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The ST segment represents the isoelectric period when the ventricles are in between depolarization and repolarization. Interpretation ...
The rapid depolarization of the cell, during phase 0, causes the membrane potential to approach sodium's equilibrium potential (i.e. the membrane potential at which sodium is no longer drawn into or out of the cell). As the membrane potential becomes more positive, the sodium channels then close and lock, this is known as the "inactivated" state.
Ventricular contraction occurs between ventricular depolarization and repolarization. During this time, there is no movement of charge, so no deflection is created on the ECG. This results in the flat ST segment after the S wave. [70] Frames 24–28 in the animation depict repolarization of the ventricles.
This results in altered pathways for ventricular depolarization. Since the electrical impulse can no longer use the preferred pathway across the bundle branch, it may move instead through muscle fibers in a way that both slows the electrical movement and changes the directional propagation of the impulses.
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]
Ventricular relaxation, or diastole, follows repolarization of the ventricles and is represented by the T wave of the ECG. It too is divided into two distinct phases and lasts approximately 430 ms. [1] During the early phase of ventricular diastole, as the ventricular muscle relaxes, pressure on the remaining blood within the ventricle begins ...
Electrical waves track a systole (a contraction) of the heart. The end-point of the P wave depolarization is the start-point of the atrial stage of systole. The ventricular stage of systole begins at the R peak of the QRS wave complex; the T wave indicates the end of ventricular contraction, after which ventricular relaxation (ventricular diastole) begins.
When this happens, the troponin changes back to its original shape, blocking the binding sites on actin and preventing the formation of crossbridges. This decrease in Ca 2+ within the cell is brought about by a variety of proteins , known collectively as ion transporters .