Lidocaine is classified as a sodium channel blocker and is a frequently used antiarrhythmic. Sodium channel blockade increases the refractory period of the cardiac myocyte (24). When cardioplegia is given in an ideal environment without washout, this action is prolonged because the lidocaine remains in adequate concentrations to continually affect the myocardium. Additionally, sodium channel blockade helps counteract the negative effects of a hyperkalemic depolarized arrest by polarizing the cell membrane to some degree and preventing sodium and calcium accumulation within the cell. Depolarized arrest can allow for sodium and calcium accumulation through exchange mechanisms and blocking the sodium channels helps prevent this (30). A 2009 study by O’Brien et al. (31) showed that del Nido cardioplegia reduced calcium accumulation during myocardial ischemia in a setting of a depolarized arrest. It may be helpful to note that del Nido cardioplegia can therefore be classified as a modified depolarizing agent, primarily as a result of the properties of lidocaine and magnesium.