USMLE

Class II Antiarrhythmics

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Cardiovascular Pharm
  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

Summary

The Class 2 antiarrhythmics describe beta-blockers that are used to treat arrhythmias of the heart in the acute setting. Just like all other beta-blockers, these drugs end with the suffix -lol, as in: metoprolol, atenolol, carvedilol and esmolol.

These drugs work as antiarrhythmics mainly by blocking beta-1 signaling at nodal tissue in the heart, especially the AV node. Blocking beta-1 signaling results in decreased calcium levels, which inhibits the nodal action potentials. This reduces pacemaker rate and AV nodal conduction, making beta-blockers good drugs for rate control in arrhythmias like atrial fibrillation. A side effect to watch out for in the acute use of beta-blockers is bronchospasm, so these drugs should be avoided in patients with COPD or asthma.

Key Points

  • Class 2 Antiarrhythmics
    • Drugs
      • Beta-Blockers
        • Includes all drugs that target beta-1 receptors, including
          • Beta-1 selective (atenolol, esmolol, metoprolol)
          • Beta-2 and beta-2 non-selective (timolol, propranolol)
          • Combined alpha and beta (carvedilol, and labetalol)
    • Mechanism
      • Beta-1 receptor blockade
        • Decrease SA/AV nodal activity (rate control)
          • Blocking beta-1 receptors prevents Gs cascade, reducing cAMP and decreasing Ca2+ currents
          • Reduces slope of phase 4 (and phase 0) at nodal tissue, since nodal tissue has Ca2+-dependent action potentials (see: CV Pharmacology)
    • Clinical Use
      • Ventricular rate control
        • Supraventricular arrhythmias
          • E.g. atrial fibrillation/flutter
    • Adverse Effects
      • Acute effects more important than chronic effects for antiarrhythmic function
      • Cardiovascular Depression (e.g. bradycardia, AV block)
        • Due to beta-1 receptor blockade at heart
      • Bronchospasm
        • Due to beta-2 receptor blockade at bronchioles
        • May lead to acute exacerbation of COPD and Asthma
      • Unopposed alpha agonism
        • Does not affect combined alpha and beta blockers (carvedilol and labetalol)
        • Severe vasoconstriction (esp. at coronary arteries) and hypertension seen in pheochromocytoma or cocaine toxicity
        • May worsen vasospasm (Prinzmetal angina)