Page 282 - Cardiac Nursing

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258 P A R T III / Assessment of Heart Disease
destruction, loss from hemorrhage, and dilution from massive ratio. The INR is equivalent to the PT ratio that would have been
blood transfusions that contain few platelets. obtained if the patient’s PT had been compared to a PT value ob-
Specific conditions that may cause a decrease in platelets in- tained using the International Reference Preparation, a standard
clude hemorrhage, hypersplenism, leukemia, lymphoma, pros- human brain thromboplastin prepared by the World Health Or-
thetic heart valves, heparin-induced thrombocytopenia, idio- ganization. With the INR, standardized PT results are available
pathic thrombocytopenic purpura, disseminated intravascular for health care providers in different parts of the country and the
coagulation (DIC), systemic lupus erythematosus, hemolytic world. These standardized results are independent of the reagents
anemia, and infection. Medications that decrease the platelet used and adjust for the type of instrument used. The therapeutic
count include acetaminophen, aspirin, chemotherapy, hista- INR in most situations ranges from 2.0 to 3.5. However, different
mine-blocking agents, heparin, hydralazine, quinidine, and thi- ranges have been established for deep vein thrombosis prophylaxis
azide diuretics. Nonsteroidal anti-inflammatory drugs may (1.5 to 2.0), deep vein thrombosis (2.0 to 3.0), prevention of em-
cause a decrease in platelet aggregation. The concurrent use of bolus in atrial fibrillation (2.0 to 3.0), PE (2.5 to 3.5), and pros-
2
heparin with antiplatelet agents increases the risk of bleeding. thetic valve prophylaxis (2.5 to 3.5). The INR should not be used
After a large number of blood transfusions (14 units or more) to initiate warfarin therapy; it should be used only once the pa-
and after extracorporeal circulation, the platelet count is typically tient is thought to be on a stable dose.
low. 2,3
Aspirin has been incorporated into the treatment plan after
MI to prevent hypercoagulability due to platelet aggregation. Partial Thromboplastin Time and
Antiplatelet agents (clopidogrel and ticlopidine) help prevent Activated Partial Thromboplastin
platelet aggregation by inhibiting fibrinogen binding and Time
platelet–platelet interaction. Antiplatelet agents are included in
most treatment plans to prevent arterial thrombus including The partial thromboplastin time (PTT) and activated partial
post-MI, PCI/stent placement, cardiovascular surgery, and other thromboplastin time (aPTT) measure the intrinsic coagulation
vascular surgeries. Patients receiving antiplatelet drugs may have system and are used in assessing patients receiving unfractionated
a normal platelet count but have increased bleeding due to the heparin. With low-molecular-weight heparin, neither the PTT
drug. The drug alters the platelets for the life of platelets; there- nor aPTT changes, so laboratory monitoring is not required. The
fore increased bleeding may be seen for 7 to 14 days after dis- PTT measures deficiencies in all factors except factors VII and
continuation of treatment. Glycoprotein (GP) IIb/IIIa agents are XIII, whereas the aPTT measures all coagulation factors except
also used to decrease platelet aggregation in acute MI and post- platelet factor III, XIII, and VII. The aPTT is measured by adding
PCI/stent placement patients. Patients who receive GPIIb/IIIa test reagents to PTT to shorten clotting time. When clotting time
agents should be monitored for signs of bleeding and thrombo- is shortened, minor clotting defects can be detected.
cytopenia. The therapeutic range for both PTT and aPTT is maintained
Increased amounts of platelets may be seen in malignant dis- at 1.5 to 2.5 times the patient’s baseline value. The PTT and
orders including, polycythemia vera, postsplenectomy syndrome, aPTT is usually drawn 30 to 60 minutes before the patient’s next
and rheumatoid arthritis. Platelet counts may also be increased in dose of heparin. For PTT and aPTT results less than 50 seconds,
those who live at high altitude or exercise strenuously. 2 an increase in the heparin dose should be considered. Conversely,
a decrease in dose should be considered for PTT and aPTT values
greater than 100 seconds.
Prothrombin Time The PTT and aPTT are prolonged in heparin administration,
congenital clotting factor deficiencies, cirrhosis of the liver, vita-
The prothrombin time (PT) is used to evaluate the extrinsic sys-
tem and common pathway in the clotting mechanism. Specifi- min K deficiency, and DIC. Antihistamines, ascorbic acid, chlor-
3
cally, it measures the activity of prothrombin, fibrinogen, and fac- promazine, and salicylates may also cause an increase.
tors V, VII, and X. Prothrombin is synthesized by the liver. PT
may be prolonged in heart failure, vitamin K deficiency, liver dis- Activated Clotting Time
ease, bile duct obstruction, DIC, massive blood transfusion, sali-
cylate intoxication, and alcohol use. Severe liver damage may pro- The activated clotting time (ACT) is used during cardiac surgery
long PT. Drugs that may prolong PT include but are not limited and cardiac catheterization to monitor heparinization. The time it
to some antibiotics, allopurinol, amiodarone, warfarin, heparin, takes whole blood to clot reflects the activity of the intrinsic clot-
many nonsteroidal anti-inflammatory drugs, and aspirin. De- ting mechanism. During extracorporeal heparin therapy, the ACT
creased PT is seen in thyroid dysfunction, thrombophlebitis, MI, is kept at four to six times the baseline value.
and pulmonary embolus. Medications that may decrease PT in- Tests to measure ACT are simple and easy to use at the bed-
clude but are not limited to antacids, diuretics, diphenhydramine, side. The use of ACT rather than aPTT to monitor heparin ther-
and oral contraceptives. 2,3 apy in patients with unstable angina or acute MI may result in
The PT is used mainly for monitoring patients on warfarin. much steadier levels of anticoagulation and prevent ischemic re-
Warfarin inhibits vitamin K-dependent synthesis of clotting fac- currences. 2
tors II, VII, IX, and X. Therapeutic prothrombin times are con-
sidered to be 1.5 to 2 times normal, or a 15% to 50% change in Fibrinogen Level
the normal value. If the PT is allowed to prolong greater than 2.5
times the control value, there is a risk of bleeding. Fibrinogen is a plasma protein synthesized by the liver. This test
The international normalized ratio (INR) has been adopted measures the conversion of fibrinogen to fibrin by thrombin. Fib-
for reporting PT. The INR is calculated from the observed PT rinogen levels are elevated in acute infections, collagen disease,