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Atrial Fibrillation - BMH/Tele
 

Atrial Fibrillation - BMH/Tele

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    Atrial Fibrillation - BMH/Tele Atrial Fibrillation - BMH/Tele Presentation Transcript

    • Atrial Fibrillation: Too Many Atrial Chiefs!!! Natalie Bermudez, RN, BSN, MS Clinical Educator for Cardiac Telemetry Telemetry Course
    • 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
    • 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)
    • More Statistics
      • “ Occurs in 11% to 64% of patients after a CABG, valvular replacements, and heart transplantation”
      • (Smeltzer et al, 2008, p.832)
    • Electrical Chaos
      • Chaotic, irregular, rapid depolarization in atrial tissue due increased atrial irritability
      • Firing Rate = 300 – 600 times/minute
      • Causes the atria to quiver
    • Atrial Characteristics
      • No P waves are visible on an EKG
      • Fibrillatory waves (Fine or Coarse)
    • Characteristics of AF
      • Fine or Course
    • The Gatekeeper
      • AV node controls the # of electrical impulses that reach the ventricles
    • AV Conduction
      • However, the AV conduction rate is more often tachycardic with atrial fibrillation
      • Dependent on the AV node Refractory Period
    • Ventricular Response
      • Ventricular rhythm is irregularly, irregular!!!
    • Origins of AF
      • Onset is sudden
      • May be self-limiting
      • May represent a single, isolated incident
      • (Prudente, 2008, p. 21)
      Paroxysmal
      • 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
    • Origins of AF
      • Primary rhythm disturbance without underlying heart disease
      • (Prudente, 2008, p. 21)
      “ Lone AF”
    • Origins of AF
      • AF is secondary to a cardiac disease or other disease that causes atrial remodeling
      • (Prudente, 2008)
      Secondary AF
    • Secondary AF
      • Hypertension
      • CAD
      • Valvular Disease
      • Pulmonary Disease
      • Sleep Apnea
      • Obesity
      • (Prudente, 2008)
      Atrial Remodeling
    • Secondary AF
      • “ Nearly two-thirds of AF patients have underlying heart disease that may contribute to structural remodeling”
      • (Prudente, 2008, p. 21)
    • 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
    • 3 P’s: Types of AF
      • Paroxysmal AF
      • Persistent AF
      • Permanent AF
      • (Prudente, 2008, p. 21)
    • Paroxysmal AF
      • Episodes come and go, typically lasting less than 24 hours, and convert spontaneously within 7 days
      • (Prudente, 2008, p. 21)
    • Persistent AF
      • Episodes last more than 7 days and require cardioversion with drugs, electrical shock, or both
      • (Prudente, 2008, p. 21)
    • Permanent AF
      • A longstanding episode in which cardioversion fails or no cardioversion effort is made
      • (Prudente, 2008, p. 21)
    • 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
    • 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)
    • Ventricular Response
      • HR 60 – 100
      • Controlled Ventricular Response
      • HR > 100 uncontrolled
      • Or Rapid Ventricular Response (RVR)
      • HR < 50
      • Slow Ventricular Response (SVR)
    • 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)
    • Signs & Symptoms
      • None with Controlled A-fib
      • Irregular Rhythm
      • Uncontrolled or SVR:
      • Irregular Rhythm
      • Hypotension
      • Light-headedness
      • Weakness
      • Palpitations
      • SOB
    • Goals for Treatment
      • Convert to NSR
      • or
      • Rate Control with Prevention of Blood Clots & Atrial Remodeling
    • 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
    • Rhythm Control
      • Medications that Act as Chemical Cardioverters by prolonging refractory periods:
      • Antidysrhythmics:
      • Cordarone (amiodarone)
      • Corvert (ibutilide)
      • Rhythmol (propafenone)
      • Tambocor (flecainide)
      • Tikosyn (dofetilide)
    • 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
    • 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)
    • 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
    • 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!
    • 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)
    • 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)
    • Catheter Ablation
      • Contraindicated for:
      • Left atrial thrombus indicated by TEE
      • Active bleeding or the inability to achieve anticoagulation
      • (Zak, 2010, p. 70)
    • 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)
    • 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
    • Medications for Treatment of New Onset or Sudden Onset Atrial Fibrillation
      • Cardizem (diltiazem) – nondihydropyridine CCB
      • Cordarone (amiodarone) – antiarrhythmic agent
      • Lanoxin (digoxin) – cardiac glycoside
    • 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)
    • Cardizem
      • (diltiazem hydrochloride)
      • Nondihydropyridine Calcium Channel Blocker
      • Inhibits calcium ion influx across cell membrane during cardiac depolarization
      • Slows SA/AV node conduction times
    • 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
    • Cardizem Drip
      • IV Bolus administered first
      • 5 – 20 mg IVP
      • Supplied as: 25 mg/5 ml
    • 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)
    • 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!!!
    • 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???
    • 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
    • Amiodarone
      • (Cordarone)
      • 150 mg in 100 ml D 5 W bolus over 10 minutes
      • Rate = 600 ml/hr
    • Amiodarone
      • (Cordarone)
      • Concentration: 450 mg (150 mg vials x 3) in 250 ml D 5 W
      • (glass bottle)
    • 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)!!!
    • Amiodarone Infusion
      • Maintenance Drip:
      • This is not a drip that is titrated!!!
    • 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)
    • 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)**
    • 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
    • Digoxin (Lanoxin)
      • Decreased Heart Rate:
      • Negative Chronotropic Effect
      • Blocks the reuptake of norepinephrine at the adrenergic nerve terminal
    • Digoxin (Lanoxin)
      • Improved Cardiac Output:
      • Parasympathetic effects
      • Augments vagal tone (cholinergic or parasympathetic)
      • Slower heart rates allow for increased cardiac filling time
    • 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)
    • Herbal Drug Interaction
      • St. John’s wort and ginseng inhibit the metabolism of digoxin increasing the risk of toxicity
      • (Eckman, Labus, and Thompson, 2009)
    • 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???
    • 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)
    • Heparin Sodium
      • Anticoagulant
      • “ Blood Thinner”
      • Prevents conversion of fibrinogen to fibrin and prothrombin to thrombin
      • Main use is prevention of blood clot formation!!!
    • Heparin Sodium
      • Common Administration Routes:
      • Subcutaneously or Intravenously
    • 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)
    • 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.
    • 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)
    • 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)
    • 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
    • Heparin: Too Much?
      • ATTENTION!!!
      • Reversal agent for Heparin is…
      • Protamine Sulfate
      • 1 gram per 100 units of heparin (IV)
    • 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
    • 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!!!
    • 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
    • Coumadin
      • Monitor:
      • S/S of Bleeding -> gums, hematuria, black tarry stools
      • Labs -> PT/INR (Target INR = 2.0 – 3.0)
      • Avoid IM injections
    • Herbal Drug Interaction
      • St. John’s wort, ginseng, and gingko inhibit the metabolism of warfarin increasing the risk of toxicity
      • (Micromedex)
    • Coumadin: Too Much?
      • Anticoagulant Therapy
      • ATTENTION!!!
      • Reversal agent for Coumadin is…
      • Vitamin K (Oral, SQ, or IV)
    • 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.
    • 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.