Cardiac Action Potential - Overview

Overview

Action potentials are generated by the movement of ions through the transmembrane ion channels in the cardiac cells. Rate dependence of action potential repolarization is a fundamental property of cardiac cells, and its modification by disease or drugs can bring about fatal arrhythmias.

Cardiac muscle bears some similarities to skeletal muscle, as well as important differences. Like skeletal myocytes (and axons for that matter), a given cardiac myocyte has a negative membrane potential when at rest. A notable difference between skeletal and cardiac myocytes is how each elevates the myoplasmic Ca2+ to induce contraction. When skeletal muscle is stimulated by somatic motor axons, influx of Na+ quickly depolarizes the skeletal myocyte and triggers calcium release from the sarcoplasmic reticulum. In cardiac myocytes, the release of Ca2+ from the sarcoplasmic reticulum is induced by Ca2+ influx into the cell through voltage-gated calcium channels on the sarcolemma. This phenomenon is called calcium-induced calcium release and increases the myoplasmic free Ca2+ concentration causing muscle contraction. In both muscle types, after a delay (the absolute refractory period), potassium channels reopen and the resulting flow of K+ out of the cell causes repolarization to the resting state. The voltage-gated calcium channels in the cardiac sarcolemma are generally triggered by an influx in sodium during the "0" phase of the action potential (see below).

Note that there are important physiological differences between nodal cells and ventricular cells; the specific differences in ion channels and mechanisms of polarization give rise to unique properties of SA node cells, most importantly the spontaneous depolarizations (cardiac muscle automaticity) necessary for the SA node's pacemaker activity.