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Phase 0 involves rapid depolarization as sodium ions influx through fast sodium channels in atrial and ventricular myocytes. In nodal cells, depolarization occurs more slowly through calcium ion inflow via slow calcium channels, combined with potassium channel closure and slow sodium inflow. This phase initiates the electrical activity that triggers heart muscle contraction.

The plateau phase balances calcium influx and potassium outflow, maintaining a sustained depolarized state. This prolonged depolarization is crucial for extending heart muscle contraction, allowing adequate time for efficient blood ejection. Without this plateau, the heart would not pump blood effectively throughout the body.

Potassium ions exit the cell during phases 1 and 3, causing the membrane potential to decline and return to its resting state. In phase 1, initial repolarization begins as potassium efflux causes a slight decrease in membrane potential. In phase 3, potassium outflow predominates, completing repolarization and restoring the cell's negative resting charge.

Nodal cells depolarize slowly through calcium influx via slow calcium channels, potassium channel closure, and slow sodium inflow. Ventricular myocytes depolarize rapidly through fast sodium channel influx. This difference allows nodal cells to regulate heart rate and coordinate electrical conduction throughout the heart.

Refractory periods are intervals when cardiac cells cannot be restimulated. The effective refractory period spans from phase 0 to mid-phase 3, during which cells are completely unresponsive. The relative refractory period follows, where stronger stimuli can trigger early depolarization. Premature contractions during this period can cause arrhythmias, including ventricular tachycardia and fibrillation.

An electrocardiogram traces the heart's sequential depolarization and repolarization. The P wave represents atrial depolarization, the QRS complex shows ventricular depolarization, and the T wave indicates ventricular repolarization. Anomalies in these waveforms and intervals reveal underlying cardiac pathologies requiring clinical evaluation.

In the resting state, cardiac cells maintain a polarized membrane with higher sodium concentration outside and higher potassium concentration inside, creating a negative intracellular charge. This ionic gradient is essential for generating action potentials. When stimulated, sodium rapidly influxes, disrupting this balance and initiating depolarization and the subsequent cardiac action potential cycle.