Coagulation Drugs

Anticoagulation drugs

The above pathway is the short version of the coagulation process in the body.
After the formation of the clot, the process of removal of clot is called fibrinolysis. It is initiated within 24 to 48 hours of clot formation and continues until the clot is dissolved. Fibrinolysis involves several sequential steps. When fibrin clot is formed, nearby blood vessel cells secrete the enzyme tissue plasminogen activator (TPA). TPA converts the inactive protein plasminogen, which is present in the fibrin clot, to its activate form, plasmin. Plasmin then digests the fibrin strands to remove the clot.  
The drugs affects the coagulation is as follow:

Type of modification Mechanism Drug classification
Prevention of clot formation Inhibition of specific clotting factors
Inhibition of platelet actions


Removal of an existing clot Clot dissolved by the drug Thrombolytic
Promotion of clot formation Inhibition of fibrin destruction Hemostatic


Mechanism of action:
They usually interrupt the clotting pathway. They inhibit the one of the factors in the clotting mechanism and prevent clotting. They also called as the blood thinners, which is a misnomer, because they do not change the thickness of the blood. Instead, anticoagulant imparts the negative charge to the surface of the platelets, which inhibits the clumping action or aggregation of these cells. They are usually antithrombin.

  • heparin (Heparin)
  • Enoxaparin(Lovenox)
  • Dabigatran(Pradaxa)
  • Warfarin(Coumadin)


  • Unstable angina
  • Stroke (CVA) –due to ischemia
  • Heart valve disease
  • Atrialfib (a rapid, irregular heart beat)
  • Prophylaxis for high risk patients to prevent thrombus formation post surgery –i.e. hip or knee surgery
  • Immobility
  • Pulmonary embolism
  • Factor V Leiden (genetic disorder, in which abnormal clot formations occur )


  • Active bleeding
  • Anticipated bleeding

Parental anticoagulants


  • Heparin
  • Low molecular weight heparin

Mechanism of action:

Potentiates antithrombinIII (a plasma protein that inactivates Factor Xaand Thrombin

Drug Interactions

  • ASA & NSAIDs augment anticoagulation

Adverse Effects

  • Hemorrhage
  • Heparin Induced Thrombocytopenia & Thrombosis (HITT*) aka White Clot Syndrome

Considered a “High Risk Medication”


  • Protamine Sulfate IV


  • IV
  • SQ
    • Do not aspirate
    • Do not massage
    • Insert needle at 90 degree angle

Enoxaparin (Low molecular weight heparin)
Mechanism of action:

Potentiates effect of Antithrobminon Factor Xa and Thrombin. Their mechanism of action is 2 to 3 hours longer than heparin. It produces a more stable response than heparin; so, fewer follow-up lab tests are needed, and family members, caregivers, or patients can be trained to give subcutaneous injection at home.

Kinetics: Given SQ

Adverse Effects:

  • Bleeding,
  • Angioedema,
  • Thrombocytopenia
  • No HITT ?

Nursing Management

  • Pregnancy cat B

  • Allergy to pork products or heparin

Nursing Management for parental anticoagulants

  • Assessment/Analysis
    • Diagnosis, history, allergies, & baseline labs -Pregcat C

  • Planning/Implementation

  • Patient Teaching

  • Route: IV or SQ
    • SQ technique
      • Do not aspirate
      • Do not massage

  • Evaluation

    • Look at patient

  • Monitor Labs

    • Partial ThromboplastinTime (PTT)
      • Normal is 60-90 seconds
      • Therapeutic is 90-180 seconds

    • Activated Partial ThromboplastinTime (aPTT)
      • Normal is 25-35 seconds
      • Therapeutic is 50-70 seconds

    • Activated Clotting Time (ACT)
      • Normal is 70-180 seconds

    • Complete Blood Count (CBC)

Oral Anticoagulant

Mechanism of action:
They acts by inhibiting the hepatic synthesis of coagulation factors II, VII, IX, and X. The most often prescribed oral anticoagulant is Warfarin (Coumadin). It is vitamin K antagonists.  Often, patient begin anticoagulation therapy with heparin and are switched to warfarin when their condition stabilize. When transitioning, the two drugs are administered concurrently for 2 to 3 days because warfarin takes several days to achieve optimum effects.
Pantoxifylline is another oral anti-coagulant that works by a different mechanism, which is reduces the viscosity of red blood cells and increases their flexibility.
The most common adverse effect of oral anticoagulant is bleeding.
Drug interaction:

  • Aspirin, NSAIDs, and diet high in vitamin K


  • Vitamin K
  • Fresh frozen plasma

Patient teaching

  • The basic action of Coumadin
  • The reason for the prescription
  • Know how to calculate dose
  • Take at the same time each day
  • (do not double dose if dose missed)
  • Stick to usual diet
  • Wear a medic alert bracelet
  • Alert other physicians or dentists
  • Use a soft toothbrush & electric razor
  • Know signs of bleeding like dark or brown urine, black or brown stool, bleeding gums etc…
  • Have PT/INR checked as ordered

Lab values to monitor for warfarin

  • INR (International normalized ration)
    • Normal is 0.8 to 1.2
    • Therapeutic is 2-3 for DVT and 2.5-3.5 for arterial thrombosis
  • PT
    • Normal is 10.4 to 12.2 seconds
    • Therapeutic value is 1.5 or 2 times of normal value


Mechanism of action:
Antiplatelet drugs inhibit the platelet aggregation. Unlike anticoagulant are used to prevent clot formation in veins, Antiplatelet drugs are used to prevent clot formation in arteries.
There are main four different types of Antiplatelet drugs.

  1. Aspirin
  2. ADP receptors blockers
    1. They are small groups of drugs that irreversible alter the plasma membrane of platelets. This alteration changes the bindings of ADP to its receptors on platelets so they are unable to receive chemical signals required for them to aggregate.

Examples: clopidogrel



  1. Glycoprotein IIb /IIIa receptors antagonists
    1. It is the enzyme that is required for platelet aggregation. They can be given only by IV route
      1. Abciximab
      2. Eptifibatide
      3. Tirofiban
  2. Drugs for intermittent claudication
    1. Pentoxifylline
    2. Cilostazol

Clinical uses:

  • Stroke
  • Angina
  • Myocardial infarction or heart attack
  • Acute coronary syndrome
  • Thromboembolic diseases
  • Intermittent claudication


Mechanism of action:
Thrombolytic agents promote fibrinolysis, or clot destruction, by converting plasminogen to plasmin. The enzyme plasmin digests fibrin and breaks down fibrinogen, prothrombin, and other plasma proteins and clotting factors. Unlike the anticoagulants, which can only prevents clots, thrombolytics actually dissolve the insoluble fibrin within the clot.
Clinical uses:
These agents are used for disorders in which an intravascular clot has already formed, such as in acute myocardial infarction, pulmonary embolism, acute ischemic CVA, and DVT.
The goal of thrombolytic therapy is to quickly restore the blood flow to the tissue served by the blocked vessel. Delayed in establishing circulation may result in ischemia and permanent damage. The therapeutic effect of thrombolytic is greater when they are administered as soon as possible after clot formation occurs, preferably within 4 hours.

  • They have narrow margin of safety between normal and abnormal reaction, therefore it is discontinued as soon as clot is dissolved and then appropriate anticoagulant or anti platelet drugs are administered.


  • Alteplase
  • Reteplase
  • Streptokinase
  • Tenecteplase