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REVIEW :
blood coagulation
Brush up on your knowledge of these potentially
life-saving drugs.
By Amy M. Karch, RN, MS
THE
CNE
Rx
L EARNING O BJECTIVES
1. Explain the clotting mechanism.
2. Discuss the various drugs that
alter blood coagulation.
3. Describe nursing care for patients
receiving drugs that alter coagulation.
The author and planners of this CNE activity have
disclosed no relevant financial relationships with
any commercial companies pertaining to this activity. See the last page of the article to learn how to
earn CNE credit.
Volume 7, Number 11
Platelet inhibitors
Platelet inhibitors are often the first
line of defense in preventing vascular clots; they dont affect clots that
already have formed. These drugs
block platelets ability to adhere
and aggregate to form the platelet
plugthe first step in sealing the
vascular system and preventing
blood loss into body tissues.
Current platelet inhibitors include abciximab (ReoPro), anagrelide (Agrylin), aspirin, cilostazol
(Pletal), clopidogrel (Plavix), dipyridamole (Persantine), eptifibatide
(Integrilin), ticlopidine (Ticlid), ticagrelor (Brilinta), and tirofiban (Aggrastat). These drugs are used to
treat cardiovascular diseases in
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Platelets
Fibrin
Collagen
Striated muscle
After an injury to a blood vessel, the vessel constricts. With a small injury, constriction
typically seals the open space, allowing blood to flow and helping the vessel to heal.
A larger injury exposes endothelial cells lining the vessel to blood flowing through it,
causing platelets to adhere to the injured area. When a platelet adheres, it releases
chemicals that attract more platelets, in turn drawing even more platelets to the area
in a process called platelet aggregation. Consequently, a platelet plug forms. In some
cases, this is enough to seal the leak and keep pressures stable while the vessel heals.
In more severe injuries, the vessel wall injury activates Hagemann factor, a clotting
factor. Activated Hagemann factor triggers activation of other clotting factors, initiating
the clotting cascade. The cascade ends in conversion of prothrombin to thrombin;
activated thrombin initiates clot formation.
All clotting factors are made in the liver and require vitamin K for their formation.
Calcium is the catalyst that speeds the clotting cascade. Activated thrombin breaks
down fibrinogen into fibrin. An insoluble protein, fibrin forms a clot at the site. The
change of blood from fluid to solid form stops blood flow in the vessel. In this process,
called the intrinsic process, a clot forms within the vessel.
A similar process, the extrinsic process, occurs in blood that has leaked out of the
vessel at the injury site. This process produces a seal within the vessel, along with a
seal outside the vessel. While this allows the vessel wall to seal and heal, it could
interrupt blood flow to tissues beyond that point, causing ischemia or even cell death.
When Hagemann factor is activated and triggers the clotting cascade, it also causes
plasminogen conversion to plasmin. Plasmin dissolves fibrin and returns blood to the
fluid state. This is the bodys clot-dissolving mechanism. Plasminogen, made in the
liver, also is activated by such conditions as stress, fever, and various enzymes. This
process protects against the harmful effects of clot formation.
Anticoagulants
Although commonly called blood
thinners, anticoagulants dont actually thin the blood. Like platelet inhibitors, they dont dissolve clots
that have already formed but they
can prevent formation of new clots.
In patients with clots, deep vein
thrombosis, or occluded vessels
that have caused an MI or a stroke,
November 2012
27
Volume 7, Number 11
is a direct thrombin inhibitor; rivaroxaban (Xarelto) inhibits activated thrombin. Both stop the coagulation process.
Warfarin. Warfarin blocks the livers use of vitamin K to produce
clotting factors. Its commonly prescribed for chronic conditions that
might involve problems with clot
formation, such as coronary artery
disease, atrial fibrillation, knee or
hip replacement, and immobility.
However, warfarin has several
disadvantages. For one, it takes
time to deplete already-formed clotting factors; clot formation may not
decrease until 48 to 72 hours after
warfarin therapy begins. Also, if the
patient receives too much warfarin
and is bleeding, no precise antidote
exists. Although vitamin K can be
injected to trigger the liver to resume making clotting factors, clotting activity may not return for 48
to 72 hours. In severe overdose and
bleeding, blood products containing
clotting factors may be given to
stop the bleeding; however, the liver still needs time to restore a normal level of clotting factors.
Traditionally, warfarin was the
only oral anticoagulant patients
could take at home. In light of its
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angelica
cats claw
chamomile
chondroitin
feverfew
garlic
ginkgo
goldenseal
psyllium
fish oil
vitamin E
turmeric.
November 2012
29
Volume 7, Number 11
Selected references
Brunton L, Chabner B, Knollman B. Goodman and Gilmans The Pharmacological
Basis of Therapeutics. 12th ed. New York:
McGraw-Hill; 2010.
Facts & Comparisons. Drug Facts and Comparisons 2012. 66th ed. Philadelphia: Lippincott Williams & Wilkins; 2011.
Hankey GJ, Eikelboom JW. Dabigatran etexilate: a new oral thrombin inhibitor. Circulation. 2011 Apr 5;123:1436-50.
Karch AM. 2012 Lippincotts Nursing Drug
Guide. Philadelphia: Lippincott Williams &
Wilkins; 2011.
Karch AM. Focus on Nursing Pharmacology.
6th ed. Philadelphia: Lippincott Williams &
Wilkins; 2012.
Mitke M. New alternative to warfarin may
help reduce stroke in patients with AF.
JAMA. 2011 Jan 5:305(1):25-6.
Porth CM. Pathophysiology: Concepts of Altered Health States. 8th ed. Philadelphia:
Lippincott Williams & Wilkins; 2010.
Price MJ, Berger PB, Teirstein et al; GRAVITAS Investigators. Standard- vs high-dose
clopidogrel based on platelet function testing after percutaneous coronary intervention: the GRAVITAS randomized trial. JAMA.
2011 Mar 16:305(11):1079-105.
Shimoli V, Gage BF. Cost-effectiveness of
dabigatran for stroke prophylaxis in atrial
fibrillation. Circuation. 2011:123:2562-70.
Streiff MB, Haut ER. The CMS ruling on venous thromboembolism after total knee or
hip arthroplasty: weighing risks and benefits. JAMA. 2009 Mar 11:301(10):1063-5.
www.AmericanNurseToday.com
Provider accreditation
The American Nurses Associations Center for Continuing Education
and Professional Development is accredited as a provider of continuing
nursing education by the American Nurses Credentialing Centers
Commission on Accreditation. ANCC Provider Number 0023. Contact
hours: 1.4, Rx contact hours: 1.4.
ANAs Center for Continuing Education and Professional Development
is approved by the California Board of Registered Nursing, Provider
Number CEP6178.
Post-test passing score is 75%. Expiration: 12/31/14
ANA Center for Continuing Education and Professional Developments ac-
www.AmericanNurseToday.com
CNE
Rx
credited provider status refers only to CNE activities and does not imply
that there is real or implied endorsement of any product, service, or company referred to in this activity nor of any company subsidizing costs related to the activity. This CNE activity does not include any unannounced
information about off-label use of a product for a purpose other than that
for which it was approved by the Food and Drug Administration (FDA).
The planners of this CNE activity have disclosed no relevant financial relationships with any commercial companies pertaining to this CNE.
P URPOSE / GOAL
To provide nurses with the information they need to better
manage patients who are receiving drugs that alter blood
coagulation
L EARNING O BJECTIVES
1. Explain the clotting mechanism.
2. Discuss the various medications that alter blood coagulation.
3. Describe nursing care for patients receiving drugs that alter
coagulation.
November 2012
31