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Control of Respiration
Dr: Ali Mohamed ibrahim
• Like the heartbeat, breathing must occur in a
continuous, cyclic pattern to sustain life
processes.
• inspiratory muscles must rhythmically contract
and relax to alternately fill the lungs with air
and empty them automatically, without
conscious.
• Respiratory muscles (unlike cardiac muscles)
require electrical stimulation from CNS
• Basic elements of the respiratory regulation
system are :(1) control centers in CNS
(2) sensors
(3) effectors (respiratory muscles).
• the optimum matching of ventilation and
perfusion within the lungs is necessary to
maintain appropriate homeostasis for the arterial
blood gases and hence for oxygen delivery to the
tissues
respiratory control centers
• Located in the pons and medulla.
• These centers are not located in a special
nucleus or a group of nuclei but they are
rather poor defined collection of neurons.
• Respiratory control centers in the brain stem
generate the rhythmic pattern of breathing.
• The primary respiratory control center are the
medullary respiratory center.
• The pontine centers influence output from the
medullary respiratory center.
1. Medullary respiratory center
• consists of two neuronal clusters:
1)dorsal respiratory group (DRG)
• consists mostly of inspiratory neurons whose
descending fibers terminate on the motor
neurons that supply the inspiratory muscles.
When the DRG neurons fire, inspiration takes
place; when they cease firing, expiration
occurs.
• the pre-Bötzinger complex located near the
upper end of the DRG center, this region display
pacemaker activity, similar to those of the SA
node of the heart.
• Scientists believe the rate at which the DRG
inspiratory neurons rhythmically fire is driven by
the pre-Bötzinger complex.
• It sends impulses that increase gradually for 2s &
then they stop for 3s ,this produces the
inspiratory and expiratory periods of the
respiratory cycle .
• There are Opioid receptors on pre-Bötzinger
complex thus, opioids inhibit respiration.
• Depression of respiration is a side effect that
limits the use of opiates in the treatment of
pain.
• 2) ventral respiratory group (VRG):
• consists mostly of expiratory neurons
• Inactive at rest (expiration occurs passively)
• Inactivated when the dorsal group is
stimulated & vice versa (reciprocal
innervation)
• Active during forced expiration
2. Pons Respiratory Centers
• The respiratory centers in the pons exert
“fine-tuning” influences over the medullary
center to help produce normal, smooth
inspirations and expirations.
• Pneumotaxic centre:
• It is located in the upper pons
• It sends impulses to the DRG that help “switch off
” the inspiratory neurons, limiting the duration of
inspiration.
.
• Lesion of this center causes prolonged deep
inspirations and brief, limited expirations
(apneusis).
• Apneustic Centre:
• It is located in the lower pons.
• It the inspiratory neurons from being switched off
by inhibiting Pneumotaxic center .
• It stimulate the dorsal group to increase the
depth of inspiration.
• Lesions of this area causes long gasping
inspirations interrupted by occasional expirations
due to over activity of Pneumotaxic center .
• The apneustic and pneumotaxic centres
function in co-ordination in order to provide a
rhythmic respiratory cycle.
Effects of sections on respiration
• Functions of the different groups of the
respiratory center are studied by performing
sections at various levels in the brain stem
Pons
Medulla
Result is gasping
respiration
Produces prolong,
deep inspirations
Stops breathing since
no automated output
to respiratory system
Control of Respiratory
A) Voluntary control of respiration
B) Involuntary (Automatic) control
• A) Voluntary control of respiration
– is generated from cerebral cortex
– reach the respiratory motor neuron via
corticospinal or corticobulbar. (bypass the
respiratory centers)
– This pathway allows voluntary modification of
breathing during activities, such as talking, singing
& breath holding.
• B) Involuntary (Automatic) control:
• Is generated from spontaneously discharging
neurons in pons & medulla
• these centers Sends impulses to the
respiratory muscles by motor neurons in
cervical & thoracic spinal cord that innervate
the respiratory muscles via reticulospinal
tract.
• This pathway is responsible for the
spontaneous rhythm that allow automatic
breathing without conscious effort, during
waking day & during sleep.
Automatic control regulation
• The respiratory center automatic activity is
regulated by impulses coming from a large
number of receptors (sensors) according to
body needs.
• There are two main classes of receptors:
• chemoreceptor & nonchemical receptors.
Accordingly there are two modes of regulation
of respiration
• 1- chemical regulation: which involve the
variation of blood chemistry (O2, CO2, H) on
ventilation
• 2- non-chemical regulation: (neural)
• is superimposed on the basic chemical
regulation of respiration. It involves other
afferents that affect breathing in particular
situation.
non-chemical regulation(neural)
• 1)From The limbic system :
• this influence breathing during emotions
• 2) From the hypothalamus :
• this alter breathing as apart of its
thermoregulatory function e.g. exposure to
heat cause hyperpnoea in human.
• 3) From the lung’s stretch receptors :
• Marked Stretching of the lungs during forced
inspiration initiates impulses from stretch
receptors via afferent pulmonary vagal fibers.
(The Hering-Breuer inflation reflex )
• marked deflation of the lung during forced
expiration initiates impulses from stretch
receptors via afferent pulmonary vagal fibers.
(Deflation reflex)
• 4) From the irritant receptors :
• in nose and in the trachea
• produces sneezing and coughing.
• 5) From The proprioceptors in skeletal muscles
& joints :
• discharge to the nervous system Leading to
hyperpnea & tachycardia.
• These receptors help to ↑ ventilation during
exercise.
• 6)From the swallowing receptor :
• These receptors are located at the entrance of
the pharynx
• Its stimulated by food during deglutition
• It initiates inhibitory signals to the respiratory
center leading to apnea for 2-3 seconds
• This is protective reflex that prevent food
entrance into the respiratory passages.
Chemical control
• By chemoreceptors that detect chemical
changes of (PO2, PCO2, pH) in the blood or
CSF.
• There are two types of chemoreceptors
- peripheral chemoreceptors
- central chemoreceptor
peripheral chemoreceptors
• called glomus cells, present outside the CNS
• most are in the carotid sinuses & few are in
aortic arch.
Mechanism of pripheral
chemoreception
The peripheral chemoreceptors are stimulated
by:
1.)Hypoxia( PO2 <60mmHg) (main stimulus)
2.)Hypercapenia (+ PCO2 ) (slight stimulus)
3.)Acidosis ( PH) (slight stimulus)
• when peripheral chemoreceptors stimulated
send excitatory impulses via afferent nerves
(IX carotid body, X aortic body) to the
respiratory centers in the medulla.
Peripheral chemoreceptors
Respiratory center
Carotid bodies Aortic bodies
PO2, PCO2, {H+}
Effect of O2 lack on ventilation
Low PO2
Peripheral
chemoreceptor
stimulate
Respiratory center
ventilation
increase
PO2 returned
to normal
PO2 is returned
to normal
Peripheral
chemoreceptors
The central chemoreceptors
• Found on the medulla, in contact with the CSF.
• It monitor the Pco2 in the blood.
• It monitor the H+ concentration of the CSF.
• Stimulated by:
-high hydrogen ions in the CSF, including the
brain interstitial fluid( direct)
- high carbon dioxide in blood (indirect)
• Inhibited by:
-Low blood PCO2
-Low CSF H+
• Hydrogen ions in the blood can not cross the
blood brain barrier(BBB) easily but Carbon
dioxide can cross the BBB & reacts with water
in the CSF to produce carbonic acid & then
bicarbonate & hydrogen ions.
• SO carbon dioxide stimulates central
chemoreceptors indirectly .
• Ventilation increased by 2–3 L/min for 1–mm
Hg rise in PaCO2.
• At normal physiological condition the central
chemoreceptors are the main respiratory drive
of ventilation in response to change in Pco2.
• The peripheral chemoreceptors only take
control if there is dramatic decrease in Po2
Effect of increase in CO2 on ventilation
Rise in PaCO2
Respiratory center
ventilation
PO2 returned
to normal
PaCO2 is reduced
to normal
CO2 diffuses
CSF {H+}
Central
chemoreceptors
CSF
 CSF CO2
stimulate
increase
stimulate
increase
Effect of increase in H+ on ventilation
Respiratory center
ventilation
PO2 returned
to normal
PaCO2 is reduced
and {H+} is reduced
CO2 diffuses
Central
chemoreceptors
CSF
 CSF {H+}
stimulate
stimulate
increase
NOT ALL SO; GO AND READ

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Control of Respiration 36 .pptx

  • 1. Control of Respiration Dr: Ali Mohamed ibrahim
  • 2. • Like the heartbeat, breathing must occur in a continuous, cyclic pattern to sustain life processes. • inspiratory muscles must rhythmically contract and relax to alternately fill the lungs with air and empty them automatically, without conscious. • Respiratory muscles (unlike cardiac muscles) require electrical stimulation from CNS
  • 3. • Basic elements of the respiratory regulation system are :(1) control centers in CNS (2) sensors (3) effectors (respiratory muscles). • the optimum matching of ventilation and perfusion within the lungs is necessary to maintain appropriate homeostasis for the arterial blood gases and hence for oxygen delivery to the tissues
  • 4. respiratory control centers • Located in the pons and medulla. • These centers are not located in a special nucleus or a group of nuclei but they are rather poor defined collection of neurons.
  • 5.
  • 6. • Respiratory control centers in the brain stem generate the rhythmic pattern of breathing. • The primary respiratory control center are the medullary respiratory center. • The pontine centers influence output from the medullary respiratory center.
  • 7. 1. Medullary respiratory center • consists of two neuronal clusters: 1)dorsal respiratory group (DRG) • consists mostly of inspiratory neurons whose descending fibers terminate on the motor neurons that supply the inspiratory muscles. When the DRG neurons fire, inspiration takes place; when they cease firing, expiration occurs.
  • 8. • the pre-Bötzinger complex located near the upper end of the DRG center, this region display pacemaker activity, similar to those of the SA node of the heart. • Scientists believe the rate at which the DRG inspiratory neurons rhythmically fire is driven by the pre-Bötzinger complex. • It sends impulses that increase gradually for 2s & then they stop for 3s ,this produces the inspiratory and expiratory periods of the respiratory cycle .
  • 9. • There are Opioid receptors on pre-Bötzinger complex thus, opioids inhibit respiration. • Depression of respiration is a side effect that limits the use of opiates in the treatment of pain.
  • 10. • 2) ventral respiratory group (VRG): • consists mostly of expiratory neurons • Inactive at rest (expiration occurs passively) • Inactivated when the dorsal group is stimulated & vice versa (reciprocal innervation) • Active during forced expiration
  • 11. 2. Pons Respiratory Centers • The respiratory centers in the pons exert “fine-tuning” influences over the medullary center to help produce normal, smooth inspirations and expirations.
  • 12. • Pneumotaxic centre: • It is located in the upper pons • It sends impulses to the DRG that help “switch off ” the inspiratory neurons, limiting the duration of inspiration. . • Lesion of this center causes prolonged deep inspirations and brief, limited expirations (apneusis).
  • 13. • Apneustic Centre: • It is located in the lower pons. • It the inspiratory neurons from being switched off by inhibiting Pneumotaxic center . • It stimulate the dorsal group to increase the depth of inspiration. • Lesions of this area causes long gasping inspirations interrupted by occasional expirations due to over activity of Pneumotaxic center .
  • 14. • The apneustic and pneumotaxic centres function in co-ordination in order to provide a rhythmic respiratory cycle.
  • 15. Effects of sections on respiration • Functions of the different groups of the respiratory center are studied by performing sections at various levels in the brain stem
  • 16. Pons Medulla Result is gasping respiration Produces prolong, deep inspirations Stops breathing since no automated output to respiratory system
  • 17.
  • 18. Control of Respiratory A) Voluntary control of respiration B) Involuntary (Automatic) control
  • 19. • A) Voluntary control of respiration – is generated from cerebral cortex – reach the respiratory motor neuron via corticospinal or corticobulbar. (bypass the respiratory centers) – This pathway allows voluntary modification of breathing during activities, such as talking, singing & breath holding.
  • 20. • B) Involuntary (Automatic) control: • Is generated from spontaneously discharging neurons in pons & medulla • these centers Sends impulses to the respiratory muscles by motor neurons in cervical & thoracic spinal cord that innervate the respiratory muscles via reticulospinal tract.
  • 21. • This pathway is responsible for the spontaneous rhythm that allow automatic breathing without conscious effort, during waking day & during sleep.
  • 22. Automatic control regulation • The respiratory center automatic activity is regulated by impulses coming from a large number of receptors (sensors) according to body needs. • There are two main classes of receptors: • chemoreceptor & nonchemical receptors. Accordingly there are two modes of regulation of respiration
  • 23. • 1- chemical regulation: which involve the variation of blood chemistry (O2, CO2, H) on ventilation • 2- non-chemical regulation: (neural) • is superimposed on the basic chemical regulation of respiration. It involves other afferents that affect breathing in particular situation.
  • 24. non-chemical regulation(neural) • 1)From The limbic system : • this influence breathing during emotions • 2) From the hypothalamus : • this alter breathing as apart of its thermoregulatory function e.g. exposure to heat cause hyperpnoea in human.
  • 25. • 3) From the lung’s stretch receptors : • Marked Stretching of the lungs during forced inspiration initiates impulses from stretch receptors via afferent pulmonary vagal fibers. (The Hering-Breuer inflation reflex )
  • 26. • marked deflation of the lung during forced expiration initiates impulses from stretch receptors via afferent pulmonary vagal fibers. (Deflation reflex)
  • 27. • 4) From the irritant receptors : • in nose and in the trachea • produces sneezing and coughing.
  • 28. • 5) From The proprioceptors in skeletal muscles & joints : • discharge to the nervous system Leading to hyperpnea & tachycardia. • These receptors help to ↑ ventilation during exercise.
  • 29. • 6)From the swallowing receptor : • These receptors are located at the entrance of the pharynx • Its stimulated by food during deglutition • It initiates inhibitory signals to the respiratory center leading to apnea for 2-3 seconds • This is protective reflex that prevent food entrance into the respiratory passages.
  • 30. Chemical control • By chemoreceptors that detect chemical changes of (PO2, PCO2, pH) in the blood or CSF. • There are two types of chemoreceptors - peripheral chemoreceptors - central chemoreceptor
  • 31. peripheral chemoreceptors • called glomus cells, present outside the CNS • most are in the carotid sinuses & few are in aortic arch.
  • 32.
  • 33. Mechanism of pripheral chemoreception The peripheral chemoreceptors are stimulated by: 1.)Hypoxia( PO2 <60mmHg) (main stimulus) 2.)Hypercapenia (+ PCO2 ) (slight stimulus) 3.)Acidosis ( PH) (slight stimulus)
  • 34. • when peripheral chemoreceptors stimulated send excitatory impulses via afferent nerves (IX carotid body, X aortic body) to the respiratory centers in the medulla.
  • 35. Peripheral chemoreceptors Respiratory center Carotid bodies Aortic bodies PO2, PCO2, {H+}
  • 36. Effect of O2 lack on ventilation Low PO2 Peripheral chemoreceptor stimulate Respiratory center ventilation increase PO2 returned to normal PO2 is returned to normal Peripheral chemoreceptors
  • 37. The central chemoreceptors • Found on the medulla, in contact with the CSF. • It monitor the Pco2 in the blood. • It monitor the H+ concentration of the CSF. • Stimulated by: -high hydrogen ions in the CSF, including the brain interstitial fluid( direct) - high carbon dioxide in blood (indirect) • Inhibited by: -Low blood PCO2 -Low CSF H+
  • 38. • Hydrogen ions in the blood can not cross the blood brain barrier(BBB) easily but Carbon dioxide can cross the BBB & reacts with water in the CSF to produce carbonic acid & then bicarbonate & hydrogen ions. • SO carbon dioxide stimulates central chemoreceptors indirectly . • Ventilation increased by 2–3 L/min for 1–mm Hg rise in PaCO2.
  • 39.
  • 40. • At normal physiological condition the central chemoreceptors are the main respiratory drive of ventilation in response to change in Pco2. • The peripheral chemoreceptors only take control if there is dramatic decrease in Po2
  • 41. Effect of increase in CO2 on ventilation Rise in PaCO2 Respiratory center ventilation PO2 returned to normal PaCO2 is reduced to normal CO2 diffuses CSF {H+} Central chemoreceptors CSF  CSF CO2 stimulate increase stimulate increase
  • 42. Effect of increase in H+ on ventilation Respiratory center ventilation PO2 returned to normal PaCO2 is reduced and {H+} is reduced CO2 diffuses Central chemoreceptors CSF  CSF {H+} stimulate stimulate increase
  • 43. NOT ALL SO; GO AND READ