The membrane potential is determined
primarily by the concentration of sodium,
potassium, and calcium ions across the
cell membrane, and by the relative con-
ductances of the membrane to these ions.
The resting membrane potential is very
close to the potassium equilibrium
potential (calculated from Nernst equa-
tion) because the relative conductance
of potassium is much higher than the
relative conductances of sodium and
calcium in the resting cell.
Ions move across the cell membrane
through ion-selective channels, which
have open (activated) and closed
(inactivated) states that are regulated
by either membrane voltage or by
receptor-coupled mechanisms.
Concentrations of sodium, potassium,
and calcium across the cell membrane
are maintained by the Na+
/K +-ATPase
pump, the Na+
/Ca++ exchanger, and the
Ca++-ATPase pump.
Nonpacemaker cardiac action potentials
are characterized as having very nega-
tive resting potentials (approximately
-90 mV), a rapid phase 0 depolarization
produced primarily by a transient
increase in sodium conductance, and
a prolonged plateau phase (phase 2)
generated primarily by inward calcium
currents through L-type calcium chan-
nels; increased potassium conductance
repolarizes the cells during phase 3.
Pacemaker action potentials (e.g.,
those found in SA nodal cells) spon-
taneously depolarize during phase 4,
owing in part to special pacemaker cur-
rents (lf). Upon reaching the threshold
for action potential generation, cal-
cium conductance increases as L-type
calcium channels become activated,
which causes depolarization (phase 0).
As the calcium channels close, potas-
sium conductance increases and the
cell repolarizes (phase 3).
At rest, SA nodal pacemaker activity
is strongly influenced by vagal activ-
ity (vagal tone), which significantly
reduces the intrinsic SA nodal firing
rate. Pacemaker activity is increased
by sympathetic activation and vagal
Conduction of action potentials within
the heart is primarily cell-to-cell,
although specialized conduction path-
ways exist within the heart that ensure
rapid distribution of the conducted
action potentials. Conduction velocity
is increased by activation of sympa-
thetic nerves and decreased by para-
sympathetic activation.
The low conduction velocity within the
AV node ensures sufficient time for
atrial contraction to contribute to ven-
tricular filling.
Cells located within the AV node and
ventricular conducting system can also
serve as pacemakers if the SA node
fails or conduction is blocked between
the atria and ventricles (AV block).
The ECG evaluates rhythm and con-
duction by examining the appearance
(amplitude, duration, and shape) of
specific waveforms that represent atrial
depolarization (P wave), ventricular
depolarization (QRS complex), and
ventricular repolarization (T wave).
Different ECG leads view the electri-
cal activity of the heart from different
angles. Each limb lead can be repre-
sented by an electrical axis on a fron-
tal plane from which the direction of
depolarization and repolarization vec-
tors within the heart can be determined
using standard rules of interpretation
(e.g., a wave of depolarization traveling
toward a positive electrode produces
a positive voltage in the ECG). Chest
leads (V, to V6) measure the electri-
cal activity in a horizontal plane that is
perpendicular to the frontal plane.
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