What ECMO Is, and the Two Modes
"Extracorporeal membrane oxygenation is not a treatment; it is a bridge. It buys time — time for the lung to recover, time for the heart to recover, time to reach a decision or a durable device. It does nothing to the underlying disease. A patient placed on ECMO without a credible answer to 'a bridge to what?' has merely had their dying prolonged and made more complicated."
Extracorporeal Life Support: The ELSO Red Book, 6th Edition. Extracorporeal Life Support Organization; 2022.The circuit (common to every mode)
- Drainage cannula pulls deoxygenated blood from a large vein → pump (centrifugal) → membrane oxygenator (gas exchange) → return cannula delivers oxygenated blood back.
- Sweep gas flows across the membrane and controls CO₂ removal; blood flow (pump speed) + FiO₂ of the sweep control oxygenation. These are two independent dials — this is the single most important concept at the bedside.
VV ECMO — respiratory support
- Drains and returns to the venous system (e.g. femoral drain → IJ return, or dual-lumen single cannula)
- Supports gas exchange only; the patient's own heart provides the circulation
- Requires an adequate native cardiac output and blood pressure
- Blood is oxygenated before the right heart → lungs → systemic circulation
VA ECMO — cardiac ± respiratory support
- Drains from a vein, returns to an artery (e.g. femoral vein → femoral artery)
- Supports both circulation and gas exchange — a temporary heart-lung bypass
- Creates retrograde aortic flow that competes with native LV output
- Risk of differential hypoxia (Harlequin) and LV distension
A hypoxaemic patient with a good heart needs VV. A patient in cardiogenic shock or arrest needs VA. Putting a patient in isolated respiratory failure on VA "to be safe" exposes them to arterial cannulation, limb ischaemia, LV distension and differential hypoxia for no benefit. Conversely, VV will not rescue a failing circulation, however perfect the SpO₂ on the circuit.
How ECMO Actually Delivers Oxygen & Removes CO₂
"Oxygen delivery on ECMO is a flow problem, and carbon dioxide removal is a ventilation problem — of the sweep gas, not the lung. Once you separate these two in your mind, the machine stops being a black box: a desaturating VV patient needs more flow (or a bigger drainage cannula), while a rising CO₂ needs more sweep."
Marino PL. The ICU Book, 5th Ed. Extracorporeal Support. Wolters Kluwer; 2025.- Pump speed (RPM) → blood flow (L/min): the master control for oxygenation. Higher flow = more oxygenated blood delivered. Limited by drainage ("chugging"/suck-down = under-filled or cannula against vessel wall).
- Sweep gas flow (L/min): controls CO₂ clearance. Doubling sweep roughly doubles CO₂ removal; it has little effect on oxygenation. Drop CO₂ slowly to avoid cerebral vasoconstriction.
- Sweep FiO₂: the O₂ concentration of the gas across the membrane (usually 100%). A fine-tune for oxygenation.
In peripheral (femoro-femoral) VA ECMO, the oxygenated return runs up the aorta, against the native LV ejection. Two consequences dominate care:
- Differential hypoxia (Harlequin / North–South syndrome): if the native lungs are poor and the LV recovers enough to eject, poorly oxygenated blood from the LV perfuses the coronaries and brain (upper body), while well-oxygenated ECMO blood perfuses the lower body. The right arm/right ear SpO₂ can be dangerously low while the legs look pink. Always monitor the right radial artery / right-hand SpO₂.
- LV distension & pulmonary oedema: retrograde aortic flow raises LV afterload. If the LV cannot open the aortic valve, it distends, pressure backs up into the lungs, and the LV may not recover. Watch for absent arterial pulsatility and a rising PA/wedge — may need LV venting (IABP, Impella, atrial septostomy, surgical vent).
Once the oxygenator is doing the gas exchange, the ventilator can be dialled to ultra-protective, "lung-rest" settings (low plateau pressure, low driving pressure, low FiO₂, low rate). The injured lung is spared ventilator-induced injury while it heals. Ventilating a VV patient aggressively "to help the numbers" defeats the reason they were cannulated.
Indications, Evidence & Contraindications
• PaO₂/FiO₂ <50 mmHg for >3h, or <80 for >6h, or
• pH <7.25 with PaCO₂ ≥60 mmHg for >6h despite RR up to 35 and plateau ≤32.
EOLIA (NEJM 2018) was stopped for futility, but 28% of the control arm crossed over to ECMO, and a Bayesian post-hoc analysis plus the EOLIA/CESAR meta-analysis support a mortality benefit. Early referral to an ECMO centre (as in CESAR) is the practical message.
ECMO-CS (2023) found no benefit of immediate VA ECMO over an early-conservative strategy in rapidly deteriorating AMI cardiogenic shock — ECMO is not automatic in every shock.
ECPR (ECMO during CPR) for refractory VF/VT arrest with a shockable rhythm and short low-flow time: ARREST and the Prague study support benefit in highly selected witnessed arrests with good CPR; INCEPTION was neutral — selection and speed are everything.
• Irreversible underlying disease with no transplant/device option
• Severe irreversible brain injury; unwitnessed arrest / prolonged low-flow
• Advanced age with frailty; disseminated malignancy
• Uncontrolled bleeding or absolute contraindication to any anticoagulation
• Prolonged high-pressure ventilation (>7 days) is a relative marker of poorer lung recovery.
Decide the exit before the entrance: recovery, transplant, durable device, or planned withdrawal.
Transfuse restrictively — a haemoglobin near-normal is not required; target platelets typically >50–100 ×10⁹/L if bleeding. Modern circuits run at lower anticoagulation intensity than historically taught. Bleeding, not clotting, is the commoner and more lethal complication.
ECMO is concentrated in tertiary and private centres and is resource- and cost-intensive (circuits, oxygenators, 1:1 nursing, perfusion support). Patient selection and honest family counselling about cost and prognosis are critical before initiation.
H1N1 and severe viral pneumonia (and the COVID-19 surges) drove much of India's VV ECMO experience; national ECMO networks and referral pathways have grown around this. Fulminant myocarditis and poisoning-related cardiotoxicity (e.g. aluminium/yellow phosphide, oleander) are recognised VA ECMO indications where a reversible insult justifies support.
Drug Reference — ECMO
| Drug | Indication | Dose | Notes |
|---|---|---|---|
| Unfractionated heparin | Circuit anticoagulation (standard) | Bolus ~50–100 U/kg at cannulation → infusion titrated to anti-Xa 0.3–0.7 (or unit ACT/aPTT target) | Anti-Xa preferred; monitor AT-III if heparin resistant |
| Bivalirudin | Anticoagulation (HIT / heparin resistance) | ~0.03–0.05 mg/kg/h, titrate to aPTT; no bolus | Direct thrombin inhibitor; watch for clot in stagnant circuit areas if flow low |
| Fentanyl / midazolam | Analgesia & sedation | Infusions titrated (higher requirements — circuit sequestration) | Lipophilic drugs adsorb to the circuit → doses often higher; reassess as circuit ages |
| Noradrenaline | Vasoplegia / low SVR on VV | 0.05–0.5+ µg/kg/min titrated to MAP ≥65 | VV ECMO does not support BP — treat distributive shock conventionally |
| Dobutamine / adrenaline | Native cardiac support on VA (aid LV ejection) | Titrated low-dose | Maintaining pulsatility helps prevent LV distension & stasis |
| Platelets / fibrinogen / FFP | Bleeding, consumption | Platelets to >50–100 ×10⁹/L; fibrinogen >1.5 g/L if bleeding | Acquired von Willebrand & thrombocytopenia are near-universal on ECMO |
| Antibiotics | Proven infection only | Dose-adjust for altered Vd & circuit sequestration | No routine prophylaxis; ECMO alters PK of many drugs (larger Vd) |
From Candidacy to Weaning
Candidate assessment — "a bridge to what?"
- Confirm the insult is potentially reversible or there is a transplant/device pathway
- Exclude futility (irreversible brain injury, disseminated malignancy, uncontrolled bleeding)
- Choose mode: hypoxaemia + good heart → VV; shock/arrest → VA
- Refer early to an ECMO centre — outcomes are better before multi-organ failure sets in
Cannulate & initiate
- Ultrasound-guided cannulation; confirm cannula position (echo / X-ray)
- VA femoral arterial line: place a distal perfusion cannula to prevent limb ischaemia
- Start heparin; establish flow; wean toxic vent/vasopressor settings to rest the failing organ
Daily management & troubleshooting
- Desaturation (VV): ↑ flow, check recirculation, treat fever/high output, upsize/reposition cannula
- Rising CO₂: ↑ sweep gas
- VA — monitor right radial ABG / right-hand SpO₂ for differential hypoxia; watch pulsatility & LV distension
- Lung-rest ventilation; daily anticoagulation, haemolysis (LDH, plasma free Hb) & circuit inspection
Assess for weaning
- VV: as lungs recover, reduce sweep gas to zero (trial off) while keeping blood flow; observe gas exchange on ventilator settings for hours
- VA: reduce ECMO flow stepwise with echo assessment of LV/RV function ("turn-down/flow-reduction trial"); ensure native output & pulsatility recover
Decannulate or transition
- Decannulate when native organ function sustains the patient; arterial site often needs surgical repair
- If no recovery: transition to durable device / transplant, or hold a goals-of-care discussion for planned withdrawal
Common Mistakes in ECMO
ECMO does not treat disease; it buys time. Starting it in irreversible illness with no path to recovery, transplant or a device simply prolongs dying and consumes vast resources. Define the destination before you cannulate.
Turning up the sweep gas for a low SpO₂ (a flow problem) or cranking flow for a high CO₂ (a sweep problem) wastes time. Oxygenation follows blood flow (and sweep FiO₂); CO₂ follows sweep gas rate.
If you monitor only the left arm or a leg, you can miss dangerously hypoxic blood reaching the brain and coronaries as the LV recovers. Sample and pulse-oximeter the right upper limb. Manage with better native lung oxygenation or by converting to V-A-V.
Retrograde flow raises LV afterload; a non-ejecting, distending LV floods the lungs and cannot recover. Watch arterial pulsatility and PA pressures, and vent the LV (IABP/Impella/septostomy) when needed.
Bleeding kills more ECMO patients than clotting. Modern low-intensity anticoagulation and restrictive transfusion are safer than the old "keep them thin and topped up" approach. Anti-Xa guidance beats ACT alone.
The purpose of VV ECMO is to rest the lung. Reverting to high plateau/driving pressures because a number looks off perpetuates ventilator-induced lung injury and defeats the therapy.
Femoral arterial cannulation for VA ECMO can cause a threatened, then dead, lower limb. Place a distal perfusion cannula and monitor the limb (colour, Doppler, NIRS) relentlessly.
Exam Pearls
Q: What controls oxygenation vs CO₂ removal on ECMO?
Oxygenation ← blood flow (pump speed) and sweep FiO₂. CO₂ removal ← sweep gas flow rate. They are independent controls.
Q: VV vs VA — how do you choose?
VV supports gas exchange only and needs an adequate native circulation → isolated respiratory failure. VA supports circulation and gas exchange → cardiogenic shock or arrest.
Q: What is differential hypoxia (Harlequin / North–South syndrome)?
On peripheral VA ECMO, if native lungs are poor and the LV ejects, deoxygenated blood perfuses the upper body (coronaries, brain) while ECMO oxygenates the lower body. Monitor the right radial artery / right-hand SpO₂.
Q: What did EOLIA and CESAR show?
CESAR (2009): referral to an ECMO centre improved 6-month survival without severe disability. EOLIA (2018): stopped for futility but with high crossover; Bayesian/meta-analysis supports a mortality benefit. Early ECMO referral in severe ARDS is reasonable.
Q: What is recirculation on VV ECMO?
Freshly oxygenated return blood is drained straight back into the circuit without passing through the body, so systemic saturation falls despite high circuit flow. Caused by cannula proximity; increasing flow can worsen it. Reposition the cannula.
Q: Why does LV distension occur on VA ECMO and how is it managed?
Retrograde aortic flow ↑ LV afterload; if the LV can't eject it distends → pulmonary oedema and no recovery. Manage by maintaining pulsatility/inotropy and venting (IABP, Impella, atrial septostomy, surgical vent).
Q: Bleeding or clotting — which is the bigger problem?
Bleeding. Acquired von Willebrand syndrome, thrombocytopenia and anticoagulation make haemorrhage the commonest serious complication. Modern practice uses lower-intensity anticoagulation and restrictive transfusion.
Q: How do you wean VV vs VA ECMO?
VV: reduce sweep gas to zero (keep blood flow) and watch gas exchange on ventilator settings. VA: stepwise flow reduction with echo assessment of native cardiac recovery and pulsatility.
References
- Combes A, Hajage D, Capellier G, et al. (EOLIA). Extracorporeal Membrane Oxygenation for Severe Acute Respiratory Distress Syndrome. N Engl J Med. 2018;378:1965–1975.
- Peek GJ, Mugford M, Tiruvoipati R, et al. (CESAR). Efficacy and economic assessment of conventional ventilatory support versus extracorporeal membrane oxygenation for severe adult respiratory failure. Lancet. 2009;374:1351–1363.
- Goligher EC, Tomlinson G, Hajage D, et al. Extracorporeal Membrane Oxygenation for Severe ARDS: A Bayesian post-hoc analysis of EOLIA. JAMA. 2018;320:2251–2259.
- Ostadal P, Rokyta R, Karasek J, et al. (ECMO-CS). Extracorporeal Membrane Oxygenation in the Therapy of Cardiogenic Shock. Circulation. 2023;147:454–464.
- Yannopoulos D, Bartos J, Raveendran G, et al. (ARREST). Advanced reperfusion strategies for refractory ventricular fibrillation out-of-hospital cardiac arrest. Lancet. 2020;396:1807–1816.
- Suverein MM, Delnoij TSR, Lorusso R, et al. (INCEPTION). Early Extracorporeal CPR for Refractory Out-of-Hospital Cardiac Arrest. N Engl J Med. 2023;388:299–309.
- Extracorporeal Life Support Organization (ELSO). General Guidelines for All ECLS Cases, v1.4. Ann Arbor, MI; 2017 (with subsequent ELSO guideline updates).
- Tonna JE, Abrams D, Brodie D, et al. Management of Adult Patients Supported with VV ECMO: ELSO Guideline. ASAIO J. 2021;67:601–610.
- Marino PL. Marino's The ICU Book, 5th Edition. Extracorporeal Support. Philadelphia, PA: Wolters Kluwer; 2025.