🎓 DNB Anaesthesiology — December 2025, Paper I (Solved)

Organisation — "Randy Travis Drinks Cold Beer" (Roots → Trunks → Divisions → Cords → Branches)

The brachial plexus provides the entire cutaneous and muscular innervation of the upper limb (except trapezius and a strip of medial arm skin). It is formed from the ventral rami of C5–T1.

• Roots (C5–T1): lie between anterior and middle scalene muscles (interscalene groove).
• Trunks: Upper (C5+C6), Middle (C7), Lower (C8+T1) — cross the posterior triangle / cross the first rib.
• Divisions: each trunk splits into an anterior and posterior division (behind the clavicle).
• Cords (named by relation to the axillary artery): Lateral (ant. divisions of upper+middle trunk, C5–7), Posterior (all 3 posterior divisions, C5–T1), Medial (ant. division of lower trunk, C8–T1).
• Terminal branches: musculocutaneous, axillary, radial, median, ulnar.

Branches at each level

• From roots: dorsal scapular nerve (C5), long thoracic nerve (C5–7), branches to scalenes & longus colli, and a contribution to the phrenic nerve.
• From trunks (upper trunk only): suprascapular nerve and nerve to subclavius.
• Lateral cord: lateral pectoral nerve, musculocutaneous nerve, lateral root of median nerve.
• Medial cord: medial pectoral nerve, medial root of median nerve, medial cutaneous nerve of arm, medial cutaneous nerve of forearm, and the ulnar nerve.
• Posterior cord ("ULTRA"): Upper subscapular, Lower subscapular, Thoracodorsal (nerve to latissimus dorsi), Radial, Axillary.

Approaches (level of block determines coverage)

• Interscalene (at roots/trunks) — for shoulder and proximal humerus surgery; spares the ulnar (inferior trunk, C8–T1) — "ulnar sparing".
• Supraclavicular (at trunks/divisions) — the "spinal of the arm"; most complete, dense block for the whole upper limb below the shoulder.
• Infraclavicular (at cords) — for elbow, forearm and hand; good for catheter placement.
• Axillary (at terminal branches) — for forearm and hand; safest (no risk of pneumothorax), but misses the musculocutaneous nerve (must be blocked separately).

Techniques: landmark/paraesthesia (Winnie), peripheral nerve stimulator, and ultrasound-guided (roots/trunks appear as the hypoechoic "bunch of grapes / traffic-light sign" in the interscalene groove between the scalenes).

Complications of interscalene block

• Phrenic nerve palsy → ipsilateral hemidiaphragmatic paresis — virtually 100%; avoid in significant respiratory compromise.
• Horner's syndrome (ptosis, miosis, anhidrosis) from stellate ganglion spread.
• Recurrent laryngeal nerve block → hoarseness.
• Vertebral artery injection → immediate seizures / LA systemic toxicity (LAST).
• Inadvertent neuraxial spread — epidural, subarachnoid (total spinal) via a dural cuff.
• Pneumothorax (lower with interscalene than supraclavicular), nerve injury, haematoma, infection.

1. As bicarbonate — ~70% (major form)

• CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻; the reaction is accelerated ~13,000× by carbonic anhydrase inside the red cell.
• HCO₃⁻ diffuses out of the RBC in exchange for Cl⁻ — the chloride shift (Hamburger phenomenon); H⁺ is buffered by haemoglobin.

2. As carbamino compounds — ~23%

• CO₂ binds to the terminal amine groups of the globin chains of haemoglobin (carbaminohaemoglobin), and to plasma proteins.
• Deoxygenated Hb carries CO₂ far better than oxygenated Hb — the basis of the Haldane effect.

3. Dissolved in plasma — ~7%

• Governed by Henry's law (CO₂ is ~20× more soluble than O₂); this fraction determines the PaCO₂.

Haldane effect

• The effect of oxygenation on the affinity of Hb for CO₂.
• In the lungs: O₂ loading ↓ the affinity of Hb for CO₂ → CO₂ is unloaded and expired.
• In the tissues: deoxygenation ↑ CO₂-carrying capacity, so deoxy-Hb picks up more CO₂. (HbO₂ + CO₂ ⇌ HbCO₂ + O₂).

Bohr effect

• The effect of CO₂ and H⁺ (pH) on the affinity of Hb for O₂.
• In the tissues: ↑CO₂ and ↑H⁺ ↓ the affinity of Hb for O₂ → the O₂ dissociation curve shifts right → O₂ unloading (enhanced delivery). Factors: ↑CO₂, ↑temperature, ↓pH, ↑2,3-DPG.

How they are related

They are reciprocal / complementary aspects of the same interaction between O₂, CO₂ and haemoglobin. The Bohr effect promotes O₂ release in the tissues (CO₂/H⁺ drive O₂ off Hb); the Haldane effect simultaneously allows that same deoxygenated Hb to pick up more CO₂. In the lungs the process reverses. Together they make gas exchange maximally efficient at both ends of the circulation.

Definition

The diffusing capacity of the lung (DLCO) is the ability of a gas to transfer from the alveoli to the pulmonary capillary blood per unit driving pressure. It reflects the function of the alveolar–capillary membrane. Carbon monoxide is used to measure it (single-breath DLCO) because it is diffusion-limited and avidly bound by Hb.

Diffusion is governed by Fick's law: V̇gas = [A × D × (P₁ − P₂)] / T, where A = surface area, T = membrane thickness, (P₁ − P₂) = partial-pressure gradient, and D = diffusion coefficient (∝ gas solubility ÷ √molecular weight — Graham's law).

Factors affecting diffusing capacity

• Surface area — ↓ in emphysema, lung resection, pneumonectomy; ↑ with exercise.
• Membrane thickness — ↑ thickness ↓ DLCO: pulmonary fibrosis, pulmonary oedema, ARDS.
• Partial-pressure gradient (P₁ − P₂) — a larger alveolar–capillary gradient increases diffusion (affected by alveolar O₂ tension/FiO₂).
• Haemoglobin — ↑ in polycythaemia; ↓ in anaemia (DLCO is corrected for Hb).
• Pulmonary blood flow / capillary volume — ↑ with exercise; ↓ in pulmonary embolism.
• V/Q matching, age, smoking, body position — poor V/Q matching, ageing and smoking reduce DLCO.

↓ DLCO: emphysema, pulmonary fibrosis, anaemia, pulmonary embolism. ↑ DLCO: polycythaemia, exercise, left-to-right shunt, alveolar haemorrhage, supine position.

Patient factors

• Extremes of age; obesity (↓ FRC, ↑ atelectasis).
• Pre-existing lung disease (V/Q mismatch), smoking (↑ secretions, ↓ ciliary clearance).
• Cardiac disease (pulmonary oedema); neuromuscular disease (weak respiratory muscles).

Surgical factors

• Site of surgery — upper abdominal & thoracic surgery reduce FRC most.
• Position — supine ↓ FRC; Trendelenburg ↓↓ further; lateral → V/Q mismatch.
• Duration (prolonged → atelectasis), pain (splinting), and laparoscopy/pneumoperitoneum (↑ intra-abdominal pressure, ↓ compliance).

Anaesthesia factors (general anaesthesia)

• CNS depression of respiratory drive; loss of upper-airway tone.
• Muscle relaxants and volatile agents (blunt hypoxic/hypercarbic drive, cause atelectasis).
• High FiO₂ → absorption atelectasis; mechanical ventilation → barotrauma / volutrauma.
• Loss of FRC (~15–20%) on induction is the central mechanism of intra-operative hypoxaemia.

Anaesthetic techniques

• Opioid-based general anaesthesia — high-dose opioid technique (e.g. fentanyl/sufentanil) for cardiac and major surgery to preserve haemodynamic stability.
• Balanced anaesthesia (most common) — opioid + inhalational/IV agent + muscle relaxant.
• Total intravenous anaesthesia (TIVA / TCI) — e.g. propofol + remifentanil.
• Regional analgesia with opioid adjuncts — peripheral nerve blocks and neuraxial (epidural/intrathecal) opioids.
• Post-operative analgesia techniques — PCA, neuraxial opioid, multimodal regimens.

Routes of application

• Intravenous — most rapid, titratable onset (PCA, infusion).
• Intramuscular / subcutaneous — variable, unpredictable absorption.
• Oral — significant first-pass metabolism.
• Transdermal (fentanyl, buprenorphine patch) and transmucosal / intranasal (fentanyl).
• Neuraxial — epidural and intrathecal.

Pharmacokinetic factors

• Absorption — route-dependent (IV fastest; IM/SC variable; oral limited by first-pass).
• Distribution — lipid solubility (more lipophilic → faster CNS penetration and onset, e.g. fentanyl); protein binding (only free drug is active); volume of distribution (large Vd → prolonged/context-sensitive effect).
• Metabolism — mostly hepatic; oral opioids undergo first-pass; morphine → glucuronidation, fentanyl → CYP3A4.
• Elimination — renal excretion of active metabolites; morphine-6-glucuronide accumulates in renal failure → toxicity (respiratory depression).

Pharmacodynamic factors

• Age — elderly: ↑ sensitivity, ↓ clearance; neonates: immature metabolism/BBB.
• Comorbidities — hepatic/renal disease (accumulation); CNS disease (↑ sensitivity); respiratory disease (↑ risk of respiratory depression).
• Tolerance — chronic opioid use ↓ response, needs higher doses.
• Drug interactions — additive respiratory depression with sedatives/benzodiazepines.
• Acid–base status — acidosis increases the ionised/unionised balance and CNS penetration.

Definition

Cardiac output (CO) is the volume of blood pumped by the heart per minute. CO = Heart Rate × Stroke Volume; normal ≈ 5 L/min (cardiac index 2.5–4 L/min/m²).

Factors affecting CO

• Heart rate — up to a point ↑HR ↑CO, but excessive tachycardia ↓ diastolic filling → ↓CO.
• Preload (Frank–Starling) — hypovolaemia/blood loss ↓ preload → ↓CO.
• Contractility — ↑ by sympathetic stimulation/inotropes; ↓ in ischaemia, cardiomyopathy, volatile agents.
• Afterload — ↑ afterload (↑SVR, aortic stenosis) → ↓CO.
• Rhythm — loss of atrial kick (AF) ↓CO.
• Perioperative modifiers — positive-pressure ventilation & PEEP (↓ venous return), pneumoperitoneum (↑IAP → ↓VR, ↑afterload), position (Trendelenburg ↑VR; head-up ↓VR), anaesthetic depth/drugs (propofol & volatiles depress CO), and the surgical stress response (catecholamines ↑CO).

Physical properties that demand a special vaporiser

• Boiling point 22.8 °C — close to room temperature; it would boil intermittently in a conventional vaporiser, causing wild fluctuations in output.
• High saturated vapour pressure ≈ 669 mmHg (88.5 kPa) at 20 °C — near atmospheric; a variable-bypass vaporiser would need impossibly high fresh-gas flow to dilute it and could deliver dangerously high concentrations.
• Low potency (MAC ≈ 6%) — large volumes of vapour must be delivered.

The Datex-Ohmeda Tec 6 solves this: it is electrically heated to 39 °C and pressurised (~2 atm), creating a stable vapour phase. It is a dual-circuit gas–vapour blender — fresh gas passes one circuit; pure desflurane vapour is injected via the other through a pressure-regulating valve, electronically matched (differential pressure transducer) so the set % is delivered. It is concentration-calibrated, agent-specific and heated/pressurised (unlike a variable-bypass vaporiser).

Factors influencing vaporiser output

• Fresh gas flow rate — at very low flows output rises, at very high flows it falls (incomplete saturation).
• Temperature — ↓ temperature ↓ SVP ↓ output (the Tec 6 negates this by heating).
• Ambient/barometric pressure (altitude) — the Tec 6 delivers a constant % v/v, so at altitude the delivered partial pressure falls and the dial must be increased to keep depth.
• Carrier gas composition — N₂O transiently alters output.
• Back pressure / pumping effect (intermittent PPV) and tilting (→ overdose) affect conventional vaporisers.

Definition & mechanism

Volatile anaesthetic reflectors are devices that conserve and recycle exhaled volatile agent, allowing inhalational agents to be delivered through a standard ICU ventilator without a circle system. A reflector containing an activated-carbon / zeolite matrix sits between the Y-piece and the endotracheal tube: on expiration it adsorbs the volatile agent, and on inspiration it releases it back to the patient — reducing anaesthetic consumption by ~90%. (Marketed as AnaConDa; MIRUS is a similar system.)

Where they are used

• ICU sedation — inhalational (isoflurane/sevoflurane) sedation as an alternative to propofol/dexmedetomidine.
• Difficult-to-sedate patients and status asthmaticus/refractory bronchospasm (bronchodilator effect).
• Where rapid, titratable sedation and fast wake-up are wanted.
• Advantages: stable, rapidly titratable sedation, reduced drug consumption/cost. Disadvantages: added dead space (↑ CO₂ retention risk), need for scavenging/special equipment. Avoid in small children and in hypercapnia.

Cerebral perfusion pressure (CPP)

• CPP is the pressure gradient driving cerebral blood flow: CPP = MAP − ICP (use CVP if it exceeds ICP; = MAP − ICP or CVP, whichever is higher).
• Normal CPP ≈ 60–100 mmHg; normal ICP 10–15 mmHg.
• CPP < 50 mmHg → cerebral ischaemia. Because ↑ICP or ↓MAP each lower CPP, neuroprotection = maintain MAP and lower ICP.
• Cerebral autoregulation keeps CBF constant over MAP ~50–150 mmHg; it is lost in injured brain, making CBF pressure-passive.

Cushing's triad (Cushing reflex)

A late sign of raised ICP, indicating impending/actual brain herniation. The triad is:

• Hypertension (widened pulse pressure)
• Bradycardia
• Irregular respiration (e.g. Cheyne–Stokes)

Mechanism: ↑ICP → ↓CPP → brainstem ischaemia → sympathetic surge (hypertension to restore perfusion) → the resulting hypertension triggers a baroreceptor-mediated reflex vagal bradycardia; brainstem compression disrupts respiration. It mandates urgent intervention to lower ICP.

Arterial supply

• Single anterior spinal artery — formed from both vertebral arteries; runs in the anterior median fissure; supplies the anterior two-thirds of the cord (motor tracts, spinothalamic tracts).
• Paired posterior spinal arteries — supply the posterior one-third (dorsal columns).
• Radicular (segmental) arteries reinforce these. The largest is the artery of Adamkiewicz (arteria radicularis magna), usually arising on the left between T9–L2; it supplies the lower two-thirds of the cord / lumbar enlargement — critical in thoraco-abdominal aortic surgery.

Anterior spinal artery syndrome (watershed T4–T8 region most vulnerable) → motor paralysis and loss of pain & temperature below the lesion, with preserved proprioception/vibration (dorsal columns spared).

Venous drainage

• Anterior and posterior spinal veins drain into the internal vertebral venous plexus (Batson's plexus), which is valveless → bidirectional flow.
• It communicates with azygos, caval and pelvic venous systems — a route for the spread of infection and tumour (e.g. prostate) to the vertebrae/CNS.

Definition

The p-value is the probability of obtaining a result at least as extreme as the observed one, purely by chance, assuming the null hypothesis (H₀) is true. It quantifies how likely the observed difference is a chance finding.

Interpretation

• p ≤ 0.05 → statistically significant — the null hypothesis is rejected; the difference is unlikely to be due to chance alone (at the conventional α = 0.05).
• p > 0.05 → not statistically significant — insufficient evidence to reject H₀ (we do not "prove" H₀).
• 0.05 is the significance level (α) = the accepted probability of a Type I error (falsely rejecting a true null). In a two-tailed test each tail carries α/2 = 0.025.
• A p-value indicates statistical significance, not clinical significance or effect size, and depends heavily on sample size.

Type I error (α) = rejecting a true null (false positive); Type II error (β) = accepting a false null (false negative); power = 1 − β.

Definition & formula

The odds ratio is a measure of association that compares the odds of an event (disease) in an exposed group with the odds in an unexposed group. For a 2×2 table with cells a, b, c, d: OR = (a/b) ÷ (c/d) = ad / bc.

When it is used

• Primarily in case-control studies (where incidence/risk cannot be calculated directly).
• In logistic regression and cross-sectional studies.
• In cohort studies, although relative risk (RR) is generally preferred there.

Interpretation

• OR = 1 → no association.
• OR > 1 → exposure associated with higher odds of disease.
• OR < 1 → protective association.

Example: smokers 80 lung-cancer / 20 not; non-smokers 40 / 60. OR = (80×60)/(20×40) = 6 → smokers have six times the odds of lung cancer.

Informed consent — components/issues

Informed consent is the communication of the anaesthetic plan (pre-operative preparation, intra-operative management and post-operative care) in terms the patient understands, with risks, benefits and complications discussed and questions answered. Its essential elements:

• Decision-making capacity — ability to comprehend information, reason rationally and consistently, and express a preference.
• Voluntariness — free from coercion or undue influence.
• Disclosure — adequate information; the standard used may be the professional practice standard (what local physicians disclose), the reasonable person standard (what a reasonable patient would want to know), or the subjective standard (this particular patient's wishes).
• Comprehension of risks vs benefits and the basis of the recommendation.

Special situations: emergency (patient lacks capacity → act in best interest), minors (parental/guardian consent), and the pregnant patient (an autonomous competent woman's refusal is respected).

Informed refusal

The right of a competent, fully-informed patient to decline a recommended treatment or procedure — even if that refusal may be harmful or fatal. It requires the same elements as consent (capacity, adequate disclosure of the consequences of refusing + alternatives, voluntariness) and must be documented. Process: explain the situation → explain the risks of refusal → offer alternatives → confirm understanding → document.

Specific ethical issues

• Withholding vs withdrawing treatment — not starting vs stopping ongoing therapy; ethically and legally regarded as equivalent.
• Medical futility — treatment unlikely to benefit the patient.
• DNAR / DNR orders (withholding CPR).
• Advance directives / living wills and surrogate decision-making.
• Palliative (terminal) sedation — relieving refractory suffering (doctrine of double effect).
• Euthanasia vs assisted dying — active euthanasia is illegal in India; the Supreme Court has legalised passive euthanasia and advance directives (Aruna Shanbaug 2011; Common Cause 2018).

Resting membrane potential

≈ −70 mV, maintained by the Na⁺/K⁺-ATPase (3 Na⁺ out : 2 K⁺ in) and the high resting K⁺ permeability (K⁺ leak channels). The membrane is polarised, with Na⁺ high outside and K⁺ high inside.

Sequence of the action potential

• Depolarisation to threshold (~ −55 mV): a stimulus opens some Na⁺ channels; once threshold is reached the response is all-or-none.
• Rapid depolarisation: voltage-gated Na⁺ channels open → rapid Na⁺ influx → membrane potential overshoots to about +30 mV.
• Repolarisation: Na⁺ channels inactivate and voltage-gated K⁺ channels open → K⁺ efflux returns the potential toward resting.
• Hyperpolarisation (after-potential): K⁺ channels close slowly → transient undershoot below resting.
• Restoration: the Na⁺/K⁺-ATPase re-establishes the ionic gradients.

Refractory periods: absolute (Na⁺ channels inactivated — no AP possible) then relative. Conduction is continuous in unmyelinated fibres and saltatory (node-to-node) in myelinated fibres.

Structure & principle

LAs have a lipophilic aromatic ring — an intermediate ester/amide chain — and a hydrophilic tertiary amine. They act by disrupting ion-channel function in the neuronal membrane, blocking voltage-gated Na⁺ channels and preventing transmission of the action potential.

How they block the channel

• LAs are weak bases. The unionised (lipid-soluble) base crosses the nerve membrane; inside the axoplasm it re-ionises to the cationic (BH⁺) form, which is the active form and binds the inner pore of the voltage-gated Na⁺ channel (from the cytoplasmic side).
• This blocks Na⁺ influx → prevents/reduces depolarisation → ↓ amplitude and conduction of the action potential.
• LAs preferentially bind open/inactivated channels; rapidly firing fibres have more channels open → more block — the basis of use- (frequency-) dependent block.

Differential block

Smaller and myelinated fibres are blocked more readily than large and unmyelinated ones. Typical order of blockade: autonomic (B) → pain & temperature (C, Aδ) → touch/pressure → proprioception → motor (Aα) last. Recovery occurs in reverse.