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Group 1: Sodium Channel Blockers – Antiarrhythmic Drugs

by Pravin Shukle, MD
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    About the Lecture

    The lecture Group 1: Sodium Channel Blockers – Antiarrhythmic Drugs by Pravin Shukle, MD is from the course Cardiovascular Pharmacology. It contains the following chapters:

    • Group 1: Antiarrhythmics
    • Group 1A: Antiarrhythmics
    • Group 1B: Antiarrhythmics
    • Group 1C: Antiarrhythmics

    Included Quiz Questions

    1. a drug that has one action on a membrane that is depolarized, and another on a membrane that is not.
    2. acts on two parts of the action potential at the same time.
    3. has an increased activity after depolarization.
    4. acts differently depending upon the altitude of the state in which the patient lives.
    1. prolong the action potential by blocking sodium channels.
    2. shorten the action potential by blocking sodium channels.
    3. shorten the action potential by blocking calcium channels.
    4. prolong the action potential by blocking calcium channels.
    1. amiodarone
    2. procainamide.
    3. disopyramide.
    4. quinidine.
    1. can be inadvertently initiated by group 1A anti-arrhythmic drugs, and is treated with quinidine.
    2. can be inadvertently initiated by quinidine, and is treated with group 1A anti-arrhythmic drugs.
    1. will preferentially affect ischemic cells.
    2. will preferentially affect normal tissues.
    3. will preferentially affect depolarized tissues.
    4. will preferentially affect purkinje fibres.
    1. Type 1B anti-arrhythmic agents do not act as pro-arrhythmic drugs.
    2. Lidocaine can be used in arrhythmia in ischemic tissues.
    3. Procainamide can be used to treat digitalis induced arrhythmia.
    4. Mexeletine can be used to treat chronic arrhythmia.
    1. flecanide.
    2. mexeletine
    3. procainamide.
    4. lidocaine
    1. low potassium increases digoxin toxicity, high potassium increases procainamide toxicity.
    2. low potassium increases both procainamide and digoxin toxicity.
    3. high potassium increases both procainamide and digoxin toxicity.
    4. high potassium increases digoxin toxicity, low potassium increases procainamide toxicity.

    Author of lecture Group 1: Sodium Channel Blockers – Antiarrhythmic Drugs

     Pravin Shukle, MD

    Pravin Shukle, MD


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