Breathing Regulation - PPT KUL

Regulation of
Respiration
Suyasning HI
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 expi

(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 c
Respiratory Centers of the

CNS
The primary
portions of
the
brainstem
that control
ventilation
are the
medulla
oblongata
and the pons.
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).
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.
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.
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 O2hemoglobin 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,
stretch receptors in the muscle
portions of bronchi and bronchioles
send a signal through a branch of the
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
apnea 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.
THANK YOU

Breathing Regulation - PPT KUL

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Breathing Regulation - PPT KUL

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Regulation of

Review of Gas Exchange

1. Diaphragm contracts during inspiration and relaxes during expi

Respiratory Centers of the

Dorsal Respiratory Group

Control of Dorsal Respiratory

Ventral Respiratory Group

Chemical Signals in the CNS

In the CNS, CO2 and

H+ is the Main Stimulus (in the

CO2 and H are Linked

The blood-brain barrier

Effect of PCO2 and pH on

Acute and Chronic Elevation of

Renal Control of Acid-Base

Sensing PO2 in the CNS

Effect of Arterial PO2 on

Effect of CO2 and H+ on

Respiration During Exercise

Alveolar Ventilation and

Cheyne-Stokes Breathing Cardiac

Because of the delay in getting blood to the CNS, changes

This type of Cheyne-Stokes breathing can occur in patients

Cheyne-Stokes Breathing Brain

Cheyne-Stokes breathing can also occur in patients

Obstructive Sleep Apnea

Symptoms of Obstructive Sleep

Central Sleep Apnea

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