Yes. You heard me correctly, but I’ll repeat what I just said: you’re not really asleep when you’re under a general anaesthetic (GA).

 It’s understandable that there is confusion about exactly what a GA entails. Patients having surgery under a general anaesthetic certainly look like they’re asleep, lying still with their eyes closed, unaware of their surroundings. Anaesthetists like me don’t help the cause when we casually refer to induction of general anaesthesia as ‘going to sleep’ during our preop visits. However, regular sleep and general anaesthesia are two entirely different states.

 So if general anaesthesia isn’t sleep, what is it? Read on.

 A short history of anaesthesia

 Eeh! It were different in my day. Patients having surgery these days don’t know they’re born.

 For most of human history, if you needed surgery, you suffered pain. Severe pain. Agonising, unbearable pain. Attempts were made to alleviate the worst of your suffering, of course. Alcohol, opium, cannabis, mandrake and extracts from a whole variety of plants, flowers and herbs produced varying degrees of sedation, analgesia and stupefaction but were hardly anaesthetic. Cryoanaesthesia, when snow or ice was applied to the affected part to freeze and numb the nerves, had its uses during limb amputations – provided you lived somewhere cold. Hypnotists attempted to induce a deep trance in which their subjects’ minds became disconnected from the pain they were suffering during surgery. A less sophisticated approach simply produced unconsciousness with repeated blows to the head. Effective but potentially dangerous. Kill or cure.

 All of these techniques fell far short of the ideal, and whichever was adopted, the usual resort was to strap the patient down, give them a stick to bite down on and rely on the surgeon to complete the procedure as quickly as possible. As Ross Logan, my good friend and colleague from my books, would say, a good surgeon is a fast surgeon. The faster the better.

The big breakthrough occurred as recently as 1846, when an event took place that is among the most momentous in the history of medicine – a real game changer. William TG Morton (who was a medical student at the time, can you believe it?) publicly demonstrated the first successful use of general anaesthesia at Massachusetts General Hospital. He administered ether vapour to a 21-year-old man, who drifted off, allowing the surgeon, Dr John Collins Warren, to completely remove a tumour from his neck. Upon seeing that his patient had remained insensible throughout, experiencing no pain whatsoever, Dr Warren announced to his rapt audience, ‘Gentlemen, this is no humbug.’

 The news of this astonishing discovery crossed the Atlantic remarkably quickly for the time. A couple of months later, a dental surgeon gave ether to a patient for a tooth extraction in London. Two days after that, again in London, a leg amputation was successfully performed under general anaesthesia. Once again the anaesthetist was a medical student – these were exciting times indeed to be at medical school!

Chloroform, another volatile anaesthetic, was introduced into clinical practice the following year. Nitrous oxide (laughing gas), whose analgesic and befuddling characteristics had already been known for some time, was added to the list a few years later. Both ether and chloroform remained mainstays of anaesthetic practice for the next hundred years or so until the dawn of a new age of anaesthetic discovery in the 1940s and 1950s and the introduction of a collection of new, improved drugs. Nitrous oxide was still in use, albeit declining, when I retired, more than 200 years after its effects on the brain were first discovered.

 Anaesthesia

 If you are fluent in Ancient Greek, you will know that the word anaesthesia means ‘without sensation’. There are several types of anaesthesia, including: local anaesthesia, regional anaesthesia and general anaesthesia.

 Local anaesthesia is what you have at the dentist if you need a filling. It involves injecting a numbing agent (funnily enough, they are called local anaesthetics) directly into the tissue that is to be surgically interfered with. Other procedures where local anaesthesia can be employed include the removal of lumps, bumps and other lesions from the skin, vasectomy, and more extensive procedures such as inguinal hernia repair.

 Local anaesthetic drugs affect all types of nerves, motor and sensory. The area numbed will lose all sensory modalities to a greater or lesser extent – pain, hot, cold, touch, pressure, etc. Fortunately for patients (as well as surgeons and anaesthetists), the sensory nerve fibres most sensitive to the numbing effect of local anaesthetics are those that convey pain messages. The least sensitive are those nerves conveying touch, pressure, and vibration. This is why you may sometimes feel touch and pressure while your surgeon beavers away at that sebaceous cyst on your back, but you do not feel any pain at all. Phew!

 Regional anaesthesia uses the very same drugs as local anaesthesia. The main difference is where you place the local anaesthetic. To perform a regional anaesthetic block, you inject close to a major nerve complex where lots of nerves come together. Because of this, the effects are much more profound and widespread. For example, a brachial plexus regional nerve block is performed by injecting between 20-40ml local anaesthetic into your neck, or just above your collar bone, or in your armpit. The effect is to paralyse your entire upper limb from your shoulder down to the tips of your fingers. Sensation is similarly KO’d, including taking out those all-important pain nerve fibres.

 Two other, perhaps more familiar, examples of regional anaesthesia are spinals and epidurals. They both involve injecting local anaesthetic around the nerves in your back, close to your spinal cord. I’ll be covering these in a later post, so all I will say here is that just 2-3 ml of local anaesthetic injected in just the right place can render you temporarily paraplegic with loss of all sensation and motor power below your waist.

 So if general anaesthesia isn’t sleep, what is it?

 General anaesthesia cannot be thought of as simply local anaesthesia of the brain. It is something radically different.

 General anaesthesia is a reversible, drug-induced state of deep, unresponsive coma. Coma, not sleep. You don’t dream. You don’t unconsciously shift your position from time to time to make yourself more comfortable. A loud noise does not startle you awake. Neither does a fly tickling your nose. An earthquake could strike the hospital, and you would continue to lie where you were, ever serene and motionless. And you don’t even rouse in anguish and indignation when your surgeon amputates your left leg when all you’ve come into hospital for is to have your ingrowing toenail removed. For as long as you remain anaesthetised, you will lie perfectly still, unconscious, delicately poised between this world and the next. If a doctor were to perform brainstem function tests on a deeply anaesthetised you without knowing you were anaesthetised, they would diagnose you as brainstem dead. An anaesthetised individual is as close to death’s door as it is possible to approach without actually passing through it to the other side. You are totally reliant on your anaesthetist to ensure that you don’t take that small extra step.

 Under anaesthetic, your urge to breathe will be inhibited. In fact, there’s a good chance your brainstem will be so depressed that you will stop breathing altogether. If your anaesthetist has given you a muscle relaxant, you absolutely won’t breathe regardless of the depth of your anaesthetic because your muscles will be paralysed. Your pulse and blood pressure will be unregulated under anaesthetic. Without the vigilance and skills of your anaesthetist, your blood pressure might crash dangerously, and you could suffer a cardiac arrest. At the other extreme, if your anaesthetic is too light, you might wake up in the middle of your operation, paralysed from the effects of the muscle relaxant, unable to scream for help or lift even a finger to warn people that you are wide awake.

 What a nightmare! The good news is that a highly trained anaesthetist is constantly by your side while you are anaesthetised, keeping you safe. You will wake up when it’s all over and not a minute before.

 The holy triad of general anaesthesia

 There are three components of what is termed balanced anaesthesia: hypnosis (that is to say a state of drug-induced unconsciousness), analgesia (suppression of your nervous system’s responses to painful surgical stimulation), and immobility (often, but certainly not always, facilitated by the use of muscle relaxant drugs). A fourth component, amnesia (you don’t remember what happened afterwards), is sometimes added although you might well argue that amnesia naturally follows from hypnosis.

 In the early, pioneering days of anaesthesia, one drug, ether or chloroform, usually provided all three components. However, this is not the case in modern anaesthetic practice. The popular image of a single magical substance called ‘the anaesthetic’ that switches the brain off, often in conjunction with a second magical substance called ‘the antidote’ to switch it back on again, is simplistic and wrong. For a routine surgical procedure, your anaesthetist may give you ten or more different drugs. Let’s take a look at a common operation.

Laparoscopic cholecystectomy (keyhole surgery to remove the gallbladder)

 This operation is routine and straightforward (most of the time), and is usually performed as a day-case procedure. Here is a list of the drugs I typically gave my patients:

Midazolam – a benzodiazepine (similar to Valium) given by intravenous injection to calm and sedate you immediately before induction of general anaesthesia.

Ondansetron – an anti-emetic drug to reduce the risk of postoperative nausea and vomiting.

Fentanyl – a potent, short-acting, synthetic opioid drug (with similar effects to morphine) given to provide the analgesic component of general anaesthesia.

Propofol – an intravenous anaesthetic used to induce general anaesthesia.

Atracurium – a muscle relaxant drug given to paralyse your vocal cords, which facilitates tracheal intubation. The resulting flaccid abdominal musculature also provides the surgeon with optimal operating conditions.

Nitrous oxide – laughing gas. It has anaesthetic and analgesic properties. It is given continuously for the duration of surgery alongside a volatile agent to maintain general anaesthesia. Nitrous oxide is much maligned by newer upstart anaesthetists because of its effects on the environment (it’s a potent greenhouse gas and ozone layer destroyer) and its propensity to cause more nausea and vomiting than other agents (allegedly). So much so, it’s on its way out. I liked using it, though.

Sevoflurane – a volatile liquid whose vapour has anaesthetic properties. A whole series of similar drugs came on line at various times from the 1950s. They basically all had comparable effects, but the side-effect profile improved. For example, patients wake up more quickly and suffer fewer hangover effects with sevoflurane (1995) than isoflurane (1983), which in turn is better tolerated than halothane (1956).

Morphine – a naturally occurring opioid extracted from the opium poppy (contrast with diamorphine, aka heroin, which is a chemically modified, more potent derivative of morphine). It is given towards the end of surgery for postoperative analgesia.

Paracetamol – a familiar drug available as an injectable liquid, also given for postoperative analgesia.

Parecoxib – an injectable anti-inflammatory analgesic drug.

Neostigmine – administered at the end of surgery to reverse the effects of the muscle relaxant, atracurium. Neostigmine doesn’t, however, reverse the hypnotic or analgesic components of balanced anaesthesia.

Glycopyrrolate – given in conjunction with neostigmine to prevent the former from causing your heart to stop! It’s not the best idea to give unopposed neostigmine, therefore. An anaesthetic colleague of mine did exactly that by mistake one day (the ampoule containing a mixture of both drugs is remarkably similar to the one with only neostigmine in it). The patient promptly had a cardiac arrest, and there was a bit of a hoo-ha. Fortunately, an entire regiment of anaesthetists rapidly descended on the scene and heroically brought the patient back to life. Aren’t we marvellous! The patient suffered no ill effects, which is more than can be said for the poor anaesthetist concerned who shat her pants.

 Of course, more drugs might be given depending on circumstances – antibiotics, drugs to increase blood pressure, drugs to decrease blood pressure, drugs to speed up a slowing heart, drugs to treat bronchoconstriction, etc.

 At the end of surgery, there is no antidote to wake you up. It’s a case of turning off the vaporiser and the nitrous oxide gas flow. The inhalational agents are then excreted from the body with every exhalation until the concentration in the brain drops below a critical threshold value, whereupon, lo and behold, the reticular activating system (RAS) I spoke about in the previous post on brainstem death flicks from off to on. Simples.

 There will be anaesthetists reading this (always assuming anybody is reading this) who are jumping excitedly up and down at this point, berating me for not talking about total intravenous anaesthesia (TIVA). The TIVA brigade is evangelistic in its condemnation of all inhalational anaesthetic agents. Members use intravenous infusions of propofol and remifentanil (an ultra-short-acting, ultra-potent, synthetic opioid) to induce their patients, as well as to maintain anaesthesia. Don’t ask me why. They just do. How can you tell if your anaesthetist is a fully paid up member of the TIVA brigade? Rather like wondering if a friend you’ve invited for dinner is vegetarian, you don’t need to worry about it. They’ll tell you.

How do anaesthetics work?

 When I was studying for my anaesthetic exams, the answer to this question was far from having been fully answered. A popular theory I learnt stemmed from the fact that many anaesthetic drugs are lipid (fat) soluble. Moreover, their anaesthetic potency is directly related to how lipid soluble they are. Neurones (nerve cells), including those in the brain, communicate with each other through a combination of electrical and chemical signals at microscopic junctions between them called synapses. Crucially, the neuronal membranes, like all other cell membranes, consist predominantly of lipids.

 Putting these facts together gave rise to the idea that general anaesthetic drugs might work by dissolving into the fatty membranes of neurones, thereby interfering with the transmission of electrical and chemical signals between them at synapses. It was an attractive theory because chemically diverse substances such as nitrous oxide, xenon, ether, chloroform, sevoflurane, thiopental, propofol and ketamine all produced the same general anaesthesia.

 However, simple as the theory was, it did not tell the whole story. Attention then shifted to proteins, which are also components of cell membranes. Many of these membrane proteins function either as receptors or as microscopic channels through the membrane that allow chemical agents to pass through from one side to the other. These receptors and membrane channels are directly involved in electrical and chemical signal transmission between neurones. One of the most important is the GABAA receptor and its linked membrane channel. GABA is the brain’s main inhibitory neurotransmitter. GABA switches brain cells off. It was discovered that many general anaesthetics enhance GABA’s effects at GABAA receptors.

 However, this still wasn’t the complete picture. Ketamine and nitrous oxide, for example, work by blocking the action of NMDA, an excitatory neurotransmitter, at NMDA receptors. NMDA switches brain cells on.

 Much remains to be discovered about the mechanisms of action of general anaesthetic drugs. There are likely multiple sites of drug action rather than a single molecular ‘anaesthetic switch’.

 What actually happens when you have a general anaesthetic?

 I’m guessing that most of you will have had surgery under general anaesthesia at some time in your life. If so, perhaps you fully understood everything that happened. On the other hand, perhaps you didn’t. Whatever, here is McCluskey’s idiot’s guide: I’m having an operation under general anaesthesia. What happens when I go into hospital?

 Usually Step 1 is when you see your surgeon in the outpatient clinic and are listed for surgery. Patients come in all ages, shapes and sizes, degrees of physical fitness and with any number of associated chronic medical conditions. Your surgeon is good at operating (hopefully), but they know the square root of bugger all about anything that doesn’t either involve slicing through some delicate tissue with a scalpel or knocking seven bells out of some bone or other with a hammer.

 Thankfully, Step 2 involves a trip to the preoperative assessment clinic, where a nurse specialist puts you through the wringer. Your full medical and surgical history is reviewed, blood is taken, and special investigations, such as ECGs, chest X-rays and lung function tests, are ordered. If your nurse has any serious concerns, they will likely contact your anaesthetist, who will arrange to see you well ahead of the date of surgery to further assess you and explain your individualised risk of going ahead with surgery (and anaesthesia). Otherwise, the first time you normally meet your anaesthetist is on the day of surgery itself.

 Step 3 is when you pitch up on the preop admissions ward on the day of surgery, assuming you are a day case. You will likely have an uncomfortable feeling in your stomach. This is partly butterflies because you are worried about what lies ahead. It’s also partly hunger as you will have been instructed to fast for a minimum of six hours before the scheduled start of the operating list (still (not sparkling) water is allowed up to two hours before). Never assume this precaution is merely so you don’t feel sick afterwards. ‘I’ve got an iron constitution,’ you might say to yourself, ‘so I can safely go ahead with my full English cooked breakfast as usual.’

 Properly following preoperative fasting instructions is an essential health and safety provision. Your health and safety! The admonition doesn’t exist simply to reduce the chance of you suffering from a dicky tummy afterwards. To be fair to patients, preoperative instruction letters could be better phrased, in my view. Although they do routinely detail the fasting instructions, they do not usually explain why fasting is necessary. It always seemed to me that a few additional sentences might have avoided situations where we ended up cancelling a patient on the day of surgery because they weren’t properly fasted. Or worse, took a patient having a routine procedure to the ICU afterwards suffering from aspiration pneumonia because they had been economical with the truth when questioned about their fasting status. Something along these lines would have done the trick:

 If you don’t follow these instructions to the letter and then don’t later admit that you haven’t followed them when questioned, you are at high risk of vomiting under general anaesthesia. Gastric secretions are highly acidic and corrosive. If vomit gets into your lungs, which it will, it will burn through the delicate lining of your air passages and cause widespread inflammation, infection and respiratory failure. Your operation will be cancelled, and you’ll be admitted to the Intensive Care Unit with aspiration pneumonia, where you’ll spend the next few days in a medically induced coma on a mechanical ventilator. There is a good chance you will die.

 Surely a message to discourage even the most ardent of breakfasters.

 Your anaesthetist will assess you and discuss your anaesthetic options (general anaesthesia versus regional or local anaesthesia, postoperative pain relief), potential side effects, and complications. It’s very much not a one-size-fits-all approach. If you were expecting a premed, forget it. Anaesthetists hardly ever bother these days. Feeling shit scared is good for the soul, if not your heart.

 Seriously, though, it really isn’t that your anaesthetist can’t be arsed. There are several reasons why premeds went out of fashion during my career. Firstly, in the past, a good sedative premed helped ensure induction of anaesthesia went more smoothly. However, modern anaesthetic drugs have rendered premeds unnecessary in this regard. Secondly, most patients nowadays undergo surgery as day cases, which certainly was not the case when I began my anaesthetic career. A sedative premed can delay postoperative recovery and interfere with the drive to get you up and about as soon as possible after day case surgery. It may even mean you have to be admitted overnight if you are too drowsy to discharge home safely. Finally, operating theatre logistics make it virtually impossible to time a premed to be effective exactly when it needs to be. Depending on whether a patient arrives in theatre earlier or later than expected, the premed either isn’t yet effective and would only serve to interfere with postoperative recovery when it eventually does reach peak effect, or the patient is fast asleep on the ward but wide awake and scared stiff by the time they belatedly reach theatre.

 After you arrive in the operating theatre suite, you often need to wait a while in the reception area until the team is ready for you. When it is your turn, you will be taken to the anaesthetic room rather than directly into the operating theatre itself. Your anaesthetist and/or their assistant (an anaesthetic nurse or an Operating Department Practitioner, ODP) will complete a final check of who you are, what you’re having done, and any special circumstances. Your baseline heart rate, blood pressure and blood oxygen saturation observations are recorded, an intravenous cannula is inserted and, if I’m your anaesthetist, a quick injection of midazolam immediately follows to calm you down if you’re anxious and to make you forget ever having been in the anaesthetic room afterwards – courtesy of the anterograde amnesic effect of midazolam. It means we can tell bawdy jokes or make fun of you, and you won’t remember a thing. Marvellous.

 Despite this ritual abuse, my patients universally loved midazolam. It made them euphoric, relaxed and disinhibited. I had patients of both sexes tell me they loved me. I had patients share innermost secrets about their personal life that they would not ordinarily have divulged to anyone. All very interesting and good fun, but the main reason I used midazolam was that it smoothed induction of general anaesthesia, reducing unwanted complications such as combative behaviour, coughing, hiccoughing, laryngospasm, etc. Midazolam worked as a sort of instant premed.

 I routinely preoxygenated all of my patients immediately before induction of anaesthesia, handing them the mask to hold onto themselves. When I was ready, an injection of propofol rendered my patient unconscious within 20-30 seconds. Many of them expected to be told to count forwards or backwards, but I preferred to tell my patients a joke. Or even better, for them to tell me a joke as they drifted off. If neither of us could think of a joke, I used to engage in banal conversation about the previous evening’s TV, the weather or how Manchester City were doing.

 If my patient was talking as the bolus of propofol reached their brain, they would hesitate mid-sentence, perhaps slur their words or sound confused, and then become silent. Their eyes, previously bright with emotion and recognition of their surroundings, would glaze over and become dull and lifeless. Or they would roll up into the back of the patient’s head. More often than not, my patient would stop breathing. Not breathing is an unmitigated disaster in the outside world. It usually either means you’re dead already or you very soon will be. The situation is not much better on a general hospital ward. But not breathing is par for the course in the anaesthetic room with an anaesthetist present. No big deal.

 If my patient wasn’t breathing, I might wait a few moments to see if they started up again before gently ventilating them with a bag-valve-mask apparatus and then inserting a laryngeal mask airway for the duration of surgery. If I’d given them a muscle relaxant, they definitely wouldn’t breathe, of course, and I would pass a tracheal breathing tube between their vocal cords and attach them to the mechanical ventilator. Then, I’d do a quick check of my patient’s obs to make sure we had a green light, and we would be off into the operating theatre.

 I always found inducing general anaesthesia enthralling. I never lost my wonder and fascination with the process up until the day I retired. It was one of the big reasons why I became an anaesthetist in the first place, and it is high on the (relatively small) list of things I miss about work now that I am retired.

 While you’re lying on the operating table, dead to the world, I tell my anaesthetic nurse or ODP to call me back when it’s all over and nip off to the coffee room. Only kidding! I’m going nowhere. Your brain, and in particular your brainstem, which you rely on to breathe, regulate your blood pressure and heart rate, switch your RAS back on when your general anaesthetic is discontinued, and generally keep you safe and alive, is temporarily out of commission. It’s now my job to do all these tasks for you.

 When your operation is over, you’re taken to the recovery room. I might hand you over to the recovery nurse and head straight back into the anaesthetic room to start the next case, or stay with you until you emerge from general anaesthesia. Whichever course I take depends on whether or not you are a risky patient (eg you are morbidly obese, have severe COPD or heart problems) and how pressed for time I am. Whether I stay or go, recovery nurses are highly trained to manage anaesthetised patients safely until they emerge from anaesthesia and can be safely discharged back to the ward.