Ions move across the cell membrane through specific ion channels. When these channels open, the permeability and electrical conductance to their respective ion increases, which leads to a change in the membrane potential.
The membrane potential in a resting cell is near the equilibrium potential for K+. That occurs because the membrane is relatively more permeable in the resting state to K+ than to the other ionic species such as Na+ and Ca++. Therefore, the membrane potential reflects not only the concentration gradients of individual ions (i.e., the equilibrium potentials), but also the relative permeability of the membrane to those ions. If the membrane has a very high permeability to one ion over all the others, then that ion will have a greater influence on determining the membrane potential. One way to express this relationship is as follows:
Em = g'K EK + g'Na ENa + g'Ca ECa + g'Cl ECl
The membrane potential (Em) depends on the sum of the individual equilibrium potentials times the relative membrane conductance of each ionic species. The relative conductance (g’X) of a given ionic species is the conductance for that single ion divided by the total conductance for all of the ionic species (i.e., g’X = gX/gTotal).
If the equilibrium potential values for a typical myocyte are incorporated into the equation describing Em, then
Em = g'K (-96 mV) + g'Na (+52 mV) + g'Ca (+134 mV) + g'Cl (-90 mV)
In a cardiac cell, the individual ion concentration gradients change very little, even when Na+ and Ca++ enter the cell, and K+ leaves the cell during action potentials. Therefore, changes in Em are primarily due to changes in ionic conductances and the associated changes in ion currents. For example, in a resting cell, g'K is very high relative to all the other ionic conductances so the Em is near the EK. At the peak of an action potential, g'Na is very high relative to the other ions, therefore the Em approaches ENa. In the heart, the most important ions determining the membrane potential are Na+, K+ and Ca++.
Ion conductances are altered by antiarrhythmic drugs that block specific ion channels. Sodium-channel blockers such as quinidine inactivate fast-sodium channels and thereby reduce the conductance of sodium ions into the cell. Calcium-channel blockers such as verapamil and diltiazem decrease calcium conductance into the cell. Potassium-channel blockers decrease potassium conductance.