Case 3

The diagnosis is membrane lung dysfunction from progressive clot deposition. 

The three major consequences are: 

(1) Hemolysis and coagulopathy—the non-biologic surface activates inflammatory and coagulatory pathways, leading to a DIC-like syndrome (evidenced by rising pfHb, dropping fibrinogen, elevated D-dimer). 

(2) Obstruction to blood flow—clot deposition increases internal resistance, reflected by the rising pressure drop across the membrane lung from 30 to 65 mmHg. 

(3) Impaired gas exchange—moisture buildup in the gas phase or debris in the blood phase impairs the membrane’s ability to oxygenate and clear CO₂, evidenced by the poor CO₂ clearance despite increasing sweep gas.

A CO₂ clearance of less than 10 mmHg between pre- and post-membrane lung blood gases despite maximal sweep gas flow rate suggests a failing membrane lung. In this case, the clearance is only 7 mmHg (55 − 48), which meets this threshold. For oxygen, a maximal VO₂ less than 100–150 mL/min despite maximal effective blood flow rate and FdO₂ of 1.0 suggests a failing membrane lung. VO₂ can be calculated using the Fick equation across the membrane lung: VO₂ = blood flow × (post-membrane O₂ content − pre-membrane O₂ content).

Answer: B. Sighing the membrane lung is the appropriate initial intervention before committing to an exchange. This involves increasing the sweep gas flow rate to 10–15 L/min for 10 seconds, which hyperventilates the membrane lung in an attempt to clear moisture buildup in the hollow fibers. This technique is only effective for removing water—not clot. If CO₂ clearance improves after sighing, moisture was the problem. If not, the membrane is failing from clot deposition and exchange is needed. 

Giving a heparin bolus (A) will not dissolve established thrombus and increases bleeding risk. Increasing blood flow (C) against high resistance worsens hemolysis. Switching anticoagulants (D) does not address the existing clot burden

Membrane lung dysfunction refers to failure of the membrane lung itself—from clot deposition, hemolysis/coagulopathy, or impaired gas exchange through the membrane fibers. Gas failure refers to loss of gas supply to the membrane lung, which can occur at the gas blender (incorrect settings), the gas line (disconnection), or the gas source (empty tank or malfunction). 

To distinguish: in gas failure, the membrane lung pressures and hemolysis labs are normal because the membrane itself is intact—the problem is that no gas is being delivered. The key bedside check is to ensure the gas blender settings are correct, the gas line is connected, and the gas source is functional. In membrane lung dysfunction, you see rising pressure drop, evidence of hemolysis/DIC, and impaired gas exchange despite confirmed gas delivery. Importantly, exchanging the membrane lung will NOT correct gas failure.

The pattern of prolonged clotting time, hypofibrinogenemia, thrombocytopenia, and elevated D-dimer is consistent with a DIC-like syndrome caused by the membrane lung’s non-biologic surface activating inflammatory and coagulatory pathways. This consumption coagulopathy occurs as fibrin and clot deposit on the membrane lung surface, consuming clotting factors and platelets. 

Choice A describes a normal coagulation profile. Choice C (isolated thrombocytopenia) might suggest HIT but not membrane-induced coagulopathy. Choice D (elevated haptoglobin) is the opposite of what is expected—haptoglobin would be decreased or depleted in hemolysis as it binds free hemoglobin.