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