Principles of Anaesthesia & Airway for Surgeons

Meet the patient

A 48-year-old obese man with a distended abdomen from a small-bowel obstruction is rolled into theatre for an emergency laparotomy. His Mallampati is III, his oxygen saturation falls to 89 percent sitting upright, and he has not fasted for ten hours. The decision that decides his next hour is whether this is a routine intravenous induction — or a rapid sequence induction with a trained assistant, suction on, and a surgical airway on the trolley.^[1]

Two questions decide every induction, and they decide every examiner stem. First, is this stomach full or empty (obstruction, pregnancy beyond 20 weeks, opioids, trauma all mean full)? Second, is the airway easy or hard — look externally for beard, receding mandible, large neck, scars, then run the bedside tests (Mallampati, mouth opening, thyromental distance, neck movement; LEMON if trauma).^[10] Hold those two questions and the rest of anaesthesia — drugs, monitors, ladder — falls into place.

The triad — unconsciousness, analgesia, paralysis

General anaesthesia is not one drug; it is three drugs working on three targets. Miss one limb and the patient either wakes up, screams, or moves. The examiner who says "define anaesthesia" wants the triad first, then the understanding that each limb has its own pharmacology and its own catastrophe.^[3]

^{[13] [9] [15]}

The classic trap: assuming the patient who is not moving is asleep. Neuromuscular blockade paralyses but does not sedate. A patient on an adequate dose of rocuronium with an inadequate volatile concentration will be paralysed and awake — this is the mechanism of accidental awareness, the subject of the NAP5 audit^[12] and the single most feared complication of anaesthesia. Watch end-tidal volatile and BIS if available, and do not rely on movement.

The induction agents in one breath

Propofol is the default because it is fast, smooth, anti-emetic and short-acting, but it drops blood pressure 20 to 30 percent in the volume-depleted or elderly. Its mechanism is GABA-A potentiation with downstream chloride influx, producing hypnosis in one arm-brain circulation (about 30 to 45 s). It is not an analgesic, so severe pain will still provoke movement and tachycardia unless an opioid or regional block is on board.^[3]

Propofol has displaced thiopentone in most centres, though thiopentone remains a noteworthy barbiturate alternative apart from its slow elimination kinetics. Ketamine and etomidate have the favourable haemodynamic profiles, so they are preferred over propofol when the patient is haemodynamically unstable.^[16][13]

The surgical question is rarely academic: the morning-list bowel obstruction, the bleeding ruptured AAA, the septic peritonitis patient all need the agent that keeps blood flowing while you get a tube in. Choose ketamine or a reduced-dose propofol with concurrent vasopressor cover, not a textbook dose of propofol on a flat tank.^[13]

Inhalational agents and MAC — the number examiners love

Minimum alveolar concentration (MAC) is the alveolar concentration of an inhalational agent at which 50 percent of patients do not move in response to surgical incision. It is a dose–response ED50 for movement, not unconsciousness. Age adjusts it (MAC falls about 6 percent per decade over 40), opioids reduce it, hyperthermia raises it, and obesity has little effect. Modern practice targets MAC 0.7 to 0.9 age-adjusted as the unconsciousness threshold, and 1.0 to 1.3 for surgical immobility.^[15]

The practical implication for the surgeon: the dose on the vaporiser dial is a vaporiser setting, not a patient dose. It is the end-tidal concentration that defines depth, and it is what the anaesthetist watches — along with train-of-four, blood pressure, heart rate, and the capnograph — to keep the patient asleep, still and alive.^[15]

Capnography is the safety check — the NAP4 lesson

Continuous end-tidal capnography is the single immediate test that an endotracheal tube is in the trachea, and its absence is the single commonest cause of death or brain damage in airway disasters. NAP4 analysed every major airway complication in the United Kingdom over one year and identified 184 anaesthesia events, 36 intensive-care events and 15 emergency-department events that resulted in death, brain damage, emergency surgical airway or unanticipated ICU admission. Failure to use capnography, or misinterpretation of a trace, contributed to 74 percent of ICU and ED deaths.^[1][2]

^{[1] [2]}

Minimal monitoring during anaesthesia — pulse oximetry, capnography, ECG, non-invasive blood pressure every 3 to 5 min, temperature for any case over 30 minutes, and neuromuscular monitoring whenever blockade is used — is mandated by the ASA, ANZCA and AAGBI-derived national standards. The surgeon waits until the tube is confirmed and the trace is rising before allowing the incision.^[9]

Airway assessment — look, then the bedside tests

The patient who will be difficult to ventilate is not always the patient who will be difficult to intubate, and the two skill sets are different. A rational exam starts outside (beard, obesity, receding mandible, short immobile neck, scars from radiotherapy or surgery, and evidence of trauma), then inside (mouth opening, dentition, Mallampati class, thyromental distance, jaw protrusion). The LEMON mnemonic (Look, Evaluate 3-3-2, Mallampati, Obstruction, Neck mobility) organises the same anatomy for the trauma bay.^[10]

^[10]

The two numbers examiners want are in Detsky's 2019 JAMA meta-analysis: a Mallampati III or IV carries a likelihood ratio around 4 for difficult intubation, but the combination of Mallampati, mouth opening and neck movement is far better than any single sign. The upper lip bite test (class III, inability to bite the upper lip with the lower incisors) was the best single bedside test. No single sign rules out difficulty; always have a rescue plan.^[10]

The DAS 2015 algorithm — the ladder that saves lives

When intubation fails, the Difficult Airway Society 2015 guideline replaces the old linear attempt-after-attempt with a four-plan ladder designed to maintain oxygenation first, and secure the airway second. The order is deliberate — each step is quicker and less invasive than the last, and the whole team knows the sequence.^[3]

^[3]

Viva gold: the can't-intubate-can't-oxygenate call and the single horizontal stab through the cricothyroid membrane with a scalpel then bougie into the trachea is the DAS-endorsed final rescue. It is the only step that requires a knife, and it belongs to whoever is trained and nearest — in theatre, that is often the surgeon. This is the one moment every surgical trainee must rehearse.^[3]

Rapid sequence induction and aspiration — cricoid in doubt

Rapid sequence induction remains the standard approach for the full stomach, but its pharmacology has moved on. Aspiration complicates 3 to 6 percent of rapid sequence inductions, yet desaturation and haemodynamic collapse now cause most of the harm, so preoxygenation and a good first attempt matter more than speed. Cricoid pressure is increasingly questioned; contemporary practice applies it selectively, mainly when active regurgitation is visible, and gentle facemask ventilation after induction is considered safe and useful when desaturation risk is high. Rocuronium has largely replaced suxamethonium as the relaxant.^[13]

Sellick described cricoid pressure in 1961 from a case series of 26 patients^[5], but its role was formally tested in the IRIS trial (about 3400 patients, 2019), which found no difference in pulmonary aspiration between cricoid and a sham procedure — non-inferiority confirmed. Modern practice continues cricoid by default, but releases it if it worsens the laryngoscopic view or ventilation.^[4]

Aspiration of gastric content in NAP4 occurred in roughly one fifth of all anaesthesia airway disasters and had an attributable mortality around 4 percent. Antacid prophylaxis (H2 blocker or proton-pump inhibitor, sodium citrate before emergency section) reduces the volume and raises pH; at caesarean section, metoclopramide plus an H2 blocker reduces aspiration pneumonia rates in the Cochrane review of over 2500 women.^[11] At the other extreme, the empty-stomach rule — ASA standard 6 hours solids, 2 hours clear fluids — is the surgical version of seat belts.

The toxic catastrophes a surgeon must not miss

Two anaesthetic emergencies land on the surgeon's radar because the trigger is the surgical patient, the drug, or the incision. Both are time-critical and both kill if recognition is slow.^[7]

Malignant hyperthermia is a rare pharmacogenetic disorder of skeletal muscle, most often caused by pathogenic variants in the ryanodine receptor gene RYR1; the triggers are the potent volatile agents and suxamethonium. Dantrolene acts at that receptor, blocking abnormal calcium release from the sarcoplasmic reticulum, and it remains the only specific treatment: stop the volatile, then give dantrolene immediately, dosed on actual body weight and repeated until the reaction settles. Complications rise with every 10 minutes of treatment delay. Mortality in modern series runs 1 to 10 percent.^{[19][18][17][7]}

Laryngospasm is forceful glottic closure in the light plane of anaesthesia, set off by airway instrumentation, suctioning, blood or secretions in PACU, and it is commoner in children and with upper-airway sepsis. Call for help, give 100 percent oxygen with firm jaw thrust and continuous positive airway pressure, and if the spasm does not break, give a small dose of suxamethonium IV and reintubate if ventilation stays poor.^[14]

Anaphylaxis under anaesthesia classically presents as profound hypotension and bronchospasm immediately after an antibiotic or muscle relaxant; treatment is adrenaline 50 micrograms boluses IV, 100 percent oxygen, stopping the trigger, aggressive fluids, and a mast-cell tryptase one and four hours later; the details and antibiotic-allergy labelling are covered in the surgical-safety topic.^[2]

Neuromuscular blockade — monitoring and reversal

Residual neuromuscular blockade at extubation is the hidden driver of postoperative pulmonary complications — the unrecognised weak patient who aspirates or hypoventilates in PACU. The ASA 2023 neuromuscular monitoring guideline mandates quantitative train-of-four monitoring (acceleromyography or mechanomyography), not a subjective twitch count, at the adductor pollicis whenever a non-depolarising blocker is given; extubation is allowed only when the train-of-four ratio is 0.9 or more.^[9]

Reversal follows the agent. Neostigmine antagonises the blockade indirectly through acetylcholinesterase inhibition, but it is slow, limited by muscarinic side effects, and cannot reverse deep block. Sugammadex reverses rocuronium blockade even when profound, and in the multicentre STRONGER matched cohort of over 45,000 patients it cut major postoperative pulmonary complications by about 30 percent compared with neostigmine: pneumonia fell 47 percent and respiratory failure 55 percent. Sugammadex is the default when cost and availability permit.^[8]

Special populations and practical lessons

The obstetric patient combines a full stomach, reduced functional residual capacity, rapid desaturation, aortocaval compression and mucosal oedema. Left lateral tilt or wedge, preoxygenation in ramped position, antacid prophylaxis and rapid sequence induction are the pillars; airway management carries roughly double the rate of complications of the non-pregnant population.^[2][11]

The obese patient with obstructive sleep apnoea desaturates within 60 to 90 seconds even with complete preoxygenation because the abdominal mass compresses the functional residual capacity; ramp, nasal cannula oxygen during apnoea, and videolaryngoscopy on the first attempt are standard. The septic patient receives reduced induction doses with vasopressors ready — the circulating catecholamines that were holding the pressure together vanish the moment sympathetic tone falls. The paediatric patient has a higher oxygen consumption and smaller functional residual capacity, so desaturation is faster still, and laryngospasm is the leading airway complication of extubation^[14].

Exam pearls

• Anaesthesia = triad: hypnosis (GABA or NMDA), analgesia (mu), blockade (nicotinic acetylcholine receptor); reversal drugs match the class.
• MAC 0.7 to 0.9 age-adjusted = unconsciousness; 1.0 to 1.3 = immobility.^[15]
• Capnography absent = oesophageal intubation until proven otherwise; remove the tube and reoxygenate; NAP4 lesson.
• DAS 2015 ladder: Plan A mask + intubate (max 3 attempts), Plan B supraglottic airway, Plan C facemask, Plan D scalpel-bougie cricothyroidotomy.
• Malignant hyperthermia: rising end-tidal CO2 and tachycardia after volatile or suxamethonium; dantrolene 2.5 mg/kg IV immediately.^[17]
• Laryngospasm: 100 percent O2 then suxamethonium 0.1 to 0.5 mg/kg IV, not the intubating dose.
• IRIS trial (2019): cricoid pressure was non-inferior to sham for aspiration at RSI; many keep it by tradition or release it if it worsens the view.
• Train-of-four ratio 0.9 is the extubation threshold; sugammadex reduces postoperative pulmonary complications compared with neostigmine (STRONGER, 2020).
• Paralysis does not equal unconsciousness — inadequate volatile with full blockade produces awareness (NAP5).

Educational synthesis; verify local protocol and drug doses against institutional guidelines before clinical use.

References19ShowHide

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2. [2]Cook TM, Woodall N, Harper J, et al. Major complications of airway management in the UK: results of the Fourth National Audit Project of the Royal College of Anaesthetists and the Difficult Airway Society. Part 2: intensive care and emergency departments Br J Anaesth, 2011.PMID 21447489
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