ECMO & Mechanical
Circulatory Support

Correct answer: B — Harlequin (North-South) syndrome.

In peripheral VA-ECMO via femoral cannulation, oxygenated blood is returned retrogradely up the descending aorta. As the native heart begins even minimal recovery, it ejects poorly oxygenated blood (from congested, poorly ventilated lungs) directly into the ascending aorta — supplying the coronaries, carotid, and subclavian arteries. The ECMO circuit oxygenates the lower body adequately; the upper body receives hypoxic native cardiac output. The right radial ABG is the sentinel monitor for this reason.

Key diagnostic clue: flat pulseless femoral waveform = full ECMO support of lower body. Hypoxic right radial ABG = upper body getting native hypoxic ejection. There is no sign of oxygenator failure — the femoral arterial blood is well oxygenated (PaO₂ 350 mmHg).

Management: Improve pulmonary oxygen transfer — increase FiO₂, PEEP, recruitment maneuvers, bronchoscopy to clear secretions, diuresis, and drainage of pleural effusions. If insufficient: (1) Add a VAV-ECMO Y-limb from the oxygenated return to an RIJ cannula, delivering oxygenated blood to the RA/pulmonary circulation. (2) Transition to central ECMO cannulation.

In patients on peripheral VA ECMO with recovering cardiac function and poor pulmonary function, the native cardiac output supplies deoxygenated blood to the coronaries, carotids, and subclavian arteries. The exact location of mixing between poorly oxygenated native cardiac output through the aortic valve and the well-oxygenated ECMO output from the femoral cannula is difficult to determine. Therefore monitoring oxygenation in the right arm (R subclavian as branch of innominate artery — first branch off the ascending aorta) is crucial.

Correct answer: C — Evaluate and address recirculation.

In VV-ECMO, recirculation occurs when oxygenated return blood is immediately re-entrained into the drainage cannula before it traverses the pulmonary circulation, effectively reducing net systemic oxygen delivery. The key clinical clue here is bright red blood in the drainage limb — drainage-line blood should look dark (mixed venous). With recent repositioning, it is possible that the oxygenated ECMO return flow is being directly drained into the ECMO drainage cannula, instead of moving forward through the tricuspid valve and RV to the pulmonary and then systemic circulation. Returning to prior patient position is the immediate next step. To adjust the ECMO cannulae, echocardiographic or fluoroscopic guidance may be needed. While various distances between the drainage and return cannulae have been described as ideal, evaluation for recirculation should be multifactorial.

Quantifying recirculation: Recirculation fraction (Rf) = (SdO₂ − SvO₂) / (SpO₂ − SvO₂), where SdO₂ is drainage-line SaO₂. Rf >20–30% is clinically significant.

Correct answer: B — RV failure causing LV underfilling.

Suction events occur when the Impella cannot aspirate sufficient volume — the LV is not filling adequately. Echo confirms correct device position, so the issue is preload, not malposition. The hemodynamic fingerprint is key: RAP 22, PCWP 28, CO 2.9, SVR 1820.

RAP:PCWP ratio = 22/28 = 0.79 — this exceeds the 0.63 threshold that predicts significant RV-mediated underfilling of the LV in patients on LVAD support (Kapur et al., RECOVER II). The RV is failing to deliver adequate preload to the left heart. In anterior STEMI, the RV often shares the ischemic territory (RV free wall branches from the LAD, and sometimes co-existing RCA disease).

Management cascade:
1. Start RV inotrope: dobutamine 5–7.5 mcg/kg/min or milrinone (caution: vasodilation may worsen MAP)
2. Consider inhaled pulmonary vasodilator (iNO or inhaled prostacyclin) to reduce RV afterload
3. Escalate to Impella RP or RVAD if refractory
4. ECPella (VA-ECMO + Impella) for biventricular collapse — ECMO provides systemic support while Impella decompresses the LV

Correct answer: B — Discuss termination of heparin, aggressively replace fibrinogen and platelets, treat the coagulopathy.

This patient has disseminated intravascular coagulation (DIC) superimposed on ECMO-related consumption: low fibrinogen (84 mg/dL), thrombocytopenia, elevated INR, markedly elevated D-dimer, and diffuse bleeding. The aPTT of 94 sec is supratherapeutic (target 60–80), compounding hemorrhage. This is not purely a surgical bleeding problem.

ECMO-specific coagulopathy drivers: (1) Contact activation → thrombin generation → fibrinogen consumption. (2) Shear stress → platelet activation and destruction. (3) Acquired von Willebrand deficiency (high-shear cleaves ULVWF multimers). (4) Hyperfibrinolysis from circuit phospholipid activation.

Management principles on ECMO:
— Discuss termination of heparin. Patients on VA ECMO are at risk of arterial thromboembolism, hence some anticoagulation is always preferred — however it is not uncommon for post-surgical patients to be maintained on ECMO without anticoagulation for short periods of time (hours to sometimes days).
— Target fibrinogen >150–200 mg/dL with cryoprecipitate (each unit raises fibrinogen ~10 mg/dL in adults; give 10–15 units)
— Transfuse platelets to >50,000/µL for active bleeding
— FFP has a role but delivers low fibrinogen concentration — cryoprecipitate is more fibrinogen-efficient
— Consider TXA or aminocaproic acid if hyperfibrinolysis confirmed on TEG/ROTEM (DIC with hyperfibrinolysis), but not empirically without TEG guidance (can cause thrombosis if DIC is thrombosis-predominant)
Viscoelastic testing (TEG or ROTEM) is invaluable in this setting — it differentiates fibrinolysis, platelet dysfunction, and factor deficiency and guides targeted product replacement far better than conventional labs.

Correct answer: B — Perform a formal ECMO-off (clamping) trial.

Echocardiographic improvement and adequate hemodynamics at low ECMO flow are necessary but not sufficient criteria for decannulation. The critical question is: can the heart sustain adequate output when the mechanical support is completely removed? VA-ECMO provides afterload support — removing it abruptly increases LV afterload, and a borderline ventricle may decompensate.

Standard ECMO weaning and off-trial protocol:
1. Patients on VA ECMO are evaluated with a wean trial before decannulation.
2. Wean flows gradually (e.g., 3→2 L/min over hours), monitoring hemodynamics and serial echo at each step
3. Once flows fall below 2 L/min, anticoagulation becomes critical — low-flow states dramatically increase the risk of circuit thrombosis and oxygenator clot. Ensure therapeutic UFH (aPTT 60–80 sec or anti-Xa 0.3–0.7 IU/mL) is confirmed before any further weaning
4. The formal clamp trial is performed in the operating room — circuit is clamped (both limbs) for 15–30 minutes while the surgical team is present and ready for emergent decannulation or re-establishment of support if needed. Continuous hemodynamic monitoring and repeat echo are performed during the trial
5. Criteria for tolerance: MAP ≥60, no new vasopressor requirement, CI ≥2.2 L/min/m², PCWP rise <5 mmHg, no significant LVEDD dilation or new MR on echo, no sustained arrhythmia
6. If tolerated → proceed to surgical decannulation with direct cannula-site repair

This patient has favorable features for weaning: LVEF 25–30% with spontaneous AoV opening (marker of native cardiac output), CO 4.1 L/min off pressors at low ECMO flow, PA pressures reasonable, neurologically intact. Myocarditis carries among the highest myocardial recovery rates on ECMO — patients with myocarditis often demonstrate remarkable recovery in days to weeks, and could progress from severe cardiogenic shock requiring VA ECMO to decannulation without requiring durable LVAD therapy.