2022-11-03T20:26:29+03:00[Europe/Moscow] en true <p>Class 1: Na+ channel blocker</p>, <p>Class 2. Beta blocker</p>, <p>K+ channel blocker</p>, <p>Ca++ channel blocker</p>, <p>Na+ channel blockers</p>, <p>beta blocker</p>, <p>K+ channel blockers</p>, <p>Ca2+ channel blockers </p>, <p>blocks potassium channels and prevents repolarization; significantly blocks inactivated sodium channels preventing new AP</p>, <p>blocks activated and non-activated L-type calcium channels</p>, <p>Vernakalant</p>, <p>Propranolol</p>, <p>Propafenone</p>, <p>Procainamide</p>, <p>Lidocaine</p> flashcards
Antiarrhythmic drugs

Antiarrhythmic drugs

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  • Class 1: Na+ channel blocker

    -change the slope of phase 0

    -can abolish tachyarrhythmia caused by reentry circuit

  • Class 2. Beta blocker

    reduces heart rate and conduction velocity

    can indirectly alter K and Ca conductance

  • K+ channel blocker

    -increased APD or ERP

    -delay repolarization

    -inhibit reentry tachycardia

  • Ca++ channel blocker

    -slows the rate of rising in phase 4 of SA node

    lowers conduction velocity in SA and AV node

  • Na+ channel blockers

    procainamide, lidocaine, propafenone

  • beta blocker

    propanolol

  • K+ channel blockers

    amiodarone, vernakalant

  • Ca2+ channel blockers

    verapamil and diltiazem

  • blocks potassium channels and prevents repolarization; significantly blocks inactivated sodium channels preventing new AP

    Amiodarone MOA?

  • blocks activated and non-activated L-type calcium channels

    Verapamil and Diltiazem MOA?

  • Vernakalant

    -multichannel blocker (potassium, sodium, etc.)

    -prolongs atrial effective refractory period; used for atrial fibrillation

    -slows AV node conduction

    -No change in ventricular refractory period

  • Propranolol

    nonselective B receptor blocker that acts as full antagonist to decrease heart rate

  • Propafenone

    slow dissociative sodium channel blocker

    -used for supraventricular arrhythmias

  • Procainamide

    -blocks sodium channels; slows AP upstroke, slows conduction, prolongs QRS

    -depresses SA & AV nodes

    -Suppresses abnormal ectopic pacemaker activity

  • Lidocaine

    blocks activated and non-activated sodium channels with rapid kinetics