Medicine & USMLE

Class IB Antiarrhythmics

Cardiovascular Pharm (Old)
  1. Adenosine
  2. Magnesium
  3. Nitroprusside
  4. Nitrates
  5. Ivabradine
  6. Digoxin/Digitalis
  7. Class IA Antiarrhythmics
  8. Class IB Antiarrhythmics
  9. Class IC Antiarrhythmics
  10. Class II Antiarrhythmics
  11. Class III Antiarrhythmics - Amiodarone
  12. Class III Antiarrythmics - Sotalol
  13. Class III Antiarrhythmics - Ibutilide, Dofetilide
  14. Class IV Antiarrhythmics - Verapamil, Diltiazem
  15. HMG-CoA Reductase Inhibitors (Statins)
  16. Ezetimibe
  17. Fibrates
  18. PCSK9 Inhibitors (Alirocumab, Evolocumab)
  19. Fish Oil and Omega-3s
  20. Milrinone
  21. Aliskiren
  22. Hydralazine
  23. Ranolazine
  24. Sacubitril


Lidocaine and Mexiletine are Class 1B antiarrhythmics. Class 1B drugs, like all other Class 1 antiarrhythmics, block sodium channels in the heart. It’s worth noting that Class 1B drugs have the lowest use dependence of all class 1 drugs, because they bind sodium channels weakly and therefore dissociate or fall off from those channels quickly. In addition, class 1b antiarrhythmics have a preference for inactivated sodium channels in depolarized tissue. These properties of the class 1B drugs make them extremely useful in treating post-MI arrhythmias. Patients taking lidocaine or mexiletine may experience CNS side effects like tremor, dizziness, and seizures, as well as some degree of cardiovascular depression.

Key Points

  • Class 1B Antiarrhythmics
    • Drugs
      • Lidocaine
        • Lidocaine also used as a Local Anesthetic
      • Mexiletine
    • Mechanism
      • Block Sodium (Na+) channels
        • Prolong phase 0 depolarization in non-nodal cardiomyocytes (rhythm control)
          • Phase 0 upstroke is mediated by Ca2+ in nodal tissue, which is less affected by sodium channel blockade (less effective for rate control)
        • Lowest binding affinity (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
        • Selective for ischemic tissue (depolarized cells)
          • 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)
      • May also decrease effective refractory period (ERP)
        • Due to small effect on potassium channels
    • Clinical Use
      • Post-MI (ischemia-induced) arrhythmias
        • Due to selectivity for ischemic or depolarized tissue described above
      • Digitalis-induced arrhythmias
    • Adverse Effects
      • Cardiovascular depression
      • CNS effects (tremor, seizures, drowsiness, altered mental status)