How Does Anaesthetic Work?

Local anaesthetics such as lidocaine block sodium channels in nerve cell membranes. Nerves transmit signals as a wave of sodium ions crossing the membrane, and blocking those channels stops the wave from propagating.

The pain signal is therefore never sent. The nerve is intact and the tissue is unaffected, but communication is interrupted at the point of injection. As the drug diffuses away and is metabolised, channels unblock and sensation returns.

General anaesthesia is not simply a strong version of the same thing. It produces a state that is not sleep and not coma, with several distinct components usually achieved by combining drugs.

Anaesthetists aim for a specific set of effects:

• •Unconsciousness, so the patient is not aware
• •Analgesia, blocking pain signalling
• •Amnesia, so no memory is formed of the period
• •Muscle relaxation, allowing surgery and ventilation
• •Suppression of reflex responses to surgical stimulation

General anaesthetics are chemically diverse, ranging from simple gases like nitrous oxide to complex molecules, and it is puzzling that such different substances produce a similar state.

An early theory linked potency to solubility in fats, suggesting the drugs act on cell membranes generally. Current thinking focuses instead on specific protein targets, particularly receptors for the neurotransmitter GABA, and on disruption of the large-scale communication between brain regions that appears necessary for consciousness.

This is why anaesthesia interests neuroscientists well beyond medicine. It provides a reversible, controllable way to switch consciousness off and on in a laboratory setting.

Brain imaging during induction shows that individual regions often keep responding to stimuli while the coordinated communication between regions breaks down. That finding has supported theories treating consciousness as arising from integration across the brain rather than from activity in any single area.

Modern anaesthesia is very safe, with serious complications rare in healthy patients, and it is continuously monitored throughout a procedure rather than administered once.

Accidental awareness under general anaesthesia does occur but is rare, with large studies putting the reported incidence at roughly one in nineteen thousand. Depth of anaesthesia monitors and careful drug management have reduced it further. It is a real phenomenon worth taking seriously without being a likely one.

Before the 1840s, surgery was performed on conscious patients, and speed was the primary surgical virtue. Public demonstrations of ether in Boston in 1846 changed medicine within a remarkably short period.

Chloroform followed shortly after and was popularised partly by its use during a royal childbirth, which reduced public objection. Early practice was dangerous by modern standards, with no reliable dosing, monitoring or airway management. Almost the entire safety record of modern anaesthesia comes from the twentieth-century development of monitoring, drug refinement and anaesthesia as a speciality in its own right.

People are often surprised that after a local anaesthetic injection they cannot feel pain but can still feel pushing and pulling. This happens because nerve fibres are not all equally easy to block. Thin fibres, including many that carry pain and temperature signals, are affected at lower drug concentrations than the thicker, heavily insulated fibres that carry touch, pressure and the sense of position. A dose that silences pain can leave some pressure sensation working.

Local anaesthetics also work less well in infected or badly inflamed tissue. To reach its target inside the nerve, the drug has to cross the cell membrane in an uncharged form. Inflamed tissue tends to be more acidic, which converts more of the drug into its charged form, and that form crosses membranes poorly. This is one reason a dentist may find a hot, infected tooth harder to numb and may need to use a different technique.

If you have ever had surgery, you were probably told to stop eating hours beforehand. The reason is linked to what general anaesthesia switches off. While you are awake, reflexes such as coughing and swallowing protect your airway, and a muscular ring at the top of the stomach helps keep its contents in place. Under anaesthesia these defences are weakened. If stomach contents come back up, they can be breathed into the lungs, a complication called pulmonary aspiration. Acidic stomach fluid and food particles can then cause serious inflammation and pneumonia.

Fasting rules aim to make sure the stomach is as empty as possible. Typical guidance asks adults to stop solid food about six hours before anaesthesia, while clear fluids such as water are often allowed until a couple of hours before, because they leave the stomach much faster. Longer fasting is not safer and can leave people dehydrated and miserable. In emergencies, when someone may have eaten recently, anaesthetists use a rapid sequence of drugs and place a breathing tube quickly, sealing the airway before anything has a chance to be inhaled.

Gas anaesthetics are dosed using a measure called the minimum alveolar concentration, or MAC. It is the concentration of the gas in the air deep in the lungs at which half of patients do not move in response to a surgical incision. Each drug has its own value. For sevoflurane, a widely used modern gas, one MAC in a middle-aged adult is roughly two percent, while nitrous oxide is so weak that its MAC is slightly above one hundred percent. It can never produce full anaesthesia on its own at normal air pressure, which is why it is used alongside other drugs.

MAC values add together roughly, which lets anaesthetists combine drugs. If a patient breathes about sixty percent nitrous oxide, that supplies a little over half a MAC, so less sevoflurane is needed to reach the same depth. Monitors measure the gas in every breath the patient breathes out, giving a continuous estimate of the concentration in the lungs. MAC also changes with the patient. It falls steadily with age, by around six percent per decade in adults, so an eighty-year-old needs noticeably less gas than a twenty-year-old. Because MAC measures movement, unconsciousness itself arrives at a lower concentration.

The first effective local anaesthetic was cocaine. In 1884 Carl Koller, a young eye doctor in Vienna, showed that a few drops of cocaine solution numbed the surface of the eye, making delicate eye surgery possible on a conscious patient. Within months surgeons and dentists were injecting it to block nerves elsewhere in the body. But cocaine was addictive and could cause dangerous effects on the heart and brain, so chemists searched for safer substitutes. Procaine, sold as Novocain, appeared in the early twentieth century, and the ending caine in so many drug names still echoes the original.

Lidocaine was made in Sweden in 1943 and came into wide use after the war, because it works quickly and causes allergic reactions far less often than procaine. Dentists usually inject it mixed with a small amount of adrenaline. Adrenaline narrows the blood vessels around the injection, so the anaesthetic is carried away more slowly, the numbness lasts longer and there is less bleeding. If a little of the mixture enters a blood vessel, your heart may race for a minute or two, which is why some people feel shaky after a dental injection. The effect passes quickly.

Local anaesthetic blocks sodium channels so nerves cannot transmit pain signals, while general anaesthesia produces unconsciousness through mechanisms still not fully explained, which is why it doubles as a research tool for studying consciousness itself.