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Group 1: Sodium Channel Blockers – Antiarrhythmic Drugs

by Pravin Shukle, MD
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    Let's take a look at how the action potential conducts electricity in and on the cell membrane. The first thing that happens in the first part of the action potential is sodium channel movement followed by calcium channel movement. The sodium channel blockers work on the movement of sodium across the cell. We call this phase 0. Another way of describing this is what we call the upstroke of the action potential. That's where the action potential is moving up. Now, the group 1 antiarrhythmics do have varying effects on the third phase of the action potential which happens later. So, these drugs are what we call "state dependant". So the action of the drug depends on what state the membrane is at. If the membrane is depolarized, it will have one type of action. If it's not depolarized, it will have another type of action. We divide up the group 1 antiarrhytmics into 3 different groups. Let's talk about group 1A. So, group 1A includes drugs like procainamide. Procainamide prolongs the upstroke of the action potential by slowing down or blocking the sodium channel. So you can see now that instead of sodium going directly in in a straight line, we've illustrated as if it's going in in a wavy line. That just shows that the sodium movement is either impaired or slowed. The action potential time is prolonged. So, have a look at the red line here, you can see that the total length or the ERP is prolonged. Now these agents, and this particular group of agents will affect the atria, the purkinje fibres, and the ventricular tissues. We use these drugs in all types of dysrrhythmias, especially during an acute myocardial infarction. The group 1A drugs are also proarrhythmic. That means that they can actually cause...

    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. Iidocaine
    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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