross the membrane unionized, then block from inside — so acidic (infected) tissue resists them.
- Esters (procaine) → plasma esterases, more allergy; amides (lidocaine) → liver, rare allergy.
- Added adrenaline (α1) prolongs the block, reduces bleeding & limits systemic absorption.
- Avoid adrenaline in end-artery areas (fingers, toes, nose, ears).
When it goes systemic: toxicity
Kept local, these drugs are very safe. The danger is when too much reaches the bloodstream — an accidental injection into a vein, or an overdose. Systemic toxicity hits the excitable tissues in a predictable order. First the central nervous system: numbness around the mouth, a metallic taste, ringing in the ears, dizziness, and then seizures. Then, at higher levels, the heart: arrhythmias and, in severe cases, cardiac arrest — bupivacaine is especially cardiotoxic. The specific rescue for severe local-anaesthetic toxicity (particularly from bupivacaine) is intravenous lipid emulsion ('lipid rescue'), which acts as a sink to soak the fat-loving drug out of the tissues, alongside standard resuscitation.
Local anaesthetics block nerves in a predictable order, smallest fibres first: autonomic and pain/temperature fibres go numb before touch and pressure, and motor function is lost last. That's why a patient under an epidural can lose pain but still feel pressure and move a little — the pain fibres blocked, the bulky motor fibres partly spared. Knowing this order explains what a partial block does and doesn't cover.
- Expecting good numbing in infected/acidic tissue. The drug can't cross well there — block proximally.
- Using adrenaline in fingers, toes, nose, or ears. It can cause tissue death (end-arteries).
- Injecting into a vessel or overdosing. Systemic toxicity → seizures then cardiac arrest.
- Forgetting bupivacaine's cardiotoxicity — severe toxicity needs IV lipid emulsion.
Why does a local anaesthetic work poorly in infected, acidic tissue?
- Local anaesthetics block sodium channels so nerves can't fire — numbness.
- They must cross unionized then block from inside; acidic (infected) tissue weakens them.
- Amides (lidocaine — two i's, liver) vs esters (procaine — plasma, more allergy).
- Adrenaline prolongs the block (avoid in end-arteries); toxicity → seizures then cardiac arrest (lipid rescue).
- Katzung BG. Basic & Clinical Pharmacology — Local Anesthetics.
- Brunton LL, et al. Goodman & Gilman's The Pharmacological Basis of Therapeutics — Local anesthetics.
- Rang HP, Dale MM, et al. Rang & Dale's Pharmacology — Local anaesthetics.
- Miller RD. Miller's Anesthesia — Local anesthetics & systemic toxicity (lipid rescue).
- Whalen K. Lippincott Illustrated Reviews: Pharmacology — Local anesthetics.
