Batch 1: Antiarrhythmics

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⚙️ Mechanism

🏥 Clinical Use

⚠️ Side Effects

💊 Class ID

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Mechanism: Block Fast Na+ Channels (Phase 0). Use dependence (bind active channels).
Class IA (Quinidine, Procainamide, Disopyramide):
- Effect: Intermediate Na+ block + K+ block. Increases AP Duration & QT.
- Toxicity: Cinchonism (Quinidine), Drug-Induced Lupus (Procainamide), Heart Failure (Disopyramide).
Class IB (Lidocaine, Mexiletine):
- Effect: Weak Na+ block. Shortens AP Duration. Best for Ischemic/Depolarized tissue (Post-MI).
- Toxicity: CNS stimulation (tremor, seizure).
Class IC (Flecainide, Propafenone):
- Effect: Strong Na+ block. No effect on AP Duration. Drastically widens QRS.
- Contraindication: Structural/Ischemic heart disease (Proarrhythmic).

Mechanism: Decrease cAMP -> Decrease Ca2+ & Funny currents. Decrease slope of Phase 4. Slows HR.
Clinical: Rate control (AFib), SVT suppression.
Toxicity: Masks hypoglycemia, bronchospasm, AV block.

Mechanism: Block K+ channels -> Prolong Phase 3 Repolarization -> Prolong QT.
Reverse Use Dependence: Bind best at slow heart rates (Risk of Torsades in bradycardia).
Amiodarone: The "dirty" drug (Blocks I, II, III, IV). Low Torsades risk but high organ toxicity:
- Lungs (Fibrosis), Liver (Hepatitis), Thyroid (Hyper/Hypo), Skin (Blue-gray), Eyes (Deposits).
Sotalol/Dofetilide: Pure K+ block. High Torsades risk.

Non-DHPs (Verapamil, Diltiazem): Block L-type Ca2+ channels. Slow Phase 0 in SA/AV nodes.
Toxicity: Constipation (Verapamil), Gingival Hyperplasia, Edema.

Adenosine: Hyperpolarizes AV node (K+ efflux).
Use: SVT termination.
SE: Flushing, Doom. Blocked by Caffeine.
Digoxin: Inhibits Na/K ATPase -> Increases Ca2+ (Contractility). Stimulates Vagus (Slows AV node).
Toxicity: Xanthopsia (Yellow vision). Worsened by Hypokalemia.
Magnesium: First-line for Torsades de Pointes.
Ivabradine: Selectively inhibits Funny current (If). Slows HR without effect on BP/Contractility.
SE: Luminous phenomena.