Antiarrhythmic medications

Vaughan-Williams Classification - The Arrhythmia Orchestra

📌 Mnemonic: Some Block Potassium Channels

-   IA (e.g., Quinidine): Intermediate on/off. ↑Action Potential Duration (APD).
-   IB (e.g., Lidocaine): Fast on/off. ↓APD.
-   IC (e.g., Flecainide): Slow on/off. No APD change.

⭐ Use-Dependence: Class IC drugs show profound effects at faster heart rates. They are contraindicated post-MI and in structural heart disease due to increased mortality risk.

Class I Agents - Salty Situation Stoppers

• Mechanism: Block voltage-gated Na⁺ channels, slowing Phase 0 depolarization. State-dependent, binding best to open/inactivated channels.

• Subtypes & Use-Dependence: (Strongest in IC > IA > IB)

  • IA: Quinidine, Procainamide, Disopyramide. Intermediate block.
    • 📌 Queen Proclaims Diso's pyramid.
  • IB: Lidocaine, Mexiletine. Weak block, fast dissociation. Preferentially affects ischemic tissue.
  • IC: Flecainide, Propafenone. Strong block, slow dissociation.

⭐ CAST Trial: Class IC agents (Flecainide, Propafenone) are contraindicated in structural and ischemic heart disease due to increased mortality.

Class II & IV Agents - Nodal Knockout Crew

• Primary Action: Slow sinoatrial (SA) and atrioventricular (AV) nodal conduction, reducing heart rate.
  • Class II (Beta-Blockers): e.g., Metoprolol. Decrease slope of phase 4 diastolic depolarization.
  • Class IV (Non-DHP CCBs): e.g., Diltiazem, Verapamil. Decrease slope of phase 0 depolarization.
• Core Use: Rate control in atrial fibrillation and atrial flutter.
• Adverse Effects: Bradycardia, AV block, heart failure exacerbation.

⭐ Beta-blockers are first-line for rate control and show a mortality benefit in post-myocardial infarction patients.

Class III Agents - Potassium's Power Play

• Mechanism: Block K+ channels, prolonging repolarization (Phase 3). This action ↑ action potential duration and the QT interval.
• Key Drugs: Amiodarone, Ibutilide, Dofetilide, Sotalol (AIDS).
• ⚠️ Major Side Effect: A prolonged QT interval significantly increases the risk for Torsades de Pointes (TdP).

⭐ Amiodarone exhibits widespread, multi-organ toxicity, affecting the lungs (fibrosis), liver (hepatitis), thyroid (hyper/hypothyroidism), skin (blue-gray discoloration), eyes (corneal deposits), and nervous system (neuropathy).

Miscellaneous Meds - The Odd Squad

• Adenosine
  • Ultra-short half-life (<10s); used to diagnose and terminate SVT.
• Digoxin
  • MOA: Directly inhibits the $Na^{+}/K^{+}$-ATPase pump, increasing intracellular calcium.
  • Toxicity: Cholinergic symptoms (nausea, vomiting), visual disturbances (yellow halos), and life-threatening arrhythmias.
• Magnesium ($Mg^{2+}$)
  • First-line treatment for Torsades de Pointes.

⭐ Adenosine causes transient flushing, chest pain, and a sense of impending doom due to its potent, brief vasodilatory and bronchospastic effects.

High-Yield Points - ⚡ Biggest Takeaways

• Class I drugs exhibit use-dependence; Class IC is strongly proarrhythmic, especially post-MI.
• Class II (beta-blockers) are crucial for rate control in AFib and reduce mortality after myocardial infarction.
• Class III agents (Amiodarone, Sotalol) prolong the QT interval, increasing the risk of Torsades de Pointes.
• Amiodarone carries significant risks of pulmonary fibrosis, thyroid dysfunction, and hepatotoxicity.
• Class IV agents (Verapamil, Diltiazem) control rate in AFib and terminate AVNRT.
• Adenosine is extremely short-acting and used for acute SVT termination.