Anesthesia

Seal Pressure Generation Features Examples (OLP) First Inflatable cuff; no gastric drainage channel; suitable for spontaneous breathing only or Classic LMA (Brain's original); Portex 15–20 cmH₂O (low generation very low-pressure IPPV; cuff repositions with each inflation; requires inflating balloon to Soft Seal; LMA Unique (single-use) — limits positive (classic) achieve seal pressure ventilation use) Second Higher seal pressures (25–30 cmH₂O); integrated gastric drainage channel (allows NGT i-gel (non-inflatable cuff); LMA 25–35 cmH₂O generation passage and decompresses stomach, reducing aspiration risk); drainage port separates ProSeal (inflatable cuff + gastric (allows positive (advanced) the respiratory and GI tracts; some have bite block and alignment features; suitable for drain); LMA Supreme (single-use + pressure ventilation positive pressure ventilation during surgery gastric drain); LMA Protector; Air-Q for most surgical procedures)

Cuff material: non-inflatable thermoplastic elastomer (TPE) gel — formulated to match the soft consistency of perilaryngeal tissues; the gel cuff moulds to the individual anatomy of the patient's hypopharynx, laryngeal inlet, and perilaryngeal anatomy at body temperature without requiring inflation; eliminates the complications of cuff inflation (cuff over-inflation, cuff herniation, cuff leak)

Structure: a short, curved airway tube connecting to a widened cuff that sits in the hypopharynx sealing around the laryngeal inlet; an integrated gastric drainage channel runs parallel to the main airway lumen, terminating at the oesophageal inlet (allows NGT insertion for gastric decompression); a bite block at the proximal end prevents jaw closure from occluding the airway

Sizes: 1 (neonates); 1.5 (infants 5–12 kg); 2 (children 10–25 kg); 2.5 (25–35 kg); 3 (small adult 30–60 kg); 4 (adult 50–90 kg); 5 (large adult >90 kg); selected by patient weight

Advantages: rapid insertion (no cuff inflation step); higher OLP (oropharyngeal leak pressure — 24–30 cmH₂O) than first-generation LMAs; integrated gastric drain (drainage of regurgitated gastric contents via the second channel reduces (but does NOT eliminate) aspiration risk); single-use (infection control); suitable for fibreoptic intubation conduit; suitable as second line (Plan B) in DAS failed intubation algorithm

Indications Contraindications Elective surgery under GA where ETT is not mandatory (most ENT, orthopaedic, Full stomach / aspiration risk (RSI with ETT preferred); predicted difficult SAD superficial surgery, gynaecological laparoscopy in non-obese); IPPV during placement (limited mouth opening <2.5 cm; fixed neck with pharyngeal surgery (2nd generation SADs can withstand 25–30 cmH₂O to allow controlled pathology; severe pharyngeal/laryngeal pathology); morbid obesity for ventilation); ambulatory anaesthesia (faster emergence, less PONV than ETT); prolonged procedures; high airway resistance/low pulmonary compliance rescue airway in failed intubation (DAS Plan B); cardiac arrest — all ILCOR requiring peak pressures >30 cmH₂O; surgery requiring full neuromuscular guidelines accept SADs as alternative to ETT in cardiac arrest (AHA 2020); bridge blockade with high airway pressures (thoracic, steep Trendelenburg in obese to fibreoptic intubation (Aintree Intubation Catheter through i-gel) patients); head-and-neck surgery where access to the SAD is lost during the case

The i-gel, once placed and ventilation confirmed, can be used as a conduit for fibreoptic-guided intubation (DAS Plan B — after failed intubation, maintain oxygenation with SAD then attempt intubation through it): pass a lubricated fibrescope through the i-gel airway tube → visualise the vocal cords through the SAD aperture → advance a tracheal tube over the fibrescope → confirm intubation with ETCO₂; then remove the i-gel over the ETT

Aintree Intubating Catheter (AIC) technique: a 56 cm catheter (4.7 mm OD) is passed through the fibrescope into the trachea; fibrescope is removed; then a 7.0–8.0 mm ETT is railroaded over the AIC through the i-gel into the trachea; the AIC is then removed; this technique allows intubation through an i-gel with a standard-sized adult ETT

Success rate: approximately 96% intubation success through second-generation SADs in multiple studies; specific i-gel success rate 93–97% for intubation via FOI conduit

Cardiac arrest: ILCOR 2020 and AHA 2020: "SADs are an acceptable alternative to tracheal intubation for airway management during cardiac arrest"; a SAD by a practitioner with limited ETT skill provides equivalent outcomes to ETT in multiple randomised trials; i-gel specifically: AIRWAYS-2 trial (Benger JR, JAMA 2018; n=9,296 out-of-hospital cardiac arrest patients): i-gel vs ETT for cardiac arrest airway management — no difference in neurologically intact survival (primary outcome); i-gel had faster insertion and fewer complications

Select size by weight; lubricate cuff with water-based lubricant (NOT silicone — degrades TPE gel); head in neutral or slightly extended position; open mouth; grasp i-gel with thumb on the bite block; introduce into the mouth aiming the cuff toward the hard palate; rotate and guide the device posteriorly along the hard palate then downward into the pharynx in a single smooth movement until resistance is felt (cuff seated against laryngeal inlet); confirm ventilation (ETCO₂ waveform, bilateral chest movement, absence of epigastric sounds); if poor seal → reinsert or change size

FGF Bag/APL Min FGF Min FGF System Efficiency Explanation Position Position (SB) (IPPV) A (Magill) Near the Near the MV 2–3× MV During SB: expired gas pushes to the patient-end APL → alveolar gas (CO₂-rich) vents first; bag patient (alveolar (10–15 fresh gas fills the space; VERY EFFICIENT for SB (least FGF). For IPPV: PPV pushes (machine (patient ventilation) L/min) mixed gas toward the bag → CO₂-rich gas is not selectively vented; fresh gas wasted — end) end APL) ≈ 4–5 INEFFICIENT for IPPV L/min B Near Near 2–2.5× MV 2–2.5× MV Intermediate efficiency; FGF near patient means fresh gas is available at each inspiration patient patient but expired gas accumulates in the same reservoir C (Waters to- Near Near 2× MV 2× MV Similar to B; CO₂ absorber canister between bag and patient; dead space includes the and-fro) patient patient absorber; largely obsolete in modern practice D (Bain — Near Machine 2–3× MV 70–100 During SB: expired gas may be inhaled from the outer tube before FGF flushes it away — coaxial) patient end (bag) (10–15 mL/kg/min INEFFICIENT for SB (high FGF needed). For IPPV: controlled pattern allows efficient (via inner L/min) (5–7 L/min) flushing of expired gas during expiration → EFFICIENT for IPPV (low FGF sufficient) coaxial tube) E (Ayre's T- Near Open- 2.5–3× MV N/A (no bag No valve or bag; all expired gas vents freely through the expiratory limb; high FGF needed piece) patient ended for IPPV) to prevent rebreathing (must flush entire expiratory limb before next inspiration); simple, (lateral expiratory low-resistance; standard for neonates/infants spontaneously breathing limb) limb (no bag/APL) F (Jackson- Near Open- 2.5–3× MV Available Modification of E with open-ended bag allowing visual monitoring of breathing, manual Rees patient ended bag (manually IPPV, and CPAP; standard paediatric anaesthesia circuit; allows TPEF (total positive modification) on compress the expiratory flow) monitoring expiratory open-ended limb bag)

Key question: at the end of expiration, just before the next inspiration, which gas is positioned nearest to the patient — fresh gas or CO₂-rich expired alveolar gas?

Mapleson A during SB: FGF enters at the bag end (far from patient); during expiration, the patient exhales → dead space gas first (CO₂-free) → then alveolar gas (CO₂-rich); the alveolar gas pushes toward the patient-end APL valve, which vents it out; the fresh gas from the machine end fills the remaining space; at end-expiration, fresh gas + dead space gas are nearest the patient — essentially no CO₂ near the patient; next breath = minimal rebreathing; only needs FGF ≈ alveolar ventilation (3–5 L/min) to maintain this; MOST EFFICIENT for SB

Mapleson D (Bain) during SB: FGF enters at the patient end (via inner tube); expired gas fills the outer tube moving toward the bag; the FGF must flush the entire outer tube of expired gas during expiration before the next breath; if FGF is insufficient, the patient inhales expired gas from the nearest part of the outer tube — rebreathing; needs 2–3× MV to reliably flush; LEAST EFFICIENT for SB

Mapleson D (Bain) during IPPV: controlled pattern of expiration → predictable FGF flushing of the outer tube; lower FGF can maintain normocapnia; 70–100 mL/kg/min sufficient; EFFICIENT for IPPV

Coaxial design: inner tube carries FGF from machine end to patient end; outer corrugated tube carries expired gas from patient toward the machine-end bag/APL; counter-current heat exchange between inspired FGF (cooler) and expired gas (warmer) warms and humidifies inspired gas — an advantage over standard Mapleson D Pethick's test: mandatory pre-use safety check for inner tube integrity; occlude patient end → turn on FGF → reservoir bag should inflate (FGF is being delivered to the patient end, blocked, and fills the circuit); then release → bag should deflate (Venturi effect from FGF venturi draws the bag down); if bag does NOT inflate when occluded → inner tube disconnected (FGF not reaching patient end) → circuit unsafe → DO NOT USE

Applications: head and neck surgery (machine remote from the airway); long cases where inspiratory gas warming is beneficial; controlled ventilation where efficiency is highest; NOT ideal for spontaneous breathing cases (high FGF required)

Mapleson E (T-piece) for neonates and infants <10–15 kg under spontaneous breathing (low resistance, simple, lightweight) Mapleson F (Jackson-Rees) for manual IPPV and continuous monitoring of breathing in children; the open-ended bag provides visual confirmation of tidal volume and allows CPAP/PEEP application Adult circle system at >25–30 kg (when resistance of circle valves is proportionally less important and CO₂ absorption economics justify the setup)

Standard soda lime composition: Ca(OH)₂ (calcium hydroxide) ~80%; NaOH (sodium hydroxide) ~4%; KOH (potassium hydroxide) ~1%; SiO₂ (silica — hardening agent to reduce dust); water 14–19% (critical — desiccated absorbent is more reactive with volatile agents) Chemical reaction (two-step):

Step 1: CO₂ + H₂O → H₂CO₃ (carbonic acid forms in the water film on granules)

Step 2: H₂CO₃ + 2NaOH → Na₂CO₃ + 2H₂O; and H₂CO₃ + Ca(OH)₂ → CaCO₃ + 2H₂O

Net: CO₂ is neutralised; water and heat are produced (the canister becomes warm — indicates active absorption); Na₂CO₃ and CaCO₃ are the end products (the "spent" absorbent)

Capacity: 1 kg of soda lime absorbs approximately 100–120 L of CO₂ before exhaustion; each breath generates approximately 200 mL of CO₂ → a 1 kg canister lasts approximately 8–10 hours of normal use in a circle system

Conditions Favoring Byproduct Agent Mechanism Clinical Significance Formation Compound A Sevoflurane High temperature soda Sevoflurane + NaOH/KOH → Nephrotoxic in rats at 150+ ppm (high renal beta-lyase ONLY lime; DESSICATED base-catalysed beta-elimination activity); NOT clinically demonstrated in humans (10– absorbent; high sevoflurane → Compound A (fluoromethyl- 30× lower renal beta-lyase activity); FDA requires concentrations; low FGF 2,2-difluoro-1-[trifluoromethyl]vinyl minimum FGF 1 L/min with sevoflurane in US; Amsorb (less dilution) ether) Plus contains no NaOH/KOH → minimal Compound A generation Carbon Monoxide (CO) Desflurane DESSICATED soda lime Volatile agent haloalkyl groups + Clinically significant CO poisoning reported in patients; >> (critical — water content dessicated NaOH/KOH → CO COHb can reach 30–35% in severe cases; diagnosis Enflurane <5%); highest temperature production via free radical difficult — SpO₂ reads normally (not affected by >> Monday morning case mechanism; desflurane produces COHb); measured with co-oximetry on ABG Isoflurane (absorbent left with dry gas most CO (difluoromethyl ether (NOT flowing all weekend) group most reactive) sevoflurane, NOT halothane) Formaldehyde/Methanol Desflurane Severe dessication Further degradation products Theoretical toxicity; not prominently reported clinically + from desflurane dessicated absorbent

Feature Soda Lime Amsorb Plus Composition Ca(OH)₂ + NaOH/KOH + water Ca(OH)₂ + Ca(OH)₂ (no NaOH or KOH — no strong alkali); CaCl₂ + Ca(SO₄) hardening agents; water

Compound A Yes — NaOH/KOH catalyses Compound A Essentially ZERO — no strong alkali to catalyse beta-elimination; no FDA FGF minimum production from sevoflurane restriction needed with Amsorb Plus

CO production from Yes — dessicated NaOH/KOH reacts with Essentially ZERO — no strong alkali dessication desflurane/isoflurane → CO CO₂ absorption Slightly higher (NaOH/KOH contribute to Slightly lower CO₂ absorption capacity (pure calcium hydroxide less efficient); larger canister capacity absorption capacity) needed for equivalent capacity Cost Lower Higher; but the improved safety profile and elimination of toxic byproducts justifies the premium, particularly for sevoflurane and desflurane

Indicator dyes: ethyl violet (most common) — turns from colourless to VIOLET/PURPLE when the absorbent is exhausted (the rising CO₂ in the spent granules lowers local pH → activates the indicator); alternative: ethyl violet turns purple in acid → spent granules; some formulations use atropine red (red when fresh, colourless when spent)

Important limitation — colour regeneration: ethyl violet can regenerate (return to near-colourless) when the gas flow stops (resting in the dark); a canister that appears fresh may actually be exhausted — colour change cannot be relied upon as the SOLE indicator of absorbent exhaustion; use TIME-based replacement (replace after approximately 8–10 hours of clinical use, or based on ETCO₂ rise as the definitive functional indicator) Canister management: Never allow the absorbent to dessicate (do not leave high-flow dry gas flowing through the circuit when not in use — this is the "Monday morning phenomenon" that produces CO from desflurane)

Replace when: ≥50% of indicator has changed colour; ETCO₂ rises unexpectedly in the circle system; more than 8–10 hours of use Never pack the granules too tightly (prevents channelling of gas flow through the absorbent) Record date of installation; use the oldest canister first from storage

The CO₂ absorbent allows the circle system to operate at FGF as low as 0.35 L/min (metabolic flow) — essentially replacing only the O₂ consumed and the agent absorbed by the patient; at metabolic flow, volatile agent consumption falls by 80–90% compared to high-flow techniques; this dramatically reduces both cost (1 mL liquid sevoflurane = approximately £1.00; saving 30 mL per hour = £30/hour) and environmental volatile agent release

Volume/Capacity Definition Normal Value Measured By Tidal Volume (TV) Volume of one normal breath at rest 500 mL (7 Spirometry mL/kg) Inspiratory Reserve Volume Maximum additional volume inhaled after normal ~3000 mL Spirometry (IRV) inspiration Expiratory Reserve Volume Maximum volume exhaled after normal expiration ~1000 mL Spirometry (ERV) Residual Volume (RV) Volume remaining after maximum forced ~1200 mL NOT by spirometry — requires helium dilution, nitrogen expiration — CANNOT be exhaled washout, or body plethysmography Functional Residual Capacity Volume in the lungs at end of normal expiration — ~2200 mL Body plethysmography or gas dilution (NOT spirometry) (FRC = ERV + RV) the "resting lung volume" Total Lung Capacity (TLC = VC Maximum volume in the lungs after maximum ~6000 mL Plethysmography or gas dilution + RV) inspiration Vital Capacity (VC = IRV + TV + Maximum volume exhaled from maximum ~4500 mL Spirometry ERV) inspiration (~70 mL/kg) FEV1 Volume exhaled in the first second of a forced >80% Spirometry (forced) expiration from TLC predicted FEV1/FVC ratio The proportion of VC exhaled in the first second ≥0.70 (70%) Spirometry; FEV1/FVC <0.70 = OBSTRUCTION by ATS/ERS definition

Normal flow-volume loop: inspiration (bottom of loop) is effort-dependent and effort-independent portions; expiration (top of loop) shows a sharp early peak (maximum flow = PEF) followed by a linear decline down to RV; the loop shape depends on lung mechanics Pattern Flow-Volume Loop Appearance Spirometry Clinical Examples Obstructive Scooped/concave expiratory curve (reduced flow at low lung FEV1/FVC <0.70; FEV1 reduced more COPD; asthma (reversibility: ≥12% + 200 mL volumes); expiratory peak flow reduced; loop is wider (↑ RV) than FVC; RV ↑ (air trapping); TLC may FEV1 increase post-bronchodilator); and shorter (↓ VC); the characteristic "shark fin" appearance be ↑ (emphysema) or normal; FVC may emphysema; bronchiectasis with concave expiratory limb be ↓ in severe COPD Restrictive Smaller loop (all volumes reduced proportionally); normal FVC ↓; FEV1 ↓ proportionally; Pulmonary fibrosis; obesity (FRC falls below shape (expiratory limb straight, not scooped); peak flow may FEV1/FVC NORMAL or ↑ (preserved closing capacity); neuromuscular disease be normal relative to lung size; loop is narrower and shorter ratio); TLC <80% predicted (definitive (diaphragm weakness); chest wall deformity but proportionally similar shape to normal criterion for restriction); RV normal or ↓ (kyphoscoliosis); pleural disease Fixed upper Both inspiratory AND expiratory flow plateaus are truncated FEV1/FVC may be normal or mildly Fixed tracheal stenosis; foreign body; airway (flattened) — a "box shape" loop; the fixed obstruction limits abnormal; the specific flattened loop subglottic stenosis; bilateral vocal cord palsy obstruction both inspiratory and expiratory flow equally shape is diagnostic Variable Expiratory flow plateau only (during expiration, positive Characteristic asymmetric flattening of Tracheomalacia; intrathoracic tracheal intrathoracic pleural pressure collapses the obstruction further → worsens expiratory limb tumour obstruction flow limitation); normal inspiratory limb Variable Inspiratory flow plateau only (during inspiration, negative Characteristic asymmetric flattening of Vocal cord dysfunction; large goitre; extrathoracic pleural pressure draws the extrathoracic obstruction inward inspiratory limb extrathoracic tracheal tumour; unilateral obstruction → worsens flow limitation); normal expiratory limb vocal cord palsy

Definition: DLCO (Diffusing capacity for carbon monoxide) measures the ability of the alveolar-capillary membrane to transfer gas from the alveolus to the blood; measured by having the patient inhale a small amount of CO (non-toxic test concentration) and measuring how much is absorbed into the blood over a period; CO is used because it binds haemoglobin with very high affinity (200× O₂) → its uptake is entirely membrane and Hb-limited, not flow-limited

Normal: 25–30 mL/min/mmHg; expressed as % predicted (normal ≥75% predicted) Clinical significance:

Reduced DLCO: emphysema (loss of alveolar-capillary surface area); pulmonary fibrosis (↑ membrane thickness); pulmonary hypertension (↓ blood volume in capillaries); pulmonary haemorrhage (competing CO binding)

Elevated DLCO: polycythaemia (more Hb available for CO binding); pulmonary haemorrhage (blood in alveoli binds CO); left-to-right cardiac shunt (increased pulmonary blood flow) DLCO is the single best preoperative predictor of postoperative pulmonary complications and mortality after lung resection — superior to FEV1 alone; ppoDLCO <40% = very high risk regardless of FEV1

Predicted postoperative values (ppo): both ppoFEV1 and ppoDLCO must be calculated and must both exceed 40% predicted for resection to proceed safely

Formula: ppoFEV1% = preop FEV1% × [1 − (segments resected / total segments)]; total segments = 19 (right lung 10, left lung 9); e.g., right lower lobectomy = 5 segments: ppoFEV1 = FEV1% × (14/19) = FEV1% × 0.74

CPET (Cardiopulmonary Exercise Test): if ppoFEV1 or ppoDLCO <30–40% → CPET for further risk stratification; VO₂max >20 mL/kg/min → low risk; 10–20 → moderate risk; <10 → very high risk (likely inoperable) 6-minute walk test: surrogate for CPET if unavailable; <400 m → high risk; predicts post-resection outcomes

Direction Boundary Structure Clinical Notes Superior Fusion of periosteal dura and spinal dura at the foramen Epidural drugs cannot spread intracranially under normal conditions; high blocks can impair (cranial) magnum; the epidural space is a closed cavity cranially cranial nerve function if drug reaches cervical cord (but not intracranial) Inferior Sacrococcygeal membrane (sacral hiatus) — the natural Caudal block: sacral hiatus between sacral cornua; typically 5 mL LA for perineal surgery; 20 (caudal) termination of the spinal canal; accessed for caudal mL for lumbar anaesthesia in adults; 1 mL/kg in children epidural blocks Anterior Posterior longitudinal ligament covering the vertebral The anterior epidural space is narrow at the midline (epidural veins concentrate (ventral) bodies and intervertebral discs anterolaterally); catheter tip may impinge on the posterior longitudinal ligament anteriorly Posterior Ligamentum flavum (flavum = yellow; elastic, dense Loss of resistance technique targets the moment the needle tip exits the ligamentum flavum (dorsal) collagenous ligament connecting adjacent laminae); and into the epidural space; LF is thickest at L3–L4 (5–6 mm) and thinnest at C1 (1–1.5 mm) the posterior surface of the vertebral arch/laminae Lateral Pedicles of the vertebral arches and the intervertebral The lateral spread through intervertebral foramina is partially limited by the dural sleeve (bilateral) foramina; drug spreads laterally through the foramina to around each nerve root; elderly patients have calcified foramina reducing lateral leakage → surround exiting nerve roots more drug confined to the epidural space → wider spread per volume

Epidural fat: the primary content; distributed in lobules throughout the space; acts as a pharmacological depot — lipophilic drugs (opioids, particularly fentanyl and sufentanil) are taken up into epidural fat; acts as a physical spacer determining available volume for drug spread; reduced in elderly (less fat → more drug spreads per unit volume) Batson's venous plexus (epidural veins): an extensive valveless venous network of large, thin-walled veins lying predominantly anterolaterally within the epidural space; drain the spinal cord and vertebral column into the azygous, hemiazygous, and vertebral veins; valveless → blood flows in any direction depending on pressure gradients; during the Valsalva manoeuvre or in pregnancy (IVC compression → elevated epidural venous pressure → engorged veins → reduced epidural space volume → wider spread of same drug volume); veins are a source of significant risk during epidural catheter placement (catheter in vein → intravascular injection of LA → LAST)

Spinal nerve roots and dural sleeves: nerve roots pass laterally from the dural sac to the intervertebral foramina surrounded by dural sleeves (extensions of the dura); these are the primary site of LA uptake and block in epidural anaesthesia; the sleeves provide a surface for drug uptake and spread along the nerve

Radicular arteries: branches of the lumbar and intercostal arteries pass through the intervertebral foramina to supply the spinal cord; vascular injection of LA → immediate LAST; adrenaline in epidural solutions causes vasoconstriction of these vessels (decreasing LA systemic absorption and increasing block duration)

Plica mediana dorsalis: an inconstant fibrous median fold at the back of the epidural space that may divide it partially into two lateral compartments; can cause asymmetric or "one-sided" epidural blocks when a catheter tip is directed into one lateral compartment

The epidural space is a POTENTIAL space (the dura is normally pressed against the ligamentum flavum by the higher pressure in the subarachnoid space); it contains a small volume of fluid between the dural surface and the surrounding structures

Negative pressure: in most adults (particularly in the thoracic region), the epidural pressure is slightly negative relative to atmospheric pressure; mechanism: the dura is normally apposed to the surrounding structure by cerebrospinal fluid pressure + small negative epidural pressure; the negative pressure was the basis for the historical "hanging drop" technique (a drop of saline in the needle hub would be aspirated into the epidural space when the needle exits the LF) — less reliable than loss of resistance but still used by some clinicians

Pressure variation: epidural pressure rises with Valsalva, coughing, straining, and in pregnancy (engorged veins transmit pressure); abdominal compression during thoracic epidural catheter placement → veins engorge → increased risk of intravascular placement at that moment

Factor Effect on Spread Magnitude Volume of ↑ Volume → ↑ spread; THE MOST IMPORTANT FACTOR; rule of thumb: 1–1.5 mL per dermatome (segment) for adults Major — predominant injectate determinant Concentration Determines motor vs sensory block intensity but NOT spread; 0.1% bupivacaine → sensory only; 0.5% → motor + Minimal effect on spread Concentration Determines motor vs sensory block intensity but NOT spread; 0.1% bupivacaine → sensory only; 0.5% → motor + Minimal effect on spread sensory Age ↑ Age → ↑ spread per volume; elderly have reduced epidural fat, calcified foramina (less lateral leakage), and reduced Major — reduce dose 30– compliance of the space; same volume spreads ~2× further in a 70-year-old vs a 20-year-old 50% in elderly Pregnancy Engorged epidural veins (from IVC compression) → reduced epidural space volume → same volume spreads further; Major — well established reduce dose 25–30% in pregnant patients clinically Height Taller patients have larger epidural space → slightly less spread per volume; clinical effect modest Minor Weight/Obesity ↑ Intra-abdominal pressure → engorged epidural veins → reduced volume → wider spread; similar to pregnancy effect Moderate Site of Thoracic epidural spreads more cephalad than caudad from the injection point; lumbar epidural spreads more bilaterally Moderate — influences injection choice of insertion level Speed of Faster injection → slightly more turbulence → slightly wider spread; effect modest in clinical practice Minor injection Position of Gravity has modest effects on epidural drug spread (less than in spinal); lateral position → slightly more dependent side Minor for epidural (vs patient block; sitting position → sacral block more reliable major for spinal)

Dural puncture → CSF leak through the dural defect into the epidural space (at approximately 0.1–0.2 mL/min) → CSF volume in the subarachnoid space decreases → CSF pressure falls → the buoyant support of the brain in CSF is reduced → the brain descends slightly with gravity when upright → traction on pain-sensitive structures (the meningeal blood vessels, cranial nerves — particularly the trigeminal nerve = frontal/temporal headache, and the vagus and glossopharyngeal nerves = nausea and vomiting) → postural headache

The two mechanisms: (1) direct traction on pain-sensitive structures from CSF hypotension; (2) reflex cerebral vasodilation (adenosine-mediated) compensatory to the CSF loss — additional vascular headache component; the cerebral vasodilation component explains why caffeine (vasoconstrictor) provides partial temporary relief

IIH (intracranial pressure reduction): CSF pressure may fall from normal 10–15 cmH₂O to <5 cmH₂O; measured as "low opening pressure" on lumbar puncture

Risk Factor Effect Needle gauge Smaller gauge → smaller dural defect → less CSF leak → lower PDPH risk; 25G Whitacre: 1–2% PDPH; 22G Quincke: 25–30% PDPH; 16G

Tuohy (accidental ADP): 70–80% PDPH Needle type/design Pencil-point (Whitacre/Sprotte — separates rather than cuts dural fibres): much lower PDPH rate than cutting (Quincke); for equivalent gauge, pencil-point has 5× lower PDPH rate

Quincke bevel Bevel parallel to dural longitudinal fibres: lower PDPH rate (smaller functional defect); perpendicular: higher rate orientation

Age Young patients (especially obstetric population): high PDPH risk; elderly: lower risk (reduced CSF pressure and flow; more compliant meninges)

Gender Female: higher risk than male (hormonal differences and obstetric population); pregnancy further increases risk Previous PDPH Strong risk factor for recurrence — may reflect individual susceptibility in dural compliance Diagnostic criteria (IHS — International Headache Society): headache that develops within 5 days of dural puncture; worsens within 15 minutes of sitting/standing and resolves (or improves significantly) within 15 minutes of lying flat; accompanied by at least one of: neck stiffness, tinnitus, hypacusis, photophobia, nausea

Severity grades: mild (tolerated; no limitation of daily activities); moderate (limits daily activities; patient confined to bed part of the time); severe (complete bed rest; unable to ambulate); very severe (cranial nerve palsies — 6th nerve palsy from traction most common → diplopia)

Bed rest: lying flat relieves the headache by reversing the gravitational traction; but strict bed rest does NOT reduce the rate of EBP requirement or speed recovery — provide for comfort only

Analgesics: paracetamol 1 g QID; NSAIDs (ibuprofen 400 mg TID); simple analgesics for symptomatic relief while awaiting natural dural sealing

IV/oral hydration: adequate hydration supports CSF production; no evidence that supernormal hydration accelerates recovery

Caffeine: caffeine sodium benzoate 500 mg oral or IV; causes cerebral vasoconstriction (adenosine antagonist) → reduces the vascular component of PDPH → temporary partial relief (12–24 hours); does NOT seal the dural hole; approximately 70% of patients report temporary improvement; reassess at 24 hours — if still symptomatic, EBP should be discussed

ACTH/Cosyntropin: ACTH 1.5 IU/kg IV once → stimulates adrenal cortisol production → increases CSF production (aldosterone effect on choroid plexus); some trials showing modest benefit; not widely used

Sumatriptan: some evidence in case reports; not standard treatment

Reassurance: PDPH naturally resolves in most patients within 7–14 days as the dural hole heals; 85% of patients improve without EBP if managed conservatively for 14 days

Site of action: mu-opioid receptors (MOR) in the substantia gelatinosa (laminae I and II) of the dorsal horn; PRESYNAPTIC: opioid binds MOR on C/Aδ fibre terminals → ↓ Ca²⁺ influx → ↓ release of substance P, glutamate, CGRP → reduced nociceptive transmission; POSTSYNAPTIC: ↑ K⁺ conductance → hyperpolarisation → reduced responsiveness to nociceptive input The dual mechanism provides potent, segmental analgesia without affecting motor, sympathetic, or non-pain sensory modalities — the key clinical advantage over LA agents

Property Fentanyl (lipophilic, log P 4.05) Morphine (hydrophilic, log P 0.9) Onset 5–15 minutes (rapidly absorbed into spinal cord 30–60 minutes (slow diffusion through aqueous CSF) lipid) Duration 2–4 hours (rapid redistribution out of cord) 12–24 hours (persists in CSF; slow clearance)

CSF spread Minimal — absorbed before spreading rostrally Extensive — remains in CSF → bulk flow cephalad to brainstem

Delayed respiratory Minimal — early (0–4h) from systemic absorption HIGH RISK at 6–24 hours — morphine accumulates near respiratory centre in depression only medulla

Systemic vascular uptake High — much of epidural fentanyl is systemic, not Low — primarily spinal mechanism spinal IT dose (adult) 20–25 mcg added to spinal LA 100–300 mcg (100–150 mcg for CS; up to 300 mcg for major surgery) Epidural dose 50–100 mcg bolus; 2–4 mcg/mL infusion 2–4 mg epidural; 0.05–0.1 mg/mL infusion

Scenario Recommended Drug Dose Benefit Caesarean section Morphine 100–150 mcg + Fentanyl Added to hyperbaric bupivacaine 2 mL Morphine: 12–24h post-CS analgesia; Fentanyl: augments — IT 20–25 mcg intraoperative block quality Major orthopaedic Morphine 200–300 mcg Added to spinal LA 18–24h postoperative analgesia; reduces opioid surgery — IT requirements

Labour analgesia — Fentanyl 2 mcg/mL in dilute LA Bupivacaine 0.0625–0.1% + fentanyl 2 Walking epidural; dense block without motor impairment epidural mcg/mL at 5–10 mL/hr Post-thoracotomy — Fentanyl or sufentanil 0.5 mcg/mL in 5–8 mL/hr thoracic epidural infusion Facilitates extubation; reduces PPCs epidural ropivacaine 0.2%

Mechanism: morphine slowly migrates cephalad in CSF via bulk flow over 6–12 hours → reaches the fourth ventricle near the pre-Bötzinger complex (respiratory rhythm generator) → mu-receptor activation → ↓ respiratory drive → progressive hypoventilation → hypoxia

Risk factors: IT morphine >300 mcg; co-administered systemic opioids/sedatives; elderly; obesity/OSA; poor respiratory reserve

Mandatory monitoring: hourly RR and sedation score for 24 hours; SpO₂ monitoring; supplemental O₂ available; naloxone at bedside; monitored ward (HDU level)

Treatment: RR <8 or SpO₂ <90%: naloxone 0.04–0.4 mg IV titrated (start 0.04 mg increments to preserve analgesia); then naloxone infusion 2–5 mcg/kg/hr (morphine duration exceeds naloxone t½ of 45–90 min → re-narcotisation without infusion)

Pruritus: 50–100% incidence with IT morphine; direct MOR activation in trigeminal nucleus → facial and truncal itch; treat: ondansetron 4 mg IV (5-HT3 antagonism), nalbuphine 5–10 mg IV, or low-dose naloxone 0.04 mg IV

PONV: 20–40%; multimodal prophylaxis; ondansetron at emergence

Urinary retention: sacral MOR activation → detrusor relaxation; catheterise if symptomatic

At the supraclavicular level, the brachial plexus roots C5–T1 have formed into three TRUNKS: superior (C5–C6), middle (C7), inferior (C8–T1); they lie compactly as a cluster posterolateral to the subclavian artery, above the first rib, deep to the clavicle

Sonoanatomy: high-frequency linear probe (10–15 MHz) in the supraclavicular fossa, coronal oblique plane; the subclavian artery appears as a large pulsatile anechoic circle; the brachial plexus trunks appear as a "bunch of grapes" — hypoechoic cluster — posterolateral to the artery; the first rib is a bright hyperechoic line with acoustic shadow deep to the plexus; pleura visible just deep to the first rib The "corner pocket": the zone at the corner between the lateral border of the subclavian artery and the superior surface of the first rib; the inferior trunk (C8– T1 → ulnar nerve) sits specifically here; targeted injection in this corner ensures complete block of all three trunks including the ulnar nerve territory — the most commonly missed nerve with supraclavicular techniques

1. Patient supine, head turned 45° away; high-frequency probe in supraclavicular fossa; coronal oblique plane 2. In-plane needle approach lateral to medial; 22G 50 mm needle; advance toward the corner pocket first (lateral subclavian artery border + first rib superior surface) 3. Hydrolocation: 1–2 mL saline to confirm tip position (fluid surrounds inferior trunk in the corner; if fluid goes deep to first rib → withdraw — pleural puncture risk) 4. Inject 5–10 mL LA into the corner pocket (inferior trunk coverage); then reposition needle superiorly and inject 15–20 mL more to cover superior and middle trunks; total 20–30 mL 0.375% ropivacaine or 0.25% bupivacaine

Complication Incidence Mechanism Management Pneumothorax 4% landmark; <0.5% Pleura is immediately deep to the first rib — the deep margin of Small (<15%) — O₂ + observation; Large (>15%) or ultrasound-guided the injection target; needle past first rib → pleural puncture → symptomatic → chest drain; CXR if any respiratory delayed pneumothorax (may present 1–6 hours post-block) symptoms develop post-block Phrenic nerve 40–60% standard Phrenic nerve lies on the anterior scalene adjacent to the Clinically inconsequential with normal contralateral palsy volumes; 20–30% brachial plexus; LA spreads medially → baths the phrenic function; CONTRAINDICATED if: contralateral phrenic with reduced volumes nerve → ipsilateral hemidiaphragm paralysis → ↓ FVC 25% palsy, contralateral pneumonectomy, severe COPD (FEV1 (5–10 mL) <50%) Horner's 1–4% Stellate ganglion (T1 sympathetic) adjacent to plexus; LA Benign and self-limiting; reassure patient (warn them Syndrome spreads medially → sympathetic chain block → ipsilateral preoperatively) ptosis, miosis, anhidrosis LAST <1% with US Large LA volume adjacent to subclavian artery; intravascular Incremental injection with aspiration every 5 mL; LAST guidance injection protocol

Best for: surgery from the elbow to the hand; forearm fractures; wrist/hand surgery; more reliable than axillary block for elbow procedures (musculocutaneous nerve reliably blocked at this level); more reliable ulnar coverage than interscalene (with corner pocket technique)

Compared to interscalene: supraclavicular has less phrenic nerve palsy risk (though still 20–30%); better ulnar nerve coverage; less good for true shoulder surgery (interscalene preferred) Intercostobrachial nerve NOT covered (medial upper arm skin from T2); supplement with subcutaneous ring injection if medial arm tourniquet is planned

The interscalene groove lies between the anterior scalene muscle (anteriorly) and the middle scalene muscle (posteriorly); the brachial plexus roots C5, C6, and C7 exit the intervertebral foramina and enter this groove at approximately the C6 level (cricoid cartilage level)

Sonoanatomy — "traffic light sign": high-frequency linear probe transversely at C6 level; the three roots C5, C6, C7 appear as three hypoechoic oval structures stacked between the anterior and middle scalene muscles — resembling traffic lights; the vertebral artery is deep (anteromedial) and must be identified and avoided; the internal jugular vein and carotid artery are medial

Critical relation: the phrenic nerve (C3–C4–C5) lies directly on the ANTERIOR SURFACE of the anterior scalene at this level; any injection sufficient to block C5–C6 roots simultaneously bathes the adjacent phrenic nerve

The phrenic nerve forms from C3–C4–C5 roots and descends on the anterior surface of the anterior scalene muscle; at the C5–C6 interscalene level, the phrenic nerve is anatomically inseparable from the brachial plexus injection target — it lies on the muscle surface directly adjacent to the C5–C6 roots Any volume of LA sufficient to block C5–C6 (the primary targets) inevitably spreads anteriorly to the phrenic nerve; Urmey (Anesth Analg 1991) demonstrated by hemidiaphragm ultrasound that 100% of patients have ipsilateral hemidiaphragm paralysis after interscalene block regardless of technique or volume

Clinical consequence: ipsilateral hemidiaphragm paralysis → ↓ FVC ~25%; well tolerated in patients with normal contralateral function; catastrophic if contralateral reserve is limited

Contralateral phrenic nerve palsy (bilateral phrenic palsy → complete diaphragm paralysis → respiratory failure) Contralateral pneumonectomy (single functioning lung → loss of ipsilateral hemidiaphragm → severe compromise) Severe COPD (FEV1 <50% predicted) where 25% FVC reduction would cause respiratory failure Contralateral vocal cord paralysis (combined impairment) Local infection; coagulopathy; patient refusal

Procedure Block Role Total shoulder arthroplasty (TSA), Gold standard; complete shoulder anaesthesia; continuous catheter for 48–72h dramatically reduces opioid use and reverse TSA improves rehabilitation Shoulder arthroscopy (rotator cuff, Single-shot + GA or sedation; 6–12h post-op analgesia; beach chair positioning requires careful MAP management labrum) Clavicle fracture fixation May need supplemental superficial cervical plexus block (C3–C4) for medial clavicle skin not covered by brachial plexus Proximal humerus fractures Excellent coverage; continuous catheter; reduces pain and aids physiotherapy

Complication Mechanism / Management Horner's syndrome (1– Stellate ganglion (T1 sympathetic) adjacent → LA spread → ipsilateral ptosis, miosis, anhidrosis; benign, self-limiting; warn patient 4%) preoperatively Recurrent laryngeal Hoarseness and voice change; avoid bilateral interscalene in singers/voice professionals; self-limiting nerve palsy

Vertebral artery Catastrophic — even 1 mL IV → cerebral circulation → immediate seizure; deep anteromedial vessel; identify on ultrasound before needle injection insertion; always aspirate before injecting Spinal / epidural Needle through intervertebral foramen → intrathecal space → high or total spinal at cervical level → immediate respiratory arrest; use US injection guidance and advance cautiously; always aspirate

Boundaries: superior (inguinal ligament), lateral (sartorius), medial (adductor longus); floor: iliopsoas laterally + pectineus medially

Contents lateral to medial — NAVY: Nerve (femoral nerve), Artery (femoral artery), Vein (femoral vein), Y-fronts (lymphatics/lymph nodes) Femoral nerve (L2–L4) lies just lateral and slightly deep to the femoral artery; divides immediately below the inguinal ligament into anterior division (purely sensory — medial and intermediate cutaneous nerves of the thigh) and posterior division (saphenous nerve + motor branches to all four quadriceps heads)

A fascial tunnel in the middle third of the thigh; boundaries: roof = sartorius; lateral wall = vastus medialis; posteromedial wall = adductor longus then adductor magnus

Contents: saphenous nerve (PURELY SENSORY at this level — all motor branches to quadriceps have already branched off proximal to the canal); femoral artery; femoral vein; descending genicular artery

Key concept: the motor branches to the quadriceps (rectus femoris, vastus lateralis, vastus intermedius, vastus medialis) ALL originate within the femoral triangle or proximal thigh — ABOVE the adductor canal; the saphenous nerve within the canal is exclusively sensory

Feature Femoral Nerve Block (FNB) Adductor Canal Block (ACB) Target Entire femoral nerve in femoral triangle (motor + sensory Saphenous nerve within the adductor canal (sensory only at this level) branches)

Quadriceps motor COMPLETE — all four quadriceps heads paralysed; patient PRESERVED — motor branches all originate proximal to the canal; block cannot extend knee → cannot weight-bear safely completely unaffected Analgesia quality Excellent anterior knee; partial posterior knee Equivalent anterior and medial knee (same saphenous nerve territory); with for TKR IPACK for posterior → comprehensive coverage

Falls risk High — quadriceps weakness → falls documented in multiple Very low — normal quadriceps strength maintained studies Rehabilitation Delayed until block resolves (12–18h); physiotherapy postponed Day 1 physiotherapy achievable; reduces hospital LOS by ~1 day PROSPECT 2022 NOT recommended (motor weakness/falls) RECOMMENDED as primary block for TKR + IPACK for posterior knee recommendation

ACB technique: supine with thigh externally rotated; high-frequency probe at mid-thigh level; identify sartorius (superficial, triangular shape), femoral artery; saphenous nerve appears as a small hyperechoic oval adjacent to the artery within the fascial compartment; inject 15–20 mL 0.25–0.375% ropivacaine or 0.25% bupivacaine; visualise spread within the canal on ultrasound IPACK block (Infiltration between Popliteal Artery and Capsule of the Knee): complements ACB by covering the posterior knee capsule — popliteal branches of the sciatic, obturator, and genicular nerves; 15–20 mL LA injected posterior to the knee between the capsule and popliteal artery; performed at end of surgery under ultrasound or arthroscopically

Fascia Iliaca Block: large volume (40 mL) deep to fascia iliaca → spreads to femoral nerve, LFCN, sometimes obturator; landmark technique; used for hip fracture analgesia in ED by non-anaesthesiologists; less reliable for surgical anaesthesia

When the femoral nerve enters the femoral triangle below the inguinal ligament, its posterior division immediately starts giving off motor branches to the quadriceps: nerve to rectus femoris, nerve to vastus lateralis, nerve to vastus intermedius, and nerve to vastus medialis — ALL of these motor branches originate within the femoral triangle (above or at the level of the inguinal ligament); by the time the saphenous nerve (the sensory continuation of the posterior femoral nerve division) reaches the adductor canal, it has already lost ALL its motor branches and is purely sensory; therefore, an ACB at mid-thigh level blocks ONLY sensory afferents without any motor component