Surgical approach
- Access: median sternotomy (most common); occasionally minimally invasive (MIDCAB) via left anterior thoracotomy for LAD grafting
- Conduit harvest
- LIMA/RIMA (internal mammary) harvested pedicled or skeletonised; LIMA→LAD most common
- Saphenous vein (open or endoscopic) ± radial artery (requires spasm prophylaxis and adequate collateral flow)
- On-pump CABG (with CPB): cannulation and bypass
- Systemic heparinisation → aortic cannula + right atrial (two-stage) venous cannula (or bicaval)
- Initiate CPB; temperature management (often mild hypothermia); haemodilution
- Aortic cross-clamp; cardioplegia (antegrade via aortic root and/or retrograde via coronary sinus) ± topical cooling
- Distal anastomoses on arrested heart; proximal anastomoses to aorta (often during partial clamp) or using composite grafts
- De-airing; remove cross-clamp; reperfusion; wean from CPB; protamine reversal; haemostasis; pacing wires; chest drains; sternal closure
- Off-pump CABG (OPCAB): beating-heart revascularisation
- Heparinisation to lower target ACT than CPB; heart stabiliser and positioner used
- Coronary occlusion/shunt during distal anastomosis; haemodynamic instability common with heart displacement (especially posterior vessels)
Anaesthetic management (headline)
- Type of anaesthesia: General anaesthesia with awake arterial line
- Airway: cuffed ETT
- Duration: typically 3–6 hours (longer if complex/multiple grafts, redo, combined procedures)
- Pain: moderate–severe (sternotomy + chest drains). Multimodal opioid-sparing analgesia; aim early extubation where appropriate
- Key aims: maintain myocardial oxygen supply-demand balance; avoid tachycardia/hypotension; ensure anticoagulation/ACT targets; manage CPB physiology; meticulous haemostasis and temperature control
Indications and patient profile
- Indications: prognostic and/or symptomatic benefit in coronary artery disease
- Left main stem disease, triple vessel disease (esp. with LV dysfunction), proximal LAD disease, diabetes with multivessel disease, refractory angina despite optimal medical therapy/PCI
- Urgent/emergency CABG: ongoing ischaemia, failed PCI, mechanical complications (rare as isolated CABG), cardiogenic shock in selected cases
- Common comorbidity burden: LV dysfunction, valvular disease, pulmonary hypertension, CKD, carotid disease, frailty, anaemia, diabetes, COPD, obesity, OSA
- Risk stratification: EuroSCORE II (and local models). Use to inform planning (ICU bed, blood products, invasive monitoring, inotropes/MCS readiness)
Preoperative assessment and optimisation
- History/exam: angina class, recent ACS, exercise tolerance, heart failure symptoms, syncope, arrhythmias, prior PCI/stents, bleeding history, stroke/TIA, claudication
- Investigations to review
- Coronary angiography (targets, LVEDP if available), echocardiography (LV/RV function, valves, pulmonary pressures), ECG
- Bloods: FBC (anaemia/platelets), U&E (CKD/K+), coagulation, HbA1c, group & save/crossmatch; consider iron studies if anaemic and time allows
- CXR; spirometry if significant lung disease; carotid duplex if indicated (bruit, prior TIA/stroke, high-risk features per local policy)
- Medication management (typical patterns; follow local protocol)
- Aspirin usually continued; P2Y12 inhibitors (clopidogrel/ticagrelor/prasugrel) stopped pre-op when possible (bleeding vs ischaemia trade-off)
- Beta-blockers usually continued (avoid withdrawal tachycardia). Nitrates continued if symptomatic
- ACEi/ARB: often held on day of surgery if concern about vasoplegia/hypotension (institution-dependent)
- Anticoagulants: warfarin stopped and bridged only if strong indication; DOACs stopped according to renal function and bleeding risk
- Diabetes: adjust insulin/agents; SGLT2 inhibitors usually withheld pre-op to reduce ketoacidosis risk
- Optimisation: treat infection, correct anaemia if time, manage heart failure (diuresis), smoking cessation, discuss postoperative ventilation/ICU, consent for transfusion and invasive lines
Monitoring and access
- Standard: ECG (5-lead with ST analysis), SpO2, NIBP, capnography, temperature, urine output
- Invasive: arterial line pre-induction if unstable; central venous access (drug delivery, CVP trends); large-bore peripheral access
- Advanced monitoring (case-dependent): cardiac output monitoring, SvO2, pulmonary artery catheter (selected: severe pulmonary HTN/RV failure/complex), cerebral oximetry (NIRS) where available
- TOE: commonly used; essential in many centres for assessment of ventricular function, volume status, regional wall motion, valve pathology, aortic atheroma, air, and causes of instability
- Defibrillator pads; external pacing availability; warming devices; rapid infuser and cell salvage (if used locally)
Induction and maintenance (key principles)
- Goals: avoid tachycardia, hypotension, hypertension, and myocardial ischaemia; maintain coronary perfusion pressure; preserve RV function; ensure smooth laryngoscopy and sternotomy response control
- Induction: titrated opioid + hypnotic (propofol/etomidate) ± benzodiazepine; neuromuscular blockade (e.g. rocuronium). Consider vasopressor ready (metaraminol/phenylephrine/noradrenaline)
- Maintenance: volatile (isoflurane/sevoflurane) or TIVA; balanced with opioid; consider volatile myocardial preconditioning (evidence mixed but widely used). Maintain depth to prevent sympathetic surges
- Ventilation: avoid hypoxia/hypercapnia (↑PVR), avoid excessive PEEP impairing venous return; lung-protective strategy; recruitment after sternotomy/CPB
- Haemodynamic targets (typical): HR ~50–80 (avoid tachycardia), MAP often 60–80 pre-CPB (individualise; higher if critical carotid/renal disease), maintain sinus rhythm where possible
Anticoagulation, ACT and protamine
- Heparin before cannulation (on-pump) or before coronary occlusion (off-pump). Dose commonly 300–400 IU/kg for CPB (institutional variation)
- ACT targets
- On-pump: typically ACT > 480 s (or per local protocol/device)
- Off-pump: often lower target (e.g. ACT 250–350 s), per surgeon preference/protocol
- Heparin resistance: consider antithrombin deficiency (heparin exposure, sepsis, liver disease). Management: additional heparin, AT concentrate or FFP, confirm ACT device/function
- Protamine reversal post-CPB: dose guided by heparin dose/ACT/heparin concentration systems. Give slowly; watch for hypotension, pulmonary hypertension, anaphylactoid reactions
- High-risk protamine reactions: prior exposure (e.g. NPH insulin), vasectomy, fish allergy (association debated), rapid administration
Cardiopulmonary bypass (CPB): physiology and practical implications
- Core features: non-pulsatile flow, haemodilution, hypothermia (often), systemic inflammatory response, altered coagulation and platelet dysfunction, microemboli risk
- Perfusion targets (typical): pump flow ~2.2–2.6 L/min/m²; MAP often 50–80 mmHg (individualise: chronic HTN, carotid disease)
- Gas exchange on CPB: oxygenator; CO2 management; alpha-stat vs pH-stat strategies (centre-specific; pH-stat more common in deep hypothermia/paediatrics)
- Temperature: hypothermia reduces metabolic rate; rewarming must be controlled to avoid gaseous microemboli and cerebral hyperthermia; aim normothermia at separation
- Electrolytes/acid-base: monitor K+ (cardioplegia-related hyperkalaemia), lactate, ionised Ca2+; treat metabolic acidosis by addressing cause (flow/oxygen delivery)
Myocardial protection and ischaemia management
- Cardioplegia: high K+ arrests heart; may be blood or crystalloid; repeated dosing; antegrade/retrograde routes
- Recognise intra-op ischaemia: ST changes, new regional wall motion abnormality on TOE, haemodynamic deterioration, ventricular arrhythmias
- Management: optimise supply-demand (HR, BP, Hb, oxygenation), treat hypotension (vasopressors), consider nitrates for spasm, inotropes for LV failure, discuss graft issues with surgeon
Weaning from CPB: structured approach
- Prerequisites: normothermia/rewarmed, adequate ventilation, rhythm (sinus/pace), electrolytes corrected (K+, Ca2+, Mg2+), Hb acceptable, lungs recruited, surgical field ready
- Assess with TOE: LV/RV function, volume status, valve function, regional wall motion, tamponade/air, aortic pathology
- Haemodynamic support: vasopressor for vasoplegia (noradrenaline/vasopressin), inotrope for pump failure (dobutamine/adrenaline/milrinone), pacing for brady/AV block
- Common problems at separation
- LV failure (ischaemia, inadequate protection, graft issue), RV failure (PHTN, air, ischaemia), vasoplegia, bleeding/coagulopathy, tamponade, residual air, arrhythmias
- Mechanical circulatory support (MCS): IABP, VA-ECMO, Impella (centre-dependent). Indications: refractory cardiogenic shock despite optimisation
Bleeding and transfusion strategy
- Causes: surgical bleeding, residual heparin, platelet dysfunction (CPB), hypofibrinogenaemia, dilutional coagulopathy, hyperfibrinolysis
- Approach: quantify blood loss; check ACT; use point-of-care testing where available (TEG/ROTEM) to guide targeted therapy
- Typical components: RBCs (aim Hb per patient/physiology), platelets, FFP, fibrinogen (cryoprecipitate/concentrate), calcium replacement, tranexamic acid (common)
- Re-sternotomy risk: persistent high drain output, haemodynamic instability, rising lactate, tamponade signs; early surgical review
Analgesia and fast-track extubation
- Multimodal: paracetamol, opioids (fentanyl/remifentanil intra-op; morphine/oxycodone post-op), consider ketamine low-dose, magnesium; avoid NSAIDs in CKD/bleeding risk
- Regional adjuncts (centre-specific): parasternal/pectointercostal fascial plane blocks, ESP blocks; neuraxial techniques limited by anticoagulation and bleeding risk
- Fast-track: aim extubation within ~6 hours in suitable patients (stable haemodynamics, normothermia, acceptable bleeding/gas exchange, good analgesia)
Postoperative issues (ICU/HDU)
- Cardiac: low cardiac output syndrome, arrhythmias (AF common), ischaemia/infarction, pacing needs, tamponade
- Respiratory: atelectasis, pleural effusions, pneumonia, pulmonary oedema; manage with physiotherapy, recruitment, diuresis as appropriate
- Renal: AKI risk (CPB, hypotension, emboli); optimise perfusion, avoid nephrotoxins, monitor urine output/creatinine
- Neurological: delirium, stroke, cognitive dysfunction; manage BP, oxygenation, glucose; early mobilisation and delirium prevention bundle
- Glycaemic control: avoid severe hyperglycaemia and hypoglycaemia; insulin infusion protocols common
You are anaesthetising a patient for CABG. What are your key preoperative concerns and how do you assess risk?
Structure: patient factors, coronary anatomy/ventricular function, comorbidities, medications/bleeding, and planning for ICU/inotropes/blood.
- Assess severity/instability of coronary disease: recent ACS, ongoing angina, critical LMS/proximal LAD, prior stents and antiplatelets
- LV/RV function and valves on echo; pulmonary pressures; symptoms of heart failure
- Comorbidities: CKD, COPD, diabetes, carotid disease/TIA, anaemia, frailty
- Medication plan: aspirin continuation, P2Y12 cessation timing, anticoagulant management, beta-blocker continuation, ACEi/ARB strategy
- Risk scoring: EuroSCORE II; plan resources (ICU bed, blood, cell salvage, TOE, MCS availability)
Describe your monitoring for CABG and justify each component.
Answer should cover standard + invasive + adjuncts (TOE) and what decisions each informs.
- ECG with ST analysis: detect ischaemia/arrhythmias; defib pads for rapid cardioversion/defib
- Arterial line: beat-to-beat BP, blood sampling, vasopressor titration; consider pre-induction in severe disease
- Central venous access: vasoactive infusions, access reliability; CVP trends (limited as preload marker)
- TOE: ventricular function, volume, RWMA, air, tamponade; guides weaning from CPB
- Temperature (core), urine output, ABGs/electrolytes (K+, Ca2+, lactate), coagulation/ACT
How would you conduct induction of anaesthesia for CABG in a patient with critical left main stem disease?
Key themes: maintain coronary perfusion pressure, avoid tachycardia, avoid hypotension, have rescue drugs ready, gentle laryngoscopy.
- Preparation: arterial line before induction if unstable; vasopressors drawn up; defib pads; discuss plan with team
- Induction: titrated opioid + hypnotic (consider etomidate if poor LV) + muscle relaxant; avoid large boluses causing hypotension
- Haemodynamic goals: maintain MAP/diastolic pressure for coronary perfusion; avoid tachycardia (treat pain/light anaesthesia promptly)
- Intubation response: adequate depth, short-acting opioid, consider lidocaine/esmolol carefully; treat hypertension/tachycardia
What ACT targets do you use for CABG and what are the causes and management of heparin resistance?
Examiners want: numbers (typical), causes (AT deficiency), and practical management.
- Targets: on-pump commonly ACT > 480 s; off-pump often ACT 250–350 s (follow local protocol)
- Heparin resistance causes: antithrombin deficiency (prior heparin, sepsis), high factor VIII, thrombocytosis, device/measurement error
- Management: confirm sampling/device; give more heparin; administer AT concentrate (preferred) or FFP; recheck ACT
Describe the physiological changes during CPB and their anaesthetic implications.
Cover haemodilution, non-pulsatile flow, inflammatory response, coagulation changes, temperature, and organ effects.
- Haemodilution: reduced Hb and oncotic pressure → tissue oxygen delivery considerations and fluid shifts
- Non-pulsatile flow and altered autoregulation: MAP targets individualised (carotid disease/chronic HTN)
- Inflammatory response: vasoplegia, capillary leak, lung dysfunction
- Coagulation: platelet dysfunction/consumption, factor dilution, fibrinolysis → bleeding risk; need for targeted blood product therapy
- Temperature management: hypothermia reduces metabolic rate; rewarming risks (gas emboli, cerebral hyperthermia)
How do you approach weaning from CPB? Give a structured plan.
A systematic approach scores highly: temperature, ventilation, rhythm, preload/afterload/contractility, TOE, bleeding, and communication with perfusionist/surgeon.
- Check prerequisites: rewarming, ventilation on, lungs recruited, acid-base/electrolytes corrected (K+, Ca2+, Mg2+), Hb acceptable
- Rhythm: sinus preferred; pace if brady/heart block; treat AF/VT promptly
- TOE assessment: LV/RV function, volume, RWMA, valve function, air, tamponade
- Optimise haemodynamics: preload (volume), afterload (vasopressors/vasodilators), contractility (inotropes), consider pulmonary vasodilators if RV failure
- If difficulty: consider graft problem/ischaemia, inadequate myocardial protection, vasoplegia, tamponade, pneumothorax; escalate to MCS if refractory
A patient becomes hypotensive after protamine. What are the differential diagnoses and immediate management?
Need to distinguish protamine reaction from surgical bleeding/tamponade/ventricular dysfunction/vasoplegia.
- Immediate actions: stop/slow protamine, call for help, 100% oxygen, check rhythm, support BP with vasopressors/inotropes
- Protamine reactions: systemic hypotension (rapid infusion), anaphylactoid/anaphylaxis, pulmonary hypertension with RV failure
- Other causes: bleeding, tamponade, LV failure/ischaemia, vasoplegia, pneumothorax, residual heparin/ACT issues
- Management specifics: adrenaline for anaphylaxis; pulmonary vasodilators (e.g. inhaled NO) and inotropes for RV failure; TOE to diagnose tamponade/ventricular dysfunction
Discuss postoperative atrial fibrillation after CABG: risk factors, prevention, and management.
Common FRCA theme: incidence, haemodynamic impact, anticoagulation considerations, and rate vs rhythm control.
- Incidence: common (often day 2–3). Risk factors: age, atrial enlargement, inflammation, electrolyte disturbance, withdrawal of beta-blocker
- Prevention: continue beta-blockers where possible; correct K+/Mg2+; consider amiodarone prophylaxis in high-risk patients (local policy)
- Management: assess stability; if unstable → DC cardioversion. If stable → rate control (beta-blocker/amiodarone) or rhythm control (amiodarone) depending on context
- Anticoagulation: balance stroke risk vs bleeding; follow cardiology/cardiothoracic protocols (often delayed/individualised early post-op)
What are the main causes of excessive bleeding after CABG and how would you manage it in ICU/theatre?
Examiners want a logical algorithm: surgical vs coagulopathy, ACT, targeted products, and when to re-explore.
- Differentiate: surgical source vs coagulopathy (CPB platelet dysfunction, dilution, fibrinolysis, hypofibrinogenaemia, residual heparin)
- Immediate steps: quantify drain losses, check haemodynamics, send labs/POC (TEG/ROTEM), check ACT and temperature/calcium
- Treat: protamine if residual heparin; fibrinogen replacement if low; platelets for platelet dysfunction/low count; FFP for factor deficiency; TXA if hyperfibrinolysis
- Escalate: early surgical review; re-sternotomy if ongoing high losses/instability/tamponade suspicion
Compare on-pump vs off-pump CABG from an anaesthetic perspective.
Focus on haemodynamics, anticoagulation, organ effects, and practical conduct rather than surgical marketing claims.
- On-pump: controlled field and myocardial protection but CPB-related inflammation, coagulopathy, haemodilution, embolic risk
- Off-pump: avoids CPB effects but more haemodynamic instability during heart positioning; risk of ischaemia during coronary occlusion; requires close communication and vasoactive titration
- Anticoagulation: higher ACT target on-pump; lower target off-pump; protamine reversal still required
- Outcomes: patient selection matters; evidence varies by centre expertise; anaesthetist role is maintaining stability and organ perfusion
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