Flashcards in Pharmacology Lecture 1 -- Antiarrhythmic Drugs Deck (50):
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Class I antiarrhythmic drugs
Sodium channel blockers
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Effect of Class I antiarrhythmic drugs
Reduce automaticity and/or Vmax in fast channel tissue (working ventricular and atrial muscle, His-Purkinje system)
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Class II antiarrhythmic drugs
Beta blockers
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Targetted tissue of Class II antiarrhythmic drugs
Slow channel tissue (sinus and AV nodes)
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Class III antiarrhythmic drugs
Drugs that act predominantly by increasing APD in fast channel tissue (mainly potassium channel blockers)
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Class IV antiarrhythmic drugs
Calcium channel blockers ("calcium antagonists")
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Targeted tissue of Class IV antiarrhythmic drugs
Slow channel tissue
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2 examples of multiaction antiarrhythmic drugs
Sotalol (class II and III action)
Amiodarone (I, II, III, IV action)
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4 mechanisms by which drugs depress slow response action potenttials
Sympathetic antagonism
Vagal enhancement
Calcium channel blockers
Purigenic antagonists
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Define how sympathetic antagonism affects the heart
Beta-adrenergic (sympathetic) stimulation enhances Ca++ curent
Beta-blockers and other sympatholytics remove Ca++ current resulting from adrenergic stimulation
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Define how vagal enhancement affects the heart
Reduces Ca++ entry by both direct and indirect (antisympathetic) mechanisms
Includes physical maneuvers such as Valsalva, carotid sinus massage. Also, digitalis
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Define how calcium channel blockers affect the heart
Directly reduce Ca++ entry through voltage-dependent calcium channel (varapamil, diltiazem)
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Define how purigenic agonists affect the heart
Adenosine or ATP; produce vagal-like effects via purinergic receptor activation
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How to treat tachycardia due to slow tissue reentrant circuit
Block slow channel (increase refractory period) = may block reentry circuit
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How to control ventricular response in the event of atrial fibrillation
Suppress slow channel tissue to enhance filtering function of the AV node
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Ways to terminate AVN reentry
Vagal maneuvers
IV Ca++ channel blockers
IV adenosine
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Ways to prevent AVN reentry
Ca++ channel blockers, digitalis, beta blockers (non extremely effective)
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How to control rate in atrial fibrillation
Ca++ channel blockers
Digitalis
Beta blockers
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2 ways to prevent or terminate sustained tachyarrhythmias
Decrease automaticity
Increase refractory period
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Effect of decreasing automaticity for VT
Suppress extrasystoles which can act as trigger for reetrnat arrhythmias.
Can slow or stop VT due to enhanced automaticity
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The most important determinant of refractory period in fast channel tissue
Action potential duration (APD)
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Effect of decreasing Na+
Can suppress arrhythmias caused by DAD's
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What is the most common cause of the most important ventricular arrhythmias
Reetrant mechanisms
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What are the most important ventricular arrhythmias clinically?
VT associated with chronic coronary artery disease
Ventricular fibrillation
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2 classes of drugs that act predominantly on fast channel tissue
Class I and III
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General function of class I drugs
Decrease automaticity and phase 0 Na+ current in fast channel tissue
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Subcategories of Class I drugs
Class IA
Class IB
Class IC
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3 drugs that belong to class IA
Quinidine**
Disopyramide
Procainamide
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Which Class I drug is no longer used for arrhythmias due to adverse effects?
Class IA
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Define Class IB
Lidocaine** -- voltage-dependent Na+-channel blockers
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Effect of Class IB drugs
Little effect in normal tissues
Depress INa in sick depolarized tissues or automatic cells which depolarize before firing.
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When is Class IB used?
Mainly used in IV for emergency
Effective for automatic, DAD, and EAD arrhythmias (NOT reentrant)
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Define Class IC
Very strong Na+ channel blockers (i.e. flecainide***, propafenone)
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Function of Class IC
Suppress ventricular automaticity, DAD's (suppress APCs, VPCs)
Can terminate or prevent AF
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General function of class III drugs
Increase APD in fast channel tissue
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When are Class III drugs useful?
Reentrant arrhythmias (AF, AFL, some VTs)
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Main risk of using Class III drugs
Acquiring LQTS
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Define ablation
Targeted destruction of arrhythmia-generating tissue
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How is ablation performed?
Under light anesthesia or sedation with transvenous electrode catheters
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What does the effectiveness of ablation depend on?
The ability to identify discrete critical tissue zone
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When is ablation useful?
AV reentry, Atrial flutter > VT >= AF
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What is an implantable defibrillator useful for?
Highly effective in rapid termination of VT/VF
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Most changes in PR interval are due to...
Changes in conduction time through the AV node (largest part of P interval = most subject to change)
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What do longer PR intervals signify?
Slowed AV nodal conduction
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What does longer QRS duration signify?
Slowed ventricular conduction (takes longer to activate ventricles)
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What does a longer QT interval signify?
Longer APD
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What is an indication of effect on SA node?
Degree of heart rate slowing
NOTE: Pause or arrest = toxic effect
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What indicates an effect on AV node
PR interval increase
NOTE: block = toxic effect
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What indicates an effect on ventricular conduction?
Degree of QRS prolongation
NOTE: Excessive (>25%) = toxic
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