Biomedical Engineering Reference
In-Depth Information
+20mV
Plateau phase
+20mV
0mV
0mV
Repolarization
Depolarization
Depolarization
Repolarization
-40mV
Threshold potential
-60mV
Threshold potential
-60mV
-90mV
Rest potential
Rest potential
Fig. 3.3
Membrane action potential - muscle cells and cells of the conducting system
concentration about 30 times higher inside than outside the
cell. The cell membrane is readily permeable to a potassium
ion. The predominant extracellular ion is Na
+
, to which the
cell membrane is only slightly permeable. Indeed, the mem-
brane has a specific permeability to individual ions, for
example, K
+
, Na
+
, and Cl
−
ions or protein anions. This per-
meability of ion channels is mainly determined by the intra-
cellular concentration of Ca
2+
ions.
The system strives to create a thermodynamic balance by
equalizing ion concentrations on both sides of the membrane.
Ions that pass through the membrane thus diffuse into the
space where their concentration is lower. However, oppositely
charged ions do not diffuse because the membrane is not per-
meable to them. Therefore, diffusion of ions is halted by an
electrical field that occurs as a result of separation of positive
and negative ions by the membrane. The voltage occurring at
the cell membrane between intracellular and extracellular
environments is referred to as the resting membrane potential.
Ions thus indirectly affect the magnitude of the potential.
However, it is actually electric potential difference, that is,
voltage. The magnitude of this voltage ranges from a single to
hundreds of millivolts. The extracellular space is positive,
whereas the intracellular space is negative. For myocardial
contractile cells, the typical resting membrane potential is
−90 mV; in the sinoatrial node it is only about −45 mV.
The action potential is a rapid change in the electric poten-
tial on the membrane of some cells. Within milliseconds, the
intracellular space increases from a value of −90 mV to that
of +20 to +30 mV. In excitable membranes, this change in
the potential is propagated to the surroundings. An action
potential can be generated by chemical processes, external
phenomena, arrival of an impulse, or a change in the poten-
tial of the membrane - in general, by any phenomenon that
lowers the resting membrane potential of a given cell to a
threshold level. When the resting membrane potential is neg-
ative, this threshold level is at an absolute value of approxi-
mately 20 mV higher (closer to zero).
The process of action potential begins by the opening of
sodium channels, which results in a rapid rise of the potential
into positive values. This phase, accompanied by an influx of
Na
+
ions into the cell, is referred to as depolarization. Almost
simultaneously, the permeability of potassium channels is
increased and potassium ions flow out of the cell. At that
point, the rise of the potential is stopped and its subsequent
decrease occurs. This phase is called repolarization. From
the beginning of depolarization through approximately two
thirds of repolarization, the membrane is in an absolute
refractory period, that is, it is unexcitable. It cannot be depo-
larized again, not even with an intensive stimulus, because
most of the sodium channels are inactive. The channels can-
not open until the membrane voltage returns to a value of
around −40 mV. After approximately two thirds of the repo-
larization phase, depolarization can be evoked again with an
above-threshold stimulus; this phase is referred to as the rel-
ative refractory period.
The membrane temporal and voltage parameters are
dependent on the cell type and are shown in Fig.
3.3
. In myo-
cardial contractile cells, the refractory period, referred to as
the plateau, is long. It lasts 100-300 ms, and the value of
voltage is stable at approximately +15 mV. A balance between
cations flowing in and out of the cell must be maintained dur-
ing this phase. The flow of potassium cations out of the cell
is counterbalanced by an inward flow of calcium cations.
Thus, first, the heart muscle is protected against disablement
of the pumping function via sustained (tetanic) muscular
contraction. Second, this refractory period is longer than the
duration of the spread of impulse over the whole heart; there-
fore, in a healthy individual, an impulse cannot return or
spread in loops. Action potential on the membranes of the
cells of the heart's conduction system does not exhibit the
plateau phase. This is because depolarization of these cells is
caused by the opening of calcium channels and a flow of
calcium cations into the cell. Sodium cations are involved
only minimally in depolarization.
