and eject blood. The long ERP also prevents
the heart from developing sustained, tetanic
contractions like those that occur in skeletal
muscle. At the end of the ERP, the cell is in
its relative refractory period. Early in this
period, suprathreshold depolarization stim-
uli are required to elicit actions potentials.
Because not all the sodium channels have
recovered to their resting state by this time,
action potentials generated during the relative
refractory period have a decreased phase 0
slope and lower amplitude. When the sodium
channels are fully recovered, the cell becomes
fully excitable
stimuli can elicit new, rapid action potentials.
Pacemaker cells have no true resting poten-
tial, but instead generate regular, spontaneous
action potentials. Unlike most other cells that
exhibit action potentials (e.g., nerve cells, and
muscle cells), the depolarizing current of the
action potential is carried primarily by relatively
slow, inward Ca++ currents (through L-type cal-
cium channels) instead of by fast Na+ currents.
The rate of depolarization of pacemaker cells
is slow compared to “fast response” nonpace-
maker cells, and therefore they are sometimes
called “slow response” action potentials.
Cells within the sinoatrial (SA) node, located
within the posterior wall of the right atrium
(RA), constitute the primary pacemaker site
within the heart. Other pacemaker cells exist
within the AV node and ventricular conduction
system, but their firing rates are driven by the
higher rate of the SA node because the intrinsic
pacemaker activity of the secondary pacemak-
ers is suppressed by a mechanism termed over-
drive suppression. This mechanism causes the
secondary pacemaker to become hyperpolar-
ized when driven at a rate above its intrinsic
rate. Hyperpolarization
occurs because the
increased action potential frequency stimulates
the activity of the electrogenic Na+/K+-ATPase
pump as a result of enhanced entry of sodium
per unit time into these cells. If the SA node
becomes depressed, or its action potentials
fail to reach secondary pacemakers, overdrive
suppression ceases, which permits a secondary
site to take over as the pacemaker for the heart.
When this occurs, the new pacemaker outside
of the SA node is called an ectopic focus.
SA nodal action potentials are divided into
three phases: phase 0, upstroke of the action
potential; phase 3, the period of repolariza-
tion; and phase 4, the period of spontaneous
depolarization that leads to subsequent gen-
eration of a new action potential (Fig. 2.6).
Phase 0 depolarization primarily is due
to increased gCa++ through L-type calcium
channels. These voltage-operated channels
open when the membrane is depolarized to a
threshold voltage of about -4 0 mV Because the
movement of Ca++ through calcium channels
is not rapid compared to fast sodium channels
(hence, the term “slow calcium channels”),
the rate of depolarization (the slope of phase 0)
is much slower than that found in other
cardiac cells (e.g., in Purkinje cells). As the
calcium channels open and the membrane
equilibrium potential, a transient decrease in
SA Node
■ FIGURE 2.6 Changes in ion conductances
associated w ith a sinoatrial (SA) nodal pacemaker
action potential. Phase 0 (depolarization) prim ar-
ily is due to an increase in calcium conductance
through L-type Ca++ channels accompa-
nied by a fall in potassium conductance (gK+);
phase 3 (repolarization) results from an increase in
gK+ and a decrease in gCa++. Phase 4 undergoes a
spontaneous depolarization owing to a pacemaker
current (f) carried in part by Na+; decreased gK+
and increased gCa++ also contribute to the sponta-
neous depolarization.
previous page 31 Cardiovascular Physiology Concepts  2nd Edition read online next page 33 Cardiovascular Physiology Concepts  2nd Edition read online Home Toggle text on/off