Q1 / 5
A 58-year-old man is 18 hours post out-of-hospital VF arrest with ROSC after 22 minutes of CPR. He is on peripheral VA-ECMO (flows 3.8 L/min, FiO₂ 1.0) for refractory cardiogenic shock. Echo shows severely reduced biventricular function with LVEF ~10%. His femoral arterial line in the contralateral leg from the arterial ECMO cannula shows a flat, pulseless waveform and SpO₂ is 99%. A femoral arterial sample shows PaO₂ 350 mmHg. However, his right radial ABG shows: pH 7.18, PaO₂ 54 mmHg, PaCO₂ 51 mmHg.
What is the most likely explanation for the discrepancy between the upper and lower body oxygenation, and what is the immediate management priority?
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 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.
Further reading: LINK
Q2 / 5
A 44-year-old woman with severe H1N1-associated ARDS (P:F ratio 58) is on VV-ECMO via right femoral drain and right IJ return cannulas. ECMO flows 4.5 L/min, sweep 6 L/min, FiO₂ 1.0. She is on lung-rest ventilation: TV 2 mL/kg IBW, RR 10, PEEP 10, FiO₂ 0.3. SpO₂ has dropped from 94% to 88% since the patient was sat up in bed half an hour ago. Circuit pressures are unchanged. Drainage-line blood appears bright red.
Which intervention is the most appropriate first step?
Correct answer: C — Evaluate and address recirculation.
In VV-ECMO, recirculation occurs when oxygenated return blood is re-entrained into the drainage cannula before traversing the pulmonary circulation, reducing net systemic oxygen delivery. The key clue here is bright red drainage-line blood — it should look dark (mixed venous). Repositioning likely shifted the return cannula toward the drainage port; returning to the prior position is the immediate first step. If recirculation persists, echocardiographic or fluoroscopic guidance is needed to reposition or replace the cannulae.
Quantifying recirculation: Recirculation fraction (Rf) = (SdO₂ − SvO₂) / (SpO₂ − SvO₂), where SdO₂ is drainage-line SaO₂. Rf >20–30% is clinically significant.
In VV-ECMO, recirculation occurs when oxygenated return blood is re-entrained into the drainage cannula before traversing the pulmonary circulation, reducing net systemic oxygen delivery. The key clue here is bright red drainage-line blood — it should look dark (mixed venous). Repositioning likely shifted the return cannula toward the drainage port; returning to the prior position is the immediate first step. If recirculation persists, echocardiographic or fluoroscopic guidance is needed to reposition or replace the cannulae.
Quantifying recirculation: Recirculation fraction (Rf) = (SdO₂ − SvO₂) / (SpO₂ − SvO₂), where SdO₂ is drainage-line SaO₂. Rf >20–30% is clinically significant.
Further reading: LINK
Q3 / 5
A 67-year-old woman presents with anterior STEMI complicated by cardiogenic shock. After primary PCI of a mid-LAD occlusion she remains vasopressor-dependent and an Impella CP is placed. Twelve hours later: suction alarms have auto-downgraded the device from P8 to P5. MAP 58 mmHg on norepinephrine 0.25 mcg/kg/min + vasopressin 0.03 units/min. PA catheter: RAP 22 mmHg, PCWP 28 mmHg, CO 2.9 L/min, SVR 1,820 dynes·s/cm⁵. Bedside echo shows a dilated, hypokinetic RV with septal bowing into the LV and a markedly underfilled LV cavity. Echo confirms the Impella inlet is correctly positioned in the LV mid-cavity with no mitral apparatus obstruction, LVEF ~15%.
What is the most likely cause of suction events, and what is the best next management step?
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. RV inotrope — ino-constrictors (epinephrine, dopamine) preferred when MAP is tenuous; ino-dilators (milrinone, dobutamine) if systemic pressure is adequate (caution: vasodilation may worsen MAP)
2. 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
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. RV inotrope — ino-constrictors (epinephrine, dopamine) preferred when MAP is tenuous; ino-dilators (milrinone, dobutamine) if systemic pressure is adequate (caution: vasodilation may worsen MAP)
2. 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
Further reading: LINK
Q4 / 5
A 52-year-old man on VA-ECMO for post-cardiotomy shock (post-CABG day 3) develops oozing from all cannula sites, mediastinal drain output 100 mL/hr, and petechiae. Labs: Hgb 7.1 g/dL, platelets 38,000/µL, PT 22 sec (INR 1.9), aPTT 94 sec (target 60–80), fibrinogen 84 mg/dL, D-dimer markedly elevated, anti-Xa 0.62 IU/mL. He is on UFH 1,200 units/hr. Circuit flows stable at 3.6 L/min, no visible oxygenator clots.
What is the most appropriate immediate management strategy?
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:
— Hold heparin. Post-surgical patients can be maintained on ECMO without anticoagulation for short periods; the bleeding risk here outweighs the thrombotic risk of a brief pause.
— Target fibrinogen >150–200 mg/dL with cryoprecipitate (a 10-unit pool raises fibrinogen ~50–70 mg/dL in a bleeding cardiac surgery patient)
— 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.
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:
— Hold heparin. Post-surgical patients can be maintained on ECMO without anticoagulation for short periods; the bleeding risk here outweighs the thrombotic risk of a brief pause.
— Target fibrinogen >150–200 mg/dL with cryoprecipitate (a 10-unit pool raises fibrinogen ~50–70 mg/dL in a bleeding cardiac surgery patient)
— 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.
Further reading: LINK · Ref: Hastings et al. ASAIO J 2020; ELSO Anticoagulation Guidelines 2021
Q5 / 5
A 48-year-old man has been on VA-ECMO for 9 days following fulminant myocarditis. He was initially in complete electromechanical dissociation. Today, serial echos show LVEF recovering to 25–30% with spontaneous aortic valve opening on each beat. ECMO flows have been weaned to 1.5 L/min. Hemodynamics off vasopressors: MAP 72, CVP 10, PA pressures 38/18 (mean 25), CO 4.1 L/min by thermodilution, PCWP 16. He remains intubated but is awake and following commands. Creatinine 1.8 (baseline 0.9). No neurological deficits.
Regarding decannulation from VA-ECMO, which statement best represents current evidence-based practice?
Correct answer: B — Perform a formal ECMO-off (clamping) trial.
Echocardiographic improvement and adequate hemodynamics at low ECMO flow are necessary but not sufficient for decannulation. The key question is whether the heart can sustain output without mechanical support — VA-ECMO provides afterload assistance, and its abrupt removal can unmask a borderline ventricle.
Standard weaning and off-trial protocol:
1. Wean flows gradually (e.g., 3→2 L/min over hours), monitoring hemodynamics and serial echo at each step
2. Below 2 L/min, anticoagulation becomes critical — confirm therapeutic UFH (aPTT 60–80 or anti-Xa 0.3–0.7 IU/mL) before further weaning; low-flow markedly increases thrombosis risk
3. Optimize native support: adequate preload, rate-pressure product, rhythm, inotropes as needed
4. Formal clamp trial in the OR — both limbs clamped 15–30 min, surgical team present, continuous hemodynamic monitoring and echo
5. Tolerance criteria: MAP ≥60, no new vasopressors, CI ≥2.2, PCWP rise <5 mmHg, no significant LVEDD dilation or new MR, no sustained arrhythmia
6. If tolerated → surgical decannulation with direct site repair
This patient's favorable features: LVEF 25–30% with spontaneous AoV opening, CO 4.1 L/min off pressors at low flow, reasonable PA pressures, neurologically intact. Myocarditis carries among the highest recovery rates on ECMO — progression to decannulation without durable LVAD is common.
Echocardiographic improvement and adequate hemodynamics at low ECMO flow are necessary but not sufficient for decannulation. The key question is whether the heart can sustain output without mechanical support — VA-ECMO provides afterload assistance, and its abrupt removal can unmask a borderline ventricle.
Standard weaning and off-trial protocol:
1. Wean flows gradually (e.g., 3→2 L/min over hours), monitoring hemodynamics and serial echo at each step
2. Below 2 L/min, anticoagulation becomes critical — confirm therapeutic UFH (aPTT 60–80 or anti-Xa 0.3–0.7 IU/mL) before further weaning; low-flow markedly increases thrombosis risk
3. Optimize native support: adequate preload, rate-pressure product, rhythm, inotropes as needed
4. Formal clamp trial in the OR — both limbs clamped 15–30 min, surgical team present, continuous hemodynamic monitoring and echo
5. Tolerance criteria: MAP ≥60, no new vasopressors, CI ≥2.2, PCWP rise <5 mmHg, no significant LVEDD dilation or new MR, no sustained arrhythmia
6. If tolerated → surgical decannulation with direct site repair
This patient's favorable features: LVEF 25–30% with spontaneous AoV opening, CO 4.1 L/min off pressors at low flow, reasonable PA pressures, neurologically intact. Myocarditis carries among the highest recovery rates on ECMO — progression to decannulation without durable LVAD is common.
Further reading: LINK · Ref: Aissaoui et al. Crit Care Med 2017; Pappalardo et al. JACC HF 2017; ELSO Weaning Guidelines 2021