Cardiovascular Physiology
371
Recall that excitation travels from the SA node to both
ventricles only through the AV node; therefore, drug- or
disease-induced malfunction of the AV node may reduce or
completely eliminate the transmission of action potentials
from the atria to the ventricles. If this occurs, autorhythmic
cells in the bundle of His and Purkinje network, no longer
driven by the SA node, begin to initiate excitation at their
own inherent rate and become the pacemaker for the ventri-
cles. Their rate is quite slow, generally 25 to 40 beats/min,
and it is completely out of synchrony with the atrial con-
tractions, which continue at the normal, higher rate of the
SA node. Under such conditions, the atria are ineffective
because they are often contracting against closed AV valves.
Fortunately, atrial pumping is relatively unimportant for car-
diac function except during strenuous exercise.
The current treatment for all severe
AV conduction dis-
orders,
as well as for many other abnormal rhythms, is per-
manent surgical implantation of an
artifi
cial pacemaker
that
electrically stimulates the ventricular cells at a normal rate.
The Electrocardiogram
The
electrocardiogram
(
ECG
or EKG—the
k
is from the
German
electrokardiogramm
) is primarily a tool for evaluating
the electrical events within the heart. The action potentials
of cardiac muscle cells can be viewed as batteries that cause
charge to move throughout the body fl uids. These moving
charges, or currents, are caused by all the action potentials
occurring simultaneously in many individual myocardial cells
and can be detected by recording electrodes at the surface of
the skin.
Figure 12–14a
illustrates a typical normal ECG
recorded as the potential difference between the right and left
wrists. (Review Figure 12–11 for an illustration of how this
waveform corresponds in time with the spread of an action
potential through the heart.) The fi rst defl ection, the
P wave,
corresponds to current fl
ows during atrial depolarization. The
second defl ection, the
QRS complex,
occurring approxi-
mately 0.15 s later, is the result of ventricular depolarization.
It is a complex defl ection because the paths taken by the wave
of depolarization through the thick ventricular walls differ
from instant to instant, and the currents generated in the body
uids change direction accordingly. Regardless of its form
(for example, the Q and/or S portions may be absent), the
defl ection is still called a QRS complex. The fi nal defl ection,
the
T wave,
is the result of ventricular repolarization. Atrial
repolarization is usually not evident on the ECG because it
occurs at the same time as the QRS complex.
A typical clinical ECG makes use of multiple combina-
tions of recording locations on the limbs and chest (called
ECG leads
) so as to obtain as much information as possible
concerning different areas of the heart. The shapes and sizes of
the P wave, QRS complex, and T wave vary with the electrode
locations. For reference, see
Figure 12–15
and
Table 12–2
,
which describe the placement of electrodes for the different
ECG leads.
To reiterate, the ECG is not a direct record of the changes
in membrane potential across individual cardiac muscle cells.
Instead, it is a measure of the currents generated in the extra-
cellular fl uid by the changes occurring simultaneously in many
cardiac cells. To emphasize this point,
Figure 12–14b
shows
the simultaneously occurring changes in membrane potential
in a single ventricular cell.
Because many myocardial defects alter normal impulse
propagation, and thereby the shapes and timing of the waves,
the ECG is a powerful tool for diagnosing certain types of
heart disease.
Figure 12–16
gives one example. However,
note that the ECG provides information concerning only the
electrical activity of the heart. Thus, if something is wrong
with the heart’s mechanical activity, but this defect does not
give rise to altered electrical activity, the ECG will not be of
diagnostic value.
Excitation-Contraction Coupling
The mechanisms linking cardiac muscle cell action potentials
to contraction were described in detail in the chapter on mus-
cle physiology (Chapter 9; review Figure 9–40). The small
amount of extracellular calcium entering through L-type cal-
cium channels during the plateau of the action potential triggers
the release of a larger quantity of calcium from the ryanodine
receptors in the sarcoplasmic reticulum membrane. Calcium
activation of the thin fi
lament and cross-bridge cycling then
lead to generation of force, just as in skeletal muscle (review
0.3
Time (s)
+20
–90
+1
0
P
R
T
Q
S
ECG
Potential (mV)
Membrane potential (mV)
Ventricular
action potential
(a)
(b)
Figure 12–14
(a) Typical electrocardiogram recorded from electrodes placed on
the wrists. P represents atrial depolarization; QRS, ventricular
depolarization; T, ventricular repolarization. (b) Ventricular action
potential recorded from a single ventricular muscle cell. Note the
correspondence of the QRS complex with depolarization and the
correspondence of the T wave with repolarization.
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