Respiratory Areas
in the Brainstem
• Medullary respiratory center
– Dorsal groups stimulate the
diaphragm
– Ventral groups stimulate the
intercostal and abdominal
muscles
– This section is especially sensitive
during infancy, and the neurons can
be destroyed if the infant is dropped
and/or shaken violently. The result
can be death due to "shaken baby
syndrome”
• Pontine (pneumotaxic)
respiratory group
– Involved with switching between
inspiration and expiration (fine
tunes the breathing pattern-----there is
a connection with medullary resp.
center but precise function unknown)
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Rhythmic Ventilation
• Starting inspiration
– Medullary respiratory center neurons are continuously active
– Center receives stimulation from receptors (that monitor blood gas levels)
and simulation from parts of brain concerned with voluntary respiratory
movements and emotion
– Combined input from all sources causes action potentials to stimulate
respiratory muscles
• Increasing inspiration
– More and more neurons are activated (to stimulate respiratory muscles)
• Stopping inspiration
– Neurons stimulating the muscles of respiration also stimulate the neurons
in the medullary respiratory center that are responsible stopping
inspiration. They also receive input from pontine group and stretch
receptors in lungs. Inhibitory neurons activated and relaxation of
respiratory muscles results in expiration.
– Note: although the medullary neurons establish the basic rate & depth of
breathing, their activities can be influenced by input from other parts of 23-2
the brain & by input from peripherally located receptors.
Rhythmic Ventilation
• Apnea. Cessation of
breathing. Can be conscious
decision, but eventually
PCO2 levels increase to point
that respiratory center
overrides
• Hyperventilation. Causes
decrease in blood PCO2 level,
which causes respiratory
alkalosis (high blood pH).
Fainting, leads to changes in
the nervous system fires and
leads to the paresthesia (pins
& needles)
• Cerebral (cerebral cortex)and
limbic system. Respiration
can be voluntarily controlled
and modified by emotions
(ex: strong emotions can cause
hyperventilation or produce the
sobs & gasps of crying)
• Chemical control
– Carbon dioxide is major
regulator, but indirectly through
p H change
• Increase or decrease in pH can
stimulate chemo-sensitive area,
causing a greater rate and depth
of respiration
– Oxygen levels in blood affect
respiration when a 50% or greater
decrease from normal levels
exists
•
CO2.
– Hypercapnia: too much CO2
– Hypocapnia: lower than normal
CO2
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Modifying Respiration
23-4
Chemical Control of Ventilation
• Chemoreceptors: specialized neurons that respond
to changes in chemicals in solution
– Central chemoreceptors: chemosensitive area of the
medulla oblongata; connected to respiratory center
– Peripheral chemoreceptors: carotid and aortic
bodies. Connected to respiratory center by cranial
nerves IX and X (9 & 10)
• Effect of pH : chemosensitive area of medulla
oblongata and carotid and aortic bodies respond to
blood pH changes
– Chemosensitive areas respond indirectly through
changes in carbon dioxide
– Carotid and aortic bodies respond directly to p H
changes
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Chemical Control of Ventilation
• Effect of carbon dioxide: small change in carbon
dioxide in blood triggers a large increase in rate and
depth of respiration
- ex: an increase PCO2 of 5 mm Hg causes an increase in
ventilation of 100%.
– Hypercapnia: greater-than-normal amount of carbon
dioxide
– Hypocapnia: lower-than-normal amount of carbon
dioxide
• Chemosensitive area in medulla oblongata is more
important for regulation of PCO2 and pH than the
carotid & aortic bodies (responsible for 15% - 20% of response)
• During intense exercise, carotid & aortic bodies
respond more rapidly to changes in blood pH than
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does the chemosensitive area of medulla
Chemical Control of Ventilation
• Effect of oxygen: carotid and aortic body
chemoreceptors respond to decreased PO2
by increased stimulation of respiratory
center to keep it active despite decreasing
oxygen levels (50% or greater decrease----------bec. of
oxygen-hemoglobin dissociation curve-------at any PO2
above 80 mm Hg nearly all of hemoglobin is saturated
with oxygen)
• Hypoxia: decrease in oxygen levels below
normal values
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Regulation of Blood pH and Gases
23-8
Hering-Breuer Reflex
• Limits the degree of inspiration and prevents
overinflation of the lungs
• Depends on stretch receptors in the walls of
bronchi & bronchioles of the lung.
• It is an inhibitory influence on the respiratory
center & results in expiration. (as expiration proceeds,
stretch receptors no longer stimulated)
– Infants
• Reflex plays a role in regulating basic rhythm of
breathing and preventing overinflation of lungs
– Adults
• Reflex important only when tidal volume large as in
exercise
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Effect of Exercise on Ventilation
• Ventilation increases abruptly
– At onset of exercise
– Movement of limbs has strong influence (body movements
stimulate proprioceptors in joints of the limbs)
– Learned component (after a period of training, the brain “learns”
to match ventilation with the intensity of exercise)
• Ventilation increases gradually
– After immediate increase, gradual increase occurs (4-6
minutes it levels off)
– Anaerobic threshold: highest level of exercise without
causing significant change in blood pH. If exercise
intensity is high enough to exceeded anaerobic threshold,
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lactic acid produced by skeletal muscles
Other Modifications of
Ventilation
• Activation of touch, thermal and pain
receptors affect respiratory center
• Sneeze reflex (initiated by irritants in the nasal cavity),
cough reflex (initiated by irritants in the lungs)
• Increase in body temperature yields increase
in ventilation
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Respiratory Adaptations to
Exercise
• Athletic training
– Vital capacity increases slightly; residual volume
decreases slightly
– At maximal exercise, tidal volume and minute
ventilation increases
– Gas exchange between alveoli and blood increases at
maximal exercise
– Alveolar ventilation increases
– Increased cardiovascular efficiency leads to greater
blood flow through the lungs
23-12
Effects of Aging
• Vital capacity and maximum minute
ventilation decrease (these changes are related to
weakening of respiratory muscles & decreased compliance
of thoracic cage caused by stiffening of cartilage & ribs)
• Residual volume and dead space increase
• Ability to remove mucus from respiratory
passageways decreases
• Gas exchange across respiratory membrane
is reduced
23-13