medulla.
28
In addition, the nucleus of the soli-
tary tract provides both direct and relayed excit-
atory inputs to the cardiac decelerator neurons
in the nucleus ambiguus.
27
Thus, a rise in blood
pressure results in a reflex fall in heart rate and
vasomotor tone, re-establishing a normal arte-
rial pressure. Conversely, a fall in blood pres-
sure causes a reflex tachycardia and vasocon-
striction, re-establishing the necessary arterial
perfusion pressure. As a result, on assuming an
upright posture, there is normally a small in-
crease in both heart rate and blood pressure.
On occasion, loss of consciousness may re-
sult from failure of this baroreceptor reflex arc.
In such patients, measurement of standing and
supine blood pressure and heart rate discloses
a fall in blood pressure on assuming an upright
posture that is clinically associated with symp-
toms of insufficient CBF. Rigid criteria for di-
agnosing orthostatic hypotension (e.g., a fall
in blood pressure of 10 or 15 mm Hg) are not
useful, as systemic arterial pressure is usually
measured in the arm but the symptoms are
produced by decreased blood flow to the brain.
A pressure head that is adequate to perfuse
the arm (which is at the same elevation as the
heart) will be reduced by 15 to 23 mm Hg at
the brain in an upright posture, and if perfu-
sion pressure to the brain falls even a few mm
Hg below the level needed to maintain auto-
regulation, the drop in cerebral perfusion may
be precipitous.
The most common nonneurologic causes of
orthostatic hypotension, including low intravas-
cular volume (often a consequence of diuretic
administration or inadequate fluid intake), car-
diac pump failure, and medications that impair
arterial constriction (e.g., alpha blockers or di-
rect vasodilators), do not impair the tachycardic
response. Most neurologic cases of orthostatic
hypotension, including peripheral autonomic
neuropathy or central or peripheral autonomic
degeneration, impair both the heart rate and
the blood pressure responses. Put in other
words, the hallmark of baroreceptor reflex fail-
ure is absence of the elevation of heart rate
when arterial pressure falls in response to an
orthostatic challenge.
Respiration
The brain cannot long survive without an ad-
equate supply of oxygen. Within seconds of
being deprived of oxygen, brain function be-
gins to fail, and within minutes neurons begin
to die. The physician must ensure that respi-
ration is supplying adequate oxygenation. To
do this requires examination of both respiratory
exchange and respiratory pattern. Listening to
the chest will ensure that there is adequate
movement of air. A normal patient at rest will
regularly breathe at about 14 breaths per min-
ute and the exchange of air can be heard at
both lung bases. The physician should estimate
from the rate and depth of respiration whether
the patient is hypo- or hyperventilating or
whether respiration is normal. The patient’s
color is a gross indicator of oxygenation: cya-
nosis indicates deficient oxygenation; a cherry
red color may also indicate deficient oxygena-
tion because of CO intoxication. A better esti-
mate of oxygenation can be achieved by plac-
ing an oximeter on the finger; many intensive
care units and some emergency departments
also measure expired CO
2
, which correlates
well with PCO
2
.
This section considers the neuroanatomic
basis of respiratory abnormalities that accom-
Table 2–2 Neuropathologic Correlates
of Breathing Abnormalities
Forebrain damage
Epileptic respiratory inhibition
Apraxia for deep breathing or breath holding
‘‘Pseudobulbar’’ laughing or crying
Posthyperventilation apnea
Cheyne-Stokes respiration
Hypothalamic-midbrain damage
Central reflex hyperpnea (neurogenic
pulmonary edema)
Basis pontis damage
Pseudobulbar paralysis of voluntary control
Lower pontine tegmentum damage or
dysfunction
Apneustic breathing
Cluster breathing
Short-cycle anoxic-hypercapnic periodic
respiration
Ataxic breathing (Biot)
Medullary dysfunction
Ataxic breathing
Slow regular breathing
Loss of autonomic breathing with preserved
voluntary control
Gasping
46
Plum and Posner’s Diagnosis of Stupor and Coma
pany coma (Table 2–2, Figure 2–3). Chapter 5
discusses respiratory responses to metabolic
disturbances. Because neurogenic and meta-
bolic influences on breathing interact exten-
sively, respiratory changes must be interpreted
cautiously if there is evidence of pulmonary
disease.
The pattern of respiration can give impor-
tant clues concerning the level of brain dam-
age. Once assured that there is adequate ex-
change of oxygen, the physician should watch
the patient spontaneously breathe. Irregulari-
ties of the respiratory pattern that provide clues
to the level of brain damage are described in
the paragraphs below.
PATHOPHYSIOLOGY
Breathing is a sensorimotor act that integrates
nervous influences arising from nearly every
level of the brain and upper spinal cord. In hu-
mans, respiration subserves two major func-
ACh
Muscarinic
Medulla
Midbrain
Spinal Cord:
NE
Xn.
IX
and X Nerves
Cervical
Thoracic
Lumbar
Sacral
Cortex
Infralimbic
Cortex
Insular
Cortex
Hypothalamus
Rostral Ventrolateral
Medulla
Nucleus of the
Solitary Tract
Caudal
Ventrolateral
Medulla
Amygdala
Parabrachial Nucleus
VP Thalamus
Nucleus Ambiguus
1-receptor
␣1-receptor
Pons
Figure 2–3. A diagram summarizing the cardiovascular control pathways in the brain. Visceral afferent information (gray)
arrives from nerves IX and X into the nucleus of the solitary tract. This information is then distributed to the parabrachial
nucleus, which relays it to the forebrain, and to the ventrolateral medulla, where it controls cardiovascular reflexes. These
include both vagal control of heart rate (red) and medullary control (purple) of the sympathetic vasomotor control area of
the rostral ventrolateral medulla (orange), which regulates sympathetic outflow to both the heart and the blood vessels
(dark green). Forebrain areas that influence the cardiovascular system (brown) include the insular cortex (a visceral
sensory area), the infralimbic cortex (a visceral motor area), and the amygdala, which produces autonomic emotional
responses. All of these act on the hypothalamic sympathetic activating neurons (light green) in the paraventricular and
lateral hypothalamic areas to provide behavioral and emotional influence over the blood pressure and heart rate. ACh,
acetylcholine; NE, norepinephrine; VP, ventroposterior.
Examination of the Comatose Patient
47