CHAPTER 6 • NEUROHUMORAL CONTROL OF THE HEART AND CIRCULATION
133
Aortic
Pressure
Heart
Rate
Phases:
I
II
III
IV
Valsalva
■ FIGURE 6.9 Baroreceptors responses during a Valsalva maneuver. During Phase I, which occurs at the
beginning of the forced expiration, aortic pressure increases (due to aortic compression) and heart rate
decreases reflexively. Aortic pressure falls during Phase II because compression of thoracic veins reduces
venous return and cardiac output; reflex tachycardia occurs. Phase III begins when normal respiration
resumes, and is characterized by a small transient fall in aortic pressure (because of removal of aortic
compression) and a small increase in heart rate. A ortic pressure increases (and heart rate reflexively
decreases) during Phase IV because resumption of normal cardiac output occurs while systemic vascular
resistance is elevated from sym pathetic activation that occurred during Phase II.
becomes compressed, venous return to the
heart is compromised, causing cardiac out-
put and aortic pressure to fall (Phase II). As
aortic pressure falls, the baroreceptor reflex
increases heart rate. A decrease in stroke vol-
ume accounts for the fall in pulse pressure.
After several seconds, arterial pressure (both
mean and pulse pressure) is reduced, and
heart rate is elevated. W hen the subject begins
breathing again, the sudden loss of compres-
sion on the aorta causes a small, transient
dip in arterial pressure and a further reflex
increase in heart rate (Phase III). W hen com -
pression of the vena cava is removed, venous
return suddenly increases, causing a rapid rise
in cardiac output several seconds later, which
leads to a transient increase in arterial pres-
sure (Phase IV). Arterial pressure overshoots
during Phase IV because the systemic vascu-
lar resistance is increased by sympathetic acti-
vation that occurred during Phase II owing to
the baroreceptor reflex. Heart rate reflexively
decreases during Phase IV in response to the
transient elevation in arterial pressure.
In addition to arterial baroreceptors, stretch
receptors are located at the venoatrial junctions
of the heart (cardiopulmonary receptors) and
respond to atrial filling and contraction. These
tonically active receptors are innervated by
myelinated vagal afferents. Increased stretch
caused by an increase in venous return can
under some conditions increase heart rate via
medullary activation of sympathetic efferent
activity to the SA node. This response, which
is called the Bainbridge reflex, increases heart
rate when the initial heart rate is low.
An increase in blood volume and venous
pressure stimulates other types of cardiopul-
monary receptors
to
decrease
antidiuretic
hormone (ADH, vasopressin) release by the
posterior
pituitary.
Decreased
circulating
ADH causes diuresis, which leads to a fall in
blood volume and venous pressure. If blood
volume is lost as a result of dehydration or
hemorrhage,
these
receptors
will
increase
ADH release so that the kidneys excrete less
water.
Unmyelinated vagal afferents are found
throughout the atria and ventricles. Receptors
associated with these vagal afferents respond
to stretch such that the firing rate of these
receptors is enhanced with increased atrial
and ventricular pressures. The effects of these
receptors on sympathetic and vagal outflow
are similar to those on the arterial barore-
ceptors. Depending upon the circumstances,
however, these receptors can either oppose
or reinforce arterial baroreceptor function.
In heart failure, atrial and ventricular filling
pressures
are
increased,
whereas
arterial
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