ECMO Physiology and Pathophysiology 4 — Questions and Answers
Question 1: What is the physiological mechanism by which ECMO improves coronary perfusion in cardiogenic shock?
- ECMO increases heart rate, improving coronary flow velocity
- VA-ECMO raises aortic diastolic pressure, which is the primary determinant of coronary perfusion pressure (Correct answer)
- ECMO reduces myocardial oxygen demand by eliminating all mechanical work
- ECMO oxygenates coronary blood directly via the circuit
Correct answer: VA-ECMO raises aortic diastolic pressure, which is the primary determinant of coronary perfusion pressure
Coronary perfusion occurs primarily during diastole and depends on aortic diastolic pressure; VA-ECMO's continuous retrograde flow elevates aortic diastolic pressure, improving coronary perfusion pressure.
Question 2: In a patient on peripheral VA-ECMO, which monitoring site best reflects cerebral oxygenation?
- Pulse oximetry on the left foot
- Right radial arterial blood gas (pre-mixing zone) (Correct answer)
- Femoral arterial line (ECMO return side)
- Central venous oxygen saturation
Correct answer: Right radial arterial blood gas (pre-mixing zone)
The right radial artery reflects blood ejected from the native heart before it mixes with retrograde ECMO flow, providing the best estimate of oxygen delivery to the brain and coronary arteries.
Question 3: How does systemic inflammatory response syndrome (SIRS) triggered by ECMO circuit contact activation alter vascular physiology?
- SIRS increases systemic vascular resistance, necessitating higher ECMO flows
- SIRS causes vasodilation and capillary leak, increasing volume requirements and reducing effective circulating volume (Correct answer)
- SIRS primarily affects pulmonary vascular resistance without systemic effects
- SIRS triggers compensatory venoconstriction that maintains preload
Correct answer: SIRS causes vasodilation and capillary leak, increasing volume requirements and reducing effective circulating volume
Contact of blood with artificial circuit surfaces activates complement and inflammatory cascades, producing vasodilation and endothelial permeability that manifests as distributive physiology requiring volume resuscitation.
Question 4: What is the physiological basis for using prone positioning concurrently with VV-ECMO in severe ARDS?
- Prone positioning reduces ECMO recirculation by changing cannula orientation
- Prone positioning redistributes ventilation-perfusion matching and reduces dorsal alveolar overdistension, complementing ECMO's gas exchange support (Correct answer)
- Prone positioning lowers intrathoracic pressure, increasing ECMO venous drainage
- Prone positioning prevents oxygenator thrombosis by reducing blood viscosity
Correct answer: Prone positioning redistributes ventilation-perfusion matching and reduces dorsal alveolar overdistension, complementing ECMO's gas exchange support
Prone positioning recruits dorsal lung regions, improves V/Q matching, and reduces cyclic alveolar stress, providing additive benefit to VV-ECMO's extracorporeal gas exchange in ARDS.
Question 5: A patient on VV-ECMO has SvO2 of 85% from the drainage cannula but SpO2 of 82%. What does this pattern indicate?
- Membrane lung failure causing inadequate oxygenation of circuit blood
- High recirculation: oxygenated blood is being re-drained before reaching the systemic circulation (Correct answer)
- Pulmonary shunting exceeding ECMO capacity
- Incorrect placement of the drainage cannula in the right atrium
Correct answer: High recirculation: oxygenated blood is being re-drained before reaching the systemic circulation
When pre-membrane SvO2 (drainage cannula) is nearly as high as or higher than patient SpO2, a large fraction of blood draining into the circuit is already oxygenated, indicating recirculation rather than true mixed venous blood.
Question 6: Which coagulation abnormality is uniquely associated with ECMO and results from destruction of high-molecular-weight von Willebrand factor multimers?
- Heparin-induced thrombocytopenia (HIT)
- Acquired von Willebrand syndrome (AVWS) (Correct answer)
- Disseminated intravascular coagulation (DIC)
- Fibrinolysis shutdown syndrome
Correct answer: Acquired von Willebrand syndrome (AVWS)
High shear stress generated by the ECMO pump cleaves large vWF multimers via ADAMTS-13, producing an acquired von Willebrand syndrome that impairs primary hemostasis and contributes to bleeding complications.
Question 7: Why does LV end-diastolic pressure rise during VA-ECMO in patients with severely impaired systolic function?
- ECMO retrograde flow increases systemic venous return directly to the left ventricle
- Increased LV afterload from retrograde aortic flow impedes LV ejection, causing blood to accumulate in the ventricle (Correct answer)
- ECMO reduces heart rate, prolonging diastolic filling time excessively
- Anticoagulation therapy causes myocardial edema and reduced compliance
Correct answer: Increased LV afterload from retrograde aortic flow impedes LV ejection, causing blood to accumulate in the ventricle
VA-ECMO raises aortic pressure retrograde, increasing LV afterload; if the failing LV cannot eject against this pressure, stroke volume falls, residual volume accumulates, LVEDP rises, and pulmonary edema may worsen.
ECMO Physiology and Pathophysiology 4
What is the physiological mechanism by which ECMO improves coronary perfusion in cardiogenic shock?