The cardiac transmembrane potential consists of five phases:

1. Phase_0: upstroke or Rapid Depolarisation

The upstroke of the cardiac action potential in atrial and ventricular muscle and His-Purkinje fibers is due to the sudden increase in membrane conductance to Na+. When the membrane voltage reaches threshold, Na+ rushes through ion-specific channels into the cell. Upstrokes of slow_responses (sinus and AV nodes) are mediated by a slow inward, predominantly Ca++ current (I_Ca) rather than the fast inward I_Na.

2. Phase_1: Early Rapid Repolarization

Following phase_0, the membrane repolarizes rapidly and transiently to near 0 mV, partly owing to inactivation of I_Na or activation of a transient outward current carried mostly by K ions.

3. Phase_2: Plateau

During the plateau phase membrane conductance to all ions falls rather low values.

4. Phase_3: Final Rapid Repolarization

Repolarization proceeds rapidly, owing at least in part to two-currents: time-dependent inactivation of I_Ca-I, so that intracellular movement of positive changes decreases, and activation of an outward K+ current (called the delayed rectifier or I_K, the major current-causing repolarization), so that extracellular movement of positive charges increases.

5. Phase_4: Diastolic Depolarization or Resting Membrane Potential

Under normal conditions, the membrane potential of atrial and ventricular muscle cells remains steady throughout diastole. K+ is the major ion determinating the resting potential. Because of the Na-K pump, which pumps Na+ out of the cell against its electrochemical gradient and simultaneously pumps K+ into the cell against its chemical gradient, intracellular K+ concentration remains high and intracellular Na+ concentration remains low. I_K1 is the current responsible for maintaining the resting potential near the K+ equilibrium potential in atrial, AV nodal, His-Purkinje, and ventricular cells. I_K1 is the inward rectifier, shutting off during depolarization. It is absent in sinus nodal cells.