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

Definition

THRIVE (Trans-nasal Humidified Rapid-Insufflation Ventilatory Exchange) is the use of high-flow (30–70 L/min) heated and humidified oxygen delivered via nasal cannulae to prolong the safe apnoea time during airway management. It combines the benefits of high-flow nasal oxygen (apnoeic oxygenation) with a degree of CO₂ clearance.

Physiology & mechanism (three principles)

• Apnoeic oxygenation — high FiO₂ maintains a continuous alveolar-to-pharyngeal O₂ gradient; as O₂ is absorbed faster than CO₂ is produced, a mass flow of oxygen is drawn down into the alveoli ("aventilatory mass flow"), sustaining oxygenation without tidal breathing.
• CO₂ clearance / dead-space flushing — the high flow flushes the nasopharyngeal anatomical dead space and generates turbulent gas mixing, slowing the rise of CO₂ (≈ 2–3 mmHg/min vs ~4–6 with classical apnoeic oxygenation).
• Positive airway pressure & humidification — the flow creates a low-level CPAP/PEEP effect (≈ 3–7 cmH₂O) that splints alveoli open (↓ atelectasis, ↑ FRC); heating and humidification prevent mucosal drying, improve comfort/tolerance and preserve mucociliary function.

Physiological effects

• ↑ Oxygenation and prolonged safe apnoea time; ↓ atelectasis; ↓ work of breathing; some CO₂ washout.

Uses

• Difficult airway management — extends the safe apnoeic window for intubation attempts.
• Pre-oxygenation and apnoeic oxygenation during rapid sequence induction (RSI).
• Shared-airway / airway procedures — awake fibreoptic intubation, microlaryngeal/laryngeal ("tubeless") surgery, ENT and airway endoscopy.
• Hypoxaemic respiratory failure (as HFNO) and post-extubation oxygen therapy.
• Obese, obstetric and paediatric patients, and other rapid-desaturators.

Definition & cascade

Haemorrhagic shock is a form of hypovolaemic shock due to acute blood loss (trauma, surgical, obstetric or GI haemorrhage) leading to inadequate tissue perfusion and oxygen delivery.

• ↓ Blood volume → ↓ venous return → ↓ stroke volume and cardiac output → ↓ tissue perfusion.
• Compensation: baroreceptor-mediated sympathetic activation → tachycardia, vasoconstriction (redistributes flow to heart/brain); RAAS and ADH release → fluid/sodium retention.
• Decompensation: sustained hypoperfusion → anaerobic metabolism → lactic acidosis, cellular injury, capillary leak, and ultimately multi-organ dysfunction.
• ATLS classes: I (<15% loss, normal vitals) → II (15–30%, tachycardia, narrowed pulse pressure) → III (30–40%, hypotension, ↓ urine output) → IV (>40%, marked hypotension, anuria, obtunded).

Anaesthetic triggering

Malignant hyperthermia (MH) is a potentially fatal, autosomal-dominant pharmacogenetic disorder of skeletal muscle. The commonest defect is in the ryanodine receptor (RYR1) gene on chromosome 19q (also CACNA1S). On exposure to a trigger, there is uncontrolled release of Ca²⁺ from the sarcoplasmic reticulum → sustained muscle contraction and a hypermetabolic state with massive ATP consumption.

• Triggers: all volatile anaesthetic agents (halothane, iso/sevo/desflurane) and the depolarising relaxant suxamethonium (the most common trigger, often with masseter spasm).
• Safe drugs (non-triggering): nitrous oxide, propofol, etomidate, ketamine, benzodiazepines, opioids, barbiturates, non-depolarising relaxants and all local anaesthetics.
• Cascade: ↑ CO₂ and O₂ consumption, tachycardia/tachypnoea, mixed (respiratory + metabolic) acidosis, rising temperature, sweating, and — later — rhabdomyolysis → ↑CK, hyperkalaemia, myoglobinuria → AKI, arrhythmias, DIC.
• Earliest and most sensitive sign: a rising end-tidal CO₂ (EtCO₂) unresponsive to increased ventilation. (Fever is a late sign.)

Associated syndromes (mnemonic "CK-MEN")

• C — Central Core Disease — the strongest association (allelic RYR1 disorder).
• K — King–Denborough syndrome — dysmorphic facies, skeletal abnormalities, myopathy, high MH risk.
• M — Multiminicore disease (often RYR1-related; variable susceptibility).
• E — Evans myopathy; and N — Native American myopathy (STAC3-related; weakness, cleft palate, scoliosis).
• Not true MH (need precautions but not classic MH): Duchenne/Becker & myotonic dystrophy (sux → rhabdomyolysis/hyperkalaemia), Noonan syndrome, osteogenesis imperfecta.

Immediate

• Stop all triggering agents and the surgery (or finish rapidly); call for help and the MH kit.
• Hyperventilate with 100% O₂ at high fresh-gas flow (>10 L/min); use a clean circuit / activated-charcoal filters.
• Dantrolene — the mainstay: 2.5 mg/kg IV bolus, repeated every 5 min until control, up to ~10 mg/kg. Reconstitute in sterile water, not saline (poor solubility); newer formulation (Ryanodex) dissolves faster.

Supportive & monitoring

• Active cooling to ~38 °C then stop (cold IV fluids, surface cooling, lavage) — avoid over-cooling.
• Treat hyperkalaemia (calcium, insulin-dextrose, bicarbonate) and acidosis (sodium bicarbonate 1–2 mEq/kg); treat arrhythmias (avoid calcium-channel blockers with dantrolene).
• Maintain urine output >2 mL/kg/h (fluids ± diuretics, urine alkalinisation) to prevent myoglobinuric renal failure.
• Monitor EtCO₂, core temperature, ABG, electrolytes, CK, coagulation (DIC) and urine myoglobin; continue in ICU ≥24 h (recrudescence risk) and refer for MH testing/counselling.

Definition

The appearance of signs and symptoms of respiratory distress within the first 48 hours after extubation. It requires immediate attention to prevent reintubation and its consequences.

Causes (classify: anatomical & physiological)

• Upper-airway obstruction — laryngospasm, laryngeal/glottic oedema, vocal-cord palsy, residual neuromuscular paralysis, extrinsic compression (neck haematoma, oedema). Signs: stridor, see-saw respiration.
• Lower-airway / pulmonary — bronchospasm, aspiration, pneumothorax, atelectasis, pulmonary oedema (cardiogenic — LV failure/MI; or non-cardiogenic — negative-pressure pulmonary oedema).
• Physiological failure — failure of oxygenation, of ventilation, to protect the airway, or to clear secretions (secretion obstruction is a leading cause of post-extubation respiratory failure).

High-risk patients

• Age >70, anaemia (Hb <10 g/dL), severe illness, prolonged ventilation, continuous IV sedation, unplanned extubation, positive fluid balance.

Management

• General: 100% O₂ by non-rebreather mask, monitor SpO₂/EtCO₂/TOF; ABG; sit up; treat residual paralysis (reverse, correct electrolytes); clear secretions.
• Cause-directed: laryngospasm → CPAP/Larson's manoeuvre/deepen ± suxamethonium; oedema → nebulised adrenaline, steroids, head-up; bronchospasm → bronchodilators/steroids; pulmonary oedema → diuretics + vasodilators/NIV; haematoma → open sutures & evacuate.
• NIV (early) for established distress in selected patients; reintubate if failing — treat the underlying factor before the next extubation attempt.

Definition

A bronchial blocker is a device passed through (or alongside) a single-lumen tube to occlude a main bronchus (or lobar bronchus) and achieve lung isolation / one-lung ventilation, with the operative lung collapsing distal to the inflated balloon.

Advantages

• Useful when a double-lumen tube is difficult/impossible — paediatric patients, difficult airway, tracheostomy, in-situ single-lumen tube.
• No tube exchange needed if post-operative ventilation is planned (leave the SLT in situ) — convenient in ICU.
• Allows selective lobar isolation.

Disadvantages

• Slower lung collapse (takes time to inflate/deflate); poor/limited suctioning and CPAP to the operative lung.
• Can be dislodged into the trachea → loss of isolation (potentially disastrous); needs repositioning.
• Requires a fibreoptic bronchoscope for placement and confirmation.

Types

• Arndt — nylon wire guide-loop (railroaded over the bronchoscope).
• Cohen — tip-deflecting wheel.
• Fuji Uniblocker — pre-shaped/pre-angled ("hockey-stick") tip.
• EZ-Blocker — distal Y-shape with two balloons that straddle the carina.
• Univent tube — a single-lumen tube with an enclosed, retractable bronchial blocker in a separate channel.

Insertion: coaxial (through the tube) or parallel (alongside it), positioned under fibreoptic guidance.

Definition & mechanism

Aortocaval compression syndrome occurs when, from about 20 weeks' gestation, the gravid uterus compresses the inferior vena cava and aorta in the supine position. IVC compression ↓ venous return from the lower body → ↓ cardiac output → maternal hypotension; aortic compression additionally ↓ utero-placental blood flow → fetal compromise.

Features & diagnosis

• Supine hypotension, tachycardia (or paradoxical bradycardia), pallor, sweating, nausea, dizziness — and fetal heart-rate changes.
• Marked when sympathetic tone is abolished — e.g. after spinal/epidural anaesthesia the compensatory vasoconstriction is lost, producing profound hypotension.

Prevention & management

• Left uterine displacement — 15° left lateral tilt or a wedge under the right hip (the single most important measure); full left-lateral if needed.
• Fluid co-loading, and a phenylephrine infusion (first-line vasopressor for spinal hypotension in caesarean section) to maintain baseline BP.
• During resuscitation/CPR: continuous manual left uterine displacement and prompt delivery if no response.

Changes

• Plasma volume ↑ ~40–50% and red-cell mass ↑ ~20–30% → the plasma rises more → dilutional ("physiological") anaemia of pregnancy.
• Physiological gestational thrombocytopenia (mild fall in platelets) and a physiological leukocytosis.
• Hypercoagulable state — ↑ fibrinogen and factors VII, VIII, X, XII and von Willebrand factor; ↓ protein S and ↓ fibrinolysis; antithrombin ~unchanged. TEG/ROTEM show hypercoagulability.

Anaesthetic implications

• Dilutional anaemia — interpret Hb in context; ensure iron/folate; the increased blood volume gives some reserve against peripartum blood loss (but PPH risk remains).
• Thrombocytopenia — usually safe for neuraxial block if platelets are adequate (commonly ≥70–80 ×10⁹/L and stable); distinguish benign gestational thrombocytopenia from pre-eclampsia/HELLP and ITP.
• Hypercoagulability → high VTE risk — thromboprophylaxis; carefully time neuraxial blocks around LMWH dosing (bleeding vs epidural haematoma).
• Be ready for rapid, major obstetric haemorrhage — group-and-save/crossmatch, TXA, and a massive-transfusion pathway.

Modalities

• Somatosensory evoked potentials (SSEP) — stimulate a peripheral nerve (e.g. posterior tibial); record cortical (scalp) and spinal (epidural) responses. Monitors the dorsal columns / sensory pathway. Alarm: >50% amplitude drop or >10% latency increase.
• Motor evoked potentials (MEP) — transcranial electrical stimulation of the motor cortex; record the spinal D-wave or muscle CMAP. Monitors the corticospinal (motor) tract — the more critical pathway (anterior cord).
• EMG (spontaneous/triggered) for nerve-root/pedicle-screw monitoring.
• Wake-up (Stagnara) test — largely obsolete: intra-operative emergence to test lower-limb motor function; risks accidental extubation, line/implant displacement, recall.

Anaesthetic implications (critical for signal quality)

• Use TIVA (propofol + an opioid/low-dose ketamine) — the technique of choice.
• Volatile agents and nitrous oxide depress evoked potentials (dose-dependently, MEP most sensitive) — keep volatiles <0.5–1 MAC or avoid; avoid N₂O.
• No neuromuscular blockade during MEP recording (only for intubation).
• Ketamine and etomidate augment amplitudes; maintain steady anaesthetic depth and stable physiology (BP, temperature, PaCO₂) — changes alter signals.

Definition & pathophysiology

Impaired ventricular relaxation and filling. Normal diastole has active early relaxation and passive late filling; in diastolic dysfunction, ↓ LV compliance → ↑ LV filling (end-diastolic) pressure, an increased dependence on the atrial "kick" for filling, pulmonary congestion, and a fall in stroke volume/CO. Causes: LVH/hypertension, ischaemia, aortic stenosis, hypertrophic/restrictive cardiomyopathy, constrictive pericarditis; and age, diabetes, amyloidosis/infiltrative disease.

Grading (echo — E/A ratio & E/e′)

• Grade I — impaired relaxation (E/A <0.8); Grade II — pseudonormal (E/A 0.8–2, E/e′ >14 — the HFpEF pattern); Grade III–IV — restrictive (E/A ≥2), reversible then fixed.

Anaesthetic goals

• Rate: avoid tachycardia (it shortens diastolic filling) — control with β-blockers; treat pain/light anaesthesia.
• Rhythm: maintain sinus rhythm — the atrial kick is essential; new AF can precipitate acute decompensation → cardiovert if unstable.
• Preload: a narrow window — avoid both hypovolaemia and fluid overload (stiff ventricle → easily flips to pulmonary oedema).
• Afterload: avoid sudden falls in SVR; maintain coronary perfusion pressure (especially with LVH/AS).
• Practical: arterial line ± TOE; titrated induction avoiding hypotension; postoperative fluid balance and monitoring for pulmonary oedema.

The core problem

Congenital diaphragmatic hernia (CDH — usually a left posterolateral Bochdalek defect) allows abdominal viscera into the thorax, producing pulmonary hypoplasia and persistent pulmonary hypertension of the newborn (↑PVR → right-to-left shunting). The key concept: CDH is a physiological emergency, not a surgical one — surgery is deferred until the neonate is stabilised.

Considerations

• Respiratory: hypoplastic lungs, poor compliance, risk of pneumothorax/barotrauma; scaphoid abdomen, bowel sounds in chest, mediastinal shift.
• Pulmonary hypertension: labile PVR — worsened by hypoxia, hypercarbia, acidosis, hypothermia and pain → pulmonary hypertensive crises with right-to-left shunt.
• Associated anomalies (cardiac defects, malrotation, trisomy 13/18/21) — screen with echocardiography.
• Neonatal factors — hypothermia, hypoglycaemia, immature organs, small margins for error.

Pre-operative stabilisation (goals)

• Awake endotracheal intubation; avoid bag-mask ventilation (gas distends herniated bowel and worsens lung compression). Nasogastric tube to decompress the stomach.
• Gentle ("lung-protective") ventilation — PIP <25 cmH₂O, permissive hypercapnia, preductal SpO₂ ≥ ~85–90%.
• Minimise PVR (avoid hypoxia/hypercarbia/acidosis/cold/pain); correct metabolic acidosis; maintain volume/perfusion.
• For refractory pulmonary hypertension: inhaled nitric oxide, HFOV, and ECMO as rescue. Operate only once stable.

Induction & maintenance

• Continue the ET tube; avoid positive-pressure mask ventilation and avoid N₂O (bowel distension).
• Balanced technique — high-dose opioid (fentanyl) + non-depolarising relaxant ± low-dose volatile/air-oxygen; titrate to haemodynamic stability (obtund the pulmonary-hypertensive stress response).
• Continue gentle ventilation (low PIP, permissive hypercapnia); maintain oxygenation without hyperoxia/barotrauma.

Monitoring & supportive care

• Pre-ductal (right hand) and post-ductal SpO₂ — the difference indicates the degree of right-to-left ductal shunting.
• ECG, invasive/non-invasive BP (right radial arterial line = preductal for ABG), temperature (prevent hypothermia), glucose, capnography.
• Treat pulmonary-hypertensive crises: 100% O₂, hyperventilate transiently, deepen anaesthesia/analgesia, inhaled NO, optimise pH.

Surgical & postoperative

• Avoid tight abdominal closure after reduction (↑ intra-abdominal pressure → IVC compression/↓ venous return, splinted diaphragm, compromised ventilation) — a staged/silo or ventral-hernia closure may be needed.
• Beware sudden fall in compliance / contralateral pneumothorax after reduction.
• Postoperative ICU ventilation and analgesia; continue pulmonary-hypertension management; do not aggressively re-expand the ipsilateral hypoplastic lung.

Definition & advantages

Drugs added to the intrathecal local anaesthetic to enhance, prolong or modify the block. Advantages: ↑ duration and quality of block, a local-anaesthetic-sparing effect (↓ dose → ↓ toxicity), and prolonged post-operative analgesia.

Agents

• Opioids (act on dorsal-horn opioid receptors): fentanyl — lipophilic, rapid onset, short duration, minimal respiratory depression; morphine — hydrophilic, long duration but risk of delayed respiratory depression (6–12 h) plus pruritus, nausea, urinary retention.
• α₂-agonists — clonidine, dexmedetomidine: prolong block/analgesia; side-effects bradycardia and hypotension (dexmedetomidine > clonidine).
• Vasoconstrictors — adrenaline (phenylephrine): ↓ systemic absorption, prolong block; caution in cardiac patients (tachycardia).
• NMDA antagonists — ketamine, magnesium sulfate.
• Neostigmine — analgesia via spinal cholinergic mechanism but limited by severe nausea and vomiting.

Neurological complications of spinal anaesthesia

• Early: direct nerve/root injury, spinal (epidural) haematoma (the most feared — needs emergency decompression), spinal/epidural abscess, and total spinal anaesthesia.
• Delayed: post-dural-puncture headache (the most common), transient neurological symptoms (TNS), adhesive arachnoiditis, meningitis, cauda equina syndrome, and persistent neurological deficit.

Factors affecting PDPH

• Patient: young age, female sex, pregnancy, low BMI, and previous PDPH/chronic headache (more common).
• Needle: larger gauge → more PDPH; cutting (Quincke) tips cause more than pencil-point (Whitacre/Sprotte) needles; orienting a cutting bevel parallel to the longitudinal dural fibres reduces it; multiple dural punctures increase it.

Mechanism: CSF leak through the dural puncture > production → ↓ CSF pressure → traction on pain-sensitive intracranial structures and compensatory cerebral vasodilatation → a postural (upright-worsened) fronto-occipital headache, ± neck stiffness, photophobia, tinnitus and CN VI palsy.

Focused assessment

• Morbid obesity with multiple comorbidities — screen for IHD/CAD, assess functional capacity in METs, restrictive/obstructive lung disease and nutritional deficiencies.
• OSA — apply the STOP-BANG score; ask about sleeping habits (able to lie supine or not) and CPAP use.
• Airway — anticipate difficult mask ventilation and difficult intubation; assess for difficult IV access.
• Investigations: baseline CBC, KFT, LFT, TFT, coagulation; ABG (pulmonary); ECG and echocardiography (cardiac); and where indicated PFT and a sleep study.

Optimisation

Weight reduction, CPAP use, an optimised diet, physical exercise, chest physiotherapy with incentive spirometry, and a plan for multimodal analgesia. Optimise cardiac and respiratory status before an elective list.

Anticipated problems

• Difficult mask ventilation and difficult airway (anatomical & physiological); difficult IV cannulation.
• Logistical: need a large BP cuff, a table rated for the weight, and drug doses adjusted to lean/ideal body weight; difficult positioning; ↑ risk of peripheral nerve injury.
• ↑ blood loss, longer duration, and attention to fluid, electrolyte and acid–base balance.

Anaesthesia goals & technique

• Technique: general anaesthesia with a controlled ventilation via ETT ± thoracic epidural.
• Pre-oxygenation: 3 min tidal breathing / vital-capacity breaths, in head-up (ramped) position, ± CPAP with FiO₂ 100% (NIV may also be used).
• Induction: modified rapid sequence induction — titrated propofol (dosed to lean body weight ~2 mg/kg) + opioid (1–1.5 µg/kg) + a relaxant (e.g. atracurium 0.5 mg/kg); confirm ETT position and place a Ryle's tube.
• Maintenance: volatile in air/O₂ — desflurane is ideal (low blood solubility → rapid emergence); lung-protective ventilation with permissive hypercapnia, plateau pressure <30 cmH₂O and peak <35 cmH₂O.
• Fluids: avoid overload — use goal-directed fluid therapy; maintain haemodynamic stability with appropriate monitoring (IBP, CVP, airway pressures).

Extubation & recovery

• Awake extubation after return of reflexes, in the head-up position with O₂ supplementation ± CPAP.
• Multimodal analgesia — paracetamol, NSAIDs (if not contraindicated), thoracic epidural, TAP or quadratus lumborum block; minimise systemic opioids.
• Respiratory: chest physiotherapy, incentive spirometry, bronchodilators and steroids as needed.
• DVT prophylaxis (mechanical + pharmacological) and early mobilisation.

Basis

Spinal cord transection causes loss of supraspinal control over autonomic pathways, leading to acute and chronic cardiovascular, thermoregulatory and visceral dysfunction. The sympathetic outflow is thoracolumbar (T1–L2) and the parasympathetic is craniosacral; loss of descending sympathetic control leaves unopposed parasympathetic activity below the lesion.

Acute phase — spinal shock (hours to weeks)

• Cardiovascular: hypotension and bradycardia from loss of sympathetic tone; peripheral vasodilatation → warm, dry skin.
• Reflexes: areflexia below the lesion.
• Temperature: poikilothermia — cannot regulate temperature.

Chronic phase — after spinal shock resolves

• Autonomic dysreflexia (lesions above T6): a stimulus below the lesion (bladder/bowel distension, pain) triggers a massive sympathetic discharge → hypertension, reflex bradycardia, and sweating/flushing above the lesion. Treatment: remove the stimulus and give antihypertensives.
• Cardiovascular: persistent bradycardia and orthostatic hypotension.
• Thermoregulation: loss of sweating below the lesion; cannot regulate temperature.
• Bladder & bowel: neurogenic bladder, constipation, sexual dysfunction; reflexes return.

Anaesthetic implications

• Hypotension → fluids + vasopressors; bradycardia → atropine.
• Prevent autonomic dysreflexia — avoid triggers, ensure bladder/bowel decompression, and provide deep anaesthesia; regional (spinal/epidural) anaesthesia is preferred as it blocks the afferent limb of the reflex.
• Avoid suxamethonium after the acute phase (hyperkalaemia risk from receptor upregulation).

Concept & vulnerable window

Sedatives and anaesthetic agents may have harmful effects on the developing brain. Brain development begins in the 3rd trimester, is not complete at birth, and continues over the first years of life. The period of maximal synaptogenesis — roughly 34 weeks of gestational age to ~24 months post-partum (the first 2–3 years) — is the most vulnerable. A single brief exposure appears to have no adverse effect; repeated/prolonged exposure has been linked to neuronal apoptosis and neurodegeneration in animal models.

Mechanisms

• Dose- and concentration-dependent damage to neuronal and glial architecture; neuroinflammation; inhibition of neurotrophic factors.
• Generation of reactive oxygen species; activation of apoptosis via NMDA antagonism and GABA agonism.
• Suppression of neurogenesis, altered neuronal differentiation, loss of neural stem cells, and impaired synaptogenesis; variation in neuronal excitability and receptor expression.

Clinical evidence

• Association with later learning, behavioural and memory problems; note that uncontrolled pain itself can promote neuronal apoptosis (ketamine may be neuroprotective in this context).
• Prospective human studies: the PANDA study (single exposure <36 months for inguinal hernia; tested at 8–15 y vs siblings) showed no difference in IQ; the GAS trial (infants <6 months, GA vs awake spinal, tested at 2 and 5 y) showed no neurodevelopmental deficit; the MASK study compared exposed vs unexposed children <3 years.

Practical approach

• For an elective procedure, if delay adds no risk, postpone until after the brain growth spurt; minimise dose and duration of exposure.
• Reassure parents that there is no evidence that a single, well-conducted anaesthetic harms the brain.