Everything we didn’t want to know about anesthesia


The first successful surgery using anesthesia was performed by John Collins Warren in 1846 at Massachusetts General Hospital. Before then, patients would have to undergo surgeries with little or no pain relief, and experience the full process of having a limb or organ removed while awake. It’s no wonder, therefore, that anesthesia is hailed as one of the most important developments in modern medicine. But how does it actually work?

What is it?

Anesthetics are a combination of multiple drugs, usually inhalable gases such as nitrous oxide, that together create the ideal outcome for anesthesia: analgesia (the inability to feel pain), amnesia and hypnosis (the loss of memory and consciousness) so you don’t remember the experience of the operation, and immobility (the inability to move) so the doctors can perform the surgery precisely. There are two types of anesthetic – general, which puts you into a fully unconscious slumber, and local, which localises the numbing properties to a specific localized area and keeps the patient awake.

Lipid theory

It has been known for a long time that there is a strong correlation between how well the anesthetic dissolves in olive oil, and the potency of the drug. This led to a popular theory called the “lipid theory”, that said the anesthetic causes nerve cells to malfunction by disrupting or binding to their lipid (fatty) membrane. It has since been discovered, however, that anesthetics also bind to proteins without the presence of cell membranes, blocking their receptors, which is how a lot of conventional drugs work. The likelihood is, then, that it is a combination of the two; the more soluble the anesthetic is in oil, the easier it can reach the receptors found in the lipid membrane of the nerve cell. But how does this affect the nerve cells, and in turn produce the anesthetic effect?

No one really knows

The reality is, how anesthetics work have been a mystery since they were invented. We’re getting closer to the answer now, but there are elements that we still are unsure about. Part of the problem is that in order to determine what causes an induced lack of consciousness, we would first have to understand what causes consciousness in the first place, or at least where it is located. This has been a bio-philosophical debate for hundreds of years, which would have far-reaching complications when answered.

The problem with consciousness

It is largely accepted that consciousness is a multi-level, widely distributed process across the whole brain, rather than localized to one region. So, to stop consciousness, and therefore achieve unconsciousness, this spread of information and activity across the brain must be stopped. This is supported through some experiments using MRI scans, that show that some areas of the brain are lit up following an external stimulus while unconscious, but that these regions of activity do not spread to other areas like they do during wakefulness.

So, during anesthesia, the loss of consciousness and lack of sensation is caused by a disruption in communication between the different areas of the brain. It’s as though the message has been sent to your inbox, but no-one is there to read it. Although this may sound alarming, there are specially trained doctors whose main role is to monitor those people under sedation. Luckily, there are drugs that reverse the effects of anesthesia, and believe us – you wouldn’t want to have an operation without it!