ECMO Physiology and Pathophysiology 3 — Questions and Answers
Question 1: A patient on VV-ECMO develops worsening hypercapnia despite maximal sweep gas flow. What is the most likely explanation?
- Plasma leak into the gas phase of the oxygenator
- Oxygenator thrombosis reducing effective membrane surface area (Correct answer)
- Excessive recirculation washing out CO2
- Patient's metabolic rate has decreased
Correct answer: Oxygenator thrombosis reducing effective membrane surface area
Oxygenator thrombosis progressively reduces functional membrane surface area, impairing both oxygen transfer and CO2 elimination despite maximal sweep gas flows.
Question 2: What is the physiological rationale for maintaining a target ACT of 160-200 seconds during ECMO rather than full anticoagulation (ACT >400)?
- Higher ACT causes excessive pump speed reduction
- Balancing thrombosis prevention against hemorrhagic complications given the procoagulant surface of the circuit (Correct answer)
- Full anticoagulation causes hemolysis in the pump head
- ACT above 200 impairs membrane lung function
Correct answer: Balancing thrombosis prevention against hemorrhagic complications given the procoagulant surface of the circuit
The ECMO circuit's artificial surfaces activate coagulation, but excessive anticoagulation dramatically increases bleeding risk, so moderate heparin targets balance clot prevention with hemorrhage avoidance.
Question 3: How does ECMO-induced hemolysis contribute to renal injury?
- Free hemoglobin causes renal tubular toxicity and vasoconstriction of the renal microvasculature (Correct answer)
- Hemolysis reduces oxygen delivery to the kidneys by decreasing hematocrit
- Hemolyzed red cells cause glomerular mechanical obstruction
- Hemolysis triggers a cytokine storm that damages renal endothelium
Correct answer: Free hemoglobin causes renal tubular toxicity and vasoconstriction of the renal microvasculature
Free plasma hemoglobin released during hemolysis is directly nephrotoxic, causing oxidative tubular injury and scavenging nitric oxide to produce renal vasoconstriction and ischemia.
Question 4: In ARDS patients on VV-ECMO, why is ultra-protective ventilation (TV 2-4 mL/kg) physiologically preferable?
- It reduces the work of breathing imposed by the ventilator
- It minimizes ventilator-induced lung injury while ECMO maintains gas exchange, allowing lung rest (Correct answer)
- It increases functional residual capacity more than conventional tidal volumes
- It prevents oxygen toxicity from high FiO2 requirements
Correct answer: It minimizes ventilator-induced lung injury while ECMO maintains gas exchange, allowing lung rest
VV-ECMO assumes the gas exchange burden, permitting extremely low tidal volumes that minimize cyclic alveolar stretch, barotrauma, and biotrauma, facilitating lung recovery.
Question 5: What hemodynamic consequence occurs when ECMO flow is abruptly reduced in a patient with severe cardiogenic shock on VA-ECMO?
- Immediate improvement in LV function due to reduced afterload
- Precipitous drop in mean arterial pressure and end-organ perfusion (Correct answer)
- Reflex bradycardia from baroreceptor activation
- Pulmonary edema due to increased venous return
Correct answer: Precipitous drop in mean arterial pressure and end-organ perfusion
In cardiogenic shock, systemic perfusion depends on ECMO flow; abrupt reduction removes the primary driver of cardiac output and tissue oxygen delivery, causing immediate hemodynamic collapse.
Question 6: Which metabolic disturbance is most commonly associated with massive blood product transfusion during ECMO circuit prime or resuscitation?
- Hypernatremia from saline-preserved blood products
- Hypocalcemia from citrate chelation impairing ionized calcium (Correct answer)
- Metabolic alkalosis from bicarbonate excess
- Hyperkalemia from cellular potassium release in fresh blood
Correct answer: Hypocalcemia from citrate chelation impairing ionized calcium
Citrate used as anticoagulant in stored blood products chelates ionized calcium, causing hypocalcemia that impairs myocardial contractility and coagulation cascade function.
Question 7: Why does the right ventricle typically dilate and fail before the left ventricle in massive pulmonary embolism requiring ECMO?
- The RV free wall has less myocardium than the LV
- Acute pulmonary vascular obstruction causes sudden RV pressure overload beyond its adaptive capacity (Correct answer)
- Pulmonary embolism directly damages RV myocardium via inflammatory mediators
- The RV coronary supply is more vulnerable to ischemia than the LV
Correct answer: Acute pulmonary vascular obstruction causes sudden RV pressure overload beyond its adaptive capacity
The RV is a thin-walled, low-pressure chamber not adapted to acute pressure loads; sudden obstruction of the pulmonary vascular bed raises RV afterload acutely, causing dilation, ischemia, and failure.
ECMO Physiology and Pathophysiology 3
A patient on VV-ECMO develops worsening hypercapnia despite maximal sweep gas flow.
What is the most likely explanation?