Cardiovascular Physiology
369
the right atrium. The action potential spreading through the
muscle cells of the right atrium causes depolarization of the
AV node. This node has a particularly important characteris-
tic:
The propagation of action potentials through the AV node
is relatively slow
(requiring approximately 0.1 s). This delay
allows atrial contraction to be completed before ventricular
excitation occurs.
After leaving the AV node, the action potential propa-
gates down the wall—the interventricular septum—between
the two ventricles. This pathway has conducting-system fi bers
called the
bundle of His
(or atrioventricular bundle) after its
discoverer (pronounced
Hiss
). The AV node and the bundle
of His constitute the only electrical connection between the
atria and the ventricles. Except for this pathway, the atria are
completely separated from the ventricles by a layer of noncon-
ducting connective tissue.
Within the interventricular septum, the bundle of His
divides into
right and left bundle branches,
which even-
tually leave the septum to enter the walls of both ventricles.
These fi bers in turn make contact with
Purkinje fi
bers,
large
conducting cells that rapidly distribute the impulse through-
out much of the ventricles. Finally, the Purkinje fi bers make
contact with ventricular myocardial cells, which spread the
impulse through the rest of the ventricles.
The rapid conduction along the Purkinje fi bers and the dif-
fuse distribution of these fi bers cause depolarization of all right
and left ventricular cells more or less simultaneously and ensures
a single coordinated contraction. Actually, though, depolar-
ization and contraction do begin slightly earlier in the bottom
(apex) of the ventricles and then spread upward. The result is
an effi cient contraction that moves blood toward the exit valves,
like squeezing a tube of toothpaste from the bottom up.
Cardiac Action Potentials and Excitation
of the SA Node
The mechanism by which action potentials are conducted along
the membranes of heart cells is basically similar to that seen in
other excitable tissues like neurons and skeletal muscle cells.
However, different types of heart cells express unique combi-
nations of ion channels that produce different action potential
shapes. This specializes them for particular roles in the spread
of excitation through the heart.
Figure 12–12a
illustrates a typical ventricular myo-
cardial cell action potential. The plasma membrane perme-
ability changes that underlie it are shown in
Figure 12–12b
.
As in skeletal muscle cells and neurons, the resting mem-
brane is much more permeable to potassium than to sodium.
Therefore, the resting membrane potential is much closer to
the potassium equilibrium potential (–90 mV) than to the
sodium equilibrium potential (+60 mV). Similarly, the depo-
larizing phase of the action potential is due mainly to the
opening of voltage-gated sodium channels. Sodium entry
depolarizes the cell and sustains the opening of more sodium
channels in positive feedback fashion. At almost the same
time, the permeability to potassium decreases as potassium
channels that were leaking at rest close, and this also contrib-
utes to the membrane depolarization.
Also like in skeletal muscle cells and neurons, the increased
sodium permeability is very transient because the sodium
channels inactivate quickly. However, unlike these other excit-
able tissues, in cardiac muscle the reduction in sodium perme-
ability is not accompanied by membrane repolarization. The
membrane remains depolarized at a plateau of about 0 mV (see
Figure 12–12a). The reasons for this continued depolariza-
tion are (1) potassium permeability stays below the rest-
ing value (i.e., the potassium channels mentioned previously
remain closed), and (2) a marked increase occurs in the mem-
brane permeability to calcium. The second reason is the more
important of the two, and the explanation for it follows.
In myocardial cells, the original membrane depolarization
causes voltage-gated calcium channels in the plasma membrane
0
P
Ca
2+
(L)
P
K
+
P
Na
+
0
0.15
0.30
Time (s)
–50
–100
10.0
1.0
0.1
Membrane potential (mV)
Relative membrane permeability
(a)
(b)
0
0.15
0.30
Time (s)
Na
+
enters
K
+
exits
Ca
2+
enters
Figure 12–12
(a) Membrane potential recording from a ventricular muscle cell.
Labels indicate key ionic movements in each phase.(b) Simultaneously
measured permeabilities (
P
) to potassium, sodium, and calcium
during the action potential of (a). Several subtypes of potassium
channels contribute to
P
K
+
.
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