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Mechanical assist devices


Bleeding can be divided into:

  1. “Medical” bleeding secondary to defects in the coagulation cascade, platelets, or fibrinogen;
  2. “Surgical” bleeding secondary to operative trauma including leaks at sites of vascular anastomosis or cannulation sites or bleeding from small mediastinal arteries or veins. Surgical bleeding requires a return to the OR for re-exploration and hemostasis.

Surgical bleeding

Consider a “surgical” source of bleeding in the following situations:

  1. Persistent bleeding in the absence of a specific haemostatic defect (normal coagulation parameters)
  2. Sudden onset of fresh, rapid bleeding; especially if associated with a preceding sudden increase in BP. Note that repositioning the patient (turning on their side) may also cause the drainage of a pre-existing collection of “old” darker blood that had pooled in the thorax.
  3. Greater than 500 cc of bleeding in the first post-op hour.
  4. > 400 cc/hr x 2 hours.
  5. > 300 cc/hr x 3 hours
  6. > 200 cc/hr x 4 hours

If any of the above criteria are noted you must notify the ICU Fellow or Attending and the Cardiac Surgery Fellow immediately. The ICU Fellow or Attending should be notified about any significant bleeding whether it is believed to be “medical” or “surgical.”

Etiology of “medical” bleeding:

  1. Residual heparin effect; patients are anticoagulated before going on CPB with a large dose of heparin to maintain their ACT >400. The heparin is ‘reversed’ at the end of the case with protamine. Occasionally, the calculated dose of protamine given is not sufficient to completely reverse the heparin effect. Patients may also receive additional heparin if they are given back blood that remained in the bypass circuit when the patient was disconnected from CPB (“pump blood”). A “heparin rebound phenomenon” can also occur several hours post-op. An ACT will be done as soon as the patient arrives in the ICU. Normal values are between 100 and 120 seconds.
  2. Qualitative platelet defects. Platelet function may be impaired for several reasons. Many patients are on anti-platelet agents pre-operatively. CPB also leads to impaired platelet function, and the longer the duration of CPB, the greater the impairment.
  3. Quantitative platelet defects. Platelet numbers can be decreased following CPB due to hemodilution, destruction, and aggregation.
  4. Clotting factor deficits. Hemodilution on CPB or consumption. Pre-operative defects secondary to hepatic disease.
  5. Fibrinogenolysis; plasminogen activation during CPB. Clinical DIC is rare.