How does hyperkalemia affect the resting membrane potential?

In hyperkalemia, the resting membrane potential is decreased, and the membrane becomes partially depolarized. Initially, this increases membrane excitability. However, with prolonged depolarization, the cell membrane will become more refractory and less likely to fully depolarize.

How does hypokalemia affect membrane potential?

The threshold cell membrane potential Hypokalemia increases the resting potential (i.e., makes it more negative) and hyperpolarizes the cell, whereas hyperkalemia decreases the resting potential (i.e., makes it less negative) and initially makes the cell hyperexcitable (Fig. 5-2).

How does calcium affect resting membrane potential?

Resting calcium conductance is exceedingly small. Therefore, calcium does not contribute to the resting membrane potential.

How does hyperkalemia affect repolarization?

Effects of hyperkalemia At levels greater than 5.5 mEq/L, the increase in the conductance of potassium channels increases lkr current, leading to rapid repolarization in the form of a peaked T wave on the surface ECG.

Why does hypokalemia lengthen action potential?

Hypokalemia prolongs APD by reducing outward current through both K+ channels and Na+-K+ ATPase. The prolonged APD results in increased Ca2+ influx through Ca2+ channels.

What effect does hypokalemia have on the movement of potassium across the cell membrane?

Serum hypokalemia causes hyperpolarization of the RMP (the RMP becomes more negative) due to the altered K+ gradient. As a result, a greater than normal stimulus is required for depolarization of the membrane in order to initiate an action potential (the cells become less excitable).

How does calcium affect the action potential?

A critical component of the action potential is the rise in intracellular calcium that activates both small conductance potassium channels essential during membrane repolarization, and triggers transmitter release from the cell.

Why does hypercalcemia cause short QT?

Hypercalcemia changes the shape of the ventricular action potential into that of an atrial action potential, shortening the duration of phase 2. The electrocardiographic translation of a short phase 2 is short- ening in the QT interval and shortening or absence of the S T segment.

What effect does the elevated K concentration in the interstitial fluid have on the resting membrane potential of the myocardial cells in the ischemic zone?

The main effect of [K+]o elevation is resting depolarization, which causes decreased availability of Na+ channels and slow recovery of the Na+ channel inactivation gates, thus resulting in depressed excitability and prolonged postrepolarization refractoriness in ischemic cardiomyocytes.