Understanding Antiarrhythmics: from cell to bed side

posted Jan 25, 2017, 11:23 PM by sourav ghosh
Praloy Chakraborty
Associate Professor, Cardiology, Vardhman Mahavir Medical College and Safdarjang Hospital, New Delhi, India

Although antiarrhythmics have versatile mechanisms of action, they suppress arrhythmias either by preventing enhanced automaticity or by altering the electrophysiological properties of reentrant pathways. Inhibition of reentry occurs due to reduction of conduction velocity or due to increase in the refractory period. Sodium channel blockers(Class I agents) reduce the conduction velocityof fast conducting tissue(i.e Ventricular Myocardium, accessory pathways)where as calcium channel antagonists exerts action by slowing conduction through slow conducting tissue(i.e AV node). So, Sodium channel antagonists terminate accessory pathway dependent reentry (AVRT) as well as atrial and ventricular tachycardias whereas calcium channel antagonists terminate AV node dependant tachycardias. Calcium channel antagonists also inhibit after depolarization induced triggered activities. Repolarization blocking agents(Class III agents), by prolonging the action potential duration, increase the refractory period of reentry circuit and terminate large numbers of atrial and ventricular tachyarrhythmias.Beta blockers block multiples steps in arrhythmogenesis. Other AV nodal blocking agents block AV node directly or via vagomimetic action and terminate AV node dependent tachyarrhythmias.