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The standard model used to understand the cardiac action potential is that of the ventricular myocyte. Outlined below are the five phases of the ventricular myocyte action potential, with reference also to the SAN action potential. Figure 2a: Ventricular action potential (left) and sinoatrial node action potential (right) waveforms.
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] Phase 4: Resting membrane potential remains stable at ≈−90 mV. [1]
As an action potential (nerve impulse) travels down an axon there is a change in electric polarity across the membrane of the axon. In response to a signal from another neuron, sodium- (Na +) and potassium- (K +)–gated ion channels open and close as the membrane reaches its threshold potential.
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.
Transmission of a cardiac action potential through the heart's conduction system. It is not very well known how the electric signal moves in the atria. It seems that it moves in a radial way, but Bachmann's bundle and coronary sinus muscle play a role in conduction between the two atria, which have a nearly simultaneous systole.
The cardiac action potential has five phases. I to1 is active during phase 1, causing a fast repolarization of the action potential. The cardiac transient outward potassium current (referred to as I to1 or I to [1]) is one of the ion currents across the cell membrane of heart muscle cells.
Unlike that in nerve cells, the cardiac action potential duration is closer to 100 ms (with variations depending on cell type, autonomic tone, etc.). After an action potential initiates, the cardiac cell is unable to initiate another action potential for some duration of time (which is slightly shorter than the "true" action potential duration).
Figure FHN: To mimick the action potential, the FitzHugh–Nagumo model and its relatives use a function g(V) with negative differential resistance (a negative slope on the I vs. V plot). For comparison, a normal resistor would have a positive slope, by Ohm's law I = GV, where the conductance G is the inverse of resistance G=1/R.
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