The term ‘arrhythmia’ refers toany change from the normal sequence of electrical impulses of heart. Theelectrical impulses may happen too fast, too slowly or erratically. A heartbeattoo fast is called tachycardia and a heartbeat too slow is calledbradycardia. The four main types ofarrhythmias are premature (extra) beats, supraventricular arrhythmias,ventricular arrhythmias and bradyarrythmias 1. The types ofarrhythmias and their mechanisms is mentioned in Table 1.
1 2 . Table 1.1 Arrhythmia Common mechanism Premature atrial, nodal or ventricular depolarisations Unknown Atrial fibrillation Disorganised functional re-entry Atrial flutter Stable re-entrant circuit in the right atrium Atrial tachycardia Enhanced automaticity, DAD-related automaticity, or re-entry in atrium AV nodal re-entrant tachycardia (PSVT) Re-entrant circuit within or near AV node Ventricular tachycardia Re-entry near the rim of the healed MI or DADs triggered by increased sympathetic tone.
Ventricular fibrillation Disorganised re-entry The therapy of arrhythmia begins with properdiagnosis, since many pharmacological interventions are themselves arryhthmogenic3. Despite the emergence of several forms of nonpharmacologicaltherapy for cardiac arrhythmias, antiarrhythmic drugs play an important role inits management 4. Antiarrhythmic drugs (AADs) suppress cardiacarrhythmias through their effects on various ion channels and receptors 5.AADs have been classified by Vaughan Williams and Singh based on the primaryelectrophysiological action of the drug that may severe to indicate the typesof clinical effects and therapeutic utility. The classes of drugs with theiraction is given in Table 1.2 6 . Table 1.
2 Class Actions I. Membrane stabilising agents (Na+ channel blockers) II. Antiadrenergic agents III. Agents widening AP IV. Calcium channel blockers The benefit of antiarrhythmictherapy is reduction of arrhythmia related symptoms and reduction in long-termmortality in asymptomatic patients 7. But ADA carries with it anumber of risks like proarrhythmias and systemic toxicity.
Aggravation ofarrhythmias is a common complication of of antiarrhtymatic drugs therapy.Patients with a history of congestive heart failure or any heart disease are ata greater risk and AADs should be used cautiously in them 8. Therefore the goals ofpharmacologic therapy of cardiac arrhythmia are to provide the maximum benefitin terms of arrhythmia suppression while maintaining patient’s safety 4.To accomplish these goals, a deliberate treatment strategy guided by themorphological criteria of the arrhythmia modified by the rate and duration ofcomplexes, noting symptoms and adhering to the guidelines of AHA/ACC 2017 forthe management of arrhythmias is desirable9.