Phase 0 of the action potential: sodium in working muscle versus calcium in the nodes

Phase 0 is the rapid upstroke of the action potential, the first rise in voltage that starts the brief electrical signal a heart cell fires.

Working atrial and ventricular muscle uses the fast action potential. Its phase 0 begins when voltage-gated sodium channels (pores in the cell membrane that open when the voltage changes) let sodium rush in, and the membrane potential swings positive.

The sinoatrial (SA) node, the heart's natural pacemaker, is the small cluster of cells in the right atrium that sets the heart rate. The atrioventricular (AV) node is the relay that delays the signal on its way to the ventricles. Both use the slow action potential, and their cells have few fast sodium channels. Instead, phase 0 is carried by L-type calcium channels (voltage-gated channels that open when the voltage changes and let calcium in).

Nodal cells also lack a stable resting voltage. Their phase 4, the slow upward drift between beats, is driven mainly by the "funny" current (an inward current of sodium and potassium), which gives the node automaticity, the ability to fire without an outside signal. That drift sets the timing between beats, but it does not produce the phase 0 upstroke.

Antiarrhythmic drugs (drugs for heart rhythm problems) that block sodium channels are class I in the Vaughan-Williams classification (the standard way of grouping antiarrhythmic drugs by the channel or receptor they act on), and they act mainly on working muscle, where they slow phase 0. Verapamil and diltiazem, the non-dihydropyridine calcium channel blockers (the group that acts on the heart's nodes), block the L-type channels instead, so the node fires less often and the heart rate falls. At the AV node the same block slows conduction (the spread of the electrical impulse from cell to cell).