NEW Added to close a syllabus gap — "cardiothoracic or neurosurgery" is named under special requirements.

Cardiothoracic & neuroanaesthesia

One-lung ventilation, cardiopulmonary bypass, and the principles of anaesthesia for the injured or operated brain.

One-lung ventilation

Double-lumen tube — usually left-sided, because the right upper lobe bronchus arises early (about 2.5 cm from the carina) and is easily occluded. Confirm position with fibreoptic bronchoscopy.
Hypoxaemia is the main problem: the non-ventilated lung is still perfused, creating a large shunt. Hypoxic pulmonary vasoconstriction diverts blood away, reducing shunt from about 50% to 20–30% — and volatile agents inhibit HPV, which is an argument for TIVA.
Management of desaturation, in order: check tube position → 100% oxygen → CPAP to the non-dependent lung → PEEP to the dependent lung → intermittent two-lung ventilation → ask the surgeon to clamp the pulmonary artery.
Ventilation settings: tidal volume 4–6 ml/kg, plateau <30 cmH₂O, permissive hypercapnia — protective ventilation, because the dependent lung takes the whole tidal volume.
Lateral position: the dependent lung is better perfused but less well ventilated (compressed by mediastinum and abdominal contents) — worsening V/Q mismatch.

Circuit: venous cannula → reservoir → pump (roller or centrifugal) → oxygenator → heat exchanger → arterial filter → aortic cannula.
Anticoagulation: heparin 300 units/kg to an ACT >400–480 seconds before cannulation. Reversed with protamine 1 mg per 100 units.
Non-pulsatile flow at 2.4 L/min/m², MAP 50–70 mmHg. Haemodilution is deliberate, to a haematocrit around 0.25.
Myocardial protection: cold cardioplegia — high-potassium solution arresting the heart in diastole — plus topical cooling.
Systemic effects: systemic inflammatory response, coagulopathy (platelet dysfunction, factor dilution, residual heparin), haemolysis, hypothermia, fluid shifts, and neurocognitive dysfunction from microemboli.
Coming off bypass — check: rewarmed, rhythm, rate, electrolytes (especially K⁺), acid-base, ventilation restarted, and inotropes ready.

Target	Value	Rationale
CPP	60–70 mmHg	CPP = MAP − ICP
ICP	<20–22 mmHg	Above this, treat
PaCO₂	4.5–5.0 kPa	CBF varies linearly with CO₂; over-hyperventilation causes ischaemia
PaO₂	>13 kPa	Avoid hypoxia absolutely
Sodium	140–145 mmol/L	Avoid hyponatraemia — worsens oedema
Glucose	Normoglycaemia	Hyperglycaemia worsens ischaemic injury

Propofol, thiopentone and etomidate reduce CMRO₂, CBF and ICP with flow-metabolism coupling preserved — hence TIVA is favoured.
Volatiles UNCOUPLE flow from metabolism: they reduce CMRO₂ but cause dose-dependent cerebral vasodilation, raising CBF and ICP. Keep below 1 MAC if used.
Ketamine and nitrous oxide raise ICP — traditionally avoided, though the ketamine position is now debated.
Osmotherapy: mannitol 0.25–1 g/kg (osmotic diuretic, risk of hypovolaemia and rebound) or hypertonic saline (expands intravascular volume — better if hypovolaemic).

Sitting position — risk of venous air embolism. Most sensitive practical monitor is a fall in ETCO₂; transoesophageal echo and precordial Doppler are more sensitive. Management: flood the field, N₂O off, 100% oxygen, aspirate via central line, left lateral head-down.
Subarachnoid haemorrhage — nimodipine for vasospasm, triple-H therapy historically, and avoid hypotension.
Posterior fossa surgery — brainstem handling causes sudden arrhythmias and haemodynamic swings.
Emergence should be smooth: coughing and straining spike ICP and risk haematoma.