NURS 3664 Study Guide - Final Guide: Direct Thrombin Inhibitor, Protamine Sulfate, Argatroban
Final Exam Review
Neurovascular Assessment and Complications
• Pedal pulses, lower extremity temps
Know all the anticoagulants and their reversal agents
• IV Heparin
o Obtain a baseline PTT, repeat PTT in 6 hrs to adjust dosage to reach goal PTT
o Therapeutic level: 1.5-2.5x baseline
o NOMOGRAMS – standing orders
o SE: bleeding (electric razor, falls, sports)
▪ Assess mental status, peritoneal cavity, bruising
▪ Lab work: H/H, CBC
▪ Thrombocytopenia – check platelets
o HIT and HITT – stop and use alternative
▪ Argatroban – direct thrombin inhibitor
o Antidote: protamine sulfate
▪ Watch for hypotension and bronchoconstriction
o Used as bridge to warfarin therapy
• LMWH
o Derived from heparin
o Inhibit factor Xa
o Lower incidence of bleeding, decrease incidence of HIT
o Does not require lab monitoring
• Warfarin
o Inhibits activation of Vitamin K dependent coagulation factors
o Administer PO
o Onset: 12-24hrs, Peak: 3-4 days, Half Life 0.5-3 days
o Obtain baseline PT/INR, monitor daily until stable, check q week, then q month
o Start Coumadin several days before DCing Heparin to reach therapeutic PT/INR
o Therapeutic level: 2.5-3.5 (for pts. High risk for clotting); 2-3 for prophylaxis –
heparin can be stopped when you reach level and warfarin continues
o Above therapeutic: withhold or lower dose
▪ Bleeding or higher INR – decrease or skip daily dose
o May need FFP (clotting factors) for quick reversal
o SE: bleeding
o Antidote: vitamin K (Aquamephyton)
o Dietary considerations: vitamin K rich foods (beef and pork liver, green leafy veg,
crucifers) will interfere with obtaining a therapeutic PT/INR level
▪ Low levels → clot or thrombus
▪ Alcohol interferes – large amounts may affect liver fx- increase bleeding
o Many drug interactions
▪ Drugs that increase effects:
• High dose Tylenol, ASA, NSAIDS, vitamin E, broad spectrum
antibiotics
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▪ Drugs that decrease effects:
• Barbiturates, amiodarone, GI drugs like sucralfate
o Take at same time daily, do not skip dose or take two doses together
Prioritize anticoagulation!!
• Clots – tissue is dying
Neurovascular diseases
• CAD vs PVD be able to distinguish between them
o CAD
▪ Abnormal thickening of coronary arteries and hardening of the arteries
(atherosclerosis) → loss of elasticity → impairs auto-regulation of the
heart to respond to changing demands (hard to dilate and constrict)
▪ Progressive development of atherosclerotic plaque → decrease lumen
size → less O2 to cells (exacerbated by increasing O2 demands)
▪ Risk factors:
• Cigarette smoking (cardiac stimulant, peripheral vasoconstriction,
CO competes with oxygen for Hgb binding), hyperlipidemia, HTN,
DM, obesity, high triglycerides, high uric acid levels, family hx,
sedentary lifestyle, stress, c-reactive protein, ferritin,
homocysteine
• Modifiable: smoking, weight, exercise
• Non-modifiable: age, gender, ethnicity
▪ Trajectory
• Increase demands for O2 → diseased coronary artery (narrowed
lumen, decrease elasticity) → decrease O2 to cardiac muscle →
ischemia → angina → pain (release norepinephrine, increase
platelet aggregation and thromboxane A2) → MI → ACS
▪ Slow progression – atherosclerosis
▪ Sudden cut off – thrombus, emboli, spasm
▪ Syndromes resulting – classic angina pectoris, unstable angina, coronary
artery spasm, MI
o PVD
▪ Atherosclerosis – plaque ruptures → thrombus travel to other places,
blood clot breaks off – emboli
▪ Risk Factors:
• Cigarette smoking, hyperlipidemia, HTN, DM, obesity, high
triglycerides, high uric acid levels, family hx, sedentary lifestyle,
stress, c-reactive protein, ferritin, homocysteine
▪ Blood not delivered effectively to peripheral extremities
▪ Classic symptom = intermittent claudication (pain with exercise relieved
by rest)
▪ Check for pallor, check for color return, ankle brachial index
▪ Complications: ischemia → necrosis → gangrene → septicemia →
amputation
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• Atherosclerosis
• Ankle brachial index
o With Doppler take Systolic BP on both arms and then Systolic BP on affected leg
o Calculate: Ankle Systolic BP/Brachial BP
o Resting vs exercise
o Above 0.90 normal
o 0.70-0.90 mild
o 0.40-0.70 moderate
o 0.30-0.40 severe
o < 0.30 critical limb ischemia
• Venous thrombosis
o Virho’s Triad
▪ Venous stasis
▪ Endothelial damage
▪ Hypercoagulability of blood
Aspirin vs Plavix
• Aspirin
o Inhibits cyclooxygenase → formation of thromboxane A2 → blood vessel dilation
and decrease platelet aggregation and prevent clot from forming
o Irreversible – effect for life span of platelet – 7 days
▪ Platelets will not become functioning platelets
o Need to stop 7 days before surgery
o Dosage: 75-325 mg daily; low dose 81 mg
o SE: bleeding, CNS – dizziness, flushing, confusion, GI – N/V/D, heart burn,
hematologic – thrombocytopenia, agranulocytosis, leukopenia, neutropenia
• Plavix
o Alters platelet surface membrane by inactivating the GIIb/IIIA receptor site →
inhibits platelet aggregation
o Dosage 75 mg daily
o SE: bleeding, CV – chest pain, HTN, edema, CNS – headache, dizzy, fatigue, GI –
abdominal pain, dyspepsia, N/D
o Drug interaction:
▪ PPI Omeprazole (Prilosec) – significantly reduces the anti-platlet effect
Anticoagulants (prevent clot formation)
• Vitamin K antagonists
o Coumadin (Warfarin)
▪ Inhibits activation of vitamin K dependent coagulation factors
▪ PO
▪ Bridge with heparin 3-4days until therapeutic INR
• Indirect Thrombin Inhibitors
o Heparin, LMWH
▪ Binds to antithrombin III which is needed for activated II (thrombin) to
convert fibrinogen to fibrin
▪ Administered IV or SC
find more resources at oneclass.com
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Document Summary
Neurovascular assessment and complications: pedal pulses, lower extremity temps. Know all the anticoagulants and their reversal agents. Inhibit factor xa: lower incidence of bleeding, decrease incidence of hit, does not require lab monitoring, warfarin. Prioritize anticoagulation: clots tissue is dying. Co competes with oxygen for hgb binding), hyperlipidemia, htn, Dm, obesity, high triglycerides, high uric acid levels, family hx, sedentary lifestyle, stress, c-reactive protein, ferritin, homocysteine: modifiable: smoking, weight, exercise, non-modifiable: age, gender, ethnicity, trajectory. Inhibits cyclooxygenase formation of thromboxane a2 blood vessel dilation and decrease platelet aggregation and prevent clot from forming. Anticoagulants (prevent clot formation: vitamin k antagonists, coumadin (warfarin) Inhibits activation of vitamin k dependent coagulation factors: po, bridge with heparin 3-4days until therapeutic inr. Cardiac cycle: ventricular diastole (relaxation, rapid filling, slow filling, atrial kick, ventricular systole (contraction) Stroke volume: amount ejected from ventricles per beat, sv = edv esv. Conduction system: sa node pacemaker of the heart.
