CLASS ROOM TEACHING ON ANTI ARRHYTHMIC DRUGS

SUBMITTED TO
MRS.MALATHI, MSC [N],PhD LECTURER CHRI

SUBMITTED BY
S.SURESH MSC [N] II YR CHRI

SUBMITTED ON: 21.06.2011

NAME OF THE STUDENT TEACHER SUBJECT UNIT TOPIC PREVIOUS KNOWLEDGE OF THE STUDENTS

: S.SURESH : CLINICAL SPECIALITY-II : UNIT XI [ PHARMACOLOGY] : ANTI ARRHYTHMIC DRUGS

: THE STUDENTS HAVE PREVIOUS KNOWLEDGE ON ANTI ARRHYTHMIC DRUGS DURING THEIR BSC(N) PROGRAMME AND ALSO HAVE CLINICAL EXPOSURE. : LECTURE CUM DISCUSSION : MSC NURSING II YEAR : 8 : LECTURE HALL : 21.6.2011 & 2.30 PM -3.00 PM : 30 MINUTES : MRS. MALATHI, MSC [N], PhD, LECTURER, CHRI : LCD, OHP, BLACK BOARD,CHART

METHODS OF TEACHING COURSE & YEAR NO OF STUDENTS VENUE DATE & TIME DURATION EVALUAT\OR A.V AIDS

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

S.NO

TIME

SPECIFIC OBJECTIVES

CONTENT

TEACHER/LEARNER ACTIVITY

2 mts

Introduction

INTRODUCTION : Normally cardiac contraction includes five step process: a. Spontaneous development of action potential in the SA node. b. Spread of the impulse through the atrium. c. Temporary delay of the impulse at the atrioventricular (AV node). d. Rapid spread of the impulse along the two branches of the bundle of His and the purkinje fibres. e. Spread of the impulse along the cardiac muscle fibres of the ventricles. Arrhythmia are irregularities in heart rhythm that results from disturbances in pulse formation,impulse conduction or both. Anti arrhythmic drugs produce effects by altering one or more of the following factors:  Automaticity.  Conduction velocity.  Refractory period.  Membrane responsiveness.

Teacher : Introducing the topic

Student : Listening

Announcement of topic Now we will see about ANTI ARRHYTHMIC DRUGS

Teacher : Announcing the topic

Teacher : 2 2 mts Define Anti arrhythmic drugs DEFINITION Antiarrhythmic drugs are medicines that correct irregular heartbeats and slow down hearts that beat too fast. Student : Listening Defining by using LCD

3.

3mts

describe the purpose of Anti arrhythmic drugs 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. Student : Listening Teacher : Defining by using LCD

3 mts

Discuss the classification of anti arrhythmic drugs

CLASSIFICATION  Class I Membrane-stabilizing, inhibit fast sodium channel. Restriction of sodium current  Class II Inhibition of sympathetic stimulation  Class III Delayed repolarization  Class IV Calcium antagonists. Inhibit slow calcium channel. Restriction of calcium current

Teacher : Explaining by using OHP

Student: Listening Taking down notes

 Class IA Quinidine Disopyramide Procainamide

 Class IB Lidocaine Mexiletine Phenytoin ** Tocainide

 Class IC Flecainide Encainide Propafenone

 Class II Betablockers  Class III Amiodarone Sotalol

 Class IV Verapamil Diltiazem

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

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 Ik channel, 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 3 hours 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.

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

DOSAGE Cardiac Arrest 2 mg/min IV infusion (max dose 17 mg/kg); in refractory VF/VT, 100 mg IV push doses given every 5 minutes are acceptable Other indications 20 mg/min IV infusion until one of the following 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 500cc D5W or NS)

Additional adverse effect induces systemic lupus erythematous.

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 and shortening of the refractory period. Has a higher affinity for ischemic tissue, suppressing spontaneous depolarizations 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

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 is acceptable  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.

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 of the 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

CLASS II DRUGS: beta adrenergic receptor antagonist. Ex: proponolol,metaprolol,esmolol.

Class II drugs slow phase 4 depolarization in the SA node.

MECHANISM OF ACTION:
1) Blockade of beta receptors. 2) Reduce heart rate. 3) Reduce myocardial contractility. 4) Prolong AV conduction. 5) Prolong the AV refractory period.

Proponolol:

 Total dose: 0.1 mg/kg by slow IV push divided into 3 equal doses at 2-3 minute 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.

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

DOSAGE:  0.5 mg/kg over 1 minute, followed by continuous infusion at 0.05 mg/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.

CLASS III: POTASSIUM CHANNEL BLOCKERS

EX:sotalol, amiodarone, dofetilide.

Class III drugs increase the duration of action potential.

MECHANISM OF ACTION:

Prolong repolarization. Increase the ERP.

Amiodarone:

PHARMACOKINETICS: Long half time (13 -103 days). Time required to achieve steady state therapeutics level;15 to 30 days.

USE: Approved for atrial and ventricular arrhythmias; the 2000 guidelines recommend that intravenous amiodarone be used prior to lidocaine in patients receiving life support for ventricular fibrillation/ pulseless ventricular tachycardia.

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 1-3 weeks. 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.

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.

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.

7 mts

Discuss the nursing management NURSING CARE nurse should monitor for Heart block Diarrhea, Hypotension, EKG changes, Cinchonism, Interacts with many common drugs Instruct licent to monitor pulse rate & rhythm; monitor EKG; monitor tinnitus and visual 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

Teacher : Giving Hand out Discussing

Student: Listening Participate in discussing

CLASS III:
Nurse Should monitor for
y y y y y y Ventricular dysrhythmias Hypertension Muscle weakness Tremors Photophobia Monitor vitals and ECG

Instruct the client taking amiodarone to wear sunglass and sunscreens.

CLASS IV:
Nurses should monitor and assess for  Bradycardia  Chest pain, urinary retention and dry mouth.  Heart rate and rhythm ;assess chest pain,urinary retention.

7.

2mt

summary and conclusion

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 8. 1mt Reinforcement of the topic Submit on: 02.07.2011 Total marks: 10

BIBLIOGRAPHY: Books :

1. K.D.Tripathi. Essentials Of Medical Pharmacology,5th Edition, Jaypee Publishers 2. 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 & Wilkins 6. Debra k. Moser; Barbara Riegel, Cardiac Nursing: A Companion To Braunwald's Heart Disease, 2008, Saunders Elsevier 7. 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". Circulation 91 (6): 17617. Net references : 1. www.wikipedia.org 2. www.medscape.com 3. www.cvpharmacology.org