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Research Applied to Clinical Practiceimgtchr1.gif (1235 bytes)
by Robert C. Knies, RN MSN CEN
Section Editor

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Activated Clotting Time (ACT)
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      The use of ACT as a coagulation measurement that ED nurses need to know about, has arisen secondary to our increased use of glycoprotein IIb/IIIa receptor inhibitors (ReoPro, and Aggrastat). During the research about this test some interesting information about heparin arose, and my lack of knowledge about this triggered the idea that many others may also benefit from it.

        Activated Clotting Time (ACT) is a measure of the anticoagulation affects of heparin. ACT was originally described by Hatterseley in 1966. The main use of this diagnostic test is in cardiac catheterization labs and CABG surgery, where they need to keep track and have specific measures of bleeding times. The study can be done on fresh whole blood and citrated whole blood. The end point is the detection of fibrin (clot) formation.
        ACT is a good indicator of the heparin affect, when heparin is the ONLY variable, but when other variables are altered, it becomes non-specific to heparin. Although ACT has been indicatd as the global test for coagulation. There are many instances that may affect the results:
  • The ACT may decrease slightly with the process of surgery
  • It may increase if the measuring equipment is not warmed to 37º C
  • Catheter material and method for clearing heparin flush
  • Patient hypothermia
  • Increased hemodilution
  • Lysed platelets
  • Protamine sulfate administration

        The way they measure the time of fibrin is by placing the blood in a cartridge that has an activating agent in it (kaolin) that interacts with the blood to take out any outside effects that may affects the clot formation. Then the machine drops a plunger that has a small flag attached and electronically measures the time it takes for the flag to stop falling. Which means it becomes stopped by the fibrin fibers.

        A quick review of how heparin works is indicated. Heparin is a polysaccharide, (or complex sugar), that is obtained from natural sources, e.g., porcine intestines or bovine lungs. It must be given parenterally since it is not effectively absorbed from the GI tract. Heparin has no anticoagulant properties by itself, it must have ATIII (a natural anticoagulant that occurs in the intrinsic clotting pathway) as a cofactor. ATIII binds activated factors, so they are unavailable to participate in clot formation cascade, but this happens slowly.

        When combined with heparin, ATIII binds clotting factors instantaneously in the cascade process, and by binding thrombin, there is less to form fibrin, aggregate platelets and amplify clotting. No other anticoagulant developed has been shown to be as effective.

        Heparin sensitivity, like many drugs, varies significantly among patients (1). This variance may be due to inherited tendencies, an acquired disease, and the effects of drugs, such as nitroglycerin (2). Therefore, heparin therapy must be individualized. Heparin therapy may be directed at either of the following goals; prevent the adverse affects which may result from thrombus formation, and/or preserving clotting factors.

        Heparin therapy itself has been shown to potentiate heparin resistance, possibly due to a decrease in the ATIII availability and function. Other factors reported to decrease the anticoagulant response to heparin are platelets-thrombocytosis and thrombocytopenia, age of patient, hemoglobin concentration, NTG, oral anticoagulants, and pH and protein effects (3).

        The distinction between anticoagulant and antithrombotic and which action heparin performs requires some clarification. Anticoagulant and antithrombotic can be the same, but there are times when they are not and that distinction can be important. Anticoagulants prolong clotting times, heparin is an anticoagulant. Hypothermia can be considered an anticoagulant because clot formation rate is slowed, however, thrombin is still formed and there is nothing done via cooling to bind or inhibit the thrombin, therefore thrombin can further amplify clot formation. This is significant when you consider a trauma patient who is hypothermic on arrival and progresses into DIC.

        Alternate methods for monitoring heparin therapy are gaining considerable interest due to questions that have been raised as to the correlation between therapeutic effects versus proper anticoagulation monitoring. There are three general methods available for monitoring the anticoagulant effects of heparin in blood:

  • Tests that quantify heparin in the blood.
  • Tests that reflect the in vivo generation of thrombin.
  • Qualitative tests that measure the anticoagulation effects of heparin in the blood (4).

Tests that reflect the effect of heparin



Lee-White Clotting Time  Fresh Whole Blood
Activated Clotting Time (ACT) Fresh Whole Blood
Recalcified Activated Clotting Time Citrated Whole Blood
Whole Blood Partial Thromboplastin Time (PTT) Fresh Whole Blood
Activated Partial Thromboplastin Time (aPTT) Citrated Whole Blood


Tests that reflect the concentration of heparin



Protamine Sulfate Titration Fresh Whole Blood, Citrated Whole Blood or Citrated Plasma
Polybrene Titration Fresh Whole Blood, Citrated Whole Blood or Citrated Plasma
Thrombin Time Fresh Whole Blood, Citrated Whole Blood or Citrated Plasma
Hep Test Citrated Plasma
Synthetic substrates (anti-Xa and anti-IIa tests) Citrated Plasma


Tests that reflect the in vivo thrombin generation (fibrin formation)



Fibrinopeptide A Citrated Plasma
Fibrin monomer Citrated Plasma

       Therapeutic goals for heparin monitoring have been classified into:

  • Straight protocol

  • Measuring heparin effect

  • Measuring heparin concentration

  • Correlating the heparin effect to heparin concentration

    Titrating the dose of the drug is advocated by those who want to measure actual heparin concentration in the blood. Others choose the method of plasma assays, assuming they represent the in vivo pharmacologic affects of the drug.

        Many of the tests commonly used to monitor heparin anticoagulation are not capable of differentiating between the absence of clotting factors and the presence of heparin because they are non-specific and non-quantitative tests; that is, they are global or partially-global tests. These global and partially-global tests, like the ACT and aPTT, may give falsely extended or shortened clotting time results. These erroneous results may lead to improper heparin therapy.

        To summarize, this article was intended to inform the reader about ACT but also to review the action of heparin, and heparin measuring tests. As the reader can summarize this process is complicated one and will require more research to effectively, efficiently ad cost effectively control the clotting and antithrombotic effects within the human body.


1. Monitoring heparin therapy. Lab Report for Physicians. 1982;(March) 4:17.
2. Habbab, M.A., et al. Heparin resistance induced by intravenous nitroglycerin. Arch. Inter. Med. 1987;47:857-860.
3. Gravlee, G. Cardiopulmonary Bypass-Principles and Practice 1993;p.351, 353, 363, 375; Williams and Wilkins.
4. Chiu, H.M., et al. Relationship between the anticoagulant and antithrombotic effects of heparin in experimental venous thrombosis. Blood 1997;49 (2):171-184.

"Research Applied to Clinical Practice: Activated Clotting Time (ACT)"
is a webarticle by  Robert C. Knies, RN MSN CEN [[email protected]]]
©Robert C. Knies, RN MSN CEN
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