Surgical approach (cannulation & circuit set-up)
- Usually performed in ICU/theatre/cath lab by cardiothoracic surgeon, intensivist, or ECMO team; ultrasound + fluoroscopy/echo guidance where available
- Cannulation strategy chosen by indication and patient size/anatomy
- VV ECMO: typically femoro-jugular (drain femoral, return IJ) or dual-lumen cannula (IJ) with tip in IVC and return jet directed at tricuspid valve
- VA ECMO: peripheral femoral artery + femoral vein (common), or central cannulation (RA + aorta) post-cardiotomy
- Percutaneous Seldinger technique; serial dilatation; secure cannulae; confirm position (US/echo/CXR) and flows
- For femoral arterial cannulation: consider distal limb perfusion catheter to reduce limb ischaemia
- Prime circuit (crystalloid/blood depending on size/haematocrit targets), de-air, connect, commence flow and sweep gas; adjust anticoagulation
- Ongoing surgical tasks: manage bleeding at cannulation sites, reposition cannulae, manage vascular complications, decannulation and vessel repair/closure
Anaesthetic management (for cannulation/decannulation or theatre transfer)
- Type of anaesthesia: commonly GA or deep sedation; regional techniques usually avoided if anticoagulated/unstable; local infiltration for percutaneous cannulation in selected cases
- Airway: usually already intubated/ventilated; if not, plan RSI with haemodynamic support; SGA generally unsuitable (aspiration risk, need for controlled ventilation)
- Duration: cannulation typically 30–90 min (longer if difficult anatomy/complications); decannulation 30–120 min depending on surgical repair
- How painful: moderate (large-bore cannulae, groin/neck dissection if surgical cut-down); ensure analgesia and immobility
- Monitoring: full ICU-level monitoring; invasive arterial line (ideally right radial in VA ECMO), central access, capnography, temperature, urine output; consider TOE for cannula positioning and cardiac assessment
- Induction/maintenance: haemodynamically gentle (ketamine/etomidate/opioid); vasopressors/inotropes ready; avoid hypoxia/hypercapnia during airway manipulation
- Anticoagulation: coordinate heparin bolus/infusion with cannulation; balance bleeding vs thrombosis; correct coagulopathy before decannulation where possible
- Ventilation strategy once on ECMO: lung-protective/ultra-protective ventilation; avoid derecruitment; titrate PEEP; manage oxygenation largely via ECMO settings (esp VV)
- Transport: secure cannulae/lines; ensure battery/oxygen supply for pump and sweep gas; contingency for pump failure and accidental decannulation
Definition and aims
- Extracorporeal life support providing gas exchange (oxygenation and/or CO2 removal) and/or circulatory support via an extracorporeal circuit with pump + membrane oxygenator
- Aims: support failing organ(s) while underlying pathology treated/recovery occurs; bridge to decision/recovery/transplant/VAD
Configurations and key differences
- VV ECMO (venous drainage → oxygenator → venous return): respiratory support only; requires adequate native cardiac output
- Indications: severe ARDS, refractory hypoxaemia/hypercapnia, bridge to lung transplant, severe asthma with hypercapnia (selected), airway catastrophe (selected)
- VA ECMO (venous drainage → oxygenator → arterial return): provides circulatory + respiratory support; increases afterload and may impair LV ejection
- Indications: cardiogenic shock (MI, myocarditis), post-cardiotomy failure, refractory cardiac arrest (ECPR), massive PE with shock, severe sepsis with myocardial depression (selected)
- VAV / VV-A / hybrid: used when combined respiratory + circulatory needs or differential hypoxaemia management
Circuit components (what each part does)
- Drainage cannula: removes venous blood; position affects recirculation and achievable flow
- Pump (centrifugal common): generates flow; sensitive to preload/afterload; excessive negative inlet pressure risks cavitation/haemolysis
- Membrane oxygenator: diffusion of O2 into blood and CO2 out; performance affected by surface area, blood flow, sweep gas flow, and clot burden
- Heat exchanger: temperature control
- Gas blender/sweep: controls fraction of delivered O2 to oxygenator and sweep flow (main determinant of CO2 clearance)
Gas exchange physiology on ECMO (high-yield relationships)
- Oxygenation depends mainly on ECMO blood flow (L/min), patient cardiac output, Hb, and oxygenator function; sweep gas FiO2 also contributes
- CO2 removal depends mainly on sweep gas flow rate; also influenced by blood flow and metabolic CO2 production
- Recirculation (VV): oxygenated return blood is immediately drained again → reduced effective oxygen delivery; worsened by poor cannula position, high flows, low intravascular volume
- VA mixing and differential hypoxaemia: oxygenated ECMO blood mixes with native LV output; distribution depends on cannulation site and relative flows
Haemodynamics on VA ECMO (key exam concepts)
- VA ECMO increases aortic root pressure/afterload → may reduce LV stroke volume; risk of LV distension, pulmonary oedema, thrombus if aortic valve not opening
- Need to ensure some LV ejection and pulsatility; consider inotropes/vasodilators, IABP, Impella, atrial septostomy, or surgical venting in severe cases
- Right radial arterial line reflects cerebral/coronary oxygenation in peripheral VA ECMO (upper body supplied by native heart); femoral arterial line may reflect ECMO-only oxygenation
Indications and contraindications (typical FRCA framing)
- VV ECMO: potentially reversible severe respiratory failure despite optimal ventilation, paralysis, prone positioning, and adjuncts
- VA ECMO: refractory cardiogenic shock with potentially reversible cause or bridge strategy; ECPR in selected witnessed arrests with short no-flow time and treatable cause
- Relative contraindications: irreversible disease without exit strategy, severe irreversible neurological injury, uncontrolled bleeding, inability to anticoagulate, advanced frailty/poor baseline function, prolonged injurious ventilation (VV)
Anticoagulation and haematology
- Pro-thrombotic circuit surfaces + high shear → need anticoagulation but bleeding risk is high; balance is dynamic
- Common strategy: unfractionated heparin infusion; monitoring may include aPTT, anti-Xa, ACT, viscoelastic testing; interpret in context of haemolysis, inflammation, factor consumption
- Heparin resistance: consider antithrombin deficiency; management includes AT supplementation or alternative anticoagulant (e.g., argatroban) depending on local protocol
- HIT: suspect with falling platelets/thrombosis; stop heparin and use non-heparin anticoagulant (argatroban/bivalirudin) with specialist input
- Transfusion targets vary; consider Hb (oxygen delivery), fibrinogen, platelets; avoid unnecessary transfusion (TRALI/TACO, sensitisation for transplant candidates)
Ventilation and sedation on VV ECMO
- Ultra-protective ventilation: low tidal volume, low plateau pressure, adequate PEEP; aim to minimise VILI while ECMO provides gas exchange
- Wean sedation where feasible to facilitate neuro assessment and early mobilisation (in selected centres); balance against cannula safety and patient-ventilator synchrony
- Prone positioning can still be used on VV ECMO in selected cases with experienced team
Complications (categorise for viva)
- Bleeding: cannulation site, GI, pulmonary, intracranial; exacerbated by anticoagulation, thrombocytopenia, acquired vWD, factor consumption
- Thrombosis/embolism: circuit clot, oxygenator failure, stroke; risk increased with low flows and inadequate anticoagulation
- Haemolysis: high shear/negative inlet pressure; leads to AKI, hyperkalaemia, pigment nephropathy; monitor plasma-free Hb, LDH, dark urine
- Infection: line/cannula-related, ventilator-associated; immunomodulation and prolonged ICU stay increase risk
- Vascular: limb ischaemia (peripheral VA), compartment syndrome, pseudoaneurysm, dissection, venous thrombosis
- Neurological: ICH, ischaemic stroke, seizures, hypoxic brain injury (esp ECPR)
- Mechanical: air embolism, pump failure, oxygenator clotting, tubing rupture, accidental decannulation
- VA-specific: LV distension, pulmonary oedema, myocardial ischaemia, differential hypoxaemia (Harlequin/North–South syndrome)
Differential hypoxaemia (Harlequin / North–South syndrome) on peripheral VA ECMO
- Mechanism: femoral arterial return sends oxygenated blood retrograde up aorta; if lungs are failing but LV ejects poorly oxygenated blood, upper body (coronaries/brain) may receive desaturated blood while lower body appears well-oxygenated
- Recognition: low right radial SpO2/PaO2 with preserved femoral arterial oxygenation; cerebral desaturation; worsening lactate/ECG changes
- Management options: improve lung oxygenation (ventilation, recruitment), increase ECMO flow (if feasible), reduce native LV output only if appropriate, change configuration to VAV, move arterial return to axillary/subclavian/aortic (central) cannulation
Weaning and decannulation (principles)
- VV ECMO: assess lung recovery; reduce sweep gas (CO2) and ECMO FiO2; trial off sweep with acceptable gas exchange on lung-protective settings
- VA ECMO: assess myocardial recovery with echo, pulsatility, reduced vasoactive requirement, adequate MAP and end-organ perfusion; reduce flows stepwise with close monitoring; consider formal weaning study
- Decannulation: plan anticoagulation hold, blood products, vascular control/repair; monitor for bleeding, thrombosis, limb perfusion; post-decannulation haemodynamic/respiratory deterioration
You are asked to review a patient on VV ECMO with worsening hypoxaemia. How would you assess and manage?
Structure: patient factors → circuit factors → ventilator factors → diagnosis-specific actions.
- Immediate assessment: ABC, confirm SpO2 waveform, check right radial ABG (if any concern about VA/hybrid), lactate, haemodynamics
- Circuit checks: ECMO blood flow (L/min), pre/post-oxygenator pressures, visible clot, oxygenator performance, sweep gas connected and set, gas supply failure, recirculation suspicion
- Recirculation: check cannula position (US/echo/CXR), high flows relative to venous return, hypovolaemia; consider repositioning, reducing flow slightly, optimise preload
- Patient factors: anaemia (Hb), fever/shivering (↑VO2), sepsis, high CO states, pulmonary embolism, pneumothorax, atelectasis, mucus plugging
- Ventilator: ensure lung-protective settings with adequate PEEP; check for derecruitment; consider recruitment/proning if appropriate and experienced team
- Escalation: consider oxygenator change if failing (poor post-oxygenator PaO2, rising transmembrane pressure, clot); involve ECMO specialist team early
Explain how oxygenation and CO2 clearance are controlled on ECMO.
Core relationships are frequently examined.
- Oxygenation: mainly determined by ECMO blood flow relative to patient cardiac output, Hb, and oxygenator function; sweep FiO2 contributes
- CO2 clearance: mainly determined by sweep gas flow rate (↑sweep → ↓PaCO2); also affected by blood flow and metabolic CO2 production
- VV recirculation reduces effective oxygenation without necessarily affecting CO2 clearance proportionally
A patient on peripheral VA ECMO has a normal femoral arterial saturation but low right radial saturation. What is happening and what will you do?
This is differential hypoxaemia (Harlequin/North–South syndrome).
- Diagnosis: upper body supplied by poorly oxygenated native LV output; lower body supplied by oxygenated ECMO return
- Confirm: right radial ABG, cerebral oximetry if available, echo for LV function and mixing point
- Treat lungs: increase ventilator FiO2/PEEP, recruitment, treat pneumothorax/atelectasis/secretions
- ECMO strategy: increase ECMO flow if possible; consider VAV configuration or move arterial return to axillary/subclavian/aorta (central) to preferentially oxygenate upper body
- Avoid simplistic reduction of native output unless specifically indicated; ensure coronary oxygenation is prioritised
Describe the major complications of ECMO and how you would monitor for them.
Use categories: bleeding, thrombosis, haemolysis, infection, vascular, neurological, mechanical.
- Bleeding: inspect cannulation sites, drains; monitor Hb, coagulation, fibrinogen; neuro checks/CT if concern for ICH
- Thrombosis: rising transmembrane pressure, visible clot, oxygenator dysfunction, stroke signs; monitor anti-Xa/aPTT/ACT per protocol
- Haemolysis: plasma-free Hb/LDH, hyperkalaemia, dark urine, AKI; check inlet pressures and cannula position
- Vascular: limb perfusion checks, Doppler, compartment pressures if needed; ensure distal perfusion catheter function in femoral VA
- Neurological: sedation holds where safe, pupils, seizures; low threshold for imaging
- Mechanical: air in circuit, pump alarms, gas failure; emergency plan for accidental decannulation and massive haemorrhage
How does VA ECMO affect the left ventricle and why might you need LV venting?
A common viva theme: afterload and distension.
- VA ECMO increases aortic pressure/afterload → LV may fail to eject; aortic valve may not open → LV distension and pulmonary oedema
- Consequences: raised LVEDP, worsening subendocardial perfusion, stasis and LV thrombus, impaired recovery
- Signs: loss of pulsatility, rising pulmonary oedema, echo showing distended LV/closed aortic valve, high LV filling pressures
- Management: optimise inotropes/vasodilators, reduce ECMO flow if safe, add IABP/Impella, atrial septostomy, surgical LV vent
Outline an anaesthetic plan for emergency peripheral VA ECMO cannulation in cardiogenic shock.
Focus on haemodynamic stability, anticoagulation, and logistics.
- Preparation: brief team roles; blood products available; vasopressors/inotropes running; defib pads; ultrasound; difficult airway plan
- Monitoring: arterial line (right radial preferred), large-bore IV/central access, capnography, temperature; consider TOE if available
- Induction: RSI if not intubated; choose haemodynamically stable agents (etomidate/ketamine + opioid); anticipate peri-intubation collapse
- Ventilation: avoid severe hypoxia/hypercapnia/acidosis; lung-protective settings; be mindful that once on VA ECMO, ETCO2 may not reflect systemic perfusion
- Anticoagulation: coordinate heparin timing with cannulation; consider bleeding risk (CPR, trauma, recent surgery)
- After initiation: reassess perfusion, lactate, ABGs (right radial), echo for LV distension; adjust vasoactive support and consider venting strategy early
What are the key differences between ECMO and cardiopulmonary bypass (CPB) that matter to the anaesthetist?
Examiners often want practical differences and implications.
- Duration/setting: ECMO is prolonged support in ICU; CPB is short-term intraoperative support
- Anticoagulation: CPB typically requires full heparinisation; ECMO often uses lower-intensity anticoagulation (or occasionally heparin-sparing) depending on bleeding risk
- Circuit: ECMO uses membrane oxygenator + centrifugal pump; usually closed circuit, lower flows than CPB; less haemodilution (but variable)
- Physiology: VA ECMO increases afterload; CPB fully bypasses heart and lungs with controlled flows and often cardioplegia
A patient on ECMO is bleeding from cannulation sites. How would you approach this problem?
Balance haemostasis with circuit thrombosis; use a structured approach.
- Resuscitate: ABC, quantify blood loss, activate massive haemorrhage protocol if needed, maintain perfusion and oxygen delivery
- Local measures: direct pressure, surgical review for source control, check cannula fixation and insertion site
- Review anticoagulation: check anti-Xa/aPTT/ACT; consider reducing/pausing heparin with ECMO team; assess thrombosis risk (flows, clot burden)
- Correct coagulopathy: platelets, fibrinogen/cryoprecipitate, FFP, calcium; use viscoelastic testing if available; consider acquired vWD/platelet dysfunction
- Exclude catastrophic bleeding: neurological deterioration (ICH), haemoptysis, GI bleed; image early if concern
How would you troubleshoot high transmembrane pressure across the oxygenator?
Often indicates clot burden or flow issues.
- Confirm readings and trends; correlate with reduced oxygenator performance and haemolysis markers
- Check anticoagulation adequacy and circuit inspection for clot
- Assess for mechanical causes: kinked tubing, malpositioned cannula, high flows causing excessive pressure gradient
- Escalate early: plan oxygenator/circuit change with ECMO team; ensure standby oxygenation/ventilation strategy during change
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