16.2 Extracorporeal Circulation
Key Takeaways
- Cardiopulmonary bypass (CPB) circuits must be primed with crystalloid, colloid, or blood before use, and that prime volume dilutes the patient's hematocrit and coagulation factors as soon as bypass begins.
- Unfractionated heparin (targeting an ACT of roughly 400-480 seconds) anticoagulates the CPB circuit; protamine sulfate reverses it afterward, and a history of heparin-induced thrombocytopenia requires a non-heparin anticoagulant such as bivalirudin.
- Post-bypass "bypass coagulopathy" combines hemodilution, mechanical platelet dysfunction, residual heparin, and hyperfibrinolysis, and is best sorted out with viscoelastic testing (TEG/ROTEM) rather than PT/PTT alone.
- Prolonged extracorporeal support (ECMO, ventricular assist devices) causes acquired von Willebrand syndrome from shear-induced loss of high-molecular-weight vWF multimers, producing a mechanical bleeding tendency.
- Neonatal and small pediatric bypass circuits often use a blood prime (RBC unit plus FFP) with fresh, irradiated, leukoreduced units because circuit volume can rival or exceed the patient's own blood volume.
16.2 Extracorporeal Circulation
Extracorporeal circulation (ECC) pumps a patient's blood through an external mechanical circuit outside the body. The main clinical forms are cardiopulmonary bypass (CPB) for cardiac surgery, extracorporeal membrane oxygenation (ECMO) for prolonged cardiac or respiratory failure, ventricular assist devices (VADs) for chronic mechanical circulatory support, and intraoperative cell salvage. Each interacts with blood bank practice differently, but all share the same root problem tested on the SBB exam: contact between blood and a large synthetic surface area causes dilution, platelet injury, and factor consumption that the blood bank must anticipate and support.
The Cardiopulmonary Bypass Circuit
A basic CPB circuit has a venous cannula draining blood by gravity or vacuum assist into a venous reservoir, a membrane oxygenator that adds oxygen and removes carbon dioxide, a heat exchanger, an arterial pump (roller or centrifugal) that returns oxygenated blood to the patient, cardiotomy suction that recovers shed surgical-field blood back into the circuit, and inline filters.
Circuit Priming and Dilutional Effects
Before a patient is connected, the tubing, oxygenator, and reservoir must be filled ("primed") with fluid - typically 1-2 liters in an average adult, less with mini-circuits or vacuum-assisted venous drainage - predominantly balanced crystalloid, sometimes with added colloid such as albumin. The instant bypass starts, this prime volume mixes with the patient's own blood, producing acute hemodilution: hematocrit drops (dilutional anemia) and plasma concentrations of coagulation factors, fibrinogen, and platelets fall in proportion.
Because the prime volume is comparatively large relative to a small patient's total blood volume, hemodilution is far more severe in infants and children than in adults. For many pediatric and neonatal cases, the prime itself uses reconstituted whole blood (an RBC unit combined with FFP), a so-called blood prime, rather than crystalloid alone, to avoid starting bypass with the patient already anemic and coagulopathic. Blood bank practice for these units generally calls for red cells that are fresh (limiting potassium load and preserving 2,3-DPG), irradiated (preventing transfusion-associated graft-versus-host disease in an immunologically immature patient), and leukoreduced (reducing CMV transmission risk and febrile reactions), often also CMV-seronegative depending on institutional policy.
Anticoagulation: Heparin and Protamine
Bypass requires full systemic anticoagulation, because blood contacting the circuit's large synthetic surface would otherwise clot rapidly. Unfractionated heparin, dosed at roughly 300-400 units/kg, is given before cannulation, and the activated clotting time (ACT) is monitored, targeting greater than 400-480 seconds throughout bypass (institution-dependent). After separating from bypass, protamine sulfate reverses the heparin, roughly 1 mg of protamine per 100 units of remaining heparin, adjusted by ACT or protamine titration.
Two failure modes of this heparin/protamine pairing matter for SBB-level blood bank practice:
- Heparin resistance: an inadequate ACT rise despite an adequate weight-based heparin dose, usually caused by antithrombin III (AT-III) deficiency (congenital, or acquired from prior heparin exposure and consumption). It is treated with FFP, which contains AT-III, or with a purified AT-III concentrate.
- Heparin-induced thrombocytopenia (HIT): a patient with a documented HIT history cannot safely receive heparin for bypass and instead needs a direct thrombin inhibitor such as bivalirudin or argatroban - a major intraoperative management problem, because neither agent has a reversal drug equivalent to protamine.
- Protamine reactions: protamine itself can trigger anaphylaxis or severe hypotension, with higher risk in patients with fish allergy, prior NPH insulin exposure, or vasectomy (pre-formed anti-protamine antibodies).
Post-Bypass ("Bypass") Coagulopathy
Bleeding after separation from CPB is multifactorial: residual dilution of factors and platelets from the prime, mechanical platelet activation and consumption from shear stress and foreign-surface contact within the circuit, incompletely reversed heparin, hypothermia-impaired clotting-factor enzyme function, and contact-activation-driven hyperfibrinolysis. Because standard PT/PTT poorly distinguish these overlapping causes and turn around too slowly for an actively bleeding patient, cardiac programs increasingly use point-of-care viscoelastic testing (thromboelastography/TEG or rotational thromboelastometry/ROTEM) to identify the dominant defect - platelet dysfunction, low fibrinogen, residual heparin, or hyperfibrinolysis - and target blood component therapy accordingly: platelets for dysfunction or thrombocytopenia, cryoprecipitate or fibrinogen concentrate for hypofibrinogenemia, additional protamine for a residual heparin signal, and antifibrinolytics (tranexamic acid, aminocaproic acid) for fibrinolysis, which many centers also give prophylactically before bypass begins.
Cell Salvage
Intraoperative cell salvage ("cell saver") aspirates shed surgical-field blood, anticoagulates it, then washes and centrifuges it to return a concentrated, saline-suspended red cell product to the patient, reducing allogeneic RBC exposure. Because washing removes plasma, salvaged blood contains no platelets and no coagulation factors, so it cannot substitute for FFP or platelet transfusion in a coagulopathic patient. Salvage is generally avoided in surgical fields grossly contaminated with bacteria, and its use in oncologic surgery is institution- and leukoreduction-filter-dependent because of a theoretical risk of reinfusing tumor cells.
ECMO and Ventricular Assist Devices
ECMO extends extracorporeal support from the hours typical of CPB to days or weeks, in either venoarterial (VA-ECMO) configuration, which supports both the heart and lungs, or venovenous (VV-ECMO) configuration, which supports the lungs only. ECMO uses a lower, continuous heparin infusion (ACT target roughly 180-220 seconds) rather than the high single-dose bolus used for bypass. Prolonged blood-circuit contact produces ongoing, low-grade consumption of platelets and coagulation factors, so ECMO patients typically need scheduled RBC and platelet support throughout their run.
Shear stress across the ECMO pump and oxygenator also cleaves high-molecular-weight von Willebrand factor multimers, producing an acquired von Willebrand syndrome analogous to that seen with ventricular assist devices - a mechanical, non-inherited bleeding tendency that resolves only when the device is removed. Mechanical hemolysis from the pump is monitored with plasma free hemoglobin and haptoglobin, and AT-III depletion during a long ECMO run can again cause heparin resistance, managed the same way as in CPB (FFP or AT-III concentrate).
A patient going onto cardiopulmonary bypass receives a standard weight-based heparin dose, but the activated clotting time (ACT) does not rise to target. What is the most likely cause and the appropriate treatment?
A cardiac surgery patient has a documented history of heparin-induced thrombocytopenia (HIT). Which anticoagulation strategy is appropriate for cardiopulmonary bypass?
A patient on venovenous ECMO for two weeks develops a new bleeding tendency despite a normal platelet count and normal factor VIII level. What is the most likely mechanism?
Why do many neonatal cardiopulmonary bypass protocols prime the circuit with reconstituted whole blood (an RBC unit plus FFP) rather than crystalloid alone?