Cardiac Arrythmogenosis and conductance + Antiarrythmics

What are the two types of cardiac action potentials?

Pacemaker action potentials and ventricular (muscle) action potentials.

What ion is responsible for Phase 0 in ventricular action potentials?

Sodium (Na+).

What occurs during Phase 2 of the ventricular action potential?

Calcium (Ca2+) influx through L-type Ca2+ channels creating the plateau phase.

What maintains resting membrane potential in cardiomyocytes?

IK1 potassium channels.

What triggers calcium-induced calcium release (CICR)?

Ca2+ influx through L-type Ca2+ channels during Phase 2.

What are early afterdepolarisations (EADs) associated with?

K+ channel blockade during phase 2 or 3.

What are delayed afterdepolarisations (DADs) associated with?

Ca2+ overload, e.g., digoxin toxicity.

What defines re-entry arrhythmias?

Self-perpetuating circuits due to heterogeneous conduction and recovery times.

What are examples of supraventricular arrhythmias?

Atrial fibrillation, atrial flutter, sinus tachycardia, AV blocks.

What are examples of ventricular arrhythmias?

Ventricular tachycardia, ventricular fibrillation, ventricular premature beats.

What is the Vaughan Williams classification based on?

Mechanism of action of antiarrhythmic drugs.

What is the Sicilian Gambit classification based on?

Pathophysiological mechanism of arrhythmias and drug action.

Class IA antiarrhythmic effect?

Moderate Na+ channel block, prolong repolarization, increase AP duration.

Class IB antiarrhythmic effect?

Weak Na+ channel block, shorten repolarization, little effect on APD.

Class IC antiarrhythmic effect?

Strong Na+ channel block, minimal effect on repolarization.

Class II antiarrhythmic effect?

β-blockers; decrease sympathetic activity, reduce HR and conduction through AV node.

Class III antiarrhythmic effect?

K+ channel blockers; prolong repolarization and AP duration.

Class IV antiarrhythmic effect?

Ca2+ channel blockers; slow AV node conduction.

What is Torsades de Pointes?

A polymorphic ventricular arrhythmia associated with prolonged QT interval.

Which classes of drugs are commonly linked to Torsades de Pointes?

Class III (K+ blockers) and Class IA antiarrhythmics.

What does use-dependent blockade mean?

Preferential drug binding to ion channels in depolarized (active) states.

Which drugs show use-dependent Na+ channel blockade?

Quinidine, procainamide, disopyramide, lidocaine, flecainide.

What does reverse use-dependence mean?

More pronounced effect at slow heart rates.

Example of a drug with reverse use-dependence on K+ channels?

Quinidine and sotalol.

Key concept behind proarrhythmia risk?

Drug-induced arrhythmias, especially with QT prolongation and electrolyte imbalance.