Anti Arrhythmic Class Teaching

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    CLASS ROOM TEACHING ON

    ANTI ARRHYTHMIC DRUGS

    SUBMITTED TO SUBMITTED BY

    MRS.MALATHI, MSC [N],PhD S.SURESH

    LECTURER MSC [N] II YR

    CHRI CHRI

    SUBMITTED ON: 21.06.2011

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    NAME OF THE STUDENT TEACHER : S.SURESH

    SUBJECT : CLINICAL SPECIALITY-II

    UNIT : UNIT XI [ PHARMACOLOGY]

    TOPIC : ANTI ARRHYTHMIC DRUGS

    PREVIOUS KNOWLEDGE

    OF THE STUDENTS : THE STUDENTS HAVE PREVIOUS KNOWLEDGE ON ANTI ARRHYTHMIC DRUGS DURINGTHEIR BSC(N) PROGRAMME AND ALSO HAVE CLINICAL EXPOSURE.

    METHODS OF TEACHING : LECTURE CUM DISCUSSION

    COURSE & YEAR : MSC NURSING II YEAR

    NO OF STUDENTS : 8

    VENUE : LECTURE HALL

    DATE & TIME : 21.6.2011 & 2.30 PM -3.00 PM

    DURATION : 30 MINUTES

    EVALUAT\OR : MRS. MALATHI, MSC [N], PhD, LECTURER, CHRI

    A.V AIDS : LCD, OHP, BLACK BOARD,CHART

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    CENTRAL OBJECTIVES:

    The student gains adequate knowledge on Anti arrhythmic drugs and develops desirable attitude and skills in providing anti arrhythmic drugs to the

    patients.

    SPECIFIC OBJECTIVES:

    At the end of the session the student will be able to

    y define Anti arrhythmic drugs.y describe the purpose of Anti arrhythmic drugs.y discuss the classification of Anti arrhythmic drugs.y elaborate the mechanism of action, uses and adverse effects of the drugs of various classification.y discuss the nursing management during anti arrhythmic drugs administration.

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    2

    3.

    2 mts

    3mts

    Define Anti

    arrhythmic

    drugs

    describe the

    purpose of

    Anti

    arrhythmic

    drugs

    DEFINITION

    Antiarrhythmic drugs are medicines that correct irregular heartbeats and slow

    down hearts that beat too fast.

    PURPOSE:

    Normally, the heart beats at a steady, even pace. The pace is controlled by

    electrical signals that begin in one part of the heart and quickly spread through

    the whole heart. If something goes wrong with this control system, the result

    may be an irregular heartbeat, or an arrhythmia. Antiarrhythmic drugs correct

    irregular heartbeats, restoring the normal rhythm. If the heart is beating too fast,

    these drugs will slow it down. By correcting these problems, antiarrhythmic

    drugs help the heart work more efficiently.

    Teacher :

    Defining by using LCD

    Student :

    Listening

    Teacher :

    Defining by using LCD

    Student :

    Listening

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    4 3 mts Discuss the

    classification

    of anti

    arrhythmic

    drugs

    CLASSIFICATION

    Class I Membrane-stabilizing, inhibit fast sodium channel. Restrictionof sodium current

    Class II Inhibition of sympathetic stimulation Class III Delayed repolarization Class IV Calcium antagonists. Inhibit slow calcium channel. Restriction

    of calcium current

    Class IA Quinidine Disopyramide Procainamide

    Class IB Lidocaine Mexiletine Phenytoin ** Tocainide

    Class IC Flecainide Encainide Propafenone

    Teacher :

    Explaining by using OHP

    Student:

    Listening

    Taking down notes

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    Class II Betablockers Class III

    Amiodarone Sotalol

    Class IV

    Verapamil

    Diltiazem

    5 10 mts Describe the

    mechanism of

    action,dosage,

    adverse

    effects,uses.

    CLASS IA DRUGS: also block potassium channel; thus prolong action

    potential.

    Teacher :

    Explaining by using

    CHART and OHP

    Student:

    Listening

    Taking down notes

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    Quinidine:

    MECHANISM OF ACTION:

    Inhibition of sodium channels, extending the effective refractory period

    (ERP) of the myocardial cell membrane, thereby decreasing myocardial

    conduction velocity, excitability and contractility.

    Blockade of alpha adrenergic receptors, leading to a reflex increase in the

    SA node rate and producing vasodilatation.

    Blockade of Ikchannel, prolonging duration of action potential.

    Blockade of muscarinic receptors, thereby enhancing conduction through

    AV node.

    DOSAGE:

    Quinidine Sulfate tablets - 200 mg test dose, then 200 400 mg every 3hours X 3-4 doses then q6 hr

    Quinidine Bisulfate 500 mg BID

    USES:

    Conversion to or maintenance of sinus rhythm in patients with atrial

    fibrillation, flutter , or ventricular tachycardias.

    Treatment of paroxysmal supraventricular tachycardia

    Prevention of PSVT in patients with reentrant tachycardias including

    wolff-parkinson white syndrome.

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    ADVERSE EFFECTS:

    Torsades de pointes.

    ECG changes: prolonged QRS complex, giant U wave, ST segment

    depression , flattened T wave.

    Diarrhea.

    Cinchonism.

    Procainamide:

    The local anesthetic is equivalent to quinidine as an anti arrhythmic agent

    and has similar cardiac and toxic effects.

    INDICATIONS

    Useful for treatment of a wide variety of arrhythmias May use for treatment of PSVT uncontrolled by adenosine and

    vagal maneuvers if blood pressure stable

    Stable wide-complex tachycardia of unknown origin Atrial fibrillation with rapid rate in Wolff-Parkinson-White

    syndrome

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    DOSAGE

    Cardiac Arrest 2 mg/min IV infusion (max dose 17 mg/kg); inrefractory VF/VT, 100 mg IV push doses given every 5 minutes

    are acceptable

    Other indications 20 mg/min IV infusion until one of thefollowing occurs:

    Arrhythmia suppression Hypotension QRS widens by > 50% Total dose of 17 mg/kg given

    Maintenance dose 1-4 mg/min (usually mixed 2 gms in 500ccD5W or NS)

    Additional adverse effect induces systemic lupus erythematous.

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    CLASS IB DRUGS:

    Examples: lidocaine, tocainide and mesiletine

    Class IB drugs decrease the duration of action potential.

    Lidocaine:

    PHARMACOKINETICS:

    Short acting because of rapid hepatic metabolism. Loading dose should be followed by continuous intravenous

    infusion.

    MECHANISM OF ACTION:

    Acts primarily on the purkinje fibres, depressing automaticity andshortening of the refractory period.

    Has a higher affinity for ischemic tissue, suppressing spontaneousdepolarizations in the ventricles by inhibiting re entry mechanisms.

    INDICATIONS:

    Cardiac arrest from VF/VT Stable VT, wide-complex tachycardias of uncertain type, wide-complex

    PSVT

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    DOSAGE:

    Cardiac arrest from VF/VT Initial dose: 1.0 to 1.5 mg/kg IV For refractory VF may give additional 0.5 to 0.75 mg/kg

    IV push, repeat in 5 to 10 minutes; maximum total dose 3

    mg/kg

    A single dose of 1.5 mg/kg IV in cardiac arrest isacceptable

    Tracheal administration 2-4 mg/kg

    USE:

    Suppression of ventricular tachycardia ; the 2000 guideline now

    consider lidocaine a second choice behind other alternative agents for the

    treatment of ventricular arrhythmias associated with CPR.

    ADVERSE EFFECTS:

    Seizures.

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    Tocainide and mexiletine: orally effective congeners of lidocaine .

    PHARMACOKINETICS:

    Resistant to first pass hepatic metabolism. Half life : 8 to 20 hours.

    USE:

    Ventricular arrhythmias.

    ADVERSE EFFECTS:

    Dizziness, vertigo, nausea.

    CLASS 1C:

    Patients who can safely receive these medications are limited because ofthe pronounced effect on conduction

    Encainide (Enkaid) and flecainide (Tambocor) PO Limited to life threatening dysrhythmias

    Propafenone (Rhythmol) PO Has some mild beta blocking and Ca channel blocking effects

    All meds should be started while in the hospital Minimal side effects

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    Proponolol:

    Total dose: 0.1 mg/kg by slow IV push divided into 3 equal doses at 2-3minute intervals. Do not exceed 1 mg/min

    Repeat after 2 minutes if necessary Oldest of the beta blockers Can also be given PO. 10 30 mg tid or qid

    USES:

    Treatment and prophylaxis of PSVT and atrial fibrillation. Possible prevention of recurrent infarction in patients recovering from

    MI.

    ADVERSE EFFECTS:

    Sedation, sleep disturbances,sexual dysfunction.

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    Esmolol:

    PHARMACOKINETICS:

    Very short acting.(9 minutes). Administered by IV infusion.

    DOSAGE:

    0.5 mg/kg over 1 minute, followed by continuous infusion at 0.05mg/kg/minute (max 0.3 mg/kg/minute)

    Titrate to effect. Esmolol has a short half-life (2 to 9 minutes)

    USES:

    Short term control of SVT including ST and PSVT.

    Emergency control of ventricular rate in patients with atrial fibrillation or

    atrial flutter.

    ADVERSE EFFECTS:

    AV block, cardiac arrest.

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    DOSAGE:

    IV Loading dose: 1000 mg over 24 hours - 150mg in 100cc D5W,infuse over 10 minutes, then

    Infuse 360 mg over the next 6 hours, then Infuse 540 mg over the next 18 hours, then Maintenance dose: 0.5 mg/min. May be continued up to 96 hours

    or until rhythm is stable. Switch to oral form as soon as possible

    PO Loading dose: 800 1600 mg/day in divided doses for 1-3weeks. Then reduce to 600-800 mg/day for 1 month. If rhythm

    stable, decrease to 400 mg in 1-2 divided doses. Titrate to lowest

    dose to limit side effects

    ADVERSE EFFECT:

    Cardiovascular effects: torsades de pointes, ECG changes( prolonged QTinterval

    and QRS complex)

    OTHER EFFECTS:

    Pulmonary reactions such as pneumonitis, fibrosis.

    Photo dermatitis, paresthesia, tremor.

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    Sotalol:

    This drug is an oral, non selective beta adrenergic receptor antagonist that

    also blocks potassium channels.

    DOSAGE:

    Initial dose 80 mg PO bid. Adjust gradually (every 2-3 days) until appropriate

    response occurs. May require 240 320 mg

    USES:

    Life threatening sustained VT, AF.

    Adverse effects:

    Prolonged QT interval

    CLASS IV:

    Calcium channel blockers:

    EX: Verapamil, diltiazem.

    Class IV drugs slow phase 4 depolarition in the SA node and decrease the heart

    rate.

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    MECHANISM OF ACTION:

    Blockade of calcium uptake via a voltage sensitive channel,thereby reducing

    inward flow of calcium into myocardium cells.

    EFFECTS ON THE MYOCARDIUM:

    Reduce the rate of SA node discharge. Slow conduction through the AV node. Prolong the AV node refractory period. Decrease the myocardial contractility. Vasodilation.

    USES:

    Treatment of PSVT.

    Control of ventricular rate in atrial flutter or atrial fibrillation .

    Adverse effects: Hypotension ,dizziness,constipation.

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    6 7 mts Discuss the

    nursing

    management

    NURSING CARE

    nurse should monitor for

    Heart block

    Diarrhea, Hypotension, EKG changes, Cinchonism, Interacts with many commondrugs

    Instruct licent to monitor pulse rate & rhythm; monitor EKG; monitor tinnitus andvisual disturbances

    Ventricular dysrhythmias & Unlabelled Use: Digitalis-induced arrhythmias

    Hypotension, CNS effects, GI distress, Bradycardia

    Lidocaine given IV bolus and by infusion; give oral drugs with food & monitor EKG

    confusion, drowsiness, slurred speech, seizures, with lidocaine

    CLASS III:

    Nurse Should monitor for

    y Ventricular dysrhythmiasy Hypertensiony Muscle weaknessy Tremorsy Photophobiay Monitor vitals and ECG

    Teacher :

    Giving Hand out

    Discussing

    Student:

    Listening

    Participate in discussing

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    7.

    8.

    2mt

    1mt

    summary and

    conclusion

    Reinforcement

    of the topic

    y Instructtheclienttakingamiodaroneto wear sunglass and sunscreens.

    CLASS IV:

    Nurses should monitorand assess for

    Bradycardia Chest pain,urinary retentionand dry mouth. Heartrateand rhythm ;assess chest pain,urinary retention.

    SUMMARY AND CONCLUSION:

    so far we are discussed about anti arrhythmic drugs ,its purpose,dosage,

    classification, mechanism of action, use ,adverse effects and nursing

    management during administration of antiarrhythmic drugs.

    I hope you all understand and will impart this theory while you are practicing.

    ASSIGNMENT:Write an assignment on dysrhythmias

    Submit on: 02.07.2011

    Total marks: 10

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    BIBLIOGRAPHY:

    Books :

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    1. K.D.Tripathi. Essentials Of Medical Pharmacology,5th Edition, Jaypee Publishers2. H.P.Rang et.al, Pharmacology,5th edition 2006,Elsevier publications.3. V N Sharma,Essentials of pharmacology,3rd edition, 2009,CBS publishers.4. Richard D.Howland etal, Pharmacology, 3rd edition, 2006, Lippincott Williams & Wilkins.5. Susan l. Woods et al,Cardiac Nursing, 5th ed, 2005, Lippincott Williams & Wilkins6. Debra k. Moser; Barbara Riegel, Cardiac Nursing: A Companion To Braunwald's Heart Disease, 2008, Saunders Elsevier7. Unless else specified in boxes, then ref is: Rang, H. P.. Pharmacology. Edinburgh: Churchill Livingstone

    Journals :

    1. Niessen, K.; Karsan, A. (2008). Circulation Research 102 (10): 1169.2. Lie K.I. et al, LIdocaine in the prevention of primary ventricular fibrillation, (Nov 2008) New Eng. J.Med 291: 1324-1326.3. Roden ,D.M. et al : current status of class III anti arrhythmic drug therapy.Am.J.cardiol,2009 72: 44-49.4. 4.Vaughan Williams ,E.M. et al : Classifying an anti arrhythmic action: J.Clin. Pharmacol,2010: 32: 964-977.5. Conti JB, Belardinelli L, Utterback DB, Curtis AB (March 1995). "Endogenous adenosine is an antiarrhythmic agent". Circulation91 (6): 17617.

    Net references :

    1. www.wikipedia.org2. www.medscape.com3. www.cvpharmacology.org