Verapamil

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Abstract
The advent of intracellular microelectrode recordings has led to an understanding of the ionic changes and mechanisms involved in the cardiac action potential and in cardiac pacemaker function. Direct recordings from the sinus node have led to insight into mechanism of the sinus-node automaticity. An inward (depolarizing) current carried by calcium and sodium ions termed the "slow channel" is believed to play a major role in impulse formation within the sinus node.1 The slow channel is characterized by a slow rate of rise (low change in voltage per unit of change in time) and initiation at lower, less negative levels of membrane potential than the normal fast sodium spike. In addition to the sinus node, the atrioventricular (AV) junction appears to be largely dependent on the slow response for impulse formation and conduction. The slow channel has also been implicated in the genesis of arrhythmias. As it is activated