Introduction to Hemostasis

• Hemostasis

Introduction to Hemostasis

Upon completion of this learning module, you will be able to:

1. Define hemostasis.
2. Determine appropriate specimen types for hemostasis testing.
3. Briefly describe the 3 stages of hemostasis, including the order in which they occur.
4. Describe the blood vessels' role in hemostasis, including the secretions they contribute and the purpose of each.
5. Describe the platelets' role in hemostasis, including the secretions they contribute and the purpose of each.

Before we can discuss hemostasis we need to know what it is.
So, what is hemostasis?

1. blood cell production
2. balance between bleeding and clotting
3. the study of blood and its components
4. stopping of blood flow

Hemostasis

Hemostasis is a complex process by which the body stops bleeding and maintains blood in the fluid form within the vessels.

Simply put, it is the maintenance of balance between bleeding and clotting tendencies of the body.

OK, now we know what hemostasis is.
Why do we care about it?
Reflect for a few seconds.
Then, tell me why you think it may be important for YOU to learn about.

First, let's take a look at the components of blood:

Plasma

• the liquid portion of blood
• contains many chemical constituents which includes (for our purposes):

1. coagulation factors
2. fibrinolytic factors
3. inhibitors

Formed elements:

• are microscopically visible
• include (for our purposes):

1. WBCs (leukocytes)
2. RBCs (erythrocytes)
3. platelets (thrombocytes)

What is anticoagulated blood?

It is blood in vitro (ie: blood drawn into a tube) to which an agent (called anticoagulant) has been added to prevent clotting.  When spun in a centrifuge, the liquid portion is called plasma.  

This means it contains all plasma coagulation factors, fibrinolytic factors, and inhibitors.

The anticoagulant of choice for hemostasis (coag) testing is 3.2% sodium citrate.

What is serum?

Serum is a clear liquid, which separates from blood when it is allowed to clot.  Serum is blood plasma from which certain coagulation factors have been used up (depleted) in the process of clotting.  

The factors depleted are:

     fibrinogen

     prothrombin

     factors V, VIII, and XIII

For coagulation testing, plasma must be used instead of serum.

Which specimen would be appropriate for hemostasis testing?

1. plasma from a sodium citrate tube
2. serum from a sodium citrate tube
3. plasma from a tube with clot activator
4. serum from a tube with clot activator

Hemostasis involves the interaction of:

 

1. blood vessels
2. platelets
3. plasma coagulation factors

In most situations, balance is maintained via various inhibitors of coagulation and fibrinolysis.

The goal of hemostasis is the patient doesn't bleed (hemorrhage) nor form systemic clots (thrombosis).

Hemostasis occurs in

3 stages:

1. Primary Hemostasis
2. Secondary Hemostasis
3. Fibrinolysis

The result is a localized sealing of the vessel that subsequently undergoes slow removal by fibrinolysis and final tissue repair.

Primary Hemostasis:

platelet plug

Primary hemostasis begins when a blood vessel is damaged, causing collagen from the vessel to be exposed for platelets to attach to.  

Blood vessels and platelets interact  to form a fragile platelet plug  to stop bleeding temporarily, but it is ineffective for any duration of time and can be easily washed away.

Secondary Hemostasis:

"The Coag Cascade"

(fibrin formation)

Secondary hemostasis involves enzymatic activation of soluble proteins in the plasma called coagulation factors, resulting in formation of a fibrin mesh (strands) over the primary platelet plug to stabilize it.  

Prior to activation, coagulation factors exist in their inactive (zymogen) form until activated subsequently in a cascade effect.  Initially, the cascade is triggered by secretions released from vessel injury and primary hemostasis.

Fibrinolysis

Fibrinolysis involves breakdown and removal of the clot after it is no longer needed.

Plasmin, a serine protease, is the main contributor to dissolving the fibrin clot.  Plasminogen is its inactive precursor.

Platelet derived growth factor (PDGF) released from platelets then helps to heal the vessel by promoting smooth muscle growth.

Let's do a quick check in. . .Drag the mechanisms of hemostasis to place them in the order they occur. 

Step 1

Step 2

Step 3

Step 4

blood vessel injury

platelet plug formation

formation of fibrin mesh

fibrinolysis

What do the blood vessels contribute to hemostasis?

Blood vessels, lined with endothelial cells, are normally smooth and resistant to clot formation (thromboresistant).  When damaged, they contribute secretions involved in clot formation/regulation, such as:

• vasoconstriction:  endothelin -1
• vasodilation:  prostaglandins
• clot formation:   von Willebrand Factor,  ADP  and thromboplastin (tissue factor)
• clot prevention:  thrombomodulin
• clot lysis:  tissue plasminogen activator

Arterioles are the smallest portion of the arteries. They, along with the venules, are the main vessels where hemostasis occurs and are occluded with the primary platelet plug.

Capillaries seal directly.  They do not contribute to hemostasis because they lack the thick smooth muscle cell wall and collagen fibers.

Venules are the smallest portion of the veins.  They, along with the arterioles, are the main vessels where hemostasis occurs and are occluded with the primary platelet plug.

Vasoconstriction and the hemostatic mechanism is critical in arteries.  Blood pressure is much higher in them and the flow is rapid.  Therefore, clots cannot form as readily in them and bleeding is more likely.

Blood vessel constriction (vasoconstriction) and activation of hemostatic factors does occur in the veins.  However, because they are larger in diameter, the primary hemostatic plug takes longer to form in them and is often insufficient to stop bleeding.

Endothelial cells make up a thin layer that lines the lumen (central cavity) of all vessels.  Beneath the endothelium lies a subendothelium of collagen and basement membrane elastic tissue.

The smooth muscle cells lie beneath the endothelium.  They can contract and expand, which allows constriction and dilation of the lumen of the vessel.

Click on the blood drops to learn more about the various types of vessels and their cells.

Vasoconstriction  occurs immediately.  Constriction of the damaged vessel and (reflexively) adjacent vessels slows  blood flow to the area to minimize bleeding.  Platelets contribute by secreting serotonin and thromboxane A2. 

Vasodilation occurs later.  Its purpose is to open up the vessel to wash away the coagulation factors and reestablish blood flow to the site after the injured vessel has been  repaired.  Prostaglandins from endothelial cells help vasodilate vessels.

Which blood vessels, when damaged, do clots most easily form in?

1. capillaries
2. arterioles and venules
3. arteries
4. veins

What roles do the platelets play in hemostasis?

Platelets play important roles in both primary and secondary hemostasis.  For example, they:

Click on the star to learn more about each platelet role.

maintain vessel integrity

Platelets fill gaps between endothelial cells by attaching themselves to underlying exposed collagen fibers of the subendothelium to keep blood vessels intact. 

form primary platelet plug

Platelets are our first line of defense against bleeding by forming the primary platelet plug when blood vessel injury occurs.

provide a surface for fibrin generation

Membrane phospholipids of aggregated platelets provide a reaction surface for coag factors to form the secondary hemostatic fibrin mesh.

repair the injured vessel

Platelets promote vascular healing by stimulating intercellular adhesion of endothelial cells and smooth muscle growth via platelet derived growth factors.

Explain, in your own words, how platelets contribute to BOTH primary and secondary hemostasis.

Congratulations!

You have completed the first Hemostasis learning module.  In the next module, we will take a closer look at the details of Primary Hemostasis.