Transcript Regulation of Respiration Learning Objectives Regulation of ventilation by the CNS and PNS. • Know the basic anatomy of the CNS respiratory.

Regulation of Respiration
Learning Objectives
Regulation of ventilation by the CNS and PNS.
• Know the basic anatomy of the CNS respiratory center.
• Know how the dorsal respiratory group, ventral
respiratory group and the pneumotaxic center control
respiration.
• Understand how chemical changes in the CNS and PNS
influence the respiratory changes.
• Know how respiration is regulated during exercise.
• Understand the changes in the pulmonary system that
cause Cheyne-Stokes breathing and sleep apnea.
Review of Gas Exchange
Review Mechanics of Breathing
1. Diaphragm contracts during inspiration and relaxes during expiration
(major force during normal, quiet breathing).
2. Intercostal muscles elevate and depress the ribs.
3. Abdominal muscles contract during heavy expiration.
These are skeletal muscles that need stimulation from the CNS to contract.
Respiratory Centers of the CNS
• The primary
portions of the
brainstem that
control ventilation
are the medulla
oblongata and the
pons.
Respiratory Centers
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Two respiratory nuclei in medulla oblongata
Inspiratory center (dorsal respiratory group, DRG)
• more frequently they fire, more deeply you
inhale
• longer duration they fire, breath is prolonged,
slow rate
Expiratory center (ventral
respiratory group, VRG)
•involved in forced
expiration
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Dorsal Respiratory Group
• Sets the basic respiratory
rate.
• Stimulates the inspiratory
muscles to contract
(diaphragm).
• The signals it sends for
inspiration start weakly and
steadily increase for ~ 2 sec.
This is called a ramp and
produces a gradual
inspiration.
• The ramp then stops
abruptly for ~ 3 sec and the
diaphragm relaxes.
Control of Dorsal Respiratory Group
The vagus nerve and
glossopharyngeal nerves receive
input from:
• Peripheral chemoreceptors
• Baroreceptors
• Several pulmonary receptors
Sensory input can change 2 qualities
of the ramp:
• The rate of increase (e.g.,
increase during heavy breathing
to fill lungs more rapidly).
• The timing of the stop (e.g.,
stopping the ramp sooner
shortens the rate of inspiration
and expiration, thus increasing
the frequency of respiration).
Ventral Respiratory Group
• Inactive during normal,
quiet respiration.
• At times of increased
ventilation, signals from the
dorsal group stimulate the
ventral group.
• The ventral group then
stimulates both inspiratory
and expiratory muscles.
E.g., the abdominal muscles
are stimulated to contract
and help force expiration.
Respiratory Centers in Pons
Pneumotaxic center (upper pons)
•Sends continual inhibitory impulses to inspiratory
center of the medulla oblongata,
•As impulse frequency rises, breathe faster and
shallower
Apneustic center (lower pons)
•Stimulation causes apneusis
•Integrates inspiratory cutoff
information
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Pneumotaxic Center
• Controls stopping point of
the dorsal group ramp.
• Strong pneumotaxic
stimulation shortens the
duration of inspiration and
expiration. This increases
the breathing rate.
• Strong pneumotaxic
stimulation can increase the
rate of breathing to 30-40
breaths/min and weak
pneuomotaxic stimulation
can decrease the breathing
rate to 3-5 breaths/min.
Respiratory Structures in Brainstem
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2. Rhythmic Ventilation (Inspiratory Off Switch)
• Starting inspiration
– Medullary respiratory center neurons are
continuously active (spontaneous)
– Center receives stimulation from receptors and
brain concerned with voluntary respiratory
movements and emotion
– Combined input from all sources causes action
potentials to stimulate respiratory muscles
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•Increasing inspiration
–More and more neurons are activated
•Stopping inspiration
–Neurons receive input from pontine group and
stretch receptors in lungs.
–Inhibitory neurons activated and relaxation of
respiratory muscles results in expiration.
–Inspiratory off switch.
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3. Higher Respiratory Centers
Modulate the activity of the more primitive controlling
centers in the medulla and pons.
Allow the rate and depth of respiration to be controlled
voluntarily.
During speaking, laughing, crying, eating, defecating,
coughing, and sneezing. ….
Adaptations to changes in environmental temperature -Panting
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Respiratory Center
• We will discuss the
following groups of neurons
in the respiratory center.
• Dorsal respiratory group
(medulla).
• Ventral respiratory group
(medulla).
• Pneumotaxic center (pons).
Control of Respiratory Center
• We have discussed the CNS structures that
control ventilation.
• Now, we will go over the following:
1. How chemical changes in the CNS and PNS
influence the respiratory center.
2. Respiration during exercise.
3. Some disorders of respiration.
Chemical Signals in the CNS
• The levels of what
chemicals are going to
control respiration?
CO2, H+ ions and O2.
• In the CNS, CO2 and H+
are particularly
important.
• O2 has a greater effect
in the PNS.
H+ is the Main Stimulus (in the CNS)
• In the chemosensitive areas of
the respiratory center,
increased H+ is the main
stimulus.
• Activation of the central
chemoreceptors by H+ excites
the dorsal respiratory group of
neurons (inspiratory area) and
thus increase the respiration
rate.
• Why then, does activation of
central chemoreceptors occur
mainly after a rise in
peripheral CO2, but not so
much with peripheral H+?
CO2 and H+ are Linked
• The blood-brain barrier is
not very permeable to H+;
however, CO2 easily
diffuses across the BBB
(as usual).
• As we have discussed,
increases in CO2 cause
increases in H+.
• So, once CO2 diffuses into
the chemosensitive
regions of the CNS, H+ is
formed and stimulates
the dorsal group.
Effect of PCO2 and pH on Ventilation
Acute and Chronic Elevation of CO2
and H+
• An acute increase in CO2/H+ stimulates
respiration, which helps remove the excess
CO2/H+.
• What system regulates the long-term levels of
H+?
Renal Control of Acid-Base Balance
• Bicarbonate must react with
H+ before it can be
reabsorbed.
• If H+ is high, the kidneys
reabsorb nearly all the
bicarbonate. The excess H+
in the tubular lumen
combines with phosphate
and ammonia and is
excreted as salts.
• The extra bicarbonate will
then slowly diffuse into the
CNS and bind the excess H+.
Sensing PO2 in the CNS
Why does the CNS directly monitor levels of CO2 or H+ ions more than O2?
• Remember the O2-hemoglobin
dissociation curve.
• Hemoglobin buffers O2
delivery to the tissues even
with large changes in PO2.
• Also remember, the brain
receives a very steady supply
of blood under normal
conditions.
• So, O2 delivery in the brain is
fairly stable under normal
conditions and there is no as
much of a need to directly
monitor PO2.
Peripheral Chemoreceptors
• Peripheral chemoreceptors are
located in carotid and aortic
bodies and sense the level of
O2 (PO2).
• Blood flow to the receptors is
very high; so very little
deoxygenated (venous) blood
accumulates.
• Thus, they sense arterial O2
levels.
• Low PO2 levels stimulates the
dorsal respiratory group.
• The signal is sent to the
respiratory center via the
vagus or glossopharyngeal
nerve
Effect of Arterial PO2 on Ventilation
Effect of CO2 and H+ on Peripheral
Chemoreceptors
• Elevated CO2 and H+ also stimulate peripheral
chemoreceptors.
• This effect is less powerful than the effect on
CNS chemoreceptors, but it occurs ~ 5 x faster
than occurs in the CNS.
Hering-Breuer Inflation Reflex
• When the lungs become overinflated, streth
receptors in the muscle portions of bronchi
and bronchioles send a signal through a vagus
nerve to the dorsal respiratory group of
neurons.
• This signal switches off the inspiratory ramp
sooner. This decreases the amount of filling
during inspiration, but increases the rate of
respiration.
Respiration During Exercise
• During exercise, O2 consumption and CO2
formation can increase 20-fold.
• What happens to the partial pressures of O2
and CO2 in the blood?
The partial pressures do not change much.
This can occur if the ventilation increases in proportion to the
increase in O2 consumption and CO2 production.
O2 Consumption and Ventilation
During Exercise
• The increase in ventilation
during exercise prevents
large changes in the partial
pressure of O2 or CO2.
• The increase in ventilation
occurs before there is a
change in blood chemicals.
• Neuronal signals are sent to
the respiratory center
during exercise, possibly at
the same time signals are
being sent to the skeletal
muscles.
Alveolar Ventilation and Arterial PCO2
During Exercise
• The decrease PCO2 at the
onset of exercise
demonstrates that
increasing blood CO2 does
not trigger the increase in
ventilation during exercise.
• However, chemical changes
do fine-tune the ventilation
rate. Notice the decrease in
ventilation associated with
the decrease in PCO2 at the
onset of exercise.
Cheyne-Stokes Breathing
• Not having local control over ventilation can
be an issue if there is a delay or problem in
communication between the lungs and the
CNS.
• E.g., Cheyne-Stokes breathing occurs when
there is a long delay in the transport of blood
from the lungs to the brain.
Cheyne-Stokes Breathing – Cardiac Failure
• Because of the delay in getting blood to the CNS, changes in alveolar O2 or
CO2 progress longer than normal. Then, once the change is sensed by the
CNS, the resulting change in ventilation proceeds longer than is needed.
• This type of Cheyne-Stokes breathing can occur in patients with severe
cardiac failure because the blood flow is slow.
Cheyne-Stokes Breathing – Brain Damage
• Cheyne-Stokes breathing can also occur in patients with brain
damage. In these patients, the response to changes in blood gases
is exaggerated. As a result, changes in ventilation overcompensate
for changes on blood gases. This is a particularly bad sign, as death
often follows this breathing pattern in patients with brain damage.
Sleep Apnea
• Apnea is the temporary suspension of
breathing.
• Normally, some episodes of apea occur. In
people with sleep apnea, the episodes are
longer and more frequent.
• 2 types of sleep apnea are:
Obstructive sleep apnea
Central sleep apnea
Obstructive Sleep Apnea
• This occurs when the pharynx collapses during
sleep. The pharynx is normally held open by
muscles, which at night, relax.
• In patients with sleep apnea, the pharynx is
collapsed while the muscles relax. Some of
the factors that cause this collapse include:
– Excess fat deposits in the soft tissues of the pharynx or fat masses in
the neck.
– Nasal obstruction
– Enlarged tonsils
– Very large tongue
– Certain shapes of the palate
Symptoms of Obstructive Sleep Apnea
• Loud snoring and labored breathing that often
progressively worsens.
• Long silent periods (apnea) that cause
increases in PCO2 and decreases in PO2.
• This stimulates respiration, which results in
loud snorts and gasps.
• This repeats.
Central Sleep Apnea
• Less common than obstructive sleep apnea.
• The CNS signal to the respiratory muscles
stops.
• Can be caused by damage to the central
respiratory center or respiratory
neuromuscular junction.