Career Perfusionist: [13] The Extracorporeal Circuit

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The Extracorporeal Circuit

Diversion of blood from the operative site, via an extracorporeal circuit (ECC) is necessary to proceed with open heart surgery .  Vascular access leading to the right side of the heart (venous) and ejecting from the left side of the heart (arterial) is shunted from the patient to the heart lung machine.

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The heart

(and therefore the lungs) are effectively bypassed, and their associated functions assumed by the components of the ECC.

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Typically, blood is drained by gravity via cannulae

in the superior and inferior vena cavae (and/or right atrium) to the heart-lung machine where it passes through an artificial lung (bubble or membrane “oxygenator”) and then is pumped (usually with a roller or centrifugal pump) back into the systemic arterial system via an arterial cannula that is placed in the ascending aorta.

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Because of the need to offset the cooling

of blood passing through the ECC as well as the frequent need to intentionally cool and then rewarm the patient, a heat exchanger is included in the oxygenator either prior to or contiguous with the gas exchange unit.

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The extracorporeal circuit is a thrombogenic device.

In order to initiate cardiopulmonary bypass, systemic heparinization is required in order to establish a safe level of anticoagulation.  The current dosing regimen is 200- 300 units of heparin per kilogram of patient weight.  It’s administration is usually targeted to reach and maintain an activated clotting time of 350-500 seconds (normal range is defined as ≤130 seconds).  It is intended to inhibit the formation of clots within the ECC and oxygenator, as well as prevent thrombotic events from occurring in the patient.  This represents a significantly high level of anticoagulation, that must then be appropriately reversed upon termination of bypass.

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Protamine sulfate

is the drug of choice for heparin reversal.  It inactivates heparin by binding with it and forming an inert salt.  Utilization of protamine sulfate fails to account for the disruption that the extracorporeal circuit has upon the intrinsic and extrinsic coagulation pathways of the patients coagulation cascade.  Abundant experimental and clinical evidence demonstrates that cardiopulmonary bypass inflicts changes upon the plasma and cellular constituents of blood.  Cardiopulmonary bypass affects both platelet count and function.  As a result of hemodilution, platelet counts decrease rapidly to 50% of preoperative levels, but usually remaining above 100,000 per µL.  Bleeding time is excessively prolonged and platelet aggregation to adenosine diphosphate (ADP) or collagen is impaired.  There are predictable reductions in the plasma concentration of coagulation factors II, V, VII, IX, X and XII, which are attributed to hemodilution.

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Significant to the circuit itself, is the amount of crystalloid solution

required to “prime” the tubing, reservoir, filters, and oxygenator, and remove all entrapped air.  Most circuits require at least 2,000 cc of solution such as Normosol, Plasmalyte “A”, or Isolyte “S”, which are pH and electrolyte specific to match the composition of whole blood.  Added to this base solution are heparin, sodium bicarbonate, mannitol, hespan, albumin and possibly some sort of anti-inflammatory corticosteroid.  This can lead to volumes of 2,500+ cc’s, which when transfused to the patient at the onset of cardiopulmonary bypass, can equate to a hemodilutional level of 30-40% of the patient’s circulating blood volume.

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Turbulent flow, shear stress, changes in viscosity,

blood-oxygen interface, and blood-artificial surface interface effect proteins and the formed elements in the blood.  Trauma to the cellular elements of the blood during cardiopulmonary bypass results in destruction or alteration to red cells and platelets.  Clot-promoting and heparin-neutralizing factors released from these damaged cells result in a state of hypercoagulability.  Intravascular clotting can subsequently occur, resulting in an abnormal consumption of clotting factors.  These developments in turn stimulate production of antithrombin activity and the release of plasminogen activator which results in fibrinolysis.

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