Medscape is available in 5 Language Editions – Choose your Edition here.


Activated Clotting Time 

  • Author: Vadim Kostousov, MD; Chief Editor: Eric B Staros, MD  more...
Updated: Jan 15, 2014

Reference Range

Activated clotting time (ACT) depends on the test device used, and it can vary from 80 to 160 seconds. Each manufacturer provides its own baseline reference values and target range with the ACT testing device.



Normal activated clotting time (ACT) indicates that tested blood contains no heparin or that all heparin is inhibited by protamine (postoperative anticoagulation reversal).

ACT is intended to monitor anticoagulant effect of unfractionated heparin. Target ACT values may depend on the specific device and clinical scenario. ACT prolongation also can indicate coagulation factor deficiency, severe thrombocytopenia, or severe platelet dysfunction.


Collection and Panels

Specimen: Whole blood

Collection: Blood (usually 0.5-1 mL) from venous/arterial vessel; indwelling or extracorporeal line is collected into the plastic syringe/tube (see image below) and immediately placed/poured into the device cuvette/cartridge

Storage: Whole blood specimen should be processed within 1 minute (or 2 min if specimen contains therapeutic level of unfractionated heparin)

Glass vacuum tube. Glass vacuum tube.



Activated clotting time (ACT) is a point-of-care coagulation test designed to monitor heparin therapy in the clinical situations in which intensive anticoagulation is required.[1] Similar to partial thromboplastin time (PTT), ACT reflects time of clot formation via the intrinsic coagulation pathway by the addition of factor XII activators (eg, diatomaceous earth [Celite], kaolin, glass beads, ellagic acid) and increases linearly to relation to the heparin concentration. Clotting times may also vary between ACT analyzers manufactured by different (or the same) vendors, depending on the source and the formula of the activator, the amount of activator relative to the sample volume, or the method of clot detection. Therefore, instrument-specific protocols should be established and validated for each type of clinical procedure.[2]


ACT is used for bedside or intraoperative monitoring of unfractionated heparin therapy in the settings of invasive or operative procedures, as follows:

  • Dialysis
  • Cardiac catheterization and angiography
  • Intra-aortic balloon pumping
  • Percutaneous coronary intervention (PCI)
  • Extracorporeal membrane oxygenation (ECMO)
  • Vascular surgery
  • Valve replacements
  • Carotid endarterectomy
  • Cardiopulmonary bypass graft surgery


The following factors may affect ACT measurements:

  • Hemodilution
  • Hypothermia (in certain ACT devices)
  • Drugs: Warfarin, aprotinin, GPIIb/IIIa inhibitors (eg, abciximab)
  • Severe (< 20 X 10 9/L) but not moderate (40-60 X 10 9/L) thrombocytopenia [3]

Severe deficiency of contact activation factors (factor XII, prekallikrein, high-molecular-weight kininogen) does not cause increased bleeding risk during heparin therapy but does prolong the ACT and makes it impossible to use this test. Alternative coagulation tests (eg, anti-Xa assay) might be used for heparin monitoring in this situation.[4, 5, 6]

Lupus anticoagulant (LA) also prolongs initial ACT values, and other strategies could be considered for heparin monitoring in patients with LA, such as doubling baseline ACT or in vitro heparin-ACT curves development. Alternatively, the anti-Xa assay or protamine titration devices might be used.[7]

Contributor Information and Disclosures

Vadim Kostousov, MD Research Associate, Transfusion Medicine and Coagulation, Department of Pathology and Immunology, Texas Children’s Hospital, Baylor College of Medicine

Disclosure: Nothing to disclose.

Chief Editor

Eric B Staros, MD Associate Professor of Pathology, St Louis University School of Medicine; Director of Clinical Laboratories, Director of Cytopathology, Department of Pathology, St Louis University Hospital

Eric B Staros, MD is a member of the following medical societies: American Medical Association, American Society for Clinical Pathology, College of American Pathologists, Association for Molecular Pathology

Disclosure: Nothing to disclose.

  1. Spinler SA, Wittkowsky AK, Nutescu EA, Smythe MA. Anticoagulation monitoring part 2: Unfractionated heparin and low-molecular-weight heparin. Ann Pharmacother. 2005 Jul-Aug. 39(7-8):1275-85. [Medline].

  2. McPherson RA, Matthew R. Pincus MR, ed. Henry's Clinical Diagnosis and Management by Laboratory Methods. 22nd ed. Elsevier Saunders: Philadelphia, Pa; 2011.

  3. Wallach J. Interpretation of Diagnostic Tests. 6th ed. New York, NY: Little, Brown; 1996.

  4. Lehman CM, Thompson C. Instrumentation for the Coagulation Laboratory. Bennett ST, Lehman CM, Rodgers GM. Laboratory Hemostasis: A Practical Guide for Pathologists. Springer; 2007. 41-55.

  5. Ammar T, Fisher CF, Sarier K, Coller BS. The effects of thrombocytopenia on the activated coagulation time. Anesth Analg. 1996 Dec. 83(6):1185-8. [Medline].

  6. van Veen JJ, Laidlaw S, Swanevelder J, et al. Contact factor deficiencies and cardiopulmonary bypass surgery: detection of the defect and monitoring of heparin. Eur J Haematol. 2009 Mar. 82(3):208-12. [Medline].

  7. Davidson SJ, Burman JF, Rutherford LC, Keogh BF, Yacoub MH. High molecular weight kininogen deficiency: a patient who underwent cardiac surgery. Thromb Haemost. 2001 Feb. 85(2):195-7. [Medline].

  8. Cankovic L, Steenwyk BL, McGiffin DC, Nielsen VG. Practical approach to anticoagulation for cardiopulmonary bypass in the patient with congenital prolonged activated partial thromboplastin time. Blood Coagul Fibrinolysis. 2008 Oct. 19(7):725-6. [Medline].

  9. Mehta TP, Smythe MA, Mattson JC. Strategies for managing heparin therapy in patients with antiphospholipid antibody syndrome. Pharmacotherapy. 2011 Dec. 31(12):1221-31. [Medline].

Glass vacuum tube.
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.