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ANAESTHESIA EXAM ANSWERS

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Q1. Anatomy of the Airway and Tracheobronchial Tree - with Emphasis on Airway Management and Endotracheal Intubation

Introduction

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I. UPPER AIRWAY

A. Nasal Cavity

• Divided into right and left passages by the nasal septum (septal cartilage anteriorly; ethmoid + vomer posteriorly).
• Three turbinates (conchae) divide each passage into three meatuses. The inferior meatus is the preferred pathway for nasotracheal tubes and nasopharyngeal airways.
• Anaesthetic relevance: Nasal septum deviation is common - always assess and use the more patent nostril. Apply topical vasoconstrictors (xylometazoline/cocaine) before instrumentation to prevent epistaxis, as the mucosa is highly vascular.
• The roof is the cribriform plate - fragile; risk of intracranial entry if fractured (contraindication to nasotracheal intubation in basal skull fractures).
• Choanae are the posterior openings leading to the nasopharynx.

B. Oral Cavity

• Primary conduit for airway devices.
• Bounded by the tongue inferiorly and hard/soft palate superiorly.
• Adequate mouth opening requires rotation and subluxation of the temporomandibular joint (TMJ).
• Anaesthetic relevance: Interincisor distance (IID) >3 cm (2 fingerbreadths) is needed for comfortable laryngoscopy. IID <3 cm predicts difficult intubation.

C. Pharynx

1. Nasopharynx - behind the choanae; contains the adenoids; communicates with the eustachian tube. The posterior wall is where the nasopharyngeal airway rests.
2. Oropharynx - from soft palate to tip of epiglottis; contains the palatine tonsils and the base of tongue. The Mallampati classification assesses oropharyngeal structures to predict difficult intubation:
   • Class I: Soft palate, fauces, uvula, tonsillar pillars visible
   • Class II: Soft palate, fauces, uvula visible
   • Class III: Soft palate and base of uvula visible
   • Class IV: Soft palate not visible
3. Hypopharynx (laryngopharynx) - from epiglottis tip to the inferior border of the cricoid; leads to the oesophagus posteriorly and larynx anteriorly.

D. Larynx

• Located between the lower border of the thyroid and the upper border of the cricoid cartilage.
• Anaesthetic importance: Site of emergency cricothyrotomy (scalpel-bougie technique or surgical airway) in a "can't intubate, can't oxygenate" (CICO) scenario.

• The narrowest part of the adult larynx (in children it is the subglottic region/cricoid).
• The glottis is the opening between the true cords.
• The aryepiglottic folds form the lateral walls of the inlet.

• Superior laryngeal nerve (SLN) - branch of vagus; divides into:
  • Internal branch: sensory to the mucosa from epiglottis to vocal cords (target for SLN block)
  • External branch: motor to cricothyroid muscle
• Recurrent laryngeal nerve (RLN): Sensory below vocal cords + motor to all intrinsic laryngeal muscles except cricothyroid. Injured during thyroid surgery, causing hoarseness or stridor.
• Glossopharyngeal nerve (CN IX): Sensory to the posterior 1/3 of tongue, vallecula and posterior pharyngeal wall (target for glossopharyngeal nerve block or tonsillar pillar block).

1. Superior laryngeal nerve block - at the greater cornu of hyoid bone
2. Transtracheal (transcricothyroid) block - lidocaine injected through CTM, triggers cough and anaesthetises subglottic mucosa
3. Glossopharyngeal nerve block - suppresses gag reflex

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II. LOWER AIRWAY: TRACHEOBRONCHIAL TREE

A. Trachea

• Extends from the cricoid cartilage (C6) to the carina (T4-T5, angle of Louis/sternal angle).
• Length: 10-12 cm in adults; diameter: 1.5-2 cm.
• Composed of 16-20 C-shaped hyaline cartilage rings (open posteriorly); posterior wall is membranous (trachealis muscle).
• Anaesthetic relevance:
  • Cuff of the ETT should sit above the carina (usually 2-3 cm). Correct depth in adults: 21-23 cm at the lips in women, 23 cm in men (Orrit-Gupta rule: height in cm / 10 - 1).
  • The posterior membranous wall can be perforated by a stylet if excessively rigid.
  • Tracheomalacia or extrinsic compression (goitre, mediastinal mass) can cause post-extubation collapse.

B. Carina (T4)

• The keel-shaped ridge where the trachea divides into two main bronchi.
• Anaesthetic relevance: The carina should be confirmed to be below the ETT tip on CXR. Carina stimulation causes bronchospasm or coughing.

C. Right Main Bronchus

• Length: 2.5 cm; Angle: 25° from the midline (more vertical).
• Wider and more vertical - ETT or foreign bodies preferentially enter the right side.
• Divides into: Right upper (RUB), right middle (RMB), right lower (RLB) lobe bronchi.
• The right upper lobe bronchus originates close to the carina (~2.5 cm).

D. Left Main Bronchus

• Length: 5 cm; Angle: 45° from the midline (more horizontal).
• Longer - gives more margin before endobronchial intubation.
• Divides into: Left upper and left lower lobe bronchi.
• Importance for one-lung ventilation (OLV): Left-sided double-lumen tubes are preferred because the longer left bronchus allows safer positioning without occluding the left upper lobe.

E. Segmental Bronchi and Beyond

• Each lobe bronchus divides into segmental bronchi (tertiary bronchi): 10 on right, 8-10 on left.
• Further: subsegmental bronchi -> bronchioles (no cartilage, <1 mm) -> terminal bronchioles -> respiratory bronchioles -> alveolar ducts -> alveoli.
• Conducting zone: Trachea to terminal bronchioles (anatomical dead space ~150 mL).
• Respiratory zone: Respiratory bronchioles onward (gas exchange).

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III. KEY AIRWAY ASSESSMENT TOOLS

IV. SNIFFING POSITION

• Flexion of the lower cervical spine + extension of the atlantooccipital joint.
• Aligns oral, pharyngeal, and laryngeal axes to provide a straight line of sight to the glottis.

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Q2. Regulation of Cerebral Blood Flow, Factors Affecting ICP Perioperatively, and Methods to Decrease ICP

I. CEREBRAL BLOOD FLOW (CBF) - REGULATION

A. Cerebral Perfusion Pressure (CPP)

• Normal CPP: 70-100 mmHg; Target in neurosurgical patients: >60-70 mmHg
• Normal ICP: 5-15 mmHg; Normal MAP: 90-110 mmHg

B. Cerebral Autoregulation

• CBF is maintained constant (~50 mL/100g/min) over a MAP range of 60-150 mmHg through changes in cerebrovascular resistance.
• Mechanism: myogenic (Bayliss effect) + neurogenic + metabolic.
• Autoregulation is lost in: Head injury, severe hypoxia, hypercapnia, volatile anaesthetic agents (dose-dependent), and cerebral vasospasm.
• In chronic hypertension, the autoregulation curve shifts rightward (limits: 110-180 mmHg).

C. Chemical/Metabolic Regulation (most important)

1. Carbon dioxide (PaCO2): Most potent regulator.
   • PaCO2 ↑ → cerebral vasodilation → CBF ↑ (CBF changes ~4% per 1 mmHg change in PaCO2).
   • Hypocapnia (PaCO2 30-35 mmHg) → vasoconstriction → CBF ↓ → used to reduce ICP intraoperatively.
   • Mechanism: CO2 + H2O → H2CO3 → H+ → acts on perivascular pH sensors.
2. Oxygen (PaO2):
   • PaO2 <50 mmHg → significant cerebral vasodilation → CBF ↑.
   • Hyperoxia has minimal effect on normal CBF.
3. pH: Acidosis → vasodilation; Alkalosis → vasoconstriction (same as CO2 effect).
4. CMRO2 (metabolic coupling): Neuronal activity ↑ → local metabolite accumulation (CO2, H+, K+, adenosine) → localised vasodilation → CBF ↑ ("neurovascular coupling").

D. Neurogenic Regulation

• Sympathetic: NE → vasoconstriction (less important at normal BP; important at very high MAP to prevent "breakthrough" hyperperfusion).
• Parasympathetic: ACh/VIP → vasodilation.
• Intrinsic (perivascular neurons): modulate local flow.

E. Temperature

• CBF decreases ~5-7% per 1°C decrease in temperature.
• Hypothermia reduces CMRO2 → reduced CBF → used for brain protection.

F. Effect of Anaesthetic Agents on CBF

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II. FACTORS AFFECTING INTRACRANIAL PRESSURE PERIOPERATIVELY

A. Preoperative/Patient factors

• Intracranial mass lesion (tumour, haematoma, abscess)
• Cerebral oedema (cytotoxic or vasogenic)
• Hydrocephalus
• Hyponatraemia (cerebral swelling)
• Chronic hypertension (impaired autoregulation)

B. Intraoperative factors that raise ICP

1. Positioning: Trendelenburg position, head-down tilt, head rotation/flexion → impedes venous drainage → ICP ↑.
2. Airway/Ventilation: Hypercapnia, hypoxia, Valsalva (straining, coughing, laryngospasm) → ICP ↑. PEEP → ↓ venous return → ↑ ICP.
3. Anaesthetic agents: Volatile agents (halothane > isoflurane > desflurane/sevoflurane), ketamine, N2O.
4. Hypertension: Breakthrough hyperperfusion if MAP >150 mmHg with lost autoregulation.
5. Laryngoscopy/Intubation: Stimulation → sympathetic surge → transient ICP rise.
6. Fluid overload: Free water (hypotonic fluids, 5% dextrose) → hyponatraemia → cerebral oedema.
7. Hyperthermia: Increases CMRO2 → CBF ↑ → ICP ↑.

C. Postoperative factors

• Airway obstruction → hypercapnia
• Agitation/pain → hypertension → raised ICP
• Haematoma formation at surgical site
• Inappropriate posture

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III. METHODS TO DECREASE ICP

A. Positioning

• Head end elevated 15-30° - improves venous drainage without compromising CPP.
• Head in midline neutral position - avoids jugular vein compression.

B. Hyperventilation

• Target PaCO2: 30-35 mmHg (mild hypocapnia).
• Mechanism: ↓PaCO2 → cerebral vasoconstriction → ↓CBV → ↓ICP.
• Limitation: Prolonged hyperventilation causes tissue hypoxia (Bohr effect, vasoconstriction); not sustained beyond 24 hours as pH normalises.

C. Osmotherapy

1. Mannitol (0.25-1 g/kg IV): Osmotic diuretic; draws water from brain into plasma. Onset 10-20 min; duration 4-6 hours. Must monitor serum osmolality (keep <320 mOsm/L). Also a free radical scavenger.
2. Hypertonic saline (3% NaCl): Reduces cerebral oedema; may maintain CPP better than mannitol; effective in traumatic brain injury. Na+ goal: 145-155 mEq/L.

D. CSF Drainage

• External ventricular drain (EVD) or lumbar drain.
• Provides direct measurement of ICP + therapeutic drainage.

E. Anaesthetic Technique

• TIVA with propofol preferred for intracranial surgery (reduces CBF and CMRO2, no cerebral vasodilation).
• Avoid ketamine, halothane.
• Moderate hypocapnia with controlled ventilation.

F. Corticosteroids

• Dexamethasone (0.1 mg/kg, then 4 mg 6-hourly): Effective for vasogenic oedema (peritumoural); NOT effective for cytotoxic oedema (post-infarct, TBI).

G. Barbiturate Coma

• Thiopentone infusion: reduces CMRO2 and CBF → reduces ICP.
• Used for refractory ICP; requires EEG monitoring (burst suppression).

H. Temperature Control

• Targeted temperature management (32-34°C): reduces CMRO2 and CBF.
• Fever worsens ICP - treat aggressively.

I. Surgical Decompression

• Decompressive craniectomy for refractory raised ICP (e.g., malignant MCA infarction, TBI).

J. Miscellaneous

• Treat pain and agitation (avoid coughing, Valsalva).
• Seizure prophylaxis/treatment (seizures dramatically increase CMRO2).
• Avoid hypotonic fluids; use isotonic saline or balanced solutions.
• Diuretics (frusemide) as adjunct to mannitol.

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Q3. Working Principle of Pulse Oximetry and Factors Affecting Accuracy

I. PRINCIPLE OF PULSE OXIMETRY

A. Beer-Lambert Law

• The absorbance of light by a solution is proportional to the concentration of the absorbing substance and the path length through which light travels.
• A = ε × c × l (A = absorbance, ε = extinction coefficient, c = concentration, l = path length).

B. Spectrophotometry - Differential Light Absorption

• Oxyhaemoglobin (OxyHb) and deoxyhaemoglobin (DeoxyHb) absorb light differently at two wavelengths:
  • Red light (660 nm): DeoxyHb absorbs much more than OxyHb.
  • Infrared light (940 nm): OxyHb absorbs much more than DeoxyHb.
• The pulse oximeter probe emits these two wavelengths through the tissue and a photodetector measures transmitted light.

C. Pulsatile Signal (Plethysmography)

• The key innovation: the pulse oximeter analyses only the pulsatile (AC) component of the light signal, which corresponds to arterial blood.
• The non-pulsatile (DC) component represents venous blood, tissue, bone, and skin - these are subtracted.
• The ratio R = (AC660/DC660) / (AC940/DC940) is calculated.
• This ratio is compared to an empirical calibration curve (derived from healthy volunteers breathing hypoxic mixtures) to give SpO2.
• R = 1 corresponds to ~SpO2 85%; R <1 → higher SpO2; R >1 → lower SpO2.

D. Display

• SpO2 (peripheral oxygen saturation) is displayed as a percentage.
• Also displays a plethysmographic waveform (photoplethysmogram - PPG) and pulse rate.
• Normal SpO2: 95-100%.

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II. FACTORS AFFECTING ACCURACY OF PULSE OXIMETRY

A. Dyshemoglobins (most important clinical error)

1. Carboxyhaemoglobin (COHb): Absorbs light at 660 nm similar to OxyHb → pulse oximeter reads COHb as OxyHb → falsely HIGH SpO2 (typically reads ~98% even in CO poisoning).
2. Methaemoglobin (MetHb): Absorbs equally at both wavelengths → R→1 → SpO2 driven toward ~85% regardless of true saturation. In high MetHb, SpO2 reads ~85% even when patient is hypoxic or normoxic.
3. Fetal haemoglobin (HbF): Has similar absorption to HbA; little clinical effect on standard pulse oximeters.

B. Intravascular Dyes

• Methylene blue, indocyanine green, indigo carmine: Absorb at 660 nm → falsely LOW SpO2 reading (transient, ~1-2 min).
• Isosulfan blue: Similar effect.

C. Nail Polish / Pigmentation

• Dark nail polish (blue, black, green) absorbs at 660 nm → falsely low SpO2.
• Placing probe sideways on the finger may help.
• Dark skin pigmentation: Modern pulse oximeters corrected for this; older ones may slightly overestimate SpO2 in dark-skinned patients.

D. Motion Artefact

• Patient movement, shivering causes erratic AC signal → unreliable readings.
• New pulse oximeters (Masimo Radical) use signal extraction technology (SET) to filter motion artefact.

E. Poor Peripheral Perfusion / Vasoconstriction

• Hypotension, hypothermia, vasopressor use (vasoconstriction) → weak pulsatile signal → unreliable or no reading.
• Solution: Use forehead, ear, or nasal alar probes (better perfused).

F. Anaemia

• Severe anaemia: The device can still measure the ratio of HbO2/Hb accurately as long as there is a pulsatile signal. However, in profound anaemia, the absolute oxygen content delivered may be critically low despite normal SpO2.

G. Venous Pulsation

• Tricuspid regurgitation → pulsatile venous blood → includes venous saturation in reading → falsely LOW SpO2.

H. Ambient Light Interference

• Strong fluorescent lights, infrared warming lights, fibreoptic surgical lights can interfere.
• Shield the probe from ambient light.

I. Electrosurgical Interference

• Diathermy/electrocautery causes electromagnetic interference → erratic SpO2 readings.

J. Physiological Lag

• SpO2 lags behind arterial desaturation by 30-60 seconds (ear probe fastest, finger probe slowest).
• Ear probe has shorter lag than finger probe.

K. SpO2 Accuracy Limits

• Calibrated between 70-100% SpO2; below 70% SpO2 is extrapolated and unreliable.
• Standard pulse oximetry cannot distinguish between different Hb species beyond two (co-oximetry required for full analysis).

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Q4. Classification of Antihypertensive Agents, Mechanism of Action, and Management of Hypertension in FESS

I. CLASSIFICATION AND MECHANISM OF ACTION

A. DIURETICS

B. RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM (RAAS) BLOCKERS

C. CALCIUM CHANNEL BLOCKERS (CCBs)

D. SYMPATHOPLEGIC (ADRENERGIC BLOCKING) AGENTS

• Methyldopa: Converted to α-methylnorepinephrine → acts on α2 receptors in CNS → ↓sympathetic outflow → ↓BP. Drug of choice in pregnancy.
• Clonidine: α2 agonist centrally → ↓sympathetic tone. Also used for premedication, opioid withdrawal.
• Moxonidine: Imidazoline receptor agonist.

• Trimethaphan: Blocks nicotinic receptors at autonomic ganglia → ↓sympathetic and parasympathetic tone. Used for controlled hypotension.

• Mechanism: Block β1 receptors → ↓heart rate → ↓cardiac output → ↓BP. Some also block β2 (non-selective).
• Also ↓renin release (β1 receptor in juxtaglomerular cells).
• Selective (β1): Atenolol, Metoprolol, Bisoprolol.
• Non-selective: Propranolol, Nadolol.
• With α blocking: Carvedilol, Labetalol (IV preferred for hypertensive emergencies, pregnancy).

• Mechanism: Block postsynaptic α1 receptors → vasodilation.
• Examples: Prazosin, Doxazosin, Terazosin.
• Used also for BPH.
• Side effect: First-dose hypotension (orthostatic).

E. DIRECT VASODILATORS

F. NEWER AGENTS

• Sacubitril/Valsartan (ARNi): Neprilysin inhibitor + ARB; for heart failure with hypertension.
• Azilsartan, Fimasartan: Newer ARBs.
• Clevidipine: Ultra-short-acting CCB (IV); for perioperative hypertension.

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II. MANAGEMENT OF HYPERTENSION IN AN ADULT MALE PATIENT POSTED FOR FESS (Functional Endoscopic Sinus Surgery)

A. Preoperative Assessment

1. Full history: Duration, severity, medications (especially ACE inhibitors, ARBs, beta-blockers), end-organ damage.
2. BP optimization: JNC guidelines - BP should be <160/100 mmHg before elective surgery; ideally <140/90.
3. Continue antihypertensives on the day of surgery (except ACE inhibitors/ARBs which may be held 24 h before surgery to prevent refractory intraoperative hypotension).
4. Investigations: ECG, echo if indicated, renal function, electrolytes.
5. End-organ assessment: LVH, renal function, fundoscopy if severe.

B. Anaesthetic Goals for FESS

• Maintain a "deliberate/controlled hypotension" with MAP of 50-65 mmHg (reduces intraoperative bleeding = "hypotensive anaesthesia").
• Mean arterial pressure (MAP): Target 60-70 mmHg intraoperatively.

C. Premedication

• Continue beta-blockers, CCBs.
• Anxiolytic premedication (midazolam) reduces anxiety-driven hypertension.
• Betablocker (esmolol/metoprolol) IV can be used intraoperatively.

D. Induction

• Smooth induction to blunt laryngoscopy response:
  • Fentanyl 2-3 mcg/kg IV 3 min before laryngoscopy.
  • Lignocaine 1.5 mg/kg IV (attenuates sympathetic response).
  • Propofol titrated slowly for induction (reduces BP).
• Avoid ketamine (raises BP, ICP).
• Secure airway with ETT (better than LMA for FESS as surgical field is near the airway).

E. Maintenance (Techniques for Hypotensive Anaesthesia)

1. Reverse Trendelenburg (head-up tilt 15-30°): Reduces venous pressure in the head, decreases mucosal congestion.
2. Volatile anaesthetics: Isoflurane/Sevoflurane with moderate concentrations (1-1.5 MAC) cause dose-dependent hypotension.
3. Beta-blockers: Esmolol infusion (25-200 mcg/kg/min) - titratable; reduces heart rate and BP.
4. Remifentanil infusion: Powerful opioid with rapid offset; reduces sympathetic tone; excellent for FESS.
5. Local anaesthesia by surgeon: Surgeon infiltrates with lignocaine + 1:200,000 adrenaline for vasoconstriction.
6. TIVA (Total Intravenous Anaesthesia): Propofol + Remifentanil TIVA is the gold standard for FESS; better control, faster wake-up, reduced nausea.
7. Calcium channel blockers: Nicardipine IV or Clevidipine (0.5-3 mcg/kg/min) can be used.
8. Magnesium sulphate: 40-50 mg/kg loading, then infusion - blocks Ca2+ channels + NMDA receptors → hypotension + reduced blood loss.
9. Clonidine/Dexmedetomidine: Reduces sympathetic tone, decreases anaesthetic requirements.

F. Ventilation

• Maintain normocapnia (PaCO2 35-40 mmHg) or mild hypocapnia.
• Avoid hypercapnia (raises BP and HR).

G. Monitoring

• Continuous BP (arterial line in severe hypertensives), ECG, SpO2, ETCO2.
• Urine output.

H. Emergence and Postoperative

• Smooth extubation: Deep extubation or IV lignocaine 1.5 mg/kg to prevent coughing/hypertension.
• Pain control: NSAIDs and opioids as needed.
• Resume regular antihypertensives.
• Monitor for postoperative hypertension, bleeding, orbital haematoma.

I. Avoid in FESS

• Excessive PEEP (increases venous pressure → increases bleeding).
• Coughing/straining.
• N2O (distends cavities; use 100% O2 or O2/air).

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Q5. Anatomy of Brachial Plexus, Approaches for Block, and Management of LAST

I. ANATOMY OF BRACHIAL PLEXUS

Formation: Roots → Trunks → Divisions → Cords → Branches

Five terminal branches (MBUMA):

1. Musculocutaneous nerve (C5-C7) - from lateral cord; pierces coracobrachialis; supplies biceps, coracobrachialis, brachialis; sensory - lateral forearm (lateral cutaneous nerve of forearm).
2. Median nerve (C5-T1) - from lateral + medial cords; supplies forearm flexors (except FCU and medial FDP), thenar muscles (LOAF: Lateral 2 lumbricals, Opponens pollicis, Abductor pollicis brevis, Flexor pollicis brevis).
3. Ulnar nerve (C8-T1) - from medial cord; supplies FCU, medial FDP, hypothenar muscles, interossei, medial 2 lumbricals.
4. Radial nerve (C5-T1) - from posterior cord; passes through spiral groove; supplies all extensors; sensory - posterior arm, forearm, dorsal hand.
5. Axillary nerve (C5-C6) - from posterior cord; passes through quadrilateral space; supplies deltoid and teres minor; sensory - regimental badge area.

• Dorsal scapular nerve (C5) - rhomboids, levator scapulae
• Long thoracic nerve (C5-C7) - serratus anterior (injury: winged scapula)
• Suprascapular nerve (C5-C6) - supraspinatus, infraspinatus
• Medial cutaneous nerves of arm and forearm

• The brachial plexus is enclosed in the axillary sheath (derived from prevertebral fascia) along with the axillary/subclavian artery and vein.
• At the interscalene level, the plexus lies between scalenus anterior (medially) and scalenus medius (posteriorly), lateral to the carotid artery and internal jugular vein.
• The dome of the pleura lies adjacent to the brachial plexus at the root level - risk of pneumothorax.

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II. APPROACHES TO BRACHIAL PLEXUS BLOCK

1. Interscalene Block

• Position: Lateral head rotation to opposite side; needle at C6 level between scalenus anterior and medius (at the level of cricoid cartilage).
• Landmark: Posterior border of sternocleidomastoid at the level of cricoid.
• Indications: Shoulder arthroplasty, rotator cuff repair, proximal humerus fracture.
• Volume: 15-25 mL.
• Complications:
  • Phrenic nerve block (100%) → diaphragmatic paralysis → avoid in respiratory compromise
  • Recurrent laryngeal nerve block → hoarseness
  • Horner's syndrome (ptosis, miosis, anhidrosis)
  • Vertebral artery injection → seizures
  • Pneumothorax (rare with US)
  • Epidural/intrathecal spread
  • Spinal cord injury

2. Supraclavicular Block

• "Spinal of the arm" - most complete block of the brachial plexus.
• Trunks/divisions packed tightly around the first rib at the subclavian artery.
• Indications: Surgery on arm, elbow, forearm, wrist, hand.
• Complications:
  • Pneumothorax (most feared; 0.5-6% with blind technique; <1% with US)
  • Phrenic nerve block (~50%)
  • Subclavian artery puncture
  • Haematoma

3. Infraclavicular Block

• Target: Three cords around axillary artery.
• Indications: Elbow, forearm, wrist, hand; continuous catheter placement.
• Complications:
  • Pneumothorax (rare but possible)
  • Vascular puncture
  • Nerve injury

4. Axillary Block

• Safest approach - no risk of pneumothorax or phrenic nerve block.
• Arm abducted 90°; needle directed toward axillary artery pulsation.
• Must separately block musculocutaneous nerve (it leaves the sheath proximally to pierce coracobrachialis).
• Volume: 30-40 mL.
• Indications: Forearm and hand surgery.
• Complications:
  • Axillary artery haematoma
  • Axillary vein puncture
  • Infection
  • LAST

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III. MANAGEMENT OF LOCAL ANAESTHETIC SYSTEMIC TOXICITY (LAST)

• CNS toxicity (lower threshold): Perioral tingling/numbness, metallic taste, tinnitus, visual disturbances, dizziness → confusion, agitation → muscle twitching → tonic-clonic seizures → unconsciousness, apnoea.
• Cardiovascular toxicity (higher threshold): Hypertension/tachycardia (early) → hypotension, bradycardia, heart block → ventricular arrhythmias (bupivacaine: VF) → cardiovascular collapse.
• Bupivacaine most cardiotoxic (high lipid solubility, long protein binding); S(-) enantiomers (levobupivacaine, ropivacaine) are less cardiotoxic.

MANAGEMENT OF LAST (AAGBI/ASRA Guidelines):

• 100% oxygen; if apnoeic → intubate.
• Hyperventilation → alkalosis → reduces free fraction of LA.

• If cardiac arrest: Start CPR immediately.
• For seizures: Midazolam 0.05-0.1 mg/kg IV (or propofol in small dose, but avoid large doses - worsens cardiac depression).
• Avoid lidocaine (if it was the offending agent) and vasopressors in large doses (epinephrine in reduced doses: <1 mcg/kg).

• 20% Intralipid (lipid emulsion) - acts as a "lipid sink" trapping free LA molecules.
• Regimen:
  • Bolus: 1.5 mL/kg of 20% Intralipid IV over 1 min.
  • Infusion: 0.25 mL/kg/min for at least 10 min (continue until cardiovascular stability).
  • Can repeat the bolus twice (maximum cumulative dose ~12 mL/kg in first 30 min).
• Continue CPR throughout.

• Prolonged CPR (LAST arrests respond well to lipid + prolonged resuscitation).
• Consider ECMO (extracorporeal membrane oxygenation) if refractory - LAST is potentially reversible.
• Amiodarone for arrhythmias (NOT lignocaine).
• Sodium bicarbonate for acidosis.
• Avoid: Propofol in large doses, vasopressin, calcium channel blockers, beta-blockers.

• Use minimum effective dose.
• Ultrasound guidance.
• Aspirate before injection.
• Inject incrementally (3 mL aliquots with 30-second intervals).
• Use markers: 1:200,000 adrenaline as intravascular marker (tachycardia if intravascular).

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Q6. O2-Dissociation Curve (ODC): Factors Affecting It and Anaesthetic Implications

I. OXYGEN-HAEMOGLOBIN DISSOCIATION CURVE

• Initial binding of O2 to one haem group alters the quaternary structure of Hb → facilitates subsequent O2 binding → progressively increasing affinity.
• This allows loading at high PO2 (lungs) and efficient unloading at low PO2 (tissues).

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II. FACTORS AFFECTING THE ODC

• Product of erythrocyte glycolysis (Rapoport-Luebering shunt).
• Binds to beta chains of deoxy-Hb → stabilises T-state → facilitates O2 unloading.
• Increased in: chronic hypoxia, anaemia, high altitude, hyperthyroidism.
• Decreased in: stored blood (after 1-2 weeks of storage at 4°C), acidosis initially.

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III. ANAESTHETIC IMPLICATIONS OF THE ODC

1. Hypocapnia (hyperventilation):
   • Left shift of ODC → increased O2 affinity → impaired tissue O2 delivery despite normal SaO2.
   • Aggressive hyperventilation during anaesthesia can lead to cerebral and peripheral tissue hypoxia.
   • Caution: PaCO2 <25 mmHg → significant left shift → harmful.
2. Hypothermia (e.g., cardiac surgery with CPB):
   • Left shift → Hb holds onto O2 → reduces O2 delivery at hypothermic temperatures.
   • However, reduced metabolic demands at hypothermia partially compensate.
   • Targeted temperature management must account for this.
3. Stored Blood / Massive Transfusion:
   • Old blood (>7 days) has very low 2,3-DPG → left shift → impaired tissue O2 unloading immediately after transfusion.
   • 2,3-DPG levels recover within 24 hours of transfusion.
   • In massive transfusion, multiple units of stored blood may transiently worsen tissue oxygenation.
4. Acidosis/Alkalosis:
   • Metabolic or respiratory acidosis: right shift → enhanced O2 release. Beneficial at tissue level.
   • Iatrogenic alkalosis (bicarbonate, hyperventilation): left shift → reduces O2 availability to tissues.
5. Pulse Oximetry Limitation:
   • The flat upper part of ODC means SpO2 remains >90% even at PaO2 of 60 mmHg.
   • SpO2 is a poor marker of oxygenation reserve on the flat part. PaO2 must be measured directly.
6. Fetal Haemoglobin (HbF):
   • Left-shifted curve: allows placental O2 transfer from mother (PO2 ~50 mmHg) to fetus.
   • Anaesthetic drugs crossing the placenta (opioids, barbiturates) depress fetal respiration.
7. High Altitude / Chronic Hypoxia:
   • ↑2,3-DPG → right shift → compensatory adaptation to deliver O2 at lower PaO2.

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Q7. Buffering Systems for Acid-Base Regulation and Anaesthetic Implications

I. BUFFERS AND ACID-BASE REGULATION

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II. BUFFER SYSTEMS

A. Bicarbonate Buffer System (most important clinically, ~53% of blood buffering)

• pKa = 6.1 (not ideal, but extremely effective because both components are independently regulated).
• Respiratory regulation: Lungs regulate PaCO2 (volatile acid) - fast (minutes).
• Renal regulation: Kidneys regulate HCO3- (fixed acid/base) - slow (hours to days).
• Open buffer system: Both components are adjustable, making it highly effective despite the non-ideal pKa.
• Not effective against respiratory acid-base disorders (can't buffer CO2 with CO2/HCO3-).

B. Phosphate Buffer System (~5% of blood buffering; important in urine)

• pKa = 6.8 (near body pH - better pKa than bicarbonate but small concentration).
• Primarily important in intracellular buffering and renal tubular buffering.
• Titratable acid excretion by kidneys is largely phosphate-mediated.

C. Protein Buffer System (~45% of blood buffering)

• Haemoglobin is the most important protein buffer in blood.
• Imidazole groups of histidine residues on Hb buffer H+.
• Deoxyhaemoglobin is a better buffer than oxyhaemoglobin (Haldane effect).
• Plasma proteins (albumin) also contribute (10% of blood buffering).
• Intracellular proteins are the main buffers for fixed acid loads.

D. Haemoglobin Buffer System (part of protein buffers, but deserves separate mention)

• HbH (deoxyhaemoglobin) + CO2 → HbCO2 (carbaminohaemoglobin) + H+.
• Hb takes up CO2 from tissues + releases O2 → Bohr/Haldane effects.
• Haldane effect: Deoxy-Hb binds more CO2 than oxy-Hb → helps in CO2 transport from tissues.

E. Ammonia Buffer System (primarily renal)

• Renal tubular cells produce NH3 from glutamine → NH3 + H+ → NH4+ (ammonium) → excreted in urine.
• Important for net acid excretion; regulated by renal cortex over days.
• Enhanced in chronic acidosis.

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III. RESPIRATORY AND RENAL COMPENSATION

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IV. ANAESTHETIC IMPLICATIONS

1. Hyperventilation (deliberate hypocapnia):
   • Respiratory alkalosis → left shift of ODC → reduces tissue O2 delivery.
   • Also reduces ionised calcium (symptoms: paraesthesia, tetany).
   • Cerebral vasoconstriction → reduced CBF (used for ICP control, but dangerous if excessive).
   • Compensatory renal HCO3- excretion occurs over 24 hours (if prolonged ventilation).
2. Hypoventilation / Respiratory Acidosis:
   • PaCO2 rises → H+ accumulates → pH falls.
   • Right shift of ODC (beneficial for tissue O2 delivery but overall harmful).
   • Sympathoadrenal stimulation → tachycardia, hypertension.
   • Arrhythmias with volatile anaesthetics (especially halothane sensitises myocardium to catecholamines).
3. Metabolic Acidosis Perioperatively:
   • Causes: Hypoperfusion (lactic acidosis), sepsis, hypovolaemia, massive transfusion.
   • Impairs coagulation, myocardial contractility, drug metabolism.
   • Treat with fluid resuscitation; use bicarbonate only if pH <7.1 or in hyperchloraemic acidosis.
   • Dilutional acidosis: Large volumes of 0.9% NaCl (normal saline) → hyperchloraemic metabolic acidosis → use balanced crystalloids (Plasmalyte, Ringer's Lactate) instead.
4. Ringer's Lactate/Balanced Solutions:
   • Buffer in Ringer's Lactate = lactate, which is metabolised to bicarbonate in the liver.
   • Avoid in liver failure (can't metabolise lactate).
5. Bicarbonate Therapy:
   • 8.4% NaHCO3 (1 mEq/mL): Use for metabolic acidosis when pH <7.1 or in tricyclic antidepressant/bupivacaine toxicity (alkalinisation reduces free drug fraction).
   • Avoid in respiratory acidosis (generates CO2 → worsens respiratory acidosis if unable to ventilate).
   • Dose: Deficit (mEq) = 0.3 × weight (kg) × base deficit; give half the calculated dose initially.
6. Malignant Hyperthermia:
   • Massive metabolic acidosis (lactic acid from rhabdomyolysis + hyperthermia).
   • Treat with dantrolene, 100% O2, cooling, bicarbonate for severe acidosis.
7. TIVA and Acid-Base:
   • Propofol infusion syndrome: Rare; severe metabolic acidosis, rhabdomyolysis, cardiac arrhythmias in high-dose/prolonged propofol infusions.

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Q8. Physiological Changes in Pregnancy and Anaesthetic Implications

I. CARDIOVASCULAR CHANGES

• Gravid uterus compresses inferior vena cava (and aorta) in supine position after 20 weeks.
• Reduces venous return → ↓cardiac output → maternal hypotension + fetal hypoxia.
• Prevention: Left lateral tilt of 15° or left uterine displacement (wedge under right hip). MANDATORY for all obstetric procedures.

• Hypotension after spinal/epidural anaesthesia is common and rapid.
• Prophylactic crystalloid/colloid preload + vasopressors (phenylephrine preferred; or norepinephrine; avoid metaraminol as less data).
• Regional techniques are preferred.

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II. RESPIRATORY CHANGES

• Preoxygenation is mandatory for at least 3-5 minutes (achieve FEO2 >90%) before induction.
• Failed intubation → immediate cricothyrotomy if CICO.

• Airway oedema (laryngeal/pharyngeal oedema from oestrogen + fluid retention) → reduced airway size.
• Engorgement of the tongue, uvula, and epiglottis.
• Higher Mallampati grade in late pregnancy.
• Failed intubation is 8× more common in obstetric population vs general population.

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III. GASTROINTESTINAL CHANGES

• Progesterone relaxes the lower oesophageal sphincter (LOS) → gastro-oesophageal reflux (GORD).
• Mechanical displacement of the stomach by the uterus.
• Delayed gastric emptying in labour (opioid use, pain, anxiety).
• Result: ALL pregnant patients from 18-20 weeks are considered to have full stomach → aspiration risk.

• Rapid Sequence Induction (RSI) with cricoid pressure (Sellick's manoeuvre) for all general anaesthetics.
• Antacid prophylaxis: Ranitidine 150 mg PO the night before + morning of surgery; citrate 30 mL immediately before induction; Metoclopramide 10 mg IV.
• Regional anaesthesia preferred whenever possible.
• Avoid LMA (does not protect against aspiration).

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IV. HAEMATOLOGICAL CHANGES

• Pre-eclampsia: HELLP syndrome (Haemolysis, Elevated Liver enzymes, Low Platelets) → check platelets before regional.
• Regional anaesthesia contraindicated if platelets <70,000-80,000/μL (risk of spinal haematoma).
• Hypercoagulability → thromboprophylaxis with LMWH.

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V. RENAL CHANGES

• GFR increases by 50% from early pregnancy.
• Normal serum creatinine 0.4-0.6 mg/dL (lower than non-pregnant values).
• Glycosuria is normal.
• Progesterone causes ureteric dilatation → risk of hydronephrosis and UTI.

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VI. NERVOUS SYSTEM CHANGES

• Reduced MAC: Volatile anaesthetic requirements reduced by 30-40% (due to progesterone and endorphins).
• Reduced LA dose for spinal/epidural: Epidural venous plexus engorgement → reduced epidural space volume; epidural/spinal doses need reduction by 30%.
• Increased sensitivity to local anaesthetics.

• Lower propofol induction dose needed.
• Smaller intrathecal dose for spinal anaesthesia (hyperbaric bupivacaine 1.5-2 mL for CS vs 3 mL in non-pregnant).
• Epidural: Use 15-20% less volume.

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VII. HEPATIC CHANGES

• Plasma cholinesterase (pseudocholinesterase) decreases by ~25-30%.
• Prolongs the action of suxamethonium and mivacurium.
• Serum albumin decreases → more free drug fraction for highly protein-bound drugs.

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VIII. MUSCULOSKELETAL

• Progesterone and relaxin → laxity of ligaments and joints including the lumbar spine.
• Lumbar lordosis increases → changes spinal anatomy (affects epidural/spinal placement and spread).
• Low back pain common.

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IX. PLACENTAL TRANSFER OF ANAESTHETIC DRUGS

• All volatile agents cross the placenta freely.
• Thiopentone, propofol, benzodiazepines, opioids cross rapidly.
• Suxamethonium and non-depolarising NMBAs - quaternary ammonium compounds, highly ionised, do NOT cross placenta in clinical doses.
• Local anaesthetics: Highly protein bound; amides cross more than esters; bupivacaine more than lidocaine.
• Neonatal effects: Respiratory depression from opioids (treated with naloxone); sedation from barbiturates.

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Quick Reference - What Each Answer Covers

• Sagittal upper airway cross-section with labeled structures
• Tracheobronchial tree with the critical angle/length differences (R: 25°/2.5 cm vs L: 45°/5 cm)
• Difficult airway predictors box
• Laryngeal nerve supply

• Full formation diagram: Roots → Trunks (color-coded) → Divisions → Cords → 5 terminal branches
• Approach comparison table (interscalene to axillary) with key complications
• Red alert LAST management box with Intralipid dosing

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Answer Index

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What Each Answer Contains (Exam Checklist)

Q1 - Airway Anatomy

• Upper airway: nasal cavity, oral cavity, pharynx (naso/oro/hypo), larynx
• Laryngeal cartilages, vocal cords, glottis, CTM (CICO site)
• Laryngeal innervation (SLN, RLN, CN IX) - for awake intubation blocks
• Lower airway: trachea dimensions, carina (T4), R vs L bronchus differences
• Airway assessment: Mallampati, TMD, IID, LEMON, sniffing position

Q2 - CBF + ICP

• CBF regulation: CPP = MAP - ICP, autoregulation (MAP 60-150), CO2/O2/pH/temperature/CMRO2
• Effect of all anaesthetic agents on CBF/CMRO2/ICP table
• Monro-Kellie doctrine
• Perioperative ICP factors: positioning, ventilation, agents, fluids, laryngoscopy
• Methods to reduce ICP: positioning, hyperventilation, mannitol, hypertonic saline, propofol TIVA, dexamethasone, barbiturate coma, decompressive craniectomy

Q3 - Pulse Oximetry

• Beer-Lambert law, 660 nm vs 940 nm wavelengths
• AC vs DC signal separation, R ratio, calibration curve
• Accuracy factors: COHb (falsely high), MetHb (reads ~85%), dyes, nail polish, motion, poor perfusion, venous pulsation, ambient light, diathermy

Q4 - Antihypertensives + FESS

• Classification: diuretics, RAAS blockers (ACEi/ARB/DRI), CCBs (DHP vs non-DHP), sympathoplegics (central/ganglionic/beta/alpha blockers), direct vasodilators, newer agents
• FESS management: preop optimization, controlled hypotension (MAP 50-65), TIVA propofol+remifentanil, esmolol, reverse Trendelenburg, lignocaine for smooth extubation

Q5 - Brachial Plexus + LAST

• Formation: C5-T1, Roots → Trunks → Divisions → Cords → Branches (RTDCB)
• Terminal branches: MBUMA (Musculocutaneous, Median, Ulnar, radial, Axillary)
• 4 approaches table with indications and specific complications
• LAST: stop → O2 → seizure control → 20% Intralipid 1.5 mL/kg bolus + 0.25 mL/kg/min infusion → ECMO if refractory

Q6 - ODC

• Sigmoid shape, P50=27 mmHg, cooperative binding
• Right shift (CADET): ↑CO2, acidosis, ↑DPG, exercise/↑temp - Bohr effect
• Left shift: hypothermia, alkalosis, HbF, COHb, stored blood (↓DPG)
• Implications: hyperventilation danger, stored blood, hypothermia on CPB, FRC/SpO2 lag

Q7 - Buffering Systems

• Bicarbonate (53%), phosphate, haemoglobin/proteins (45%), ammonia (renal)
• Compensation formulae (Winter's formula, etc.)
• Implications: hyperventilation, RSI, bicarbonate therapy, dilutional acidosis (NS vs balanced), MH, PRIS

Q8 - Pregnancy

• CVS: CO ↑50%, aortocaval compression → left lateral tilt mandatory
• RS: FRC ↓20% + O2 consumption ↑20% = rapid desaturation; airway oedema → smaller ETT; RSI mandatory
• GI: full stomach from 18-20 weeks; Mendelson's syndrome; antacid prophylaxis
• Haematological: dilutional anaemia, hypercoagulable, check platelets for regional
• Pharmacology: MAC ↓30-40%, spinal dose ↓30%, pseudocholinesterase ↓ (suxamethonium prolonged)

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