anti aritmia-ijo-a.ppt

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    Depart. Of Pharmacology & Therapy

    Medical Faculty Padjadjaran University

    Dr. Rovina Ruslami SpPD

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    Antiarrhythmia 2 goals :

    Arrhythmia :

    asymptomatic life threatening

    Termination of an ongoing Arrhythmia

    Prevention of a recurrence

    Control arrythmia

    Proarrhythmic effect

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    Cardiac cycle : automaticity rhythmic AP

    SA node AV node HIS-purkinje

    system

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    0

    2

    0 mV

    -85 mV

    3

    1

    4

    eff refractory period

    Action Potential

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    Mechanisms of Cardiac Arrhythmia

    1. Enhanced automaticity / abnormal automaticity

    2. Triggered automaticity

    3. Block

    4. Reentry

    Tools

    ECG

    DC-cardioversion

    ICDs (Implantable cardioverter defiblillators)

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    Mechanisms of AAD actions :

    suppressing the initiating mechanism

    slow automaticity

    altering the reentrant circuit

    1. phase 4 slope2. threshold

    3. max. diastolic potential

    4. AP duration

    -blockersblock of Na+, Ca++

    adenosine

    block of K+

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    Normal Undirectional block

    altering the reentrant circuit

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    Principles in the clinical use of AADs

    Identify & remove precipitating factors

    Establish the goals of treatment

    - some arrhythmias shouldnt be treated

    - symptoms due to arrhythmia

    - choosing among therapeutic approach

    Minimize risks

    - proarrhythmic effect

    - monitoring of plasma concentration

    - patient-specific contra indication

    The electrophisiology of the heart as a moving target

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    IA Na+ channel blocker

    IB Na+ channel blocker

    IC Na+ channel blocker

    II -adrenoceptor blocker

    III K+ channel blocker

    IV Ca++ channel blocker

    Classification of AADs :

    class mechanism comment

    slow phase 0 depol

    shorten phase 3 repol

    markedly slow phase 0 depol

    suppress phase 4 depol

    prolongs phase 3 repol

    shorten action potential

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    Class I AADs

    Na channel blocker slow phase 0 depol

    excitability

    conductivity

    Use-dependence tachycardiaClass IA: bind to Na channel in intermediate speed

    quinidine, procainamide, disopyramide

    Class IB: bind rapidly to Na channellidocaine, mexiletine, tocainide

    Class IC: bind slowly to Na channel

    flecainide, propafenone

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    QUINIDINE

    inhibits arrhythmia caused by hyperautomaticityPrevent reentry arrhythmia

    Indications :

    Wide variety of arrhythmia

    A, AV, V - arrhythmia

    Maintain SR after DCFK : p.o

    Adverse effects : exacerbate arrhythmia--- blockproarrhythmic effect

    CI : heart block, liver disease

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    PROCAINAMIDE

    Analog of local anesthetic

    Indications :

    VT that non responsive to lidocaine

    FK : p.o liver kidney

    Adverse effects :inotropic negative, hypotensiondrug induced SLE (long-term therapy)

    Intoxication : asystole, CNS depression

    quinidine like effect

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    LIDOCAINE

    Inhibits arrhythmia caused by abnormal automaticity

    Indications :

    Arrhythmia related to myocardial ischaemia

    FK : iv excretion : liver

    Adverse effects :inotropic negative (-); CNS effects, tremorproarrhythmic effects

    CI : block, bradycardia

    rapidly bind to Na channel

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    -blocker slow phase 4 depol

    Class II AADs

    automaticity

    AV conduction

    Arrhythmia due to :- sympathetic activity

    - AF, SVT

    - post AMI prevent suddent death

    Inotropic (-) CI for HF

    HR & contractility

    Propranolol, metoprolol, esmolol, carvedilol

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    K channel blockers prolong phase 3

    Class III AADs

    AP duration

    eff. Refractory period

    sotalol, bretylium, amiodarone

    SOTALOL

    -blocker that has antiarrhythmia class III activity

    Indications : sustained VT, long-term : mortality

    Proarrhythmic effect torsade de pointes

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    iv excretion : kidney

    BRETYLIUM

    Indications : life threatening VT , recurrent VF

    FK :

    AMIODARONE

    Indications : severe refractory SVT, VT

    Class I, II, III & IV action mainly class III

    FK : p.o, EMG case :iv (bolus drip)

    clinical effect is achieved in 6 weeks (po)

    Adverse effects :

    vary toxicity effect, withdrawl effect

    liver toxicity, hyper-hypothyroidsm, muscle weaknessCI : block, bradycardia

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    Ca channel blocker shorten AP

    Class IV AADs

    AV conduction

    Inotropic (-) CI for HF

    HR & PR interval

    Verapamil, diltiazem

    Vasodilatoranti hypertension, anti anginal

    Indication : tachy-arryhthmia: SVT, VT

    FK : p.o, iv ( !! hypotension) liver

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    refractory period, conductivity, automaticity

    Shorten refractory period; AP; conductivityIndications : controll ventr respons to AF

    FK : p.o; iv

    Adverse effects : intoxication : VES VT / VF

    Indications : acute SVT

    FK : iv, short d.o.a

    Adverse effects : flushing, hypotension, chest pain

    ADENOSIN

    DIGOXIN

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