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Rapid Review·Cardiovascular

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PHARMACOLOGY

T2High yield

Class I Antiarrhythmics

FA P326

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Focus on

Three subclasses of sodium channel blocker, ranked by how tightly they bind.

Key takeaways

How sodium channel blockers work

Class I mechanism

slow or block conduction, especially in depolarized cells, by reducing the slope of phase 0.

State-dependent, so stronger at faster heart rates

a faster rate shortens diastole, so sodium channels spend less time in the resting state where the drug dissociates.

The binding-strength ranking

the effect is most pronounced in IC > IA > IB. "Fast taxi CAB." The full mnemonic scene is on the class I antiarrhythmics mnemonic.

The three subclasses, compared on the action potential

Class IA effect on the ventricular action potential: moderate sodium blockade reduces the slope of phase 0, and accompanying potassium blockade prolongs the action potential duration, so repolarization is later than the untreated grey trace. This is what lengthens the QT and creates the torsades risk.
What this shows
Class IA effect on the ventricular action potential: moderate sodium blockade reduces the slope of phase 0, and accompanying potassium blockade prolongs the action potential duration, so repolarization is later than the untreated grey trace. This is what lengthens the QT and creates the torsades risk.
Class IB effect on the ventricular action potential: weak sodium blockade slightly reduces the slope of phase 0, and the action potential duration is shortened relative to the untreated grey trace, repolarizing earlier.
What this shows
Class IB effect on the ventricular action potential: weak sodium blockade slightly reduces the slope of phase 0, and the action potential duration is shortened relative to the untreated grey trace, repolarizing earlier.
Class IC effect on the ventricular action potential: strong sodium blockade markedly reduces the slope of phase 0, while the action potential duration is essentially unchanged from the untreated grey trace.
What this shows
Class IC effect on the ventricular action potential: strong sodium blockade markedly reduces the slope of phase 0, while the action potential duration is essentially unchanged from the untreated grey trace.

Class IA, quinidine, procainamide, disopyramide

"The queen proclaims Diso's pyramid."
  • Moderate sodium blockade, plus some potassium blockade, so AP duration, ERP and QT all lengthen.
  • Use: both atrial and ventricular arrhythmias, especially reentrant and ectopic SVT and VT.
  • Adverse: cinchonism (headache, tinnitus) with quinidine, a reversible SLE-like syndrome with procainamide, heart failure with disopyramide, thrombocytopenia, and torsades from the long QT.

Class IB, lidocaine, mexiletine

"I'd Buy Liddy's Mexican tacos."
  • Weak sodium blockade (it dissociates easily), and it shortens AP duration. Preferentially affects ischemic or depolarized Purkinje and ventricular tissue, which is why it targets damaged myocardium.
  • Use: acute ventricular arrhythmias, especially post-MI, and digitalis-induced arrhythmias. "IB is Best post-MI."
  • Adverse: CNS stimulation or depression, cardiovascular depression.

Class IC, flecainide, propafenone

"Can I have fries, please?"
  • Strong sodium blockade with minimal effect on AP duration. Significantly prolongs ERP in the AV node and accessory bypass tracts, but has no effect on ERP in Purkinje and ventricular tissue.
  • Use: SVTs including atrial fibrillation, and only as a last resort in refractory VT.
  • Adverse: proarrhythmic, especially post-MI, so it is contraindicated in structural and ischemic heart disease. "IC is Contraindicated."
Class IA vs IB vs IC
FeatureIAIBIC
DrugsQuinidine, procainamide, disopyramideLidocaine, mexiletineFlecainide, propafenone
Sodium blockadeModerateWeakStrong
AP durationLengthenedShortenedMinimal change
QTLengthenedUnchangedUnchanged
UseAtrial and ventricular: reentrant and ectopic SVT and VTAcute ventricular arrhythmias post-MI, digitalis-inducedSVTs including AF; last resort in refractory VT
Signature toxicityCinchonism (quinidine), drug-induced lupus (procainamide), torsadesCNS stimulation or depressionProarrhythmic, contraindicated post-MI
A patient on quinidine develops tinnitus and headache; another on procainamide develops a malar rash and arthralgia. Name each toxicity.

Cinchonism for quinidine, drug-induced lupus for procainamide. Both are class IA, and both also prolong the QT.

How it's tested

The two rules that carry most questions are IB is Best post-MI and IC is Contraindicated in structural or ischemic heart disease, where the CAST trial showed increased mortality. Beyond that, the subclasses are separated by their effect on the action potential duration: IA prolongs it, which is why quinidine and procainamide cause torsades, IB shortens it, and IC leaves it unchanged while slowing conduction the most. Procainamide's own vignette is drug-induced lupus, and quinidine's is cinchonism.

Go deeper

First Aid 2026 — CV/Pharmacology (p.326) · B&B — Class I antiarrhythmics · Mehlman — HY Cardio (IA/IB/IC, post-MI arrhythmia)

High-yield images4
Sketchy-style mnemonic scene for the class I antiarrhythmics, with the IA, IB and IC floors of the building each carrying the drug names and toxicities for that subclass, including the quinidine, procainamide and disopyramide cues on the IA floor and the WPW and proarrhythmia cues on the IC floor.
Class IA effect on the ventricular action potential: moderate sodium blockade reduces the slope of phase 0, and accompanying potassium blockade prolongs the action potential duration, so repolarization is later than the untreated grey trace. This is what lengthens the QT and creates the torsades risk.
Class IB effect on the ventricular action potential: weak sodium blockade slightly reduces the slope of phase 0, and the action potential duration is shortened relative to the untreated grey trace, repolarizing earlier.
Class IC effect on the ventricular action potential: strong sodium blockade markedly reduces the slope of phase 0, while the action potential duration is essentially unchanged from the untreated grey trace.

Flashcards for this page

Card 1 of 5 · try-out only, nothing is saved

What is the difference regarding Na+ channel blocking properties among class IA, IB, and IC antiarrhythmics?

Class IA → (...) blocking
Class IB → (...) blocking
Class IC → (...) blocking
PreviousDigoxinNextClass II & III Antiarrhythmics

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