Anesthesia

Device Key Feature Sizes Specific Advantage Arndt Wire- Contains a wire loop at the tip that couples to the fiberoptic bronchoscope (FOB) — the FOB 5, 7, 9 Fr Most widely used; the wire-loop coupling Guided is threaded through the loop, then advanced under direct vision into the target bronchus; the makes bronchoscope-guided positioning Blocker blocker follows the bronchoscope and wire; once positioned, the wire is removed leaving the very reliable; 9 Fr has a large central channel lumen allowing CPAP to the operative lung Cohen Tip- A wheel mechanism at the proximal end deflects the blocker tip up to 90° in any direction — 9 Fr More directional control; useful when the Deflecting allows steering into the target bronchus under FOB vision; no need for wire coupling Arndt wire cannot reach the target bronchus; Blocker large central lumen for CPAP Fuji Pre-shaped curved tip; positioned under FOB guidance; no wire; simple design; the curve 5, 9 Fr Simplest design; can be used with any Uniblocker directs the blocker toward the target bronchus when rotated single-lumen ETT ≥7.5 mm ID; lower cost (Coopdech) EZ-Blocker A Y-shaped device with two cuffs — one for each main bronchus; inserted through the ETT Universal Can switch operative side quickly; positioned (Y-shaped) and positioned at the carina; one cuff is inflated to block the operative bronchus; allows at carina (very stable — rarely displaced); switching to block either side without FOB repositioning the Y-shape means it straddles the carina Torque Designed for paediatric use; smaller profile; positioned under FOB guidance Paediatric Provides OLV option in children where DLTs Control sizes are not available (<8 years, <30 kg) Blocker (Vitaid)

ETT size requirement: a standard single-lumen ETT of at least 7.5–8.0 mm ID is needed to accommodate both the bronchial blocker and the fiberoptic bronchoscope simultaneously (the FOB occupies ~4 mm; the blocker ~5–9 Fr); some centres use a dedicated multiport airway adapter that allows simultaneous passage of the blocker, bronchoscope, and ventilation circuit without circuit disconnection Step-by-step (Arndt wire-guided example): 1. Intubate with a ≥7.5 mm ETT; connect multiport adapter to ETT hub 2. Insert the Arndt blocker through the blocker port of the multiport adapter (blocker wire loop at the tip) 3. Insert the FOB through the bronchoscope port of the adapter; thread the FOB through the wire loop of the Arndt blocker 4. Advance the FOB under direct vision into the TARGET bronchus (left for left-sided surgery; right for right-sided surgery in most cases); once the FOB is in the correct bronchus, the blocker wire loop guides the blocker to follow the FOB into the same bronchus 5. Remove the FOB; inflate the blocker cuff with 5–8 mL air under direct FOB vision (re-insert FOB to confirm blocker position) — cuff inflated in the bronchus creates the seal for OLV 6. Remove the wire; ventilate the contralateral lung through the ETT lumen; the blocker allows the operative lung to collapse through passive resorption of gas through the inflated cuff

Feature Bronchial Blocker (via SLT) Double-Lumen Tube (DLT)

Ease of Easier overall — DLT requires specific technique; BB allows use of familiar SLT; FOB More complex; requires correctly-sized DLT (left DLT most insertion guidance ensures accuracy common — avoids right upper lobe orifice occlusion); DLT malposition is common Lung Adequate; but lung collapse takes LONGER (10–15 min via passive gas resorption vs 3– Faster lung collapse — the bronchial lumen can be actively isolation 5 min with DLT active venting) suctioned and the lung deflated; better surgical exposure quality more rapidly

Ability to Limited — the central lumen of the blocker is narrow (allows CPAP delivery but not Full suctioning capability through the bronchial lumen; can suction effective suctioning); cannot clear secretions from operative lung clear blood, secretions from operative lung operative lung

CPAP to Possible through the central lumen of larger blockers (9 Fr): apply 5 cmH₂O CPAP to the Possible through the bronchial lumen; same CPAP strategy operative partially collapsed operative lung to improve oxygenation available lung

Risk of HIGHER — the blocker can migrate proximally during surgical manipulation; Lower displacement risk once correctly secured; DLT is displacement displacement mid-surgery restores two-lung ventilation suddenly; displacement distally more rigid and secured at the ETT hub level can cause complete contralateral bronchial occlusion Preferred Difficult airway (use existing SLT); already intubated with SLT; children (no appropriate Elective thoracic surgery; rapid lung collapse needed; need clinical DLT size); tracheostomy; right upper lobe surgery (right-sided DLT risks RUL occlusion) for frequent intraoperative suctioning; most thoracic cases scenarios in adults Post-op Deflate cuff; remove blocker; leave SLT for post-op ventilation; can extubate from the SLT Must exchange DLT for SLT post-operatively if mechanical management directly ventilation needed (DLT is uncomfortable and highresistance for prolonged ventilation)

Risk Factor Higher Risk Lower Risk Device type Hollow-bore needle (higher volume blood inoculation — syringes, IV Solid needle (suture needle, lancet — less blood volume transferred) cannulae, blood gas needles) Depth of injury Deep puncture wound (needle passed completely through tissue) Superficial scratch

Visible blood on YES — visible blood increases viral inoculation volume No visible blood device Source patient High viral load (AIDS, untreated HIV, AIDS-defining illness, CD4 <200) Undetectable viral load on effective ART (extremely low risk — but viral load PEP still recommended) Exposure route Parenteral (needle/sharp); mucous membrane to high-titre blood Intact skin contact (essentially no risk) Bloodborne Transmission Risk (hollow-bore needle) Risk Modifiers Virus HIV ~0.3% (1 in 333) Deep injury + visible blood + high viral load → up to 0.9%; undetectable viral load → much lower but not zero HBV 6–30% depending on HBeAg status (HBeAg positive source = up to Highest risk of all three BBVs; vaccination provides near-complete protection 30%; HBeAg negative = 1–6%) HCV ~1.8% (1 in 55) No effective PEP or vaccine; higher risk if HCV RNA positive source

HBV Exposure HCW Vaccination Status Anti-HBs Titre Action Vaccinated and responder Anti-HBs ≥10 No action needed — fully protected; document and reassure mIU/mL Vaccinated but non-responder or <10 mIU/mL or Check anti-HBs titre immediately; if <10: HBIG 0.06 mL/kg IM + HBV booster dose simultaneously (in different unknown titre unknown sites); retest anti-HBs at 1–2 months Unvaccinated N/A HBIG 0.06 mL/kg IM within 24 hours of exposure (most effective within 12 hours) + initiate full HBV vaccination series (0, 1, 6 months) simultaneously HCV Exposure There is NO effective PEP for HCV and NO vaccine available

Management: baseline HCV antibody (anti-HCV) and HCV RNA at time of exposure; repeat HCV RNA at 4–6 weeks (HCV RNA becomes detectable 1–2 weeks after infection — earlier than antibody); repeat anti-HCV and ALT at 3 and 6 months

If HCV infection is confirmed (HCV RNA positive): refer to hepatologist; modern direct-acting antivirals (DAAs — sofosbuvir-based regimens) can achieve >95% SVR (sustained virological response = cure) when treatment is started in the acute phase (within weeks of infection); early treatment during acute HCV is the current management strategy

Follow-up Protocol (All BBVs)

HIV: HIV Ag/Ab (4th generation test) at baseline, 6 weeks, 3 months, 6 months post-exposure; if all negative at 6 months — exposure did not result in HIV infection

HBV: LFTs at baseline and 3 months; if HBV infection occurs — refer to hepatologist

HCV: as above; LFTs at baseline, 6 weeks, 3 months, 6 months

Counsel on risk reduction during the window period: use condoms, avoid blood donation, avoid breastfeeding, avoid sharing needles; advise on the meaning of the window period (infection may be present before tests become positive)

GOLD Stage FEV1 (% predicted) Anaesthetic Risk

I — Mild ≥80% Low; managed as routine

II — Moderate 50–79% Moderate; respiratory physiotherapy, bronchodilators, plan for regional if possible

III — Severe 30–49% High; aggressive preoperative optimisation, plan for postoperative HDU/ICU

IV — Very severe <30% Very high; multidisciplinary decision; consider alternatives to general anaesthesia; ICU post-op

Intervention Specific Action & Evidence Smoking Immediate cessation reduces carboxyhaemoglobin within 12 hours and improves mucociliary clearance within 2–4 weeks; maximum respiratory cessation benefit at 8 weeks (secretion production normalises); warn against "cutting back" — partial smoking cessation does not reduce PPC risk as much as complete cessation

Bronchodilators Optimise inhaler therapy: SABA (salbutamol MDI 100–200 mcg QID) + LABA (salmeterol 50 mcg BD) + LAMA (tiotropium 18 mcg OD); bronchodilators should be continued until morning of surgery with a sip of water; IV aminophylline if severe bronchoconstriction not responding to inhalers (monitor levels — narrow therapeutic index) Treat infection Course of oral or IV antibiotics if purulent sputum/fever — guided by sputum culture where possible; standard: amoxicillin-clavulanate or cotrimoxazole for community-acquired exacerbation Steroids Short course oral prednisolone 30–40 mg for 5 days for COPD exacerbation (GOLD Guidelines); then continue inhaled corticosteroids (budesonide/formoterol); stress dose steroids perioperatively (hydrocortisone 100 mg IV at induction) for patients on systemic steroids >2 weeks Chest Breathing exercises, incentive spirometry, postural drainage; reduces secretion retention and improves baseline lung function pre-operatively physiotherapy Pulmonary FEV1, FVC, FEV1/FVC ratio; if FEV1 <0.8 L → very high risk of post-op ventilatory failure; 6-minute walk test for functional capacity; ABG for CO₂ function tests retention (PaCO₂ >50 mmHg at rest = severe disease and high risk of post-op hypercapnic respiratory failure) Nutritional COPD + malnutrition = very high PPC risk; optimise nutrition if BMI <18 with supplemental enteral feeding pre-operatively status

Anaesthetic Technique Choice Regional anaesthesia preferred where feasible — epidural or spinal anaesthesia for abdominal surgery avoids airway manipulation, maintains spontaneous ventilation, provides excellent post-operative analgesia (reducing opioid need and splinting), and is associated with lower PPC rates than general anaesthesia

Laparoscopic radical cholecystectomy: requires GA (pneumoperitoneum + Trendelenburg not compatible with spontaneous ventilation); combine with epidural for analgesia

Open cholecystectomy: thoracic epidural (T6–T8) provides surgical anaesthesia ± sedation as an alternative to GA in selected cases; more commonly combined with GA for better intraoperative control Intraoperative Ventilator Settings for COPD

Intervention Evidence Epidural / regional analgesia Epidural analgesia reduces splinting → allows deep breathing and coughing → reduces atelectasis and pneumonia; continues for 48– post-operatively 72 hours post-op in major abdominal surgery Early mobilisation Sitting out of bed day 1 post-op → improves FRC and reduces atelectasis; nurse physiotherapist-supervised ambulation Incentive spirometry Pre- and post-operative deep breathing exercises reduce atelectasis rate by 30–50% NIV/CPAP readiness In GOLD III–IV patients: plan for NIV (BiPAP) prophylactically post-extubation; CPAP 5–8 cmH₂O + IPAP 12–16 cmH₂O in pressure support mode; reduces need for reintubation Minimise opioids Opioid-induced respiratory depression + cough suppression directly causes PPC; use multimodal analgesia (paracetamol + NSAIDs + epidural + regional) to minimise systemic opioid requirement ARISCAT risk stratification Use ARISCAT score preoperatively to predict PPC risk: includes age, SpO₂, anaemia, incision site, surgery duration, emergency status, respiratory infection

Known cause: irreversible structural brain injury (TBI, massive stroke, anoxic brain injury, hypoxic-ischaemic encephalopathy) — must be established; no unknown or reversible causes

Exclude reversible causes of coma: hypothermia (core temp must be ≥36°C); metabolic derangement (Na, glucose, ammonia within normal limits); drug intoxication (sedatives, neuromuscular blockers, barbiturates, alcohol — must have cleared; if uncertain, drug levels should be measured and/or a minimum of 4–5 half-lives must have elapsed)

Haemodynamic stability: MAP ≥60 mmHg; patient must not be in cardiovascular shock

Duration: in India, observation period of at least 6 hours from the onset of coma before first testing is recommended

Test Method Brain Dead Response GCS Standard assessment GCS = 3 (E1V1M1) — no eye opening, no verbal, no motor response to any stimulus Pupillary light Bright light in each eye Pupils fixed and dilated (4–9 mm); NO constriction to reflex light; tests CN II (afferent) and CN III (efferent — parasympathetic to iris sphincter) Corneal reflex Touch cornea gently with sterile cotton wisp No blink; tests CN V (afferent trigeminal) and CN VII (efferent facial nerve to orbicularis oculi) Oculocephalic Rapidly rotate head side-to-side (ONLY after cervical spine cleared); contraindicated if C- In brain death: eyes remain fixed and do NOT move — reflex (Doll's spine injury they move WITH the head (absent reflex); normally eyes eye) lag behind head movement (brisk reflex = intact brainstem) Oculovestibular Irrigate 50 mL ice cold water into each external auditory meatus (with head 30° elevated); Brain dead: no eye movement; normally produces tonic reflex (Cold observe for 1 minute deviation of eyes toward the irrigated side (brainstem caloric) intact); most sensitive brainstem test Gag reflex Stimulate posterior pharynx with suction catheter No gag; tests CN IX (afferent glossopharyngeal) and CN X (efferent vagus) Cough reflex Pass suction catheter to carina via ETT No cough — complete absence of cough response to tracheal suctioning Pain response Apply painful stimulus (supraorbital pressure, nail bed pressure) No motor response; spinal reflexes (limb withdrawal) may be present — these are spinal cord reflexes, NOT brainmediated, and do NOT exclude brain death Apnoea test Pre-oxygenate with 100% O₂ for 10 minutes; confirm PaCO₂ 35–45 mmHg; disconnect No respiratory effort at PaCO₂ ≥60 mmHg = confirms (most ventilator; deliver passive O₂ via catheter in trachea at 6 L/min; observe for respiratory absent respiratory drive = confirms brainstem death; important movements for 10 minutes; check ABG at end — PCO₂ must rise to ≥60 mmHg (or 20 abort test if SpO₂ <85%, haemodynamic instability, or single test) mmHg above baseline) cardiac arrhythmia

Brain Death Certification Committee (India) Under THO Act, brain death must be certified by a panel of four doctors: 1. Medical Administrator/Registered Medical Practitioner nominated by the hospital 2. Neurologist or Neurosurgeon 3. The treating doctor/intensivist 4. An independent doctor (not from the treating team)

Two sets of tests must be performed — first set, then a second set after an observation interval (minimum 6 hours from first set for adults; 24 hours for neonates/children). Both sets must confirm brain death. The time of death is certified at the time the second set of tests confirms brain death. The death certificate is then issued, and organ donation can proceed with family consent.

Investigation Finding in Brain Death When Used

EEG Electrocerebral silence — isoelectric (flat) EEG at maximum sensitivity When apnoea test cannot be performed (severe pulmonary (Electroencephalogram) for ≥30 minutes disease); drug intoxication suspected; medico-legal requirement CT/MRI Angiography Absence of intracranial blood flow — no filling of cerebral vessels Most specific — absence of cerebral circulation is definitive; above the skull base preferred confirmatory test in many guidelines Transcranial Doppler Reverberating flow or absent flow in the major intracranial arteries Bedside, non-invasive; widely available; reverberating flow = net (TCD) (MCA, ACA, PCA) — systolic spikes only, no forward diastolic flow zero flow = no cerebral circulation Radionuclide brain "Hollow skull sign" — isotope does not cross the blood-brain barrier into Highly specific; demonstrates absent cerebral blood flow and scan (99mTc HMPAO) brain parenchyma; only scalp uptake cellular metabolic activity SSEP (Somatosensory Bilateral absence of N20 cortical response (the cortical component is Useful when EEG unreliable; tests cortical function Evoked Potentials) absent bilaterally)

Difficult airway: the clinical situation in which a conventionally trained anaesthesiologist experiences difficulty with: (1) face mask ventilation; (2) direct laryngoscopy/intubation; or (3) supraglottic airway placement; or (4) surgical airway (cricothyrotomy)

Difficult mask ventilation (DMV): inability to maintain SpO₂ >90% or to prevent/reverse signs of inadequate ventilation during mask ventilation using 100% O₂ and positive pressure

Difficult laryngoscopy: inability to visualise any portion of the vocal cords with conventional laryngoscopy (Cormack-Lehane Grade III–IV)

Failed intubation: proper insertion of the ETT in the trachea cannot be achieved after multiple attempts

Test What It Assesses High-Risk Finding Sensitivity/Specificity Mallampati Pharyngeal space (size of tongue relative to pharyngeal opening); patient Class III (only soft palate visible) or IV Sensitivity ~50%, Specificity score opens mouth and protrudes tongue — no phonation (soft palate not visible): predicts difficult ~85%; poor alone but laryngoscopy valuable in combination Thyromental Distance from thyroid notch to chin in full neck extension; measures space <6.5 cm → difficult laryngoscopy; <6 cm Sensitivity ~50%, Specificity distance available for tongue displacement during laryngoscopy → strongly predictive ~80% (TMD) Sternomental Distance from sternum to chin in full extension; overall neck mobility <12.5 cm → reduced neck extension → Low sensitivity; useful in distance assessment difficult laryngoscopy combination Interincisor Distance between upper and lower incisors in maximum mouth opening <3 cm (two finger breadths) → restricted Specific but insensitive; gap (mouth mouth opening; limits laryngoscope important combined with opening) blade insertion other factors

ULBT (Upper Patient bites their upper lip with lower incisors: Class I = bite above Class III → likely difficult laryngoscopy; Sensitivity ~50%, Specificity Lip Bite Test) vermilion border, Class II = below, Class III = cannot bite at all — assesses better predictor than Mallampati in some ~85% mandibular prognathism and tongue space studies Neck Active flexion/extension range; atlanto-occipital extension; presence of Extension <80° of normal; cervical Important contextual movement collar/fusion/arthritis collar; rheumatoid C-spine instability assessment; cannot be (atlanto-axial subluxation risk) quantified easily LEMON L=Look externally; E=Evaluate 3-3-2 rule; M=Mallampati; O=Obstruction; Any LEMON component positive → Validated in ED setting; easy score N=Neck mobility anticipate difficulty; used in emergency to apply rapidly airway assessment The 3-3-2 Rule (LEMON "E") 3 fingers = interincisor gap (mouth opening); 3 fingers = hyoid-chin distance (mandibular space for tongue); 2 fingers = thyroid-floor of mouth distance (laryngeal height); any measurement less than the finger widths suggests a potentially difficult airway.

Plan Action Maximum Attempts Proceed If Plan A Direct laryngoscopy (DL) / Video laryngoscopy — optimise: HELP/BURP, 3 attempts maximum (including 1 SpO₂ maintained; can still ventilate bougie, different blade; videolaryngoscope if available; give 100% O₂; with an experienced colleague); after 3 by mask call for help after first failed attempt failed attempts → declare failed intubation → move to Plan B

Plan B Supraglottic airway device (SAD): 2nd generation SAD (i-gel or Proseal 2 SAD insertion attempts; if SAD fails Oxygenation maintained with SAD

LMA — better seal for positive pressure ventilation); use as conduit for → Plan C → use as conduit for FOI; if not → intubation via fibrescope Plan C

Plan C Face mask ventilation — 2-person technique (two-hand grip, jaw thrust, Maximum mask ventilation effort; if can Can maintain SpO₂ ≥90% → wake

Plan C Face mask ventilation — 2-person technique (two-hand grip, jaw thrust, Maximum mask ventilation effort; if can Can maintain SpO₂ ≥90% → wake +oral/nasal airway); attempt to maintain oxygenation while waking the maintain SpO₂ → wake up patient; if up patient; then consider options patient up (if not already paralysed or relaxant has worn off) CANNOT ventilate → CICO → Plan D (awake FOI, tracheostomy, LA technique, abort surgery)

Plan D — Front-of-Neck Access (FONA): scalpel-bougie-tube cricothyrotomy IMMEDIATELY — do NOT delay; this Always — CICO is immediately lifeCICO (DAS recommended technique); simultaneously give sugammadex 16 is a life-or-death emergency threatening; FONA must not be Emergency mg/kg IV if rocuronium was used; 4 mm Melker emergency delayed cricothyrotomy kit (scalpel or needle technique)

Indication: anticipated difficult airway (Mallampati IV, TMD <6 cm, cervical spine instability, obesity with obstructive airway, known previous difficult airway, upper airway mass or tumour); the patient who might lose their airway under GA must be intubated AWAKE Sedation protocol (cooperative sedation, not general anaesthesia): Glycopyrrolate 200 mcg IM 30 minutes before (dries secretions — improves visualisation; secretions coat the lens) Dexmedetomidine 1 mcg/kg over 10 minutes then 0.5–0.7 mcg/kg/hr infusion — produces cooperative sedation without respiratory depression; patient remains rousable and able to follow commands; maintains airway tone and reflexes Midazolam 1–2 mg IV (anxiolysis) ± fentanyl 1 mcg/kg IV (analgesia) — small doses only; avoid over-sedation which abolishes protective reflexes Topical anaesthesia of the airway (most important step):

Oropharynx: lidocaine spray 4% + gargle

Nasopharynx (nasal route): lidocaine gel 2% + vasoconstrictor (xylometazoline) in each nostril; co-phenylcaine spray

Supraglottic: transtracheal injection or spray-as-you-go (SAYGO) — lidocaine 4% 2–3 mL injected through the cricothyroid membrane or through the working channel of the bronchoscope as it advances Total lidocaine dose <9 mg/kg (using 4% — 1 mL = 40 mg; total <400 mg for 70 kg patient)

Technique: pass lubricated FOB through ETT (size 7.0 loaded on the scope); advance the FOB through the nasal or oral route under direct vision; identify the epiglottis, arytenoids, vocal cords; pass the FOB through the cords under direct vision; confirm tracheal rings and carina; railroad the ETT over the FOB into the trachea; remove FOB; confirm placement with ETCO₂ waveform; induce GA (propofol) only after ETT confirmed in trachea

Colour / Container Waste Category Treatment/Disposal Anaesthesia Examples YELLOW bag Human anatomical waste (tissues, organs); animal Incineration (temperature ≥1200°C) Bloody gauze swabs; blood-contaminated waste; microbiology waste; soiled waste (cotton, at CBWTF (Common Biomedical drapes; expired IV drugs; placenta (obstetric); gauze, bandages, gowns contaminated with Waste Treatment Facility); or deep surgical tissue specimens sent intraoperatively blood/body fluids); expired medicine burial in specific cases

RED bag Non-chlorinated plastic waste: IV tubing, IV bags, Chemical treatment + shredding + IV administration sets; Bain circuit; breathing catheters, single-use gloves (non-contaminated), urine recycling at authorised recycler; circuit components; LMA (single-use); face bags, oxygen masks, nasogastric tubes; any non- autoclave NOT used (risk of dioxin masks; suction catheters; ETT (after use); sharp plastic recyclable from patient care release from chlorinated plastics) syringe bodies (without needles)

WHITE/PUNCTURE- Sharps: needles, syringes with needles, lancets, Autoclave + shredding at CBWTF; or ALL needles (drawing up needles, IV cannula PROOF container blades, broken glass, glass ampoules encapsulation in cement; or needle needles, spinal needles, epidural Tuohy (Sharps bin) destruction in needle cutters needles, nerve block needles); scalpel blades; glass ampoules; broken glass vials BLUE bag/box Glassware (non-sharp), metallic implants Autoclave/microwave then disposal Empty glass drug vials (intact); glass syringes at municipal solid waste site or (if applicable) recycling

BLACK bag General municipal solid waste (non-biomedical): food Municipal solid waste disposal; no Uncontaminated outer drug packaging; waste, packaging materials NOT contaminated with special treatment needed newspaper; administrative paper waste; nonbody fluids, paper, office waste contaminated cardboard drug cartons

KEY RULE — Sharps NEVER in plastic bags; always in puncture-proof container The most common BMW violation in anaesthesia is discarding needles into soft plastic bags or bins — creating a needlestick injury risk for housekeeping staff. All sharps go ONLY into the labelled white puncture-proof sharps container. Fill to 75% capacity only; do not force needles in; never recap with two hands (one-handed scoop technique only).

Waste Type Container Special Consideration Expired anaesthetic drugs Yellow bag (expired Controlled substances (opioids) require specific documentation and destruction procedures under (propofol, fentanyl, muscle medicine) NDPS Act — witnessed destruction by two staff, signed register; cannot simply discard in yellow bag relaxants) without documentation Residual drug in Yellow bag for liquid, Red for Separate the needle from the syringe body before disposal; needle in white sharps bin; body in red bag syringes/vials plastic syringe body, White for needle

Used breathing circuits, Red bag Single-use circuits: red bag; reusable equipment (laryngoscope blades, handles, fiberscopes) require LMAs, ETTs proper sterilisation before reuse — contaminated items not BMW waste but infection control waste (decontamination) CO₂ absorbent (spent soda Yellow or black bag Soda lime directly in the breathing circuit — contaminated with exhaled patient air and humidity; treat lime) depending on patient contact as patient contact waste; yellow bag preferred level Vaporizer filling devices and Hazardous chemical waste — Spilled or expired volatile agents are hazardous chemical waste (flammable, environmental pollutant); halogenated liquid agent NOT BMW require specific chemical waste handling; NOT to be poured down drain

Term Definition Example in Anaesthesia Artificial The broad field of computer science dedicated to creating systems that perform Computer programs that interpret ECG rhythms, diagnose airway Intelligence tasks that would normally require human intelligence — reasoning, problem- images, or generate anaesthetic plans (AI) solving, learning, perception Machine A subset of AI where algorithms learn patterns from data without being explicitly An algorithm trained on thousands of hypotensive episodes learns Learning (ML) programmed with rules; the algorithm improves its performance with more data to predict the hemodynamic pattern before the event occurs and experience Deep A subset of ML using artificial neural networks with many layers (deep networks) Image recognition of airway anatomy on video laryngoscopy; Learning (DL) — most powerful for image recognition, speech, and complex pattern recognition recognition of EEG burst suppression patterns for depth of tasks anaesthesia monitoring Natural AI subset enabling machines to understand and process human language (text or Automated extraction of preoperative comorbidities from Language speech) unstructured clinical notes to populate risk scores; voice-activated Processing anaesthetic documentation (NLP)

Application System/Tool Evidence/Validation Hypotension Hypotension Prediction Index (HPI — Edwards Lifesciences): an ML algorithm that Multiple RCTs (HYPE trial) show HPI-guided Prediction analyses the arterial waveform in real-time and outputs a probability (0–100) of vasopressor use reduces duration and severity of intraoperative hypotension in the next 15 minutes; uses machine learning on >20 arterial intraoperative hypotension by 50–70%; now cleared by waveform features FDA and CE mark; available in Acumen IQ sensor Closed-loop SEDASYS (now withdrawn from market but concept continues); closed-loop propofol Multiple RCTs show closed-loop TIVA achieves better anaesthesia drug TIVA using BIS feedback — the algorithm automatically adjusts propofol infusion rate to BIS time-in-target than manual titration; closed-loop delivery maintain target BIS 40–60 without manual titration; closed-loop vasopressor systems vasopressor reduces hypotension time in trials (CLMA — phenylephrine titrated by ML algorithm to MAP target) Difficult airway ML algorithms trained on preoperative airway assessment data (Mallampati, TMD, BMI, Proof-of-concept; not yet clinical standard; accuracy prediction etc.) to predict difficult intubation probability; some systems use facial image analysis via superior to single clinical variables but not yet smartphone cameras validated at population level Preoperative risk ML-enhanced versions of ASA, ACS-NSQIP, and APACHE scoring — algorithms trained Multiple validation studies show ML risk scores scoring on large perioperative databases predict individualised mortality, ICU admission, and outperform traditional scoring on discrimination metrics complication probability more accurately than point-score calculators (AUC 0.85–0.92 vs 0.75–0.80 for conventional scores) Depth of Machine learning-based EEG analysis for depth of anaesthesia (Sedline, Masimo); AI AI-enhanced EEG depth monitoring commercially anaesthesia/brain interpretation of processed EEG spectrograms; burst-suppression detection algorithms; available; research phase for real-time awareness monitoring automated alerting for accidental awareness risk detection Postoperative ML algorithms predict PONV, delirium, readmission, and unplanned ICU admission in Several hospital-deployed systems; validation ongoing; outcome real-time during the intraoperative period using intraoperative vital sign patterns; NLP not yet standard practice prediction algorithms extract risk factors from preoperative notes

Black box problem: deep learning algorithms are not interpretable — they produce outputs without explaining their reasoning; clinicians cannot understand why the algorithm recommended a specific action; this reduces trust and makes error analysis difficult

Training data bias: algorithms trained on data from specific populations (predominantly Western, specific hospital systems) may perform poorly in different patient populations (Indian patients, paediatric, rare diseases); biased training data → biased (and potentially harmful) outputs

Regulatory approval: most AI/ML devices in anaesthesia are approved only as decision-support tools, not autonomous treatment systems; the clinician retains legal responsibility for all patient care decisions regardless of AI recommendation

Data privacy: AI systems require large datasets of patient information for training; ethical data governance, consent, and privacy regulations (DPDP Act India 2023; GDPR in Europe) must be complied with

Alert fatigue: AI systems that generate too many false-positive alerts (like all monitoring systems) can lead to alarm fatigue — the very real danger that clinicians learn to ignore AI warnings, including true positives

Fully autonomous closed-loop anaesthesia machines (induction + maintenance + emergence, all algorithm-controlled); currently regulatory frameworks prohibit fully autonomous administration without human oversight in most jurisdictions Preoperative AI-generated anaesthetic plans tailored to individual patient genomics, comorbidities, and predicted drug metabolism Real-time voice-activated anaesthetic documentation — NLP extracts and records events from the spoken intraoperative narrative without manual charting AI-assisted surgical team communication and cognitive load management — real-time situational awareness tools that alert the team to developing physiological trends

GWP (100Agent Atmospheric Lifetime Clinical Equivalent year, CO₂ = 1) Nitrous 265 114 years Also depletes stratospheric ozone; longest-persisting anaesthetic greenhouse gas — 1 L of N₂O delivered = Oxide (N₂O) 265 L CO₂ equivalent; used in huge volumes globally Isoflurane 510 3.2 years Medium impact; 1 L liquid isoflurane at 1 L/min FGF releases ~510 kg CO₂ eq over its lifetime Sevoflurane 130 1.1 years Lowest GWP of halogenated agents; preferred environmentally; short atmospheric lifetime Desflurane 2540 14 years Most potent greenhouse anaesthetic gas; 1 hour at 1 MAC, 2 L/min = driving 235 km; UK NHS banned desflurane from formulary in 2021; Australia, Canada, and several EU nations phasing out Propofol ~3.5 Metabolised — not The environmentally superior anaesthetic choice per MAC-hour; 97% less carbon footprint than desflurane (TIVA) (manufacturing exhaled into for equivalent anaesthesia time + disposal) atmosphere

Other contributors: single-use equipment manufacturing and disposal (anaesthesia circuits, LMAs, ETTs, gloves, syringes — lifecycle analysis shows a reusable LMA has 1/10th the carbon footprint of single-use equivalents over 40 uses); operating theatre energy consumption (3–6× normal hospital areas per m²); patient transport and building heating

N₂O infrastructure leakage: pipeline N₂O systems routinely leak 10–30% of delivered N₂O into the building atmosphere; reducing N₂O infrastructure use reduces both intentional and leak emissions

Strategy Impact & Evidence 1. Eliminate Single highest-impact action: switching from desflurane to sevoflurane for 1 hour at 2 L/min reduces CO₂ equivalent emissions by ~95%; UK NHS desflurane removed desflurane from national formulary 2021 citing lack of meaningful clinical advantage over sevoflurane combined with catastrophic environmental cost; at the individual clinical level — desflurane provides only marginally faster early emergence (5–10 min) vs sevoflurane, with no difference in actual PACU discharge time or patient outcomes 2. Low-flow / Fresh gas flow (FGF) directly determines volatile agent consumption and atmospheric release; reducing FGF from 4–6 L/min (high-flow) to 0.5–1 L/min minimal-flow (low-flow) in the circle system reduces volatile agent consumption by 70–80%; at metabolic flow (0.35 mL/min), only the patient's metabolic uptake is anaesthesia replaced; requires circle system with CO₂ absorber (not Bain circuit); simultaneously saves cost and reduces operating room pollution 3. TIVA (Total Propofol-based TIVA produces zero volatile greenhouse gas emissions; propofol is metabolised and excreted — not exhaled into atmosphere; the IV environmental cost is propofol manufacturing and packaging, substantially less per MAC-hour than volatile agents; TIVA is the "greenest" general Anaesthesia) anaesthetic option; growing advocacy for TIVA adoption on environmental grounds in addition to its established clinical benefits (reduced PONV, no MH triggering, no HPV inhibition) 4. Eliminate N₂O (GWP 265, atmospheric lifetime 114 years) also depletes stratospheric ozone; clinical alternatives exist for every indication (opioids provide or minimise analgesia; volatile agents provide hypnosis; ketamine provides dissociative anaesthesia); N₂O elimination from routine anaesthesia removes the longestN₂O lasting anaesthetic greenhouse gas; multiple centres have eliminated N₂O from their formulary without impact on patient outcomes 5. Regional Every regional technique (peripheral nerve block, neuraxial) that successfully avoids GA eliminates 100% of volatile agent emissions for that case; the anaesthesia "Regional First" philosophy aligns environmental sustainability with established clinical benefits (reduced opioid consumption, faster PACU discharge, preference lower PONV, superior analgesia); expanding regional anaesthesia is one of the most effective department-level environmental strategies ("Regional First") 6. Volatile Systems (SageTech MARU — Medical Agent Recovery Unit) that capture exhaled volatile agent from scavenging systems and reconstitute it into liquid agent capture form for reuse; pilot programmes in UK and Scandinavia demonstrating both environmental and economic benefit; requires regulatory framework for and recycling recycled agent use (quality assurance); prevents atmospheric release from scavenging exhaust 7. Reduce Where infection risk allows: use reusable LMAs (sterilised between cases — lifecycle analysis shows 90% reduction in carbon footprint vs single-use); single-use metal laryngoscope blades (sterilised) vs single-use plastic; reusable temperature probes; audit single-use vs reusable decisions against infection risk equipment evidence rather than defaulting to single-use for convenience

NHS Net Zero commitment (UK 2020): first national health system to commit to net-zero carbon by 2040; explicit desflurane ban (2021); anaesthesia sustainability targets in NHS contracts; green theatre champions programme

ESA Sustainability Task Force: green anaesthesia guidelines (2021); mandatory sustainability education in anaesthesia training programmes

India: desflurane is already rare in most Indian centres (cost-driven); sevoflurane predominates; formalising low-flow protocols and eliminating routine N₂O would meaningfully reduce Indian anaesthesia's carbon footprint without additional cost; TIVA availability expanding with propofol generic manufacturing

Individual anaesthesiologist: each anaesthesiologist makes hundreds of agent selection, FGF, and equipment choices annually — collectively determining a department's carbon footprint; professional responsibility now explicitly includes environmental stewardship in modern anaesthesia training frameworks

Infection: pathological process caused by microbial invasion of normally sterile tissue

Sepsis: life-threatening organ dysfunction caused by a dysregulated host response to infection; defined clinically as: suspected or confirmed infection + acute increase in SOFA score ≥2 points (indicating acute organ dysfunction); a SOFA score ≥2 is associated with >10% in-hospital mortality in the general ICU population

Septic shock: a subset of sepsis with circulatory, cellular, and metabolic dysfunction that is profound enough to substantially increase mortality; defined as: sepsis PLUS vasopressor requirement to maintain MAP ≥65 mmHg AND serum lactate >2 mmol/L despite adequate fluid resuscitation; hospital mortality for septic shock exceeds 40%

Quick SOFA (qSOFA): a bedside screening tool (not a diagnostic criterion) to identify patients outside the ICU at risk of sepsis: ≥2 of the following: altered mentation (GCS <15), RR ≥22/min, systolic BP ≤100 mmHg; qSOFA ≥2 → high risk of poor outcome → initiate full SOFA assessment and sepsis workup SOFA Parameter Score 0→4 Component Respiratory PaO₂/FiO₂ ratio ≥400 → 0; 300–399 → 1; 200–299 → 2; 100–199 + MV → 3; <100 + MV → 4 Coagulation Platelet count (×10³/ ≥150 → 0; 100–149 → 1; 50–99 → 2; 20–49 → 3; <20 → 4 μL) Hepatic Bilirubin (mg/dL) <1.2 → 0; 1.2–1.9 → 1; 2.0–5.9 → 2; 6.0–11.9 → 3; >12 → 4 Cardiovascular MAP/vasopressors MAP ≥70 → 0; MAP <70 → 1; Dopamine ≤5 or dobutamine → 2; Dopamine 5–15 or NE ≤0.1 → 3; Dopamine >15 or NE >0.1 → 4 CNS GCS 15 → 0; 13–14 → 1; 10–12 → 2; 6–9 → 3; <6 → 4 Renal Creatinine (mg/dL) / <1.2 → 0; 1.2–1.9 → 1; 2.0–3.4 → 2; 3.5–4.9 or UO<500 → 3; >5 or UO<200 → 4 UO

Pathogen (bacteria/virus/fungi) + host susceptibility → Pattern Recognition Receptors (PRRs: TLR-4 for LPS; NOD-like receptors) on innate immune cells → activation of NF-κB transcription factor → massive cytokine release (TNF-α, IL-1β, IL-6, IL-8 — the "cytokine storm") → systemic endothelial activation and injury → four simultaneous cascades producing multi-organ dysfunction: Cascade Mechanism Clinical Consequence Vascular NO overproduction (iNOS) → pathological vasodilation + increased vascular permeability; loss of Distributive shock: low MAP, high CO, low SVR; dysfunction vascular autoregulation; catecholamine resistance from downregulated adrenergic receptors warm extremities; relative hypotension despite high output Coagulation Endothelial injury + TF expression → thrombin generation → microthrombi in capillary beds → Microvascular occlusion → end-organ activation simultaneous consumption of clotting factors → fibrinolysis activation → DIC ischaemia despite normal/high CO; bleeding from factor depletion Mitochondrial Cytokines (TNF-α) + NO → inhibition of mitochondrial electron transport chain (Complex I and Rising lactate in the presence of normal or high dysfunction Complex IV) → cells cannot use oxygen even when delivered → aerobic glycolysis → lactate cardiac output; explains why improving cardiac (cytopathic production → Type B lactic acidosis in well-perfused tissue output does not always resolve lactate in hypoxia) advanced sepsis Immunoparalysis Initial hyperinflammation (cytokine storm) is followed by profound immunosuppression: Patients die of secondary nosocomial infections (late sepsis) lymphocyte apoptosis (programmed cell death), monocyte deactivation, T-cell exhaustion, HLA- (Candida, Aspergillus, reactivated CMV, MDR DR downregulation on monocytes → impaired pathogen clearance → secondary infections bacteria) rather than the original pathogen dominate late clinical course