Maintenance of the Body
, liberated by the adrenal medulla
during sympathetic nervous system activation, produces the
same cardiac eﬀects as norepinephrine released by the sym-
pathetic nerves: It enhances heart rate and contractility.
is a thyroid gland hormone that increases met-
abolic rate and production of body heat. When released in
large quantities, it causes a sustained increase in heart rate.
Tyroxine acts directly on the heart but also
fects of epinephrine and norepinephrine.
Normal heart function depends on having normal lev-
els of intracellular and extracellular ions. Plasma electrolyte
imbalances pose real dangers to the heart.
blood levels (
) depress the heart.
Conversely, above-normal levels (
) increase heart
rate and contractility—up to a point. Very high Ca
rupt heart function and life-threatening arrhythmias can occur.
High or low blood K
levels are particularly dangerous and
arise in a number of clinical conditions. Excessive K
) alters electrical activity in the heart by depolarizing the
resting potential, and may lead to heart block and cardiac arrest.
is also life threatening, in that the heart beats fee-
bly and arrhythmically.
Other Factors That Regulate Heart Rate
Age, gender, exer-
cise, and body temperature also inﬂuence HR, although they are
less important than neural factors. Resting heart rate is fastest in
the fetus (140–160 beats/min) and gradually declines through-
out life. Average heart rate is faster in females (72–80 beats/min)
than in males (64–72 beats/min).
Exercise raises HR by acting through the sympathetic ner-
vous system (Figure 18.22). Exercise also increases systemic
blood pressure and routes more blood to the working mus-
cles. However, resting HR in the physically ﬁt tends to be sub-
stantially lower than in those who are out of condition, and in
trained athletes it may be as slow as 40 beats/min. We explain
this apparent paradox below.
Heat increases HR by enhancing the metabolic rate of car-
diac cells. Tis explains the rapid, pounding heartbeat you feel
when you have a high fever and also accounts, in part, for the
eﬀect of exercise on HR (remember, working muscles generate
heat). Cold directly decreases heart rate.
HR varies with changes in activity, but marked and persistent
rate changes usually signal cardiovascular disease.
de-ah; “heart hurry”) is an abnor-
mally fast heart rate (more than 100 beats/min) that may result
from elevated body temperature, stress, certain drugs, or heart
disease. Persistent tachycardia is considered pathological be-
cause tachycardia occasionally promotes ﬁbrillation.
slow) is a heart rate
slower than 60 beats/min. It may result from low body tem-
perature, certain drugs, or parasympathetic nervous activation.
also inﬂuence HR—and consequently CO—by acting through
homeostatic mechanisms induced neurally, chemically, and
physically. Factors that increase HR are called
time) factors, and those that decrease HR are
Autonomic Nervous System Regulation of Heart Rate
autonomic nervous system exerts the most important extrinsic
controls aﬀecting heart rate, as shown on the right side of Fig-
ure 18.22. When emotional or physical stressors (such as fright,
anxiety, or exercise) activate the sympathetic nervous system,
sympathetic nerve ﬁbers release norepinephrine at their cardiac
synapses. Norepinephrine binds to β
-adrenergic receptors in
the heart, causing threshold to be reached more quickly. As a
result, the SA node ﬁres more rapidly and the heart responds by
Sympathetic stimulation also enhances contractility and speeds
relaxation. It does this by enhancing Ca
movements in the con-
tractile cells as we described above and in Figure 18.23. Enhanced
contractility lowers ESV, so SV does not decline as it would if only
increased. (Remember, when the heart beats faster, there
is less time for ventricular ﬁlling and so a lower EDV.)
Te parasympathetic division opposes sympathetic eﬀects
and eﬀectively reduces heart rate when a stressful situation has
passed. Parasympathetic-initiated cardiac responses are medi-
ated by acetylcholine, which hyperpolarizes the membranes of
its eﬀector cells by
channels. Because vagal innerva-
tion of the ventricles is sparse, parasympathetic activity has little
or no eﬀect on cardiac contractility.
Under resting conditions, both autonomic divisions continu-
ously send impulses to the SA node of the heart, but the
inﬂuence is inhibitory. For this reason, the heart is said
, and heart rate is generally slower than
it would be if the vagal nerves were not innervating it. Cut-
ting the vagal nerves results in an almost immediate increase
in heart rate of about 25 beats/min, reﬂecting the inherent rate
(100 beats/min) of the pacemaking SA node.
When sensory input from various parts of the cardiovascular
system activates either division of the autonomic nervous sys-
tem more strongly, the other division is temporarily inhibited.
Most such sensory input is generated by
spond to changes in systemic blood pressure, as we will discuss
in Chapter 19. Another example, the
atrial (Bainbridge) reﬂex
is an autonomic reﬂex initiated by increased venous return and
increased atrial ﬁlling. Stretching the atrial walls increases heart
rate by stimulating both the SA node and the atrial stretch recep-
tors. Stretch receptor activation triggers reﬂexive adjustments of
autonomic output to the SA node, increasing heart rate.
Increased or decreased CO results in corresponding changes
to systemic blood pressure, so blood pressure regulation o±en
involves reﬂexive controls of heart rate. In Chapter 19 we describe
in more detail neural mechanisms that regulate blood pressure.
Chemical Regulation of Heart Rate
present in the blood and other body ﬂuids may inﬂuence heart
rate, particularly if they become excessive or deﬁcient.