Hemostatic Agents

Patrick TitusParamedic Lecture

10/5/2016

Hemostasis A series of events in response to a tear in a blood

vessel to stop the bleeding.1. Damage to the vessel’s intima (innermost layer) exposes the underlying

collagen and triggers a release of two substances; adenosine diphosphate (ADP) and Thromboxane A2 (TXA2).

2. Both ADP and TXA2 stimulate the aggregation of platelets in the blood as well as vasoconstriction of the blood vessel.

3. The vasoconstriction decreases the flow of blood past the tear, thus allowing the new platelets to form a plug (clot) that temporarily occludes the bleeding.

Thrombi (blood clots that obstruct vessels or heart cavities) are the primary pathology in several clinical conditions; including MI, stroke, and pulmonary embolism.

3 Drugs Used to Treat Thrombi:

1. Platelet Aggregation Inhibitors (Antiplatelet)

2. Anticoagulants

3. Fibrinolytic (Thrombolytic)

Platelet Aggregation Inhibitors (Antiplatelet) Decreases the formation of a platelet plug.

Example = Aspirin (which inhibit cyclooxygenase, an enzyme needed for the synthases of Thromboxane A2 (TXA2).

- By inhibiting TXA2 aspirin decreases the formation of platelet plugs and potential thrombi.

- Aspirin is indicated in acute treatment of chest pain and possible Myocardial Infarction.

- Aspirin, as well as other antiplatelet and anti coagulant drugs, has no effect on existing thrombi; it can only curb the formation of new ones.

Other Antiplatelet include dipyridamole (Persantine)

Anticoagulants Interrupts the clotting cascade, and there are two primary

types; 1) Parenteral, and 2) Oral.1. The Parenteral Anticoagulant is Heparin (a substance derived from the lungs of a

cattle or the intestines of pigs.- Its primary mechanism of action is to enhance Antithrombin III’s ability to inhibit

the clotting cascade.- Heparin injections are indicate in treating and preventing deep vein thrombosis

(DVT), pulmonary embolism, some forms of stroke, and MI.

2. The Oral Anticoagulant is Warfarin aka Coumadin (originally developed as a rat poison that killed through uncontrolled bleeding).

- Prevents coagulation by antagonizing the effects of Vitamin K, which is needed for the synthesis of the clotting cascade.

- Prescribed for chronic use to prevent thrombi in high-risk patients such as those with artificial valve replacement of those in A-Fib.

In case of overdose, give Vitamin K as an antidote.

Fibrinolytic (Thrombolytic) Act directly on thrombi to break them up, by chemical

conversions that activate enzymes that break up clots.- The drugs of this class are; streptokinase (Streptase), alteplase (rtPA), tenecteplase

(TNKase), and anistreplase (Eminase).- These meds all dissolve clots effectively; they differ primarily in their

administration and risk of bleeding side effect.

• Streptokinase’s mechanism of action is to promote plasminogens conversion to plasmin, and since plasmin dissolves the fibrin mesh of clots it can directly treat the cause of MI and some strokes, rather than anticoagulants and antiplatelet which can only prevent future clots.

- Alteplase (rtPA) is identical to the naturally occurring tissue plasminogen activator.- The window of opportunity for fibrinolytic therapy is limited, because of this EMS

systems are able to administer fibrinolytic in the prehospital setting.

QUESTIONS???

Reference Page:

• Paramedic Care; Principe's and Practice (Volume 2)