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Atrial Fibrillation - BMH/Tele

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