Presented by Dr. Declan McKernan
Contact: declan.mckernan@universityofgalway.ie
Course: PM309 Cardiovascular Drugs
Describe targets and mechanisms of action of major classes of anti-dysrhythmic drugs with named examples.
Compare and contrast mechanisms of action, pharmacokinetics, and side effects of these drugs with named examples.
Action Potential Patterns:
Lengthened, shortened, and unchanged potentials observed with various drug actions.
Class | Effect | Membrane Effect | Examples |
---|---|---|---|
IA | QRS and Q-T interval | Sodium & Potassium channel block | Quinidine, Procainamide, Disopyramide |
IB | Q-T interval | Sodium channel block | Lidocaine, Mexiletine |
IC | QRS interval | Sodium channel block | Flecainide, Propafenone |
II | Heart rate; P-R interval | Beta-adrenergic receptor inhibition | Propranolol |
III | Q-T interval | Potassium channel block | Amiodarone, Sotalol |
IV | Heart rate; P-R interval | Calcium channel block | Verapamil, Diltiazem |
Other | P-R interval; Q-T inhibition | Na+, K+-ATPase inhibition | Digoxin, Adenosine |
Class I examples: Flecainide (Na+ blocker)
Class II examples: Propranolol (b-receptor antagonist)
Class III examples: D-sotalol (K+ blocker)
Class IV examples: Verapamil (Ca+ blocker)
Sinus Tachycardia: Propranolol
Sinoatrial Reentrant Tachycardia: Verapamil
AV Nodal Reentrant Tachycardia: IV Verapamil, IV Diltiazem
Atrial Fibrillation: IV Procainamide, IV Ibutilide
Ventricular Tachycardia: Lidocaine, IV Procainamide
Mechanism of Action: Block voltage-sensitive Na+ channels.
Effects: Decreased automaticity and upstroke velocity, prolonged effective refractory period.
Mechanism: Moderate block on open Na+ channels; also blocks K+ channels.
Examples: Quinidine, Procainamide, Disopyramide.
Side Effects: Diarrhea, nausea, drug interactions (e.g., digoxin).
Mechanism: Bind to open/inactivated Na+ channels, mild block.
Examples: Lidocaine, Mexiletine.
Clinical Use: Emergencies for ventricular arrhythmias only; safe in prolonged QT syndrome.
Mechanism: Most potent Na+ channel blockers.
Risk: Can worsen existing arrhythmias; used only in life-threatening situations.
Mechanism: B-adrenergic receptor blockade; decreases sympathetic influence on SA and AV nodes.
Examples: Propranolol, Atenolol.
Clinical Uses: Tachycardias induced by physical/emotional stress.
Mechanism: Block K+ channels, prolong plateau, and repolarization.
Example: Amiodarone (also has Class I, II, IV activities).
Mechanism: Block Ca2+ channels in nodal tissues to decrease conduction velocity.
Examples: Verapamil, Diltiazem.
Notable Drugs:
Amiodarone: 200-400 mg daily; hepatic metabolism; long half-life (~53 days).
Digoxin: 0.25 mg; renal elimination; 20-30% bioavailability.
Class I: Block Na+ channels; decrease automaticity and arrhythmia risk.
Class II: Inhibit sympathetic input at pacemaker cells.
Class III: Prolong repolarization by blocking K+ channels.
Class IV: Block Ca2+ channels, impacting conduction in nodal tissues.