Cardiac dysrhythmia, a condition where the heart beats irregularly, is treated by antidysrhythmic drugs. These drugs act in different ways to suppress aberrant heat beating and are often categorized by Vaughan William’s classification which has four classes (I to IV).

Class I

Class I drugs block voltage-gated Na channels. Thus, they target (non-nodal) cardiac cells that utilise these channels to depolarise. In doing so, they decrease domotropy (conduction speed) and protect against the generation of aberrant action potentials. Notably, there are three subdivisions of this class, A to C.Class IA drugs such as quinidine associate and disassociate with the open ion channel in an intermediate rate, blocking it and resulting in prolonged action potentials that also increase the refractory period. This is useful situations like atrial flutter.Class IB drugs such as lidocaine associate/dissociate quickly with and stabilise the inactivated channel. They shorten the action potential and being use-dependant, act best at high heart rates, when the membrane is depolarised during diastole (slowing drug dissociation) and where the action potential is longest.Lastly, rarely used class IC drugs like flecainide associate/dissociate slowly while causing no alteration in the action potential, therefore suppressing ectopic beats. Nevertheless, they tend to suppress everything else as well and therefore are associated with higher mortality rates after myocardial infarction.

Class II

Class II drugs are sympathetic antagonists (beta1-blockers like atenolol). As such they prevent catecholamines of the sympathetic system from overexciting the heart. This is especially critical as damaged heart tissue (e.g. via myocardial infarction) could sensitise the heart to sympathetic innervation where catecholamine stimulation by itself could result in depolarization and ectopic heartbeats.

Class III

Class III drugs such as amiodarone prolong the action potential and therefore the refractory period. Possibly by inhibiting repolarising K+ channels and possibly prolonging Na+ channel inactivation, it slows down the heart rate and especially prevents re-entry and circus dysrhythmias. These dysrhythmias occur when there is impaired conduction in parts of the heart (e.g. due to ischaemia from myocardial infarction). As a consequence, there is disruption to the normal flow and timing of depolarization in the different areas of the heart and one part may be stimulated again by a “re-entry” depolarization that has turned back from downstream tissue in the heart. By prolonging the refractive period, it would be possible to prevent tissue from possibly being stimulated twice resulting in dysrhythmia.

Class IV

Class IV drugs such as verapamil are L-type Ca2+ channel antagonists. Ca channels mediate depolarisation in all parts of the heart, blocking their action would slow conduction and therefore increase refractory period, especially in the AV node. Nevertheless, since Ca entry into cardiomyocytes are fundamental to excitation-contraction coupling, the drug cannot be used when heart function is compromised (e.g. after serious myocardial infarction or cardiogenic shock).