Thrombolytic therapy is the administration of drugs called lytics or “clot busters” to dissolve blood clots that have acutely (suddenly) blocked your major arteries or veins and pose potentially serious or life-threatening implications. These drugs are used to dissolve clots associated with cerebral vascular accidents and myocardial infarction (STEMI) and pulmonary embolism .

Aleteplase (tPA)

Tissue plasminogen activator (tPA)is a protein involved in the breakdown of blood clots. It is a serine protease found on endothelial cells, the cells that line the blood vessels.

Mechanism of action

Alteplase binds to fibrin rich clots via the fibronectin finger-like domain and the Kringle 2 domain. The protease domain then cleaves the Arg/Val bond in plasminogen to form plasmin. Plasmin in turn degrades the fibrin matrix of the thrombus, thereby exerting its thrombolytic action.

Side effects

  • Haemorrhage: most commonly intracerebral
  • Hypotension
  • Nausea/vomiting
  • Febrile
  • Arrhythmia


  • Active bleeding
  • Recent trauma or surgery
  • Uncontrolled hypertension

Nursing considerations

The time from CVA onset to thrombolytic use varies on the sources used. The local hospital policy states ‘Thrombolysis with alteplase within 270 minutes (4.5 hours) of stroke onset, under controlled conditions is a recommended treatment for acute ischaemic stroke according to New Zealand and International Stroke Guidelines.’ Therefore, I recommend that you use this time frame.

The inclusion criteria for alteplase use in New Zealand hospitals are:

  • Clinical diagnosis of ischaemic stroke, causing a serious, measurable focal neurological deficit (Defined as impairment of language, motor function, cognition, and/or gaze, vision, or neglect)
  • Stroke onset time reliably established – if wakes with stroke, onset is when last awake and normal. If patient unable to identify onset and no witness, onset is when last seen to be normal
  • Sufficient time to have CT scan and start t-PA treatment within 270 minutes of stroke onset.
  • Previously independent – not requiring “hands on” physical assistance with activities of daily living (home help or meals services are not exclusions).

All inclusion criteria must be met.

Additionally, the use of anticoagulant therapy is contraindicated within 24 hours of alteplase use.

Blood pressure must be measured every 15 minutes for the first 2 hours, every 30 minutes for the next 6 hours, and then every hour until 24 hours from treatment. If the patient develops severe headache, acute hypertension, nausea or vomiting, discontinue the infusion and obtain an urgent Cranial CT scan.

Perform neurological assessments every 15 minutes during the Alteplase infusion every 30 minutes for the next 6 hours, and then hourly until 24 hours.

Here’s a video showing how it works.

Antiplatelet: Clopidogrel

Mechanism of action

The active metabolite of clopidogrel selectively inhibits the binding of adenosine diphosphate (ADP) to its platelet P2Y12 receptor and the subsequent ADP-mediated activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation. This action is irreversible. Platelet function returns after one week of discontinuing the drug .

Side effects

  • Uncontrolled bleeding
  • Bruising
  • Hypertension
  • Headaches
  • Nausea

Nursing considerations

  • History: Allergy to clopidogrel, pregnancy, lactation, bleeding disorders, recent surgery, hepatic impairment, peptic ulcer
  • Physical: Skin color, temperature, lesions; orientation, reflexes, affect; P, BP, orthostatic BP, baseline ECG, peripheral perfusion; R, adventitious sounds

Here’s a video of it in action




Unfractionated heparin (UH) is a heterogenous preparation of anionic, sulfated glycosaminoglycan polymers with weights ranging from 3000 to 30,000 Da. It is a naturally occurring anticoagulant released from mast cells. It binds reversibly to antithrombin III (ATIII) and greatly accelerates the rate at which ATIII inactivates coagulation enzymes thrombin (factor IIa) and factor Xa. UH is different from low molecular weight heparin (LMWH) in the following ways: the average molecular weight of LMWH is about 4.5 kDa whereas it is 15 kDa for UH; UH requires continuous infusions; activated partial prothrombin time (aPTT) monitoring is required when using UH; and UH has a higher risk of bleeding and higher risk of osteoporosis in long term use. Unfractionated heparin is more specific than LMWH for thrombin. Furthermore, the effects of UH can typically be reversed by using protamine sulfate.

Mechanism of action

Under normal circumstances, antithrombin III (ATIII) inactivates thrombin (factor IIa) and factor Xa. This process occurs at a slow rate. Administered heparin binds reversibly to ATIII and leads to almost instantaneous inactivation of factors IIa and Xa The heparin-ATIII complex can also inactivate factors IX, XI, XII and plasmin. The mechanism of action of heparin is ATIII-dependent. It acts mainly by accelerating the rate of the neutralization of certain activated coagulation factors by antithrombin, but other mechanisms may also be involved. The antithrombotic effect of heparin is well correlated to the inhibition of factor Xa. Heparin is not a thrombolytic or fibrinolytic. It prevents progression of existing clots by inhibiting further clotting. The lysis of existing clots relies on endogenous thrombolytics.

Side effects

  • Heparin-induced thrombocytopenia (Read about it here)
  • Excessive bleeding
  • Abdo pain
  • GI upset

Nursing considerations

Heparin must be given parenterally as it is not absorbed through the gastrointestinal mucosa. It is usually given by iv infusion or deep sc injection. The onset of action is immediate after iv injection but can be delayed 20 to 60 minutes following sc injection. Plasma heparin concentrations may be increased and activated partial thromboplastin times (aPTTs) may be more prolonged in geriatric adults (older than 60 years of age) compared with younger adults.

HIT is caused by an immunological reaction that makes platelets form clots within the blood vessels, thereby using up coagulation factors. It can progress to thrombotic complications such as arterial thrombosis, gangrene, stroke, myocardial infarction and disseminated intravascular coagulation. Symptoms of overdose may show excessive prolongation of aPTT or by bleeding, which may be internal or external, major or minor. Therapeutic doses of heparin given for at least 4 months have been associated with osteoporosis and spontaneous vertebral fractures. Osteoporosis may be reversible once heparin is discontinued.

Here’s a video explaining it.



This is a low molecular weight heparin. It is considered a safer option to heparin and require less monitoring.

Mechanism of action 

The mechanism of action of enoxaparin is antithrombin-dependent. It acts mainly by accelerating the rate of the neutralization of certain activated coagulation factors by antithrombin, but other mechanisms may also be involved. The antithrombotic effect of enoxaparin is well correlated to the inhibition of factor Xa.  Enoxaparin binds to antithrombin (a circulating anticoagulant) to form a complex that irreversibly inactivates clotting factor Xa. It has less activity against factor IIa (thrombin) compared to unfractionated heparin (UFH) due to its low molecular weight.

Side effects 

  • Increased bleeding
  • Nausea
  • Diarrhea
  • Fever
  • Irritation at site of injection

Nursing considerations

  • Lab tests: Baseline coagulation studies; periodic CBC, platelet count, urine and stool for occult blood.
  • Monitor platelet count closely. Withhold drug and notify physician if platelet count less than 100,000/mm3.
  • Monitor closely patients with renal insufficiency and older adults who are at higher risk for thrombocytopenia.
  • Monitor for and report immediately any sign or symptom of unexplained bleeding.


Warfarin is a vitamin K antagonist that is used for prophylaxis or treatment of DVT, pulmonary thromboembolism, MI, AF, or in individuals with prosthetic heart vavlves.


Warfarin acts by inhibiting the synthesis of vitamin K-dependent clotting factors, which include Factors II, VII, IX, and X, and the anticoagulant proteins C and S. Vitamin K is an essential cofactor for the post ribosomal synthesis of the vitamin K-dependent clotting factors.

Side effects

  • Uncontrolled bleeding
  • Alopecia
  • Anorexia
  • Abdominal cramps
  • Luecopenia (Decreased WBC)
  • Nausea/vomiting

Nursing considerations

  • Monitor clotting time with prothrombin test (PTT)
    normal = 9 – 12 seconds
    therapeutic level = 1.5 times control
  • Monitor INR: Therapeutic level is between 2.0-3.0 (Target 2.5)

If you are not clear on INR here is a NZ article explaining the importance.

  • Monitor bleeding
  • Avoid aspirin and NSAIDs (similar to Heparin)
  • Watch for foods containing vitamin K
    (green vegetables, rice, pork, fish, yogurt, milk, some cheeses)
  • Other vitamins/herbs can affect the effectiveness of warfarin
    Vitamin C – decreases effectiveness of warfarin (ex: citrus juices)
    Vitamin E – increases effectiveness
    herbals – increases effectiveness (3Gs – garlic, gingko, ginger)

Antothrombin: Dabigatran

It is a synthetic, competitive and reversible direct thrombin inhibitor. Inhibition of thrombin disrupts the coagulation cascade and inhibits the formation of clots. Dabigatran etexilate may be used to decrease the risk of venous thromboembolic events in patients who have undergone total hip or knee replacement surgery, or to prevent stroke and systemic embolism in patients with atrial fibrillation, in whom anticoagulation therapy is indicated. In contrast to warfarin, because its anticoagulant effects are predictable, lab monitoring is not necessary.

Mechanism of action

Dabigatran, the main active principle in plasma, is a rapid-acting competitive and reversible direct inhibitor of thrombin. Thrombin, a serine protease, is responsible for the conversion of fibrinogen to fibrin in the coagulation cascade. Inhibition of thrombin consequently prevents thrombus development. Dabigatran inhibits free thrombin, fibrin-bound thrombin and thrombin-induced platelet aggregation.

Dabigatran directly inhibits thrombin in a concentration-dependent, reversible, specific, and competitive manner which results in a prolongation of aPTT (partial thromboplastin time), ECT (Ecarin clotting time), and TT (thrombin time). It may increase INR but this laboratory parameter is relatively insensitive to the activity of dabigatran.

Side effects 

  • Bleeding
  • Bruising
  • GI upset

Nursing considerations

  • Assess for the mentioned contraindications to this drug (e.g. hypersensitivity, acute liver disease, pregnancy etc.) to prevent potential adverse effects.
  • Conduct thorough physical assessment before beginning drug therapy to establish baseline status, determine effectivity of therapy, and evaluate potential adverse effects.
  • Obtain baseline status for complete blood count and clotting studies to determine any potential adverse effects.


Additionally, you can test your new found knowledge here, with a nursing anticoagulation quiz.




Bryant, B., & Knights, K. (2015). Pharmacology for health professionals (4th ed.). Sydney, Australia: Mosby Elsevier.