Question

Why doesn't the maximal membrane voltage (at the peak of the action potential) change with altered potassium?

What happens to the resting membrane potential in hyperkalemia?

What happens to the firing rate in hyperkalemia?

Explain.

Thank you!

Answer 1

The decrease in Vmax causes a slow-ing of impulse conduction through the myocardium and a prolongation of membrane depolarization; as a result, the QRS duration is prolonged. ... As potassium levels increase further, the resting membrane potential continues to become less negative, and thus progressively decreases Vmax.The early effect of mild hyperkalemia on myocyte function is to increase myocyte excitability by shifting the resting membrane potential to a less negative value and thus closer to threshold potential; but as potassium levels continue to rise, myocyte depression occurs and V countinous decreases.

If there is continued K+ permeability, the membrane potential will never reach its ... This simple hypothesis of voltage-dependent Na+ channels goes a long way ... but by the peak of the action potential, the K+ conductance begins to increase ... to alter the concentrations and the resultant Na+ and K+ equilibrium potentials.

The threshold cell membrane potential is reached when sodium permeability increases to the point that sodium entry exceeds potassium exit, depolarization becomes self-perpetuating, and an action potential develops. The ability of specialized cells to develop an action potential is crucial to normal cardiac conduction, muscle contraction, and nerve impulse transmission. The excitability of a tissue is determined by the difference between the resting and threshold potentials (the smaller the difference, the greater the excitability).