Medicine & USMLE

Class 1B Antiarrhythmics

Antiarrhythmic Drugs (New)
  1. Adenosine
  2. Class 3 Antiarrhythmics - Dofetilide & Ibutilide
  3. Class 1A Antiarrhythmics
  4. Class 1B Antiarrhythmics
  5. Class 1C Antiarrhythmics
  6. Class 2 Antiarrhythmics
  7. Sotalol
  8. Class 3 Antiarrhythmics - Amiodarone
  9. Class 4 Antiarrhythmics
  10. Digoxin


The class 1B antiarrhythmics are a group of drugs that include lidocaine, mexiletine, and phenytoin. These drugs are used as antiarrhythmics to treat abnormal heart rhythms. They are commonly used to treat ventricular arrhythmias, especially in the context of post-MI arrhythmias or digitalis-induced arrhythmias.

The class 1B drugs primarily act on non-nodal tissue by weakly blocking sodium channels, which causes a weak decrease in the slope of the phase 0 upstroke in the cardiac action potential. This leads to a slowing of conduction in the heart. The class 1B drugs also shorten the AP duration. Notably, these drugs target depolarized tissue in the heart.

Side effects of the class 1B antiarrhythmics include mixed effects on the central nervous system, including both CNS stimulation or CNS depression, depending on the patient. These drugs can also cause general cardiovascular depression, which manifests as a decrease in the heart rate and blood pressure of patients.

Key Points

  • Class 1B Antiarrhythmics
    • Drugs
      • Lidocaine
        • Lidocaine also used as a Local Anesthetic
      • Phenytoin
      • Mexiletine
    • Mechanism
      • Primarily acts at non-nodal cardiomyocytes
        • Phase 0 upstroke is mediated by Ca2+ in nodal tissue, which is less affected by sodium channel blockade
      • Weak sodium (Na+) channel blockade
        • Lowest binding strength (fastest dissociation) among Class 1 AAs; Binding affinity for Na+ receptor is 1C > 1A > 1B
        • Leads to lowest use dependence
          • Use-dependence is a phenomena in which higher rates of depolarization (e.g. high HR) and long dissociation time (e.g. strong binding affinity) lead to accumulated blockade of sodium channel blockade (e.g. compounding effect over several cardiac cycles). This leads to slowing of conduction speed out of proportion to the prolongation of the refractory period.
          • Class 1B have weak binding and fast dissociation, leading to almost no compounding over cycles → less use dependence
        • Slows conduction
          • primarily in non-nodal cardiomyocytes
        • Weak (slight) decrease in slope of phase 0 upstroke
        • Preferentially affects ischemic (depolarized) tissue
          • Ischemic tissue is more depolarized at rest
            • ischemia → low ATP → poor function of Na+/K+ ATPase (see: Klabunde)
          • Class 1B antiarrhythmics like lidocaine thought to prefer binding to inactivated Na+ channels, which are more commonly at depolarized state (see: Tulane)
      • Shortens AP duration
    • Clinical Use
      • Treats ventricular arrhythmias
        • Treats Post-MI (ischemia-induced) arrhythmia
          • Due to selectivity for ischemic or depolarized tissue described above
        • Treats Digitalis-induced arrhythmias
    • Side Effects
      • Cardiovascular depression
      • Mixed CNS effects:
        • CNS Stimulation (alertness, seizures, tremor)
        • CNS Depression (sedation, drowsiness)