rapidly blocks both activated & inactivated but not resting Na channels (cf quinidine which mainly blocks activated channels)
Thus, >50% of unblocked Na channels become blocked during each action potential in those cells with long plateaus & thus long periods of inactivation (ie. Purkinje fibers & ventricular cells).
During diastole, most of the Na channels in normally polarised cells rapidly become drug free & since it may shorten APD, diastole may be prolonged, thereby extending time for recovery resulting in little effect in normal cardiac cells.
In contrast, ischaemic depolarised cells where Na channels are inactivated remain largely blocked during diastole & more may become blocked.
Thus it suppresses electrical activity of the depolarised, arrythmogenic tissue.
It is NOT effective in arrythmias originating in normally polarised cells such as AF.
It exacerbates ventricular arrhythmias in < 10% of pts.
It ppts SA nodal standstill or worsens impaired conduction in 1% of pts with AMI.
It also may cause hypotension in high doses due to -ve inotropic activity.