Blood Clotting

Mechanism
Teri Junge, cst, cfa

INTRODUCTION

T
his article is intended as an introduction to the blood clot-
ting mechanism for the student surgical technologist
and as a review for those in practice. Effective control of
bleeding occurs through a complex process called hemo-
stasis, which will be explained in four basic steps. The basic steps of
the blood clotting process are vasoconstriction, platelet activation,
thrombus formation, and dissolution of the clot. Basic laboratory
tests used to identify blood clotting problems will also be presented.
Blood clotting is initiated in one of two ways. The first, referred to
as the intrinsic or internal pathway, occurs when a clot forms inside
of a blood vessel due to an internal abnormality or an injury to the
blood vessel itself.8 The second, referred to as the extrinsic or exter-
nal pathway, occurs following an injury, such as a cut, when blood
is exposed to the outside environment. No matter how the clotting
process is initiated, the clot forms in the same way. This is referred to
as the common pathway. Another term used to describe blood clot-
ting is coagulation.
Blood cells called platelets, along with numerous factors—pro-
teins, enzymes, vitamin K, and calcium—found in blood plasma, are
involved in the clotting process. Blood clotting factors are referred
to by Roman numerals and also have names associated with them.
Injuries leading to extrinsic blood clotting and the related chain
of events will be the focus of this article, as this is the type of injury
most commonly seen in the surgical environment. An example is
provided in the case study below.

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 274 OCTOBER 2006 1 CE CREDIT

FIGURE 1
Layers of the blood Artery Vein
vessel wall.
Tunica
adventitia

Tunica
muscularis
Elastic layer

Valve

Tunica
intima

Table 1 Glossary 4,7,8

Artery Large blood vessel that carries blood away from the heart
Arteriole Small artery that delivers blood rich in oxygen and nutrients to a capillary
Capillary Tiny blood vessel that allows oxygen and nutrients to be delivered to the tissues and carries
waste products away
Endothelium Smooth flat cells that line the heart, as well as blood and lymphatic vessels
Lumen The inside of a tubular structure (eg, the inside of a blood vessel or intestinal tract)
Tunic Coat or layer of a structure
Tunica Adventitia (Externa) Outer layer of a blood vessel consisting of connective tissue
Tunica Intima (Interna) Smooth inner layer of a blood vessel consisting of endothelium
Tunica Muscularis (Media) Middle layer of a blood vessel consisting of muscle tissue
Vein Large blood vessel that carries blood toward the heart
Venule Small vein that carries blood and waste products away from the capillary to a vein

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CASE STUDY Table 2 Blood Clotting Factors5,6
George, an eighteen-month-old male, has fallen Roman
while playing on the patio at his home. As he fell, Numeral Name
he hit his chin on a terra cotta flower pot and cut I Fibrinogen
himself. His mother rushed to his aid. First, she
Ia Fibrin
cleaned the wound with a soft moist cloth; she (a = activated)
then applied pressure and ice to help control the
II Prothrombin
bleeding and held George in a sitting position
on her lap to calm him. It was determined that IIa Thrombin
George needed stitches in his chin, and he was III Thromboplastin (also called tissue factor)
taken to the urgent care center for further treat- IV Calcium
ment. By the time of his arrival at the urgent care V Proaccelerin (also called labile factor and accelerator globulin (AcG))
center, the bleeding from his cut had stopped.
VI Accelerin
ANATOMY REVIEW VII Proconvertin (also called serum prothrombin conversion accelerator
To facilitate understanding of the process of vaso- (SPCA), cothromboplastin, autoprothrombin I, prothrombokinase and
stable factor)
constriction, blood vessel wall anatomy will be
reviewed. Please refer to Table 1 for a brief glossa- VIII Antihemophilic factor A (also called antihemophilic globulin (AHG))
ry of terms related to blood vessel wall anatomy. IX Antihemophilic factor B (also called Christmas factor, plasma
Walls of blood vessels, specifically veins and thromboplastin component (PTC), and autoprothrombin II)
arteries, consist of three main layers called tunics X Stuart-Prower factor (also called autoprothrombin C, Prower factor
(Figure 1). The outer tunic is called the tunica and thrombokinase)
externa or tunica adventitia and consists of the XI Antihemophilic factor C (also called plasma thromboplastin antecedent
connective tissue that maintains the cylindri- (PTA))
cal shape of the blood vessel. The middle tunic XII Hageman factor (also called glass, contact or activation factor)
is called the tunica media or tunica muscularis
XIII Fibrinase (also called fibrin stabilizing factor (FSF) and Laki-Lorand
and consists of smooth muscle tissue. The inner factor (LLF). The inactive form is also called protransglutaminase, and
tunic is called the tunica interna or tunic inti- the active form as transglutaminase.)
ma and consists of smooth epithelial tissue that
allows the blood to flow freely within the vessel.
Additionally, a layer of elastic tissue is present to of the blood vessel wall to constrict, narrow-
allow for expansion (vasodilation) and contrac- ing the lumen of the vessel, thereby temporar-
tion (vasoconstriction) of the vessel. ily restricting the flow of blood from the wound.
The muscular layer is thicker in arteries than This initial vasoconstriction lasts only about a
it is in veins, and veins have additional struc- minute, but then a secondary mechanism takes
tures called valves, which keep the blood from over that sustains vasoconstriction at the site of
flowing backward. The exception to the three- the wound. The secondary mechanism involves
layer structure of blood vessel walls are the cap- release of chemicals, such as serotonin and epi-
illaries that consist of only a single layer of cells. nephrine, from blood cells called platelets that
This layer allows the passage of fluids, cells, and have started to gather at the site of the injury.
molecules to and from the tissue cells.7 Platelets continue to stimulate the nerves, which
causes contraction of the muscle of the vessel for
VASOCONSTRICTION several more minutes.4
Vasoconstriction is the term used to describe First aid measures such as those described in
tightening of the muscle in the blood vessel wall. the case study—application of ice and pressure to
When an injury occurs, nerves in the tissue sur- the wounded area, as well as elevating the wound-
rounding the blood vessel stimulate the muscle ed area—all assist in the vasoconstriction process.

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 PL ATELET AC TIVATION/AGGREGATION by a thrombus.6 The platelet plug does not con-
Following damage, such as an accidental cut or tain red blood cells; therefore, it is sometimes
a surgical incision, blood is exposed to collagen referred to as the white thrombus.1
from the nearby tissues. At the time of injury,
two things happen almost instantly and simul- THROMBUS FORMATION
taneously. First, two substances—fibrinogen, A more stable clot, called a thrombus, must form
found in collagen, and prothrombin, found on to make a longer lasting seal on larger injured
the surface of the platelets—are activated. (See blood vessels. The thrombus must be able to
Table 2) The platelets, or thrombocytes, begin to maintain a seal on the damaged blood vessel wall,
adhere to the exposed collagen. This initial step especially that of an artery where the blood pres-
in blood clotting, or coagulation, is called plate- sure is higher than in a vein, even after the blood
let activation or platelet aggregation. vessel walls are no longer constricted. Fortunate-
As the platelets begin to assemble at the site ly, the clotting process is self-limiting. Substances
of the injury, several factors are released from called antithrombins prevent the clot from con-
the platelets. One of them, the von Willebrand tinuing to enlarge; otherwise the established clot
factor (vWF), binds the platelets to the collagen would block the flow of blood within the vessel.6
fibers. Several substances are also released from Activation of prothrombin in the platelet
the platelets, including adenosine diphosphate aggregation phase sets off a series of additional
(ADP), which attracts more platelets until a seal is events, starting with activation of factor X, that
formed over the opening in the blood vessel wall. leads to formation of the thrombus. Activat-
The clump of platelets is known as the platelet ed factor X (Stuart-Prower) leads to activation
plug. The platelet plug may be sufficient to seal of factor II (prothrombin). Prothrombin in its
a small vessel. However, in larger vessels, the active form is referred to as factor IIa (thrombin).
platelet plug is temporary and will be replaced Several substances, including thromboplastin

FIGURE 2
Red thrombus.

Red blood cell

Fibrin

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16
(factor III), calcium, and vitamin K, play a role in ever, knowledge of the status of the patient’s blood
activation of prothrombin to thrombin.1 clotting mechanism prior to and during surgical
Thrombin, in turn, helps to convert fibrinogen intervention is valuable to the surgical team mem-
(factor I) to fibrin (factor Ia). Fibrin is an insoluble bers in planning the care of the patient.
protein that, when it reacts with other substances, Several laboratory tests are available that
polymerizes to form strands that web together to will help determine if the patient has normal or
form the basis of the thrombus. The web of fibrin abnormal clotting ability. If an abnormality is
is referred to as fibrin mesh. Factor XIII (fibri- detected, intervention—such as providing blood
nase) is activated to serve as additional stabiliza- products, procoagulants, or anticoagulants—
tion of the fibrin mesh. When viewing the fibrin may be indicated.
mesh that has been stabilized with fibrinase under
a microscope, it is said to have the appearance of BLOOD CLOTTING TESTS
cross stitching on loosely woven fabric.3 The following is a list of some of the more com-
Within a few hours of the injury, as part of mon blood clotting tests, as well as brief descrip-
the inflammatory process that normally occurs tions of each.
following damage to tissue, leukocytes (white ฀ Bleeding time—Measures the time elapsed
blood cells) gather at the site of the injury to help from inf liction of a small cut until active
reduce the risk of infection. Local inflammation bleeding has stopped. Normal bleeding time
is identified by the presence of pain (dolor), red- is three to eight minutes.
ness (rubor), heat (calor), swelling (tumor), and ฀ Coagulation factor assay—Measures spe-
loss of function (functio laesa). Systemic inflam- cific proteins (clotting factors, as well as anti-
mation is identified by the presence of fever.7 clotting factors) in a volume of blood for nor-
The thrombus may contain red blood cells; malcy, deficiency or absence.
therefore it is sometimes referred to as the red ฀ Complete blood count—A group of sever-
thrombus (Figure 2).1 al tests performed on a volume of blood to
detect the number and size of certain cells
DISSOLUTION OF THE CLOT or cell fragments, including red blood cells,
Dissolution of the clot, also called fibrinolysis, white blood cells (including the various types
occurs when a negative feedback system signals of white cells), and platelets present in the
that sufficient healing of the blood vessel wall has blood.
occurred, and a substance called plasminogen is ฀ Fibrinogen test—Measures the levels of
activated. Plasminogen in its active form is called fibrinogen (Factor I) in the blood.
plasmin. Plasmin signals the clotting mechanism ฀ Miscellaneous—Various tests may be per-
to inactivate the procoagulant (clotting) process formed as needed to detect vitamin deficien-
and begins the anticoagulant process, with the use cies, liver malfunction, or leukemia that may
of naturally occurring heparin. This is achieved affect the blood clotting mechanism.
by digesting the fibrin, which is the main compo- ฀ Partial thromboplastin time (PTT)—Mea-
nent of the thrombus.6 The body then returns to sures the amount of time needed (in sec-
its state of balance, called homeostasis. onds) that it takes for clotting to occur when
reagents are added to plasma in vitro. Normal
IDENTIFIC ATION OF BLOOD CLOT TING partial thromboplastin time is 30-45 seconds.
PROBLEMS ฀ Platelet aggregation test—Measures the
Due to the complexity of the blood clotting mech- amount of time needed for platelets to aggre-
anism, numerous problems can occur that will gate (adhere to) and seal off the lumen of a
impact the clotting ability of the injured patient or vacuum tube that had been coated with colla-
the patient scheduled for surgery. Blood clotting gen and either epinephrine (EPI) or adenosine
disorders will not be discussed in this article; how- diphosphate (ADP). As being drawn through

OCTOBER 2006 The Surgical Technologist

17
 the tube, the coating activates the platelets ABOUT THE AUTHOR
promoting platelet aggregation. The term clo- Teri Junge, cst, cfa, is surgical technology pro-
sure time (CT) is used to refer to the amount gram director at San Joaquin Valley College
of time it takes for a clot to form inside the in Fresno, California. She is also the editorial
glass tube and prevent further blood flow. reviewer for this journal.
฀ Platelet count—Detects the number of plate-
lets present in the blood. It is typically includ-
Editor’s note: To review the main constituents of
ed in the CBC, but may be ordered indepen-
the blood, please refer to “Blood Components” by
dently. The normal platelet count is between
this author in the July, 2003 issue of this journal.
150,000 to 450,000 platelets per ML.
For more information about fibrin’s extraordinary
฀ Prothrombin time (PT)—Measures the
elasticity and strength, please visit http://www.wfu.
amount of time needed for blood to clot in
edu/wfunews/2006/2006.08.03.f.html and http://www.
vitro. Normal prothrombin time is 10–15
madgadget.com/archives/2006/08/fibrin_superher_
seconds.7
1.html.
CONCLUSION
Many factors influence hemostasis, and the clot- References
ting process is a very complex series of chemi- 1. Atkinson L, Fortunato N. Berry & Kohn’s Operating
cal interactions that are not all listed in this brief Room Technique, 10th ed. USA: Mosby; 2003.
2 Bhonoah Y. Blood Coagulation. Imperial College of
overview. Keep in mind the four basic steps of the
Science, Technology and Medicine: Department of
blood clotting process (vasoconstriction, platelet Chemistry. Available at: http://www.chemsoc.org/exem-
activation, thrombus formation, and dissolution plarchem/entries/2003/imperial_Bhono/bloodcoagulation.
of the clot) as you think back to the case study, html. Accessed June 19, 2006.
and try to answer the following questions: 3. Carlson C. How Blood Clots. Available at: http://www.
med.uiuc.edu/hematology/PtClotInfo.htm. Accessed June 1,
2006.
1. Why did George’s mother apply ice and
4. Cohen B. Memmler’s The Human Body in Health and
pressure to the wound? Disease, 10th ed. USA: Lippincott Williams & Wilkins;
George’s mother applied ice and pressure to 2005.
the wound to assist his body in achieving and 5. Corrigan D. The Blood. Englewood, CO: Association of
maintaining vasoconstriction. Surgical Technologists; 1994.
6. King M. Blood Coagulation. Available at: http://web.ind-
state.edu/thcme/mwking/blood-coagulation.html. Accessed
2. Why was George kept in a sitting position
June 3, 2006.
following his injury? 7. Price P, Frey K, Junge T, eds. Surgical Technology for
George was kept in a sitting position while the Surgical Technologist: A Positive Care Approach,
his mother was comforting him to elevate the 2nd ed. USA: Thomson Delmar Learning; 2004.
injured area allowing gravity to direct blood 8. Stedman J. Stedman’s Medical Dictionary for the Health
away from the wound. Professions and Nursing Illustrated, 5th ed. USA:
Lippincott Williams & Wilkins; 2005.
9. Tiscali Encyclopedia. Available at: http://www.tiscali.
3. Why do you think that the bleeding had co.uk. Accessed June 3, 2006.
stopped by the time George arrived at the
urgent care center for stitches?
George’s bleeding had stopped by the time he
arrived at the urgent care center for stitches,
because all the steps involved in his blood clot-
ting mechanism worked correctly.

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CEExam
1. The control system in which feedback 6. Plasmin begins the anticoagulant
concerning changes in the body’s inter- process by ...
nal environment causes a response a. Using heparin to signal the clotting mech-
that reverses these changes is called anism
274 OCTOBER 2006 1 CE CREDIT a. Homeostatic mechanism b. Digesting the fibrin
b. Negative feedback c. Activating plasminogen
c. Countercurrent mechanism d. Accelerating the negative feedback system
d. Feed-forward
7. Which platelet-released substance
2. Which of the following is NOT a basic attracts more platelets until a seal is
step of the clotting process? formed over the opening in a blood
a. Vasoconstriction vessel?
Blood clotting b. Platelet aggregation a. Adenosine diphosphate
c. Thrombin formation b. Thrombin
mechanism d. Fibrinolysis c. Proconvertin
d. Fibrinase
Earn CE credits at home 3. As platelets gather at an injury site,
You will be awarded continuing education (CE) credit(s) for which released factor binds the 8. Which of the following is NOT a layer of
recertification after reading the designated article and com- platelets to the collagen fibers? a blood vessel?
pleting the exam with a score of 70% or better. a. von Willebrand c. Hageman a. Tunica muscularis
If you are a current AST member and are certified, credit b. Stuart-Prower d. Laki-Lorand b. Tunica adventitia
earned through completion of the CE exam will automatically c. Tunica interna
be recorded in your file—you do not have to submit a CE report- 4. Which of the following does NOT play a d. Tunica serosa
ing form. A printout of all the CE credits you have earned, includ- role in the activation of prothrombin?
ing Journal CE credits, will be mailed to you in the first quarter a. Vitamin K 9. _______ polymerizes to form strands,
following the end of the calendar year. You may check the status b. Calcium which form the basis of a thrombus.
of your CE record with AST at any time. c. Fibrin a. Proconvertin c. Accelerator globulin
If you are not an AST member or are not certified, you will be d. Thromboplastin b. Fibrin d. Fibrinase
notified by mail when Journal credits are submitted, but your
credits will not be recorded in AST’s files. 5. The platelet plug… 10. During coagulation…
Detach or photocopy the answer block, include your check or a. Contains red blood cells a. Platelet aggregation begins
money order made payable to AST, and send it to the Accounting b. Sufficiently seals large blood vessels b. Antithrombins prevent an overreaction of
Department, AST, 6 West Dry Creek Circle, Suite 200, Littleton, CO c. Binds the platelets to the precollagenous the clotting process
80120-8031. fibers c. Fibrinogen and prothrombin are activated
d. Is also known as a white thrombus d. Factor X is activated and converts fibrino-
Members: $6 per CE, nonmembers: $10 per CE gen to fibrin
274 OCTOBER 2006 1 CE CREDIT

Blood clotting mechanism a b c d a b c d

Certified Member Certified Nonmember 1 6

Certification No. ________________________________________ 2 7

Name ______________________________________________ 3 8

Address _____________________________________________ 4 9

City ________________________ State ______ZIP___________ 5 10

Telephone ___________________________________________ Mark one box next to each number. Only one correct or best answer can be selected for each question.
OCTOBER 2006 The Surgical Technologist
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