Learning Objective

By the end of this section, medical students should be able to explain the mechanisms of action, clinical indications, pharmacokinetics, and major adverse effects of key unclassified antiarrhythmic agents used to manage supraventricular arrhythmias and torsade de pointes.

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UNCLASSIFIED ANTIARRHYTHMIC DRUGS

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Adenosine

Mechanism of Action

• Activates A₁ adenosine receptors
• Gi protein–coupled receptor activation →
  • ↓ cAMP
  • ↓ Ca²⁺ influx
• Results in:
  • ↓ SA nodal automaticity
  • ↓ AV nodal conduction velocity
  • Transient AV nodal block

Clinical Uses

• Drug of Choice (DOC) for:
  • Paroxysmal Supraventricular Tachycardia (PSVT)
  • AV nodal re-entrant tachycardia (AVNRT)

Pharmacokinetics

Parameter	Feature
Route	IV only
Half-life	< 10 seconds
Onset	Rapid
Duration	Very short

Adverse Effects

• Flushing
• Chest discomfort
• Dyspnea
• Sedation
• Transient asystole

Drug Interactions

• Methylxanthines antagonize adenosine:
  • Theophylline
  • Caffeine

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Magnesium

Clinical Use

• Torsade de pointes

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Activity

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Digoxin

Mechanism of Action

• Inhibits Na⁺/K⁺-ATPase pump
• ↑ Intracellular Na⁺
• ↓ Na⁺/Ca²⁺ exchange
• ↑ Intracellular Ca²⁺
• Enhances vagal tone →
  • ↓ AV nodal conduction
  • ↓ Heart rate

Clinical Use

• Supraventricular tachyarrhythmias
• Rate control in atrial fibrillation

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CLINICAL CORRELATES

Potassium Imbalance

Both electrolyte disturbances can precipitate arrhythmias:

Condition	Effect on Cardiac Rhythm
Hyperkalemia	Conduction abnormalities
Hypokalemia	Increased excitability

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Atrial Fibrillation

The most common cardiac arrhythmia.

Primary Management Goals

• Ventricular Rate Control:
  • Beta blockers
  • Calcium channel blockers
  • Digoxin
• Anticoagulation

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Wolff–Parkinson–White Syndrome (WPW)

Management Strategy

• Block accessory pathway with:
  • Class IA
  • Class III antiarrhythmics

Avoid These Drugs in WPW

• Digoxin ❌
• Beta blockers ❌
• Calcium channel blockers ❌
• Adenosine ❌

⚠️ These drugs slow AV nodal conduction and may increase conduction through the accessory pathway, potentially precipitating ventricular arrhythmias.

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Activity