Electrical Conduction System of The Heart - Electrochemical Mechanism

Electrochemical Mechanism

Cardiac neurons innervating the myocardium bear limited similarities to those of skeletal muscle as well as other important differences. Cardiac neurons are uniquely subject to influence by the sympathetic and parasympathetic influence of the autonomic nervous system unlike skeletal muscle.

Like a neuron, a given myocardial cell has a negative membrane potential when at rest. Stimulation above a threshold value induces the opening of voltage-gated ion channels with induced flow of cations into the cell. The positively charged ions entering the cell cause the depolarization characteristic of an action potential. After depolarization, there is a brief repolarization that takes place with the efflux of potassium through fast-acting potassium channels. Like skeletal muscle, depolarization causes the opening of voltage-gated calcium channels - meanwhile potassium channels have closed - and are followed by a titrated release of Ca2+ from the t-tubules. This influx of calcium causes calcium-induced calcium release from the sarcoplasmic reticulum, and free Ca2+ causes muscle contraction. After a delay, slow acting Potassium channels reopen and the resulting flow of K+ out of the cell causes repolarization to the resting state.

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 necessary for the SA node pacemaker activity.