Download Regulation of Respiration

Regulation of Respiration
What is
This
Lecture
About?
The nervous system adjusts the rate of
alveolar ventilation to the demands of the
body so that the(PO2) and(PCO2) in the
arterial blood are hardly altered even
during heavy exercise and most types of
respiratory stress.
Respiratory Center
The respiratory center is composed of3 major collections of
neurons:
(1) a dorsal respiratory group (DRG), located in the dorsal
portion of the medulla( causes Inspiration)
(2) a ventral respiratory group (VRG), located in the
ventrolateral part of the medulla, ( causes expiration)
and
(3) the pontine centers a- pneumotaxic center, located
dorsally in the superior portion of the pons, ( mainly
controls rate and depth of breathing) and b- apneustic
center
Note The DRG of neurons plays the most fundamental role
in the control of respiration.
Neural control of Respiration
Until recently, it was
thought the Dorsal
respiratory group of
neurons generate the basic
rhythm of breathing
It is now generally believed
that the breathing rhythm is
generated by a network of
neurons called the PreBrotzinger complex. These
neurons display pacemaker
activity. They are located
near the upper end of the
medullary respiratory
centre
Neural control of Respiration
anterior
The Rhythm:
inspiration followed
by expiration
Fairly normal
ventilation retained if
section above medulla
Ventilation ceases if section
below medulla
 medulla is major
rhythm generator
Dorsal Respiratory Group of Neurons
(DRG)
The DRG of neurons in medulla responsible
for the basic rhythm of respiration.
vagal and the glossopharyngeal nerves,
transmit sensory signals into the respiratory
center from:
(1) peripheral chemoreceptors,
(2) baroreceptors, and
(3) several types of receptors in the lungs.
What gives rise to inspiration?
Dorsal respiratory
group neurones
(inspiratory)
PONS
Fire in bursts
Firing leads to
contraction of
inspiratory muscles
- inspiration
When firing stops,
passive expiration
MEDULLA
SPINAL CORD
The rhythm generated in the
medulla can be modified by
neurones in the pons:
“pneumotaxic
centre” (PC)
Stimulation
terminates inspiration
PC stimulated when
dorsal respiratory
neurones fire
Inspiration inhibited
+
-
Without PC, breathing
is prolonged
inspiratory gasps with
brief expiration
The “apneustic centre”
Apneustic centre
Impulses from
these neurones
excite
inspiratory
area of
medulla
Prolong inspiration
Conclusion?
Rhythm generated in
medulla
Rhythm can be modified
by inputs from pons
The function of the pneumotaxic center is
primarily to limit inspiration. This has a
secondary effect of increasing the rate of
breathing, because limitation of inspiration
also shortens expiration and the entire
period of each respiration.
Ventral Respiratory Group (VRG)
Located in each side of the medulla
1.The neurons of the ventral respiratory
group remain almost totally inactive during
normal quiet respiration..
2.Providing the powerful expiratory signals
to the abdominal muscles during heavy
expiration.
What about “active” expiration
during hyperventilation?
Increased firing
of dorsal
neurones excites
a second group:
Ventral
respiratory
group neurones
In normal quiet
breathing, ventral
neurones do not
activate expiratory
muscles
Excite internal
intercostals,
abdominals etc
Forceful expiration
The Hering-Breuer Inflation Reflex
Stretch receptors located in the muscular
portions of the walls of the bronchi and
bronchioles throughout the lungs transmit
signals through the vagi into the DRG of
neurons when the lungs become
overstretched that “switches off” and stops
further inspiration.
This is called the Hering-Breuer inflation
reflex.
In human the Hering-Breuer reflex is a
protective mechanism & not activated until
the tidal volume (greater than about 1.5 L/
breath).
Chemical Control of Respiration
The goal of respiration is to maintain proper
conc. of O2,CO2,H+ ions in the tissues.
* ↑↑CO2 or H+ stimulate the respiratory center it
self→ ↑↑strength of insp. &exp. signals to the
resp. m.
* O2 does not have a direct effect on the
respiratory center & acts on peripheral
chemoreceptors located in the carotid &aortic
bodies. These in turn transmit signals to the
resp. center.
Chemosensitive area is located in medulla.
is highly sensitive to changes in either
blood PCO2 or H+ in turn excites the other
portions of the respiratory center.
Why does blood CO2 have a more potent
effect in stimulating the chemosensitive
neurons than do blood hydrogen ions?
CO2 can cross the blood brain barrier. But
H+ cannot .
If the blood PCO2↑↑, PCO2 of both the
interstitial fluid of the medulla and the
cerebrospinal fluid ↑↑. In both these fluids,
the CO2 reacts with the H2O to form new
H+ .
Respiratory center activity is increased very
strongly by changes in blood CO2.
A change in blood CO2 has a potent acute
effect on controlling respiratory drive and a
weak chronic effect so after a few days’
adaptation takes place (its effect gradually
declines over the next 1 to 2 days).
Notes
- very marked increase in ventilation caused
by an increase in PCO2
- By contrast, the change in respiration in the
normal blood pH is less.
Peripheral chemoreceptor system
Peripheral chemoreceptor system important for
detecting changes in oxygen in the blood
1-most of the chemoreceptors are in the carotid
bodies
2-few in the aortic bodies
When the O2 concentration in the arterial
blood ↓↓ the chemoreceptors become
strongly stimulated.
An increase in either CO2 or H+ also excites
the chemoreceptors and, indirectly
increases respiratory activity. (the central
effect is more potent).
Stimulation of peripheral chemoreceptors
occurs more rapidly than central stimulation,
so that the peripheral chemoreceptors
important in increasing the rapidity of
response to CO2 at the onset of exercise.
Chronic breathing of low oxygen
stimulates respiration
Acclimatization: Mountain climbers when they
ascend a mountain slowly, over a period of days
rather than a period of hours, they breathe much
more deeply and therefore can withstand far
lower atmospheric oxygen concentrations than
when they ascend rapidly. within 2 to 3 days
respiratory center loses its sensitivity to changes
in PCO2 and H+.
Low O2 can drive the respiratory system to a much
higher level of alveolar ventilation than under acute
conditions, after 2 to 3 days of low oxygen; the
alveolar ventilation ↑↑ and this helps in supplying
additional oxygen to the mountain climber.
Regulation of respiration during exercise
In strenuous exercise, O2 consumption and
CO2 formation can ↑↑ as much as 20-fold.
In the healthy athlete, alveolar ventilation
ordinarily ↑↑ almost exactly in step with the
↑↑ level of O2 metabolism.
The arterial PO2, P CO2, and pH remain
almost exactly normal.
Factors that increase ventilation during
exercise
Reflexes originating from body movement
Increase in body temperature
Adrenaline release
Impulses from the cerebral cortex
Later: accumulation of CO2 and H+ generated by
active muscles
What causes intense ventilation during
exercise?
The brain, *transmitting motor impulses to the
exercising muscles
*collateral impulses into the brain stem to
excite the respiratory center.
(This is analogous to the stimulation of the
vasomotor center of the brain stem during
exercise that causes increase in arterial
pressure).
Other factors affect respiration
Voluntary control of respiration
For short periods of time, respiration can be
controlled voluntarily (hyperventilate or
hypoventilate) to such an extent that
serious derangements in P CO2, pH, and
PO2 can occur in the blood.
• Irritant receptors
– Stimulated by inhaled irritants or mechanical
factors
– Cause bronchospasm, cough, sneeze,
tachypnea, and narrowing of glottis
• These are vasovagal reflexes.
– In hospital triggered by
• Suctioning, bronchoscopy, endotracheal
intubation
“J receptors.”
A few sensory nerve endings in the
alveolar walls in juxtaposition to the
pulmonary capillaries ,stimulated by
engorged pulmonary capillaries or in
pulmonary edema as in congestive heart
failure.
(Their excitation may give the person a
feeling of dyspnea).
Joint receptors
Impulses from moving limbs reflexly
increase breathing
Probably contribute to the increased
ventilation during exercise
Anesthesia. greatly depresses the
respiratory center
Effect of pH on Respiration
The effect of low arterial PO2 on alveolar
ventilation is far greater under some conditions
including the following:
*pulmonary disease: no adequate gas exchange,
too little O2 is absorbed into the arterial bl. &at
same time the arterial PCO2& H+ conc. remain
near normal or are ↑↑because of poor transport
of CO2 through the membrane.
*acclimatization to low O2
Influence of Chemical Factors on Respiration
Periodic Breathing
The person breathes deeply for a short
interval and then breathes slightly for an
additional interval, with the cycle repeating
itself over and over.
Cheyne-Stokes breathing, is characterized
by slowly waxing and waning respiration
occurring about every 40 to 60 seconds.
The basic cause of Cheyne-Stokes
breathing may occurs in everyone it can
be found in congestive heart failure,
uremia and in damage of respiratory
center.
Cheyne-Stokes breathing, showing changing PCO2
Sleep Apnea
Apnea: means absence of spontaneous
breathing.
sleep apnea: apneas occur during normal
sleep, can be caused by obstruction of the
upper airways, especially the pharynx, or
by impaired central nervous system
respiratory drive.
Periods of apnea result in significant
decreases in P O2 and increases in PCO2
which greatly stimulate respiration. causes
sudden attempts to breathe, which result
in loud snorts and gasps followed by
snoring and repeated episodes of apnea.
Summary of ventilation control
Respiration is regulated by:
PO2
via chemoreceptor (carotid bodies in
the arteries)
PCO2 via chemoreceptor for H+ in both
the brain and body.
pH via the same chemoreceptor in brain
and body Direct voluntary control.