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Rate dependence of the action potential is a fundamental property of cardiac cells and alterations can lead to severe cardiac diseases including cardiac arrhythmia and sometimes sudden death. [3] Action potential activity within the heart can be recorded to produce an electrocardiogram (ECG).
Cardiac excitation-contraction coupling (Cardiac EC coupling) describes the series of events, from the production of an electrical impulse (action potential) to the contraction of muscles in the heart. [1] This process is of vital importance as it allows for the heart to beat in a controlled manner, without the need for conscious input.
The threshold potential is the potential an excitable cell membrane, such as a myocyte, must reach in order to induce an action potential. [7] This depolarization is caused by very small net inward currents of calcium ions across the cell membrane, which gives rise to the action potential. [8] [9]
The cardiac action potential differs from the neuronal action potential by having an extended plateau, in which the membrane is held at a high voltage for a few hundred milliseconds prior to being repolarized by the potassium current as usual.
The action potential of a ventricular myocyte. In electrocardiography, the ventricular cardiomyocyte membrane potential is about −90 mV at rest, [1] which is close to the potassium reversal potential. When an action potential is generated, the membrane potential rises above this level in five distinct phases. [1]
An impulse (action potential) that originates from the SA node at a relative rate of 60–100 bpm is known as a normal sinus rhythm. If SA nodal impulses occur at a rate less than 60 bpm, the heart rhythm is known as sinus bradycardia. If SA nodal impulses occur at a rate exceeding 100 bpm, the consequent rapid heart rate is sinus tachycardia ...