Pharmacology
Antiarrhythmics — Vaughan-Williams classes
Pharmacology

Antiarrhythmics — Vaughan-Williams classes

Class I (Na channel), II (β-block), III (K channel), IV (Ca channel), plus adenosine, digoxin, ivabradine — when to pick what.

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◆Class IA — moderate Na block + ↑ AP duration

  • •Quinidine, procainamide, disopyramide
  • •Procainamide: AFib with WPW (drug of choice; AVOID AV nodal blockers), stable monomorphic VT
  • •Side effects: drug-induced LUPUS (procainamide, hydralazine, INH), torsades from QT prolongation, GI (quinidine), cinchonism
  • •Quinidine: ↑ digoxin levels (compete for renal clearance)

◆Class IB — weak Na block + ↓ AP duration

  • •Lidocaine, mexiletine
  • •Affinity for ISCHEMIC tissue — post-MI VT/VF
  • •Side effects: CNS (perioral numbness, seizures), don't cause torsades
  • •Lidocaine for stable VT if amiodarone fails or contraindicated

◆Class IC — strong Na block, no AP change

  • •Flecainide, propafenone
  • •Indication: 'pill-in-pocket' for paroxysmal AFib WITHOUT structural heart disease
  • •CONTRAINDICATED in structural heart disease (CAST trial — ↑ mortality post-MI)
  • •Pre-treat with AV nodal blocker (β-blocker or CCB) before — flecainide can convert AFib to AFlutter with 1:1 conduction

◆Class II — β-blockers (covered separately)

  • •Metoprolol, atenolol, esmolol (short-acting IV)
  • •Rate control AFib, ↓ post-MI mortality, prevent SVT recurrence
  • •Esmolol useful for ICU rate control (titratable)

◆Class III — K channel block (↑ AP duration)

  • •Amiodarone — most useful broad-spectrum; effects all classes
  • •Sotalol — also β-blocker; QT prolongation
  • •Dofetilide, ibutilide — used for AFib cardioversion
  • •Amiodarone SIDE EFFECTS: pulmonary fibrosis, hepatotoxicity, hypothyroidism OR hyperthyroidism (both!), corneal microdeposits, photosensitivity, blue-gray skin, neuropathy
  • •Amiodarone INTERACTIONS: ↑ warfarin INR; ↑ digoxin level — halve doses
  • •All Class III can cause TORSADES from QT prolongation (less with amiodarone uniquely)

◆Class IV — non-DHP CCBs

  • •Verapamil, diltiazem
  • •Rate control AFib, terminate SVT (alternative to adenosine)
  • •AVOID in HFrEF (negative inotrope), AVOID in WPW with AFib (worsens)
  • •Verapamil → constipation classic

◆Other / 'class V'

  • •Adenosine: SVT (AVNRT/AVRT) — 6 mg IV push, then 12 mg if needed; very short half-life (~10 sec); CONTRAINDICATED in asthma (bronchospasm)
  • •Digoxin: rate control AFib (esp HF or sedentary); narrow therapeutic index — toxicity = visual changes (yellow halos), AV block, arrhythmias; ANTIDOTE = digoxin-specific Fab
  • •Ivabradine: ↓ HR via funny channel (SA node); HF with sinus rhythm + HR >70 despite max β-blocker
  • •Magnesium: torsades de pointes treatment

Pick the antiarrhythmic

ScenarioFirst-line
AFib with WPWProcainamide (AVOID AV nodal blockers)
Stable VT with structural heart diseaseAmiodarone
Post-MI VTLidocaine (or amiodarone)
TorsadesIV magnesium
SVT — pharmacologic conversionAdenosine
AFib rate control (HFrEF)Carvedilol or metoprolol succinate (not CCB)
AFib rate control (no HF)β-blocker or diltiazem
Paroxysmal AFib, no structural diseaseFlecainide (pill-in-pocket)
HF + sinus + HR > 70Ivabradine added to GDMT

High-yield pearls

  • ◆Amiodarone has effects in ALL 4 classes — that's why it's the broad-spectrum choice
  • ◆Class IC (flecainide) NEVER in structural heart disease (CAST trial: ↑ mortality)
  • ◆Procainamide for AFib + WPW; never adenosine/β-blocker/CCB/digoxin (preferentially conducts down accessory pathway → VF)
  • ◆Adenosine + asthma = bronchospasm (CONTRAINDICATED). Use diltiazem or β-blocker for SVT instead
  • ◆Digoxin toxicity: yellow halos, AV block, hyperK; treat with digoxin-specific Fab
  • ◆Amiodarone pre-start workup: TSH, LFTs, CXR, PFTs (DLCO); monitor q6mo
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