ECMO Physiology and Pathophysiology 5 — Questions and Answers
Question 1: What physiological parameter best guides ECMO flow titration to ensure adequate oxygen delivery (DO2) in VA-ECMO?
- Mean arterial pressure alone
- Mixed venous oxygen saturation (SvO2) reflecting the balance between DO2 and VO2 (Correct answer)
- Arterial lactate concentration as a static threshold
- Urine output as a surrogate for cardiac output
Correct answer: Mixed venous oxygen saturation (SvO2) reflecting the balance between DO2 and VO2
SvO2 integrates oxygen delivery and consumption; a falling SvO2 indicates tissues are extracting more oxygen to compensate for inadequate delivery, signaling the need to increase ECMO flow or hemoglobin.
Question 2: In neonatal ECMO for persistent pulmonary hypertension of the newborn (PPHN), what is the primary pathophysiological target?
- Correcting metabolic acidosis to normalize pH
- Reducing pulmonary vascular resistance to enable transition from fetal to neonatal circulation (Correct answer)
- Increasing systemic vascular resistance to maintain coronary perfusion
- Eliminating intracardiac shunting through the foramen ovale
Correct answer: Reducing pulmonary vascular resistance to enable transition from fetal to neonatal circulation
PPHN results from failure of the pulmonary vasculature to dilate at birth, maintaining high PVR that drives right-to-left shunting; ECMO buys time while strategies to reduce PVR (inhaled NO, alkalosis, oxygen) take effect.
Question 3: How does increasing ECMO blood flow affect plasma-free hemoglobin levels?
- Higher flows reduce hemolysis by decreasing turbulence at the pump inlet
- Hemolysis increases with higher rpm as centrifugal pump shear stress rises proportionally (Correct answer)
- Flow rate has no effect; hemolysis depends entirely on anticoagulation status
- Higher flows decrease hemolysis by reducing suction pressure on red cells
Correct answer: Hemolysis increases with higher rpm as centrifugal pump shear stress rises proportionally
Centrifugal pump rpm and shear forces increase with flow; higher shear stress exceeds red cell membrane tolerance, causing progressive mechanical hemolysis that correlates with pump speed.
Question 4: What is the physiological consequence of excessive negative inlet pressure (high suction) at the venous drainage cannula during ECMO?
- Increased pump output from enhanced venous return
- Cavitation, hemolysis, and intermittent flow interruption as the right atrium collapses around the cannula (Correct answer)
- Increased circuit anticoagulation requirements
- Thrombus formation at the cannula tip from stagnant flow
Correct answer: Cavitation, hemolysis, and intermittent flow interruption as the right atrium collapses around the cannula
Excessive negative pressure causes the compliant right atrial wall to intermittently collapse over the drainage cannula (chatter), inducing cavitation, red cell destruction, and unstable pump flow.
Question 5: Which mechanism best explains why patients with severe right heart failure on VA-ECMO may paradoxically develop pulmonary edema?
- ECMO increases pulmonary venous pressure by augmenting left atrial return
- Improved RV unloading by ECMO increases pulmonary blood flow into the failing LV, which cannot accommodate the increased preload (Correct answer)
- ECMO anticoagulation increases pulmonary capillary permeability
- High ECMO flows cause pulmonary hypertension via increased pulmonary venous pressure
Correct answer: Improved RV unloading by ECMO increases pulmonary blood flow into the failing LV, which cannot accommodate the increased preload
When VA-ECMO decompresses the RV and restores pulmonary blood flow, a severely impaired LV that cannot empty adequately develops rising LVEDP transmitted back to the pulmonary capillaries, causing hydrostatic edema.
Question 6: In ECMO-supported patients, why does targeting a higher hemoglobin (>10 g/dL) improve oxygen delivery more efficiently than increasing pump flow alone?
- Higher hemoglobin reduces blood viscosity, lowering pump workload
- Oxygen content is linearly related to hemoglobin concentration; each g/dL increase augments DO2 proportionally without the adverse pressure effects of higher pump flow (Correct answer)
- High hemoglobin reduces recirculation fraction in VV-ECMO
- Hemoglobin acts as a buffer preventing acidosis during high-flow states
Correct answer: Oxygen content is linearly related to hemoglobin concentration; each g/dL increase augments DO2 proportionally without the adverse pressure effects of higher pump flow
Since DO2 = CO × CaO2 and CaO2 depends directly on hemoglobin, optimizing hemoglobin increases oxygen delivery without raising pump speed, which carries risks of hemolysis and afterload elevation.
Question 7: What pathophysiological process underlies 'circuit thrombosis' in ECMO, and which laboratory value best predicts impending oxygenator failure?
- Platelet aggregation only; thrombocytopenia predicts failure
- Activation of contact pathway coagulation on synthetic surfaces producing fibrin-platelet thrombi; rising pre- to post-membrane pressure gradient predicts oxygenator failure (Correct answer)
- Fibrinolysis consuming clot factors; rising D-dimer predicts failure
- Complement-mediated red cell destruction; rising LDH predicts failure
Correct answer: Activation of contact pathway coagulation on synthetic surfaces producing fibrin-platelet thrombi; rising pre- to post-membrane pressure gradient predicts oxygenator failure
Blood contact with synthetic circuit surfaces activates Factor XII and the intrinsic pathway, building fibrin-platelet thrombi; as clot accumulates in the oxygenator, resistance rises and the transmembrane pressure gradient increases, signaling impending failure.
What physiological parameter best guides ECMO flow titration to ensure adequate oxygen delivery (DO2) in VA-ECMO?