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SECTION VI
Cardiovascular Physiology
pressure rise and tachycardia produced by emotions such as
sexual excitement and anger. The connections between the
hypothalamus and the vasomotor area are reciprocal, with
afferents from the brain stem closing the loop.
Inflation of the lungs causes vasodilation and a decrease in
blood pressure. This response is mediated via vagal afferents
from the lungs that inhibit vasomotor discharge. Pain usually
causes a rise in blood pressure via afferent impulses in the
reticular formation converging in the RVLM. However, pro-
longed severe pain may cause vasodilation and fainting. The
activity in afferents from exercising muscles probably exerts a
similar pressor effect via pathway to the RVLM. The pressor
response to stimulation of somatic afferent nerves is called the
somatosympathetic reflex.
Unlike the vasculature, the heart is controlled by both sym-
pathetic and parasympathetic (vagal) nerves. The medulla is
also a major site of origin of excitatory input to cardiac vagal
motor neurons in the nucleus ambiguus (Figure 33–3). Table
33–3 is a summary of conditions that affect the heart rate. In
general, stimuli that increase the heart rate also increase
blood pressure, whereas those that decrease the heart rate
lower blood pressure. However, there are exceptions, such as
the production of hypotension and tachycardia by stimulation
of atrial stretch receptors and the production of hypertension
and bradycardia by increased intracranial pressure.BARORECEPTORS
The
baroreceptors
are stretch receptors in the walls of the
heart and blood vessels. The
carotid sinus
and
aortic arch
re-
ceptors monitor the arterial circulation. Receptors are also lo-
cated in the walls of the right and left atria at the entrance of
the superior and inferior venae cavae and the pulmonary
veins, as well as in the pulmonary circulation. These receptors
in the low-pressure part of the circulation are referred to col-
lectively as the
cardiopulmonary receptors.
The carotid sinus is a small dilation of the internal carotid
artery just above the bifurcation of the common carotid into
external and internal carotid branches (Figure 33–4). Barore-
ceptors are located in this dilation. They are also found in theCLINICAL BOX 33–1
Essential Hypertension & Neurovascular
Compression of the RVLM
In about 88% of patients with elevated blood pressure, the
cause of the hypertension is unknown, and they are said to
have
essential hypertension.
There are data available to
support the view that
neurovascular compression
of the
RVLM is associated with essential hypertension in some
subjects. In the 1970s, Dr. Peter Jannetta, a neurosurgeon
in Pittsburgh, PA, developed a technique for “microvascu-
lar decompression” of the medulla to treat trigeminal neu-
ralgia and hemifacial spasm, which he attributed to pulsa-
tile compression of the vertebral and posterior inferior
cerebellar arteries impinging on the fifth and seventh cra-
nial nerves. Moving the arteries away from the nerves led
to reversal of the neurologic symptoms in many cases.
Some of these patients were also hypertensive, and they
showed reductions in blood pressure postoperatively.
Later, a few human studies claimed that surgical decom-
pression of the RVLM could sometimes relieve hyperten-
sion. There are several reports of patients with a schwan-
noma or meningioma lying close to the RVLM whose
hypertension has been reversed by surgical decompres-
sion. Magnetic resonance angiography (MRA) has been
used to compare the incidence of neurovascular compres-
sion in hypertensive and normotensive individuals and to
correlate indices of sympathetic nerve activity with the
presence or absence of compression. Some of these stud-
ies showed a higher incidence of coexistence of neurovas-
cular compression with essential hypertension than in
other forms of hypertension or normotension, but others
showed the presences of a compression in normotensive
subjects. On the other hand, there was a strong positive re-
lationship between the presence of neurovascular com-
pression and increased sympathetic activity.TABLE 33–2
Factors affecting the activity of the RVLM.Direct stimulation
CO
2
Hypoxia
Excitatory inputs
Cortex via hypothalamus
Mesencephalic periaqueductal gray
Brain stem reticular formation
Pain pathways
Somatic afferents (somatosympathetic reflex)
Carotid and aortic chemoreceptors
Inhibitory inputs
Cortex via hypothalamus
Caudal ventrolateral medulla
Caudal medullary raphé nuclei
Lung inflation afferents
Carotid, aortic, and cardiopulmonary baroreceptors