Atrial Fibrillation - BMH/Tele

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Atrial Fibrillation - BMH/Tele

  1. 1. Atrial Fibrillation: Too Many Atrial Chiefs!!! Natalie Bermudez, RN, BSN, MS Clinical Educator for Cardiac Telemetry Telemetry Course
  2. 2. Course Objectives <ul><li>Discuss prevalence of atrial fibrillation in the United States </li></ul><ul><li>Discuss pathophysiology of atrial fibrillation </li></ul><ul><li>Discuss the main goals for treatment of atrial fibrillation </li></ul><ul><li>Discuss the electrical cardioversion versus chemical cardioversion </li></ul><ul><li>Review medications that are used to treat atrial fibrillation </li></ul>
  3. 3. Statistics <ul><li>“ More than 2.2 million Americans – nearly 15% of those older than age 85 – experience this arrhythmia” (Prudente, 2008, p. 21) </li></ul><ul><li>“… An estimated 150,000 new cases will be diagnosed each year.” (Zak, 2010, p. 68) </li></ul><ul><li>“ Experts expect the prevalence to increase to 5 million by 2050 as the population ages” (Prudente, 2008, p. 21) </li></ul>
  4. 4. More Statistics <ul><li>“ Occurs in 11% to 64% of patients after a CABG, valvular replacements, and heart transplantation” </li></ul><ul><li>(Smeltzer et al, 2008, p.832) </li></ul>
  5. 5. Electrical Chaos <ul><li>Chaotic, irregular, rapid depolarization in atrial tissue due increased atrial irritability </li></ul><ul><li>Firing Rate = 300 – 600 times/minute </li></ul><ul><li>Causes the atria to quiver </li></ul>
  6. 6. Atrial Characteristics <ul><li>No P waves are visible on an EKG </li></ul><ul><li>Fibrillatory waves (Fine or Coarse) </li></ul>
  7. 7. Characteristics of AF <ul><li>Fine or Course </li></ul>
  8. 8. The Gatekeeper <ul><li>AV node controls the # of electrical impulses that reach the ventricles </li></ul>
  9. 9. AV Conduction <ul><li>However, the AV conduction rate is more often tachycardic with atrial fibrillation </li></ul><ul><li>Dependent on the AV node Refractory Period </li></ul>
  10. 10. Ventricular Response <ul><li>Ventricular rhythm is irregularly, irregular!!! </li></ul>
  11. 11. Origins of AF <ul><li>Onset is sudden </li></ul><ul><li>May be self-limiting </li></ul><ul><li>May represent a single, isolated incident </li></ul><ul><li>(Prudente, 2008, p. 21) </li></ul>Paroxysmal
  12. 12. <ul><li>Transient rhythm disturbances are commonly caused by: </li></ul><ul><li>Thyrotoxicosis </li></ul><ul><li>Heart Failure Exacerbation </li></ul><ul><li>S/P Cardiac or Thoracic Surgery </li></ul><ul><li>Excessive Alcohol Intake </li></ul><ul><li>(Prudente, 2008) </li></ul>Origins of AF Paroxysmal
  13. 13. Origins of AF <ul><li>Primary rhythm disturbance without underlying heart disease </li></ul><ul><li>(Prudente, 2008, p. 21) </li></ul>“ Lone AF”
  14. 14. Origins of AF <ul><li>AF is secondary to a cardiac disease or other disease that causes atrial remodeling </li></ul><ul><li>(Prudente, 2008) </li></ul>Secondary AF
  15. 15. Secondary AF <ul><li>Hypertension </li></ul><ul><li>CAD </li></ul><ul><li>Valvular Disease </li></ul><ul><li>Pulmonary Disease </li></ul><ul><li>Sleep Apnea </li></ul><ul><li>Obesity </li></ul><ul><li>(Prudente, 2008) </li></ul>Atrial Remodeling
  16. 16. Secondary AF <ul><li>“ Nearly two-thirds of AF patients have underlying heart disease that may contribute to structural remodeling” </li></ul><ul><li>(Prudente, 2008, p. 21) </li></ul>
  17. 17. Etiology in a Nutshell <ul><li>Cardiac Surgery </li></ul><ul><li>MVR, MVS </li></ul><ul><li>Hyperthyroidism </li></ul><ul><li>Infection </li></ul><ul><li>AMI, CAD </li></ul><ul><li>Pericarditis </li></ul><ul><li>Hypoxia </li></ul><ul><li>Coffee, ETOH, Cigarettes </li></ul><ul><li>Fatigue or Stress </li></ul><ul><li>Meds (Digoxin or Aminophylline) </li></ul><ul><li>Catecholamine release during exercise </li></ul>
  18. 18. 3 P’s: Types of AF <ul><li>Paroxysmal AF </li></ul><ul><li>Persistent AF </li></ul><ul><li>Permanent AF </li></ul><ul><li>(Prudente, 2008, p. 21) </li></ul>
  19. 19. Paroxysmal AF <ul><li>Episodes come and go, typically lasting less than 24 hours, and convert spontaneously within 7 days </li></ul><ul><li>(Prudente, 2008, p. 21) </li></ul>
  20. 20. Persistent AF <ul><li>Episodes last more than 7 days and require cardioversion with drugs, electrical shock, or both </li></ul><ul><li>(Prudente, 2008, p. 21) </li></ul>
  21. 21. Permanent AF <ul><li>A longstanding episode in which cardioversion fails or no cardioversion effort is made </li></ul><ul><li>(Prudente, 2008, p. 21) </li></ul>
  22. 22. AF and Atrial Kick <ul><li>What is atrial kick??? </li></ul><ul><li>A-fib causes loss of Atrial Kick </li></ul><ul><li>Uncontrolled A-fib in combo with loss of Atrial Kick results in ↓ CO </li></ul><ul><li>(as much as 30% less) </li></ul><ul><li>May result in Heart Failure, Angina, and/or Syncope </li></ul>
  23. 23. Treatment of AF <ul><li>Controlled or Uncontrolled??? </li></ul><ul><li>Dependent upon AV conduction or ventricular response </li></ul><ul><li>Without heart rate controlling medications, atrial fibrillation is typically uncontrolled (rapid ventricular response) </li></ul>
  24. 24. Ventricular Response <ul><li>HR 60 – 100 </li></ul><ul><li>Controlled Ventricular Response </li></ul><ul><li>HR > 100 uncontrolled </li></ul><ul><li>Or Rapid Ventricular Response (RVR) </li></ul><ul><li>HR < 50 </li></ul><ul><li>Slow Ventricular Response (SVR) </li></ul>
  25. 25. Uncontrolled AF <ul><li>If left untreated can lead to: </li></ul><ul><li>Cardiovascular Collapse </li></ul><ul><li>Thrombus Formation </li></ul><ul><li>Systemic Arterial or Pulmonary Emboli </li></ul><ul><li>“ In AF patients, the yearly risk of ischemic stroke ranges from 3% to 8%” </li></ul><ul><li>(Prudente, 2008, p. 22) </li></ul>
  26. 26. Signs & Symptoms <ul><li>None with Controlled A-fib </li></ul><ul><li>Irregular Rhythm </li></ul><ul><li>Uncontrolled or SVR: </li></ul><ul><li>Irregular Rhythm </li></ul><ul><li>Hypotension </li></ul><ul><li>Light-headedness </li></ul><ul><li>Weakness </li></ul><ul><li>Palpitations </li></ul><ul><li>SOB </li></ul>
  27. 27. Goals for Treatment <ul><li>Convert to NSR </li></ul><ul><li>or </li></ul><ul><li>Rate Control with Prevention of Blood Clots & Atrial Remodeling </li></ul>
  28. 28. TREATMENT : <ul><li>Asymptomatic versus Symptomatic </li></ul><ul><li>If < 48 hours, synchronized cardioversion </li></ul><ul><li>If > 48 hours, anticoagulation therapy and rate control 1 st </li></ul><ul><li>Then chemical or synchronized cardioversion, if desired by physician </li></ul>
  29. 29. Rhythm Control <ul><li>Medications that Act as Chemical Cardioverters by prolonging refractory periods: </li></ul><ul><li>Antidysrhythmics: </li></ul><ul><li>Cordarone (amiodarone) </li></ul><ul><li>Corvert (ibutilide) </li></ul><ul><li>Rhythmol (propafenone) </li></ul><ul><li>Tambocor (flecainide) </li></ul><ul><li>Tikosyn (dofetilide) </li></ul>
  30. 30. Rhythm Control <ul><li>Medications that Act as Chemical Cardioverters by prolonging action potential in myocardial fibers without affecting conduction: </li></ul><ul><li>Betapace (sotalol): non-selective beta-blocker/antidysrhythmic </li></ul>
  31. 31. Rhythm Control <ul><li>Patients likely to receive chemical cardioversion: </li></ul><ul><li>First Episode of AF </li></ul><ul><li>Paroxysmal AF </li></ul><ul><li>Younger Patients with Structural Remodeling </li></ul><ul><li>Patients with Pronounced AF Symptoms </li></ul><ul><li>(Prudente, 2008) </li></ul>
  32. 32. Preparing Patients for Synchronized Cardioversion <ul><li>May occur at the bedside or in the Cath Lab! </li></ul><ul><li>Cardiologist MUST be present for intervention </li></ul><ul><li>Sedation is usually ordered prior to delivering electrical shock </li></ul><ul><li>Attach patient to pulse generator pads and the 3-lead wire system </li></ul><ul><li>Pulse generator should be set to “SYNC” (R waves are marked) </li></ul><ul><li>Shock delivery: 100J, 150J, 200J </li></ul>
  33. 33. Synchronized Cardioversion <ul><li>If the patient’s rhythm converts to NSR, then the heart rate control and antiagulation therapy is not needed </li></ul><ul><li>If the cardioversion is unsuccessful, then the patient will need medications! </li></ul>
  34. 34. Catheter Ablation <ul><li>It is the delivery of low-frequency, alternating current through a catheter electrode that produces thermal myocardial injury at the tip of the 4-mm catheter </li></ul><ul><li>These areas of injury, or lesions, create electrically unexcitable tissue, a situation that prevents depolarization and conduction of electrical impulse </li></ul><ul><li>(Zak, 2010, p. 70) </li></ul>
  35. 35. Catheter Ablation <ul><li>Indications for Ablation: </li></ul><ul><li>Primary Indication: </li></ul><ul><ul><li>Symptomatic AF that is refractory or intolerant to at least one class I or class III antiarrhythmic medication </li></ul></ul><ul><li>Documented HF or decreased EF who have increasing symptoms of HF in AF </li></ul><ul><li>Do not take antiarrhythmic meds </li></ul><ul><li>Long-term anticoagulation treatment </li></ul><ul><li>(Zak, 2010, p. 70) </li></ul>
  36. 36. Catheter Ablation <ul><li>Contraindicated for: </li></ul><ul><li>Left atrial thrombus indicated by TEE </li></ul><ul><li>Active bleeding or the inability to achieve anticoagulation </li></ul><ul><li>(Zak, 2010, p. 70) </li></ul>
  37. 37. Catheter Ablation <ul><li>The duration of the procedure is about 3 to 5 hours </li></ul><ul><li>Under moderate sedation or general anesthesia </li></ul><ul><li>Performed in an EP lab </li></ul><ul><li>(Zak, 2010, p. 70) </li></ul>
  38. 38. Rate Control <ul><li>Medications that Slow the Heart Rate: </li></ul><ul><li>May or May Not act as a Chemical Cardioverters!!! </li></ul><ul><ul><li>Beta-Blockers </li></ul></ul><ul><ul><ul><li>(decrease contractility) </li></ul></ul></ul><ul><ul><li>Calcium Channel Blockers </li></ul></ul><ul><ul><ul><li>(nondihydropyridine - decrease contractility) </li></ul></ul></ul><ul><ul><li>Cardiac Glycosides </li></ul></ul><ul><ul><ul><li>(increase contractility) </li></ul></ul></ul><ul><ul><li>Antiarrhythmics </li></ul></ul>
  39. 39. Medications for Treatment of New Onset or Sudden Onset Atrial Fibrillation <ul><li>Cardizem (diltiazem) – nondihydropyridine CCB </li></ul><ul><li>Cordarone (amiodarone) – antiarrhythmic agent </li></ul><ul><li>Lanoxin (digoxin) – cardiac glycoside </li></ul>
  40. 40. Cardizem <ul><li>(diltiazem hydrochloride) </li></ul><ul><li>Nondihydropyridine Calcium Channel Blocker </li></ul><ul><li>“ Diltiazem IV is the drug of choice for urgent rate control in patients with AF </li></ul><ul><li>A constant IV infusion brings ventricular response under control reliably </li></ul><ul><li>Sinus rhythm is achieved in only 15% and hypotension occurs in up to 33% of patients </li></ul><ul><li>(Khan, 2007, p. 260) </li></ul>
  41. 41. Cardizem <ul><li>(diltiazem hydrochloride) </li></ul><ul><li>Nondihydropyridine Calcium Channel Blocker </li></ul><ul><li>Inhibits calcium ion influx across cell membrane during cardiac depolarization </li></ul><ul><li>Slows SA/AV node conduction times </li></ul>
  42. 42. Cardizem Drip <ul><li>How is it ordered??? </li></ul><ul><li>Ordered to control heart rate </li></ul><ul><li>Titrate to keep HR between 60 – 100 </li></ul><ul><li>Need to monitor HR, B/P, & EKG rhythm closely </li></ul>
  43. 43. Cardizem Drip <ul><li>IV Bolus administered first </li></ul><ul><li>5 – 20 mg IVP </li></ul><ul><li>Supplied as: 25 mg/5 ml </li></ul>
  44. 44. Cardizem Drip <ul><li>Physician will order drip in mg/hr </li></ul><ul><li>Usually starting @ 5mg/hr </li></ul><ul><li>May titrate up to 15 mg/hr maximum </li></ul><ul><li>How Supplied: 100 mg/100 ml </li></ul><ul><li>(1 mg/ml) </li></ul>
  45. 45. Cardizem Drip <ul><li>If HR < 60 or SBP < 90 </li></ul><ul><li>Call physician for further orders (Do not stop or discontinue without physician orders!!!) </li></ul><ul><li>An order with titrating does not include orders to discontinue a medication; unless otherwise specified!!! </li></ul>
  46. 46. Cardizem Drip <ul><li>Before drip is discontinued, make sure patient is on oral Cardizem, or another rate control medication, first </li></ul><ul><li>To wean or not to wean??? </li></ul>
  47. 47. Amiodarone <ul><li>(Cordarone) </li></ul><ul><li>Acts as a chemical cardioverter </li></ul><ul><li>Prolongs refractory period of all cardiac cells </li></ul><ul><li>Nurses responsible for preparing IV bolus and first bottle for maintenance dose </li></ul>
  48. 48. Amiodarone <ul><li>(Cordarone) </li></ul><ul><li>150 mg in 100 ml D 5 W bolus over 10 minutes </li></ul><ul><li>Rate = 600 ml/hr </li></ul>
  49. 49. Amiodarone <ul><li>(Cordarone) </li></ul><ul><li>Concentration: 450 mg (150 mg vials x 3) in 250 ml D 5 W </li></ul><ul><li>(glass bottle) </li></ul>
  50. 50. Amiodarone Infusion <ul><li>Maintenance Drip: </li></ul><ul><li>1 mg/min (33 ml/hr) x 6 hours </li></ul><ul><li>followed by </li></ul><ul><li>0.5 mg/min (17 ml/hr) x 18 hours or until discontinued </li></ul><ul><li>Important: To avoid medication infiltration, use 0.22 Micron Filter (white)!!! </li></ul>
  51. 51. Amiodarone Infusion <ul><li>Maintenance Drip: </li></ul><ul><li>This is not a drip that is titrated!!! </li></ul>
  52. 52. Digoxin (Lanoxin) <ul><li>The most commonly cardiac glycoside to be used </li></ul><ul><li>The only one that is used in the United States </li></ul><ul><li>Functional Classification: Cardiac glycoside, inotropic, antidysrhythmic </li></ul><ul><li>(Lilley, Harrington, and Snyder, 2007) </li></ul>
  53. 53. Digoxin (Lanoxin) <ul><li>Increased Contractility: </li></ul><ul><li>Positive Inotropic Effects </li></ul><ul><li>It boosts intracellular calcium and sodium at the cell membrane, enabling stronger heart contractions **(requiring increased O 2 consumption)** </li></ul>
  54. 54. Digoxin (Lanoxin) <ul><li>Decreased Electrical Conduction Velocity: </li></ul><ul><li>Negative Dromotropic Effects </li></ul><ul><li>Decreases the velocity (rate) of electrical conduction </li></ul><ul><li>Mainly at the SA and AV nodes </li></ul><ul><li>Prolongs the refractory period in the conduction system </li></ul><ul><li>Atrial and Ventricular cardiac cells remain in a state of depolarization longer and are unable to start another electrical impulse </li></ul>
  55. 55. Digoxin (Lanoxin) <ul><li>Decreased Heart Rate: </li></ul><ul><li>Negative Chronotropic Effect </li></ul><ul><li>Blocks the reuptake of norepinephrine at the adrenergic nerve terminal </li></ul>
  56. 56. Digoxin (Lanoxin) <ul><li>Improved Cardiac Output: </li></ul><ul><li>Parasympathetic effects </li></ul><ul><li>Augments vagal tone (cholinergic or parasympathetic) </li></ul><ul><li>Slower heart rates allow for increased cardiac filling time </li></ul>
  57. 57. Adverse Reactions/Side Effects <ul><li>Digoxin Toxicity </li></ul><ul><li>[has a narrow therapeutic index – (0.5 – 2 ng/ml)] </li></ul><ul><li>Bradycardia </li></ul><ul><li>Arrhythmias, complete heart blocks </li></ul><ul><li>Nausea, vomiting </li></ul><ul><li>Abdominal pain, diarrhea </li></ul><ul><li>Headache, vision changes </li></ul><ul><li>Irritability, insomnia, depression </li></ul><ul><li>(Eckman, Labus, and Thompson, 2009, p. 184) </li></ul>
  58. 58. Herbal Drug Interaction <ul><li>St. John’s wort and ginseng inhibit the metabolism of digoxin increasing the risk of toxicity </li></ul><ul><li>(Eckman, Labus, and Thompson, 2009) </li></ul>
  59. 59. Anticoagulation Therapy for Patients with Atrial Fibrillation <ul><li>What is the difference between an anticoagulant, such as warfarin, and an antiplatelet agent, such as clopidogrel??? </li></ul><ul><li>Why are anticoagulants used for atrial fibrillation and not an antiplatelet agent??? </li></ul>
  60. 60. Anticoagulation Therapy for Patients with Atrial Fibrillation <ul><li>Thrombolytic events are the most feared complication of AF </li></ul><ul><li>Patients with AF are up to 7 times more likely than the general population to have a stroke </li></ul><ul><li>(Zak, 2010, p. 68) </li></ul>
  61. 61. Heparin Sodium <ul><li>Anticoagulant </li></ul><ul><li>“ Blood Thinner” </li></ul><ul><li>Prevents conversion of fibrinogen to fibrin and prothrombin to thrombin </li></ul><ul><li>Main use is prevention of blood clot formation!!! </li></ul>
  62. 62. Heparin Sodium <ul><li>Common Administration Routes: </li></ul><ul><li>Subcutaneously or Intravenously </li></ul>
  63. 63. Heparin Drip <ul><li>IV Bolus administered first according to patient’s weight </li></ul><ul><li>How Supplied: 10,000 units/ml </li></ul><ul><li>Followed by continuous drip </li></ul><ul><li>(dose determined by pharmacy) </li></ul><ul><li>How Supplied: 25,000 units/250 ml D 5 W </li></ul><ul><li>(100 units/ml) </li></ul>
  64. 64. Monitoring Heparin <ul><li>PTT measured on a regular basis; 6 hours initially and after any rate changes; otherwise every 12 hours or once daily </li></ul><ul><li>Platelet Count daily – H.I.T. </li></ul>
  65. 65. Heparin Induced Thrombocytopenia (HIT) <ul><li>Aka Heparin Associate Thrombocytopenia (HAT) </li></ul><ul><li>An allergic reaction that is mediated by by the production of immunoglobulin (Ig)G antibodies </li></ul><ul><li>The greatest risk of this condition is the paradoxical occurrence of thrombosis, something that heparin normally prevents or alleviates </li></ul><ul><li>(Lilley, Harrington, and Snyder, 2007, p. 422) </li></ul>
  66. 66. Heparin Induced Thrombocytopenia (HIT) <ul><li>Incidence is 5% to 15% of patients </li></ul><ul><li>Is higher bovine versus porcine heparins </li></ul><ul><li>Argatroban and lepirudin (Refludan) are indicated for treating HIT </li></ul><ul><li>(Lilley, Harrington, and Snyder, 2007, p. 422) </li></ul>
  67. 67. Monitoring Heparin <ul><li>Monitor: </li></ul><ul><li>S/S of Bleeding -> gums, hematuria, black tarry stools </li></ul><ul><li>Labs -> PTT (Target PTT = 60 – 80 seconds or 2 – 2.5 greater than baseline </li></ul><ul><li>Platelet Count > 100 </li></ul>
  68. 68. Heparin: Too Much? <ul><li>ATTENTION!!! </li></ul><ul><li>Reversal agent for Heparin is… </li></ul><ul><li>Protamine Sulfate </li></ul><ul><li>1 gram per 100 units of heparin (IV) </li></ul>
  69. 69. Heparin Discontinuation <ul><li>Before heparin drip is discontinued, patient needs to be on Coumadin (warfarin) and INR needs to be therapeutic (2.0 – 3.0) </li></ul><ul><li>This is not a nursing or pharmacy judgment – physician will order discontinuation of heparin or write standing orders </li></ul>
  70. 70. Coumadin <ul><li>(warfarin sodium) </li></ul><ul><li>Anticoagulant </li></ul><ul><li>“ Blood Thinner” </li></ul><ul><li>Depresses hepatic synthesis of vitamin K-dependent coagulation factors (II, VII, IX, X) </li></ul><ul><li>Main use is prevention of blood clot formation!!! </li></ul>
  71. 71. Coumadin Dosing <ul><li>Coumadin is usually ordered on a daily basis </li></ul><ul><li>Dose is adjusted by prescribing physician according to INR level. </li></ul><ul><li>Upon D/C, patient will need to be instructed to keep follow-up appointments for INR level monitoring </li></ul>
  72. 72. Coumadin <ul><li>Monitor: </li></ul><ul><li>S/S of Bleeding -> gums, hematuria, black tarry stools </li></ul><ul><li>Labs -> PT/INR (Target INR = 2.0 – 3.0) </li></ul><ul><li>Avoid IM injections </li></ul>
  73. 73. Herbal Drug Interaction <ul><li>St. John’s wort, ginseng, and gingko inhibit the metabolism of warfarin increasing the risk of toxicity </li></ul><ul><li>(Micromedex) </li></ul>
  74. 74. Coumadin: Too Much? <ul><li>Anticoagulant Therapy </li></ul><ul><li>ATTENTION!!! </li></ul><ul><li>Reversal agent for Coumadin is… </li></ul><ul><li>Vitamin K (Oral, SQ, or IV) </li></ul>
  75. 75. References <ul><li>Donofrio, J., Haworth,K., Achaeffer, L., & Thompson, G. (2005). Cardiovascular care made incredibly easy. Ambler, PA: Lippincott Wilkins & Williams </li></ul><ul><li>Eckman, M., Labus, D., & Thompson, G., (Eds). (2009). Nursing pharmacology made incredibly easy. Ambler, PA: Lippincott, Williams, and Wilkins. </li></ul><ul><li>Hodgson, B. B., & Kizior, R. J. (2007). Saunders nursing drug handbook. St. Louis, MS: Saunders Elsevier. </li></ul><ul><li>Khan, M. G. (2007). Cardiac drug therapy, (7 th ed.). Totowa, NJ: Humana Press. </li></ul><ul><li>Lilley, L. L., Harrington, S., & Snyder, J. S. (2007). Pharmacology and the nursing process, (5 th ed.). St. Louis, MO: Mosby Elsevier. </li></ul>
  76. 76. References <ul><li>Prudente, L. A. (2008). Quelling atrial chaos: Current approaches to managing atrial fibrillation. American Nurse Today, 3 (8), 21-26. </li></ul><ul><li>Skidmore-Roth, L. et al. (2007). Mosby’s nursing drug reference, (20 th ed.). St. Louis, MS: Mosby Elsevier. </li></ul><ul><li>Smeltzer et al. (2008). Brunner and suddarth’s textbook of medical-surgical nursing, (11 th ed.). Philadelphia, PA: Lippincott Williams and Wilkins. </li></ul><ul><li>Zak, J. (2010). Ablation to treat atrial fibrillation: Beyond rhythm control. Critical Care Nurse, 30 (6), 68-78. </li></ul>

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