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Excitation-contraction coupling in myocardium

Timothy W Smith, MD, PhD
James P Morgan, MD, PhD
Section Editor
Wilson S Colucci, MD
Deputy Editor
Susan B Yeon, MD, JD, FACC


Excitation-contraction (E-C) coupling refers to the series of events that link the action potential (excitation) of the muscle cell membrane (the sarcolemma) to muscular contraction. Although E-C coupling in myocardium is similar in many ways to skeletal muscle and smooth muscle, there are also critical differences. The cyclical nature of cardiac contraction and the importance of myocardial relaxation to cardiac pump function requires that any discussion of E-C coupling also consider the events terminating the muscle twitch as an integral part of the subject. Modulation of muscular function is said to affect inotropy (the speed and strength of muscular contraction) or lusitropy (the ability of the muscle to relax). Increased knowledge about E-C coupling has been a key to understanding both the inotropic and lusitropic states, and it continues to be useful in developing improved therapy for heart failure and cardiogenic shock.

This is a brief review of cardiac excitation (the myocardial action potential) followed by a description of muscular contraction. E-C coupling is then presented as the transduction of a membrane signal (the action potential) to an intracellular effector (the contractile apparatus) by way of a second messenger (intracellular free calcium [Ca2+]).


The resting membrane potential of the myocardial cell is cell interior negative (-90 mV), and is primarily determined by the ratio of intracellular-to-extracellular potassium as predicted by the Nernst equation. The action potential is a temporary depolarization of the membrane. It is caused by transient changes in membrane conductance of several charged ions, especially sodium, due to the opening and closing of ion-specific channels in the membrane. This process can be summarized as follows (figure 1 and movie 1) [1]. (See "Myocardial action potential and action of antiarrhythmic drugs".)

Rapid depolarization (phase 0) occurs when the resting cell is brought to threshold, leading sequentially to activation or opening of voltage-dependent sodium channels, rapid sodium entry into the cells down a favorable concentration gradient, and a cell interior positive potential that can approach +45 mV. The marked depolarization results in voltage-dependent inactivation of the sodium channels and cessation of the inward sodium flux. Calcium channels also open during depolarization but the onset of the inward calcium flux is much slower.

Phase 1 repolarization is primarily due to inactivation of the sodium channels with abolition of the inward sodium current.

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Literature review current through: Nov 2017. | This topic last updated: Oct 11, 2017.
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