History (general, anaesthetic history — especially risk for aspiration), Examination (CVS, Respiratory, Airway, other relevant parts), Investigations ^[1]

Anaesthetic history is critical: previous difficult intubation, adverse reactions to anaesthetic drugs, family history of malignant hyperthermia, history of PONV (post-operative nausea and vomiting).

Airway assessment combines mouth opening, dentition, tongue/oropharyngeal view, mandibular space, neck movement and previous airway records; no single bedside test reliably predicts difficulty. Examination is tailored to the planned technique—for example, inspect the lumbar spine when neuraxial anaesthesia is contemplated, as shown on the slide.

Before induction: pulse oximetry, blood pressure and ECG. Once the airway is instrumented: waveform end-tidal CO₂ monitoring. ^[1]

Why end-tidal CO₂ (ETCO₂)? Sustained waveform capnography helps confirm tracheal placement and continuously shows ventilation. The image-heavy monitor slides also identify the ECG/heart rate, plethysmographic waveform and SpO₂, non-invasive blood pressure, inspired and expired volatile-agent concentration, and capnogram/ETCO₂. Current monitoring standards additionally require temperature and, according to technique, inspired/expired oxygen and anaesthetic gases, ventilation variables, quantitative neuromuscular monitoring and processed EEG for TIVA with neuromuscular blockade. ^[9]

Induction → Maintenance → Emergence and Recovery ^[1]

Propofol, Thiopentone, Etomidate, Ketamine ^[1]

Sevoflurane, Nitrous Oxide ^[1]

• Sevoflurane ("the yellow stuff" ^[3]): Non-irritant to airways → suitable for inhalational induction, especially in children (paediatric patients who can't tolerate IV cannulation before induction)
• Nitrous oxide (N₂O, "laughing gas", Entonox when mixed 50:50 with O₂): Weak anaesthetic and analgesic adjunct. Its MAC exceeds 100%, so it is not a sole modern general-anaesthetic agent at normal pressure.

Why gas induction? In children or needle-phobic patients, you can hold a mask with sevoflurane over the face → child breathes in → loses consciousness → THEN establish IV access.

"This is one reason why we need muscle relaxants when administering general anaesthesia" ^[1] — the photograph shows an ETT passing between the vocal cords. NMBAs can improve intubating and surgical conditions, but they are not required for every GA or every airway device.

Nerve stimulator used to assess degree of neuromuscular blockade ^[1]

Train-of-Four (TOF): four stimuli at 0.5-second intervals, commonly delivered to the ulnar nerve with the response measured at adductor pollicis. A twitch count describes deeper block; once four responses return, a quantitative ratio detects residual fade that cannot be judged reliably by sight or touch. Confirm TOF ratio ≥0.9 before extubation. ^[10]

Isoflurane, Sevoflurane, Desflurane, +/- Nitrous Oxide ^[1]

Concept: MAC (Minimum Alveolar Concentration) — The concentration of inhaled anaesthetic at 1 atm that prevents movement in response to a surgical stimulus in 50% of patients. Think of it as the ED50 for volatile agents. Lower MAC = more potent agent. MAC is additive — combining agents reduces the concentration of each needed.

Reading the machine photographs: the agent-specific vaporiser converts liquid volatile anaesthetic into a calibrated vapour and its dial sets the delivered concentration. The monitor displays inspired concentration (entering the patient) and end-tidal concentration (leaving the alveoli). End-tidal concentration approaches alveolar—and, after equilibration, brain—partial pressure. The slide’s desflurane vaporiser is heated and pressurised because desflurane is unusually volatile. ^[1]

Propofol ^[1]

• Propofol infusion for both induction and maintenance, often combined with remifentanil infusion
• Target-Controlled Infusion (TCI): Computerized pump calculates dose based on patient weight and age to maintain a target plasma or effect-site concentration ^[3]
• Advantages: No atmospheric pollution, reduced PONV, smooth emergence
• Unlike a volatile technique, there is no end-tidal propofol concentration to confirm delivery. Current monitoring guidance recommends processed EEG when TIVA is combined with neuromuscular blockade, alongside close inspection of the IV cannula, tubing and pump. ^[9]

Simple: Paracetamol (PO, IV, PR), NSAIDs & COX-2 inhibitors (IV, suppositories) ^[1] Opioids: Fentanyl (IV, SC), Morphine (IV, PO), Oxycodone (IV, PO), Pethidine (IV) ^[1] Others: Tramadol, Gabapentinoids, Ketamine, Regional Techniques ^[1]

Naloxone — a short-acting opioid antagonist titrated to restore adequate ventilation while avoiding abrupt loss of analgesia and acute withdrawal. Because it may wear off before the opioid, continued observation and repeated doses or an infusion may be required. Follow the local emergency protocol rather than a single memorised dose.

Oral analgesia, Parenteral analgesia, Infusion, Patient Controlled Analgesia (PCA), Continuation of Regional Block (Epidural, Catheters along major plexus & nerves) ^[1]

Multimodal analgesia is the standard approach: combining paracetamol + NSAID + opioid ± regional technique to target different pain pathways, reduce opioid consumption, and minimize side effects (the WHO analgesic ladder adapted for acute pain).

PCA (Patient Controlled Analgesia): the patient activates a programmed opioid bolus with dose and lockout limits. These safeguards reduce risk but do not make PCA overdose-proof; monitoring, avoidance of proxy activation and adjustment for comorbidity remain essential.

Home, Ward, High Dependency Unit (HDU), Intensive Care Unit (ICU). If you are not sure, ask the anaesthesiologist. ^[1]

Factors determining disposition: premorbid status, nature/length of operation, intraoperative events, anticipated postoperative complications, level of monitoring/support needed. ^[5]

Established by the deposition of local anaesthetic in close proximity to a nerve or a group of nerve fibres. The local anaesthetic blocks transmission of signals → reduced sensation from the anatomical area supplied by the blocked nerves. ^[1]

RA may be used alone or in combination with sedation or general anaesthesia. Pain relief is provided by nerve blockade; hypnosis is provided by the sedative agent. Sometimes the regional anaesthesia technique does not cover the entire surgical field → combination with GA is required. ^[1]

How LAs work: LAs bind voltage-gated Na⁺ channels from the intracellular side and prevent action-potential propagation. Fibre diameter, myelination, firing frequency, drug concentration and geometry all influence susceptibility; in practice, autonomic and sensory function often disappear before dense motor function, producing differential block.

Neuraxial blocks (spinal, epidural), plexus blocks, nerve blocks, local infiltration, topical anaesthesia, intravenous regional technique ^[1]

How to read the neuraxial diagram: from posterior to anterior, the needle traverses skin/ligaments to reach the epidural space outside the dura; a spinal needle continues through dura into the CSF-containing subarachnoid (intrathecal) space. This anatomical difference explains why spinal anaesthesia uses a small intrathecal dose with rapid dense block, whereas an epidural can be titrated through a catheter using larger volumes.

Role of adrenaline with LA: ^[6]

• Local vasoconstriction can slow systemic absorption, prolong block and help reveal accidental intravascular injection through a haemodynamic response.
• The traditional blanket rule “never use adrenaline in fingers, toes, nose, pinna or penis” is too absolute. Dilute preparations are used safely in selected sites, but avoid them when perfusion is compromised and follow the procedure-specific/local protocol.

• 1% solution = 10 mg/mL and 0.5% = 5 mg/mL.
• If the chosen protocol sets a patient-specific maximum of 210 mg, the corresponding volume of 0.5% solution is 210 ÷ 5 = 42 mL. The arithmetic does not establish that 210 mg is safe for every patient or technique.

Inadvertent intravascular injection, Overdose, Adverse reaction to adjuvant (e.g., epinephrine, preservatives) ^[1]

Spectrum of systemic manifestations: Neurological symptoms → Convulsions → Cardiovascular collapse ^[1]

The slide presents a useful CNS → seizure → cardiovascular collapse teaching sequence, but real LAST can be atypical: cardiovascular toxicity may occur without warning CNS excitation, and onset may be delayed after infiltration or an infusion. ^[11]

Classic mechanism: lower toxic concentrations preferentially suppress inhibitory cortical pathways, producing excitation/seizures; higher concentrations cause global CNS depression and direct cardiac conduction/contractility toxicity. Do not wait for every classic prodrome before acting.

Management of potentially serious LAST: ^[11]

1. Stop injecting LA
2. Call for help, bring the LAST rescue kit/checklist and prioritise oxygenation/ventilation; hypoxia, hypercapnia and acidosis worsen toxicity
3. Treat seizures promptly, preferably with a benzodiazepine; avoid large propofol doses in cardiovascular instability
4. Give 20% lipid emulsion early for a serious event according to the weight-based checklist; propofol is not a substitute
5. If arrest occurs, use modified LAST resuscitation: smaller-than-usual adrenaline doses are preferred, avoid vasopressin, calcium-channel blockers and beta-blockers, and prefer amiodarone for ventricular arrhythmia
6. Continue monitored care after apparent recovery because recurrence/delayed toxicity can occur

Risk reduction for LAST: [6,11]

• Calculate the patient-specific cumulative dose and label/communicate every local-anaesthetic contribution
• Aspirate and inject incrementally while maintaining verbal contact and monitoring; a negative aspiration does not exclude intravascular placement
• Use ultrasound appropriately for peripheral blocks, while recognising that visualisation does not eliminate risk
• Consider an adrenaline-containing test marker when appropriate; absence of a haemodynamic response is not proof of extravascular injection
• Keep the LAST checklist and 20% lipid emulsion immediately available wherever potentially toxic doses are used

Hypotension: Sympathectomy, inadequate intravascular volume, inappropriate patient choice (cardiac/valvular disease) ^[1] Bradycardia: Blockade of cardiac sympathetic fibres ^[1]

Why? Spinal/epidural anaesthesia blocks sympathetic fibres → arteriolar vasodilation (↓SVR) and venodilation (↓venous return) → hypotension. A high block may impair T1–T4 cardiac accelerator fibres; reduced venous return also promotes vagal bradycardia. Treat promptly with positioning, appropriately selected IV fluid and vasopressor, and atropine when indicated; the exact strategy varies by setting (especially obstetrics and fixed-output lesions).

Excessive rostral spread of LA — dose too much, position head down, subdural injection ^[1] Respiratory distress: motor blockade of intercostal muscles → may require ventilatory support ^[1] The slide labels the extreme endpoint “total spinal” and attributes it to supraspinal blockade. ^[1]

Current physiological interpretation: a high/total neuraxial block is excessive cephalad spread causing profound sympathectomy and high motor block. Respiratory failure can follow intercostal and then diaphragmatic impairment; severe hypotension/bradycardia may reduce cerebral perfusion and cause loss of consciousness. It is not best understood as local anaesthetic routinely bathing and anaesthetising the brainstem. This is an emergency: call for help, give oxygen, secure/ventilate the airway as required and provide aggressive cardiovascular support.

Conversion from RA to GA may be required immediately for several reasons: ^[1]

• Total or partial failure of block (see below)
• Complications from the regional technique — LA toxicity, severe haemodynamic disturbances, excessive block
• Prolonged surgery — duration of surgery exceeds duration of block → return of sensation during surgery
• Patient factors during surgery — restlessness or becoming uncooperative

Reasons for total or partial block failure: ^[1]

Operator factors: Misplaced needle, Incorrect dosage, Drug error (including expired drugs) Patient factors: Anatomical variants