Maintenance of the Body
clean” the SA node will begin to function normally and sinus
rhythm will be reestablished. Implantable cardioverter deﬁbril-
lators (ICDs) can continually monitor heart rhythms and slow
an abnormally fast heart rate or emit an electrical shock if the
heart begins to ﬁbrillate.
A defective SA node may have several consequences. An
ik), which is an abnormal pacemaker, may
appear and take over the pacing of heart rate, or the AV node
may become the pacemaker. Te pace set by the AV node (
) is 40 to 60 beats per minute, slower than sinus
rhythm but still adequate to maintain circulation.
Occasionally, ectopic pacemakers appear even when the SA
node is operating normally. A small region of the heart becomes
hyperexcitable, sometimes as a result of too much caﬀeine (sev-
eral cups of coﬀee) or nicotine (excessive smoking), and gener-
ates impulses more quickly than the SA node. Tis leads to a
the SA node initiates the next contraction. Ten, because the
heart has a longer time to ﬁll, the next (normal) contraction is
felt as a thud. As you might guess, premature
tractions (PVCs) are most problematic.
Te only route for impulse transmission from atria to ventri-
cles is through the AV node. Tus any damage to the AV node
interferes with the ability of the ventricles to receive pacing im-
. In total heart block no impulses
get through and the ventricles beat at their intrinsic rate, which
is too slow to maintain adequate circulation. In partial heart
block, only some of the atrial impulses reach the ventricles. In
both cases, artiﬁcial pacemakers are implanted to recouple the
atria to the ventricles as necessary. Tese programmable devices
speed up in response to increased physical activity just as a nor-
mal heart would, and many can send diagnostic information to
the patient’s doctor via telephone.
Modifying the Basic Rhythm:
Extrinsic Innervation of the Heart
Although the intrinsic conduction system sets the basic heart
rate, ﬁbers of the autonomic nervous system modify the march-
like beat and introduce a subtle variability from one beat to the
next. Te sympathetic nervous system (the “accelerator”) in-
creases both the rate and the force of heartbeat. Te parasympa-
thetic activation (the “brakes”) slows the heart. We explain these
neural controls later—here we discuss the anatomy of the nerve
supply to the heart.
Te cardiac centers are located in the medulla oblongata. Te
projects to sympathetic neurons in
level of the spinal cord. Tese preganglionic neurons,
in turn, synapse with postganglionic neurons in the cervical and
upper thoracic sympathetic trunk
. From there,
postganglionic ﬁbers run through the cardiac plexus to the
heart where they innervate the SA and AV nodes, heart muscle,
and coronary arteries.
sends impulses to the para-
sympathetic dorsal vagus nucleus in the medulla, which in turn
sends inhibitory impulses to the heart via branches of the vagus
nerves. Most parasympathetic postganglionic motor neurons lie
Right and left bundle branches.
Te AV bundle persists
only brieﬂy before splitting into two pathways—the
leF bundle branches
, which course along the inter-
ventricular septum toward the heart apex.
Subendocardial conducting network.
strands of barrel-shaped cells with few myoﬁbrils, the
endocardial conducting network
, also called
je), completes the pathway through the in-
terventricular septum, penetrate into the heart apex, and
then turn superiorly into the ventricular walls. Te bundle
branches excite the septal cells, but the bulk of ventricular
depolarization depends on the large ﬁbers of the conduct-
ing network and, ultimately, on cell-to-cell transmission
of the impulse via gap junctions between the ventricular
muscle cells. Because the le² ventricle is much larger than
the right, the subendocardial conducting network is more
elaborate in that side of the heart.
Te total time between initiation of an impulse by the SA
node and depolarization of the last of the ventricular muscle
cells is approximately 0.22 s (220 ms) in a healthy human heart.
Ventricular contraction almost immediately follows the
ventricular depolarization wave. Te wringing motion of con-
traction begins at the heart apex and moves toward the atria,
following the direction of the excitation wave through the ven-
tricle walls. Tis contraction ejects some of the contained blood
into the large arteries leaving the ventricles.
Te various cardiac pacemaker cells have diﬀerent rates of
spontaneous depolarization. Te SA node normally drives the
heart at a rate of 75 beats per minute. Without SA node input,
the AV node would depolarize only about 50 times per minute.
Without input from the AV node, the AV bundle and the sub-
endocardial conducting network would depolarize only about
30 times per minute (though they conduct very rapidly). Note
that these slower pacemakers cannot dominate the heart unless
faster pacemakers stop functioning.
Te cardiac conduction system coordinates and synchro-
nizes heart activity. Without it, impulses would travel much
more slowly—0.3 to 0.5 m/s as opposed to several meters per
second in most parts of the conduction system. Tis slower rate
would allow some muscle ﬁbers to contract long before others,
reducing pump eﬀectiveness.
Defects in the intrinsic conduction system can cause irregular
heart rhythms, or
me-ahz). Tey may also
cause uncoordinated atrial and ventricular contractions, or even
, a condition of rapid and irregular or out-of-phase
contractions in which control of heart rhythm is taken away from
the SA node by rapid activity in other heart regions. Te heart in
ﬁbrillation has been compared with a squirming bag of worms.
Fibrillating ventricles are useless as pumps; and unless the heart
is deﬁbrillated quickly, circulation stops and brain death occurs.
Deﬁbrillation is accomplished by electrically shocking the
heart, which interrupts its chaotic twitching by depolarizing
the entire myocardium. Te hope is that “with the slate wiped