Learning Objectives By LessonBradyarrhythmia Mechanisms
- Describe the main mechanisms accounting for bradyarrhythmias
- Identify the phases of sinus node action potential
- Describe the underlying mechanism for sinoatrial exit block
Tachyarrhythmia Mechanisms (Part 1)
- Describe the main mechanisms accounting for tachyarrhythmias
- Describe how abnormal automaticity can result in tachyarrhythmias
- Describe how triggered activity can result in tachyarrhythmias
- Describe the difference early and delayed afterdepolarizations
- Idenitfy common associations with early and delayed afterdepolarizations
Antiarrhythmic Drug Classification
- Describe and identify different aspects of a cardiomyocyte action potential
- Describe and identify different aspects of a pacemaker cell action potential
- Assign antiarrhythmic drugs (AADs) to their associated Vaughan-Williams class
- Describe the differences in kinetics amongst class I antiarrhythmic drugs (AADs)
- Describe the mechanism of action of each antiarrhythmic drug (AAD) class
- Identify the action potential phases each antiarrhythmic drug (AAD) class effects
- Describe the effect of each antiarrhythmic drug (AAD) class on the action potential
- Describe the effect of each antiarrhythmic drug (AAD) class on the ECG
Antiarrhythmic Proarrhythmia Mechanisms
- Define proarrhythmia in relation to antiarrhythmic drugs (AADs)
- Describe three proarrhythmia mechanisms of antiarrhythmic drugs (AADs)
- Identify key components for scar-mediated reentry arrhythmias
- Describe how slow conduction can contribute to scar-mediated reentry arrhythmias
- Describe how class I and III antiarrhythmic drugs (AADs) can influence conduction in scar-mediated reentry arrhythmias
- Describe how prolonged repolarization can be proarrhythmic
- Describe the mechanism for pause-dependent polymorphic ventricular tachycardia (VT)
- Describe how intracellular calcium overload can be proarrhythmic
- Describe the mechanism for pause-independent bidirectional ventricular tachycardia (VT)
- Identify triggers for intracellular calcium overload arrhythmias
- Describe the differential diagnosis for bidirectional ventricular tachycardia (VT)
- Describe the mechanism for digoxin-induced bidirectional ventricular tachycardia (VT)
- Identify an electrolyte abnormality that can potentiate the effect of digoxin
- Describe the mechanism for catecholaminergic polymorphic ventricular tachycardia (CPVT)
Antiarrhythmic Rate Dependence
- Describe the modulated receptor hypothesis of cardiac ion channels
- Describe the difference between use dependence and reverse-use dependence
- Identify antiarrhythmic drugs (AADs) with use dependence properties
- Identify antiarrhythmic drugs (AADs) with reverse-use dependence properties
- Describe the mechanism of action of class Ic antiarrhythmic drugs (AADs)
- Describe the mechanism of action of class III antiarrhythmic drugs (AADs)
- Describe the clinical utility of class Ic antiarrhythmic drugs (AADs)
- Describe the clinical utility of class III antiarrhythmic drugs (AADs)
- Describe the proarrhythmic risk of class 1c antiarrhythmic drugs (AADs)
- Describe the proarrhythmic risk of class 1c antiarrhythmic drugs (AADs)
- Describe how to monitor class 1c antiarrhythmic drugs (AADs)
- Describe how to monitor class 1c antiarrhythmic drugs (AADs)
- Describe the rate dependence of amiodarone
- Describe the clinical utility of class Ib antiarrhythmic drugs (AADs) during myocardial ischemia
Antiarrhythmic Metabolism & Interactions
- Identify major routes of antiarrhythmic drug (AAD) elimination
- Identify renally eliminated antiarrhythmic drugs (AADs)
- Identify antiarrhythmic drugs (AADs) that act as metabolizers and inhibitors of cytochrome P450 2D6
- Identify antiarrhythmic drugs (AADs) that act as metabolizers, inhibitors, and inducers of cytochrome P450 3A4
- Describe the effects from co-administration of amiodarone with warfarin, digoxin, tacrolimus, and cyclosporine
- Identify drugs to avoid co-administering with class Ia and III antiarrhythmic drugs (AADs) due to their QT prolonging effects
Antiarrhythmic Selection & Monitoring
- Describe the antiarrhythmic drug (AAD) selection approach for atrial fibrillation (AF) management
- Identify the ideal patient candidate in which a class Ic antiarrhythmic drug (AAD) might be considered for atrial fibrillation (AF) management
- Identify the ideal patient candidate in which dofetilide or sotalol might be considered for atrial fibrillation (AF) management
- Identify the ideal patient candidate in which amiodarone might be considered for atrial fibrillation (AF) management
- Describe the antiarrhythmic drug (AAD) selection approach for ventricular tachycardia (VT) management
- Describe the baseline and follow-up monitoring approach for class Ic antiarrhythmic drugs (AADs) flecianide and propafenone
- Describe the baseline and follow-up monitoring approach for class III antiarrhythmic drugs (AADs) dofetilide, sotalol, and amiodarone
Contributors: Anthony Kashou, MD; Mahmoud Ismayl, MD; Khalid Saeed Al-Asad, MD; Adnan Halboni, MD; Adolfo Martinez Salazar, MD; Nandan Anavekar, MBBCh
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