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  1. Arrhythmias may require treatment because rhythms that are too rapid, too slow, or asynchronous can reduce cardiac output.
  2. Cardiac arrhythmias are a common problem in clinical practice, occurring in up to 25% of patients treated with digitalis, 50% of anesthetized patients, and over 80% of patients with acute myocardial infarction.
  3. Some arrhythmias can precipitate more serious or even lethal rhythm disturbances; for example, early premature ventricular depolarizations can precipitate ventricular fibrillation. In such patients, antiarrhythmic drugs may be lifesaving.
  4. On the other hand, the hazards of antiarrhythmic drugs—and in particular the fact that they can precipitate lethal arrhythmias in some patients— has led to a reevaluation of their relative risks and benefits. In general, treatment of asymptomatic or minimally symptomatic arrhythmias should be avoided for this reason.

Cardiac action potential

  • Important to learn basis of various events in cardiac action potential
  1. Phase-0: Na+ entry                          
  2. Phase-1: brief K+ exit
  3. Phase-2: Calcium entry (plateau phase) as well as potassium exit    
  4. Phase-3: potassium exit (prolonged)
  5. Early phase (early after depolarization: disturbance leads to torsa de depointes)
  6. Late phase (delayed after depolarization)


cardiac action potential

There is an abnormality in the site of origin of the impulse, its rate or regularity, or its conduction. However, all arrhythmias result from:

(1) Disturbances in impulse formation,

(2) Disturbances in impulse conduction, or

(3) Both.


Classification-Vaughen-William-Singh’1988 (mnemonic: SoBePoCa)

  1. Class-I (Na+Channel blockers)
    1. 1a-Qunidine, procainamide, disopyramide (QPD)
    2. 1b-Lidocaine, phenytoin, tocainide, mexilitine (Leave PMT)
    3. 1c-Encainide, flecainide, propafenone, moricizine
  2. Class-II- Beta blockers
    1. Metprolol                      
    2. Propanolol          
    3. ​Esmolol
  3. Class-III-K+ Channel blockers (ABDIS)
    1. Amiodarone        
    2. Dronaderone              
    3. Ibutilide              
    4. Doefetilide           
    5. Bretylium                    
    6. Sotalol                  
    7. Verenakalant
  4. Class-IV-CCBs
    1. Verapamil                    
    2. ​Diltiazem
  5. Class-V-Miscellaneous
    1. Adenosine                    
    2. Amrinone                    
    3. Milrinone            
    4. Potassium                              
    5. Magnesium                
    6. Digoxin        

Electrophysiological properties:

  • 1a & class-III have similar electrophysiological properties (delayed ventricular repolarization, prolonged QT, increase in APD)
  • 1b-increase or decrease ERP
  • 1c-have no effect on ERP/APD

General properties of antiarrhythmic

  1. Suppress conduction in fast conducting cardiac tissues
  2. Reduce conduction in aberrant tissues (e.g. WPW)
  3. Prevent reentry (MC mechanism of cardiac arrhythmias)
  4. Reduce automaticity
  5. Bind to Na+ channels tightly in presence of ischemia (e.g. lidocaine)
  6. All except lidocaine have proarrhythmic acivity  


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