CHAPTER 2 • ELECTRICAL ACTIVITY OF THE HEART
17
to 2 milliseconds. In skeletal muscle cells, the
action potential duration is approximately 2
to 5 milliseconds. In contrast, the duration of
ventricular action potentials ranges from 200
to 400 milliseconds. These differences among
nerve, skeletal muscle, and cardiac myocyte
action potentials relate to differences in the
ionic conductances responsible for generating
the changes in membrane potential.
NONPACEMAKER ACTION POTENTIALS
Figure 2.5 shows the ionic mechanisms respon-
sible for the generation of “fast response” non-
pacemaker action potentials such as those
found in atrial and ventricular myocytes, and
Purkinje fibers. By convention, the action
potential is divided into five numbered phases.
Nonpacemaker cells have a true resting mem-
brane potential (phase 4) that remains near
ERR
Ventricular Cell
■ FIGURE 2.5 Changes in ion conductances associ-
ated w ith a ventricular myocyte action potential.
Phase 0 (depolarization) primarily is due to the
rapid increase in sodium conductance
(gNa+)
accompanied by a fall in potassium conductance
(gK+); the initial repolarization of phase 1 is due to
opening of special potassium channels (/to); phase
2 (plateau) primarily is due to an increase in slow
inward calcium conductance (gCa++) through L-type
Ca++ channels; phase 3 (repolarization) results from
an increase in gK+ and a decrease in gCa++. Phase
4 is a true resting potential that primarily reflects a
high gK+.
ERP,
effective refractory period.
the equilibrium potential for K+ because gK+,
through inward rectifying potassium channels
(see Table 2-1), is high relative to gNa+ and
gCa++ in resting cells (see Equation 2-4). When
these cells are rapidly depolarized from -9 0 mV
to a threshold voltage of about -7 0 mV (owing
to, for example, an action potential conducted
by an adjacent cell), a rapid depolarization
(phase 0) is initiated by a transient increase
in conductance of voltage-gated, fast Na+-
channels. At the same time, gK+ falls. These
two conductance changes very rapidly move
the membrane potential away from the potas-
sium equilibrium potential and closer to the
sodium equilibrium potential (see Equation
2-4). Phase 1 represents an initial repolariza-
tion caused by the opening of a special type of
K+ channels (transient outward) and the inac-
tivation of the Na+ channels. However, because
of the large increase in slow inward gCa++,
the repolarization is delayed and the action
potential reaches a plateau phase (phase 2).
This inward calcium movement is through
long-lasting (L-type) calcium channels that
open when the membrane potential depolar-
izes to about -4 0 mV L-type calcium channels
are the major calcium channels in cardiac and
vascular smooth muscle. They are opened by
membrane depolarization (they are voltage-
operated) and remain open for a relatively
long duration. These channels are blocked by
classical L-type calcium channel blockers (e.g.,
verapamil
and
diltiazem).
Repolarization
(phase 3) occurs when gK+ increases through
delayed rectifier potassium channels and gCa++
decreases. Therefore, changes in Na+, Ca++,
and K+ conductances primarily determine the
action potential in nonpacemaker cells.
During phases 0, 1, 2, and part of phase 3,
the cell is refractory (i.e., unexcitable) to the
initiation of new action potentials. This is
the effective (or absolute) refractory period
(ERP, or ARP) (see Fig. 2.5). During the ERP,
stimulation of the cell does not produce new,
propagated
action
potentials
because
the
h-gates are still closed. The ERP acts as a pro-
tective mechanism in the heart by limiting the
frequency of action potentials (and therefore
contractions) that the heart can generate. This
enables the heart to have adequate time to fill
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