The propagation of action potentials through successive regions of the heart can be clinically monitored by electrocardiographic recording. The cardiac action potential typically comprises Phase 0 upstroke, early Phase 1 recovery, Phase 2 plateau and Phase 3 repolarisation to Phase 4 electrical diastole. These are driven respectively by inward Na+, early K+ transient outward, inward Ca2+, rapid and slow outward K+ currents, and inward rectifying K+ currents. The inward Ca2+ currents trigger Ca2+-induced release of sarcoplasmic reticular Ca2+ by cardiac ryanodine receptors, thereby initiating excitation-contraction coupling leading to contractile activation. With repolarisation, this is reversed through Ca2+-ATPase-mediated Ca2+ reuptake into the sarcoplasmic reticulum, and electrogenic Na+-Ca2+ exchange expelling Ca2+ into the extracellular space. These processes are modulated by feedforward autonomic, sympathetic and parasympathetic triggering of specific G-protein signaling pathways, involving their respective transmitters norepinephrine and acetylcholine. Conversely, cytosolic Ca2+ exerts feedback effects on the initiating Na+ current generation.