Presentation of respiration and reflex associated with it
REGULATION OF RESPIRATION
• The main function of respiratory system is to
maintain Pco2 ,Po2 and pH of arterial blood constant
by adjusting ventilation.
• Spontaneous respiration is produced by rhythmic
discharges from the brain to the motor neurons
that innervate respiratory muscles.
• Respiration is regulated by two mechanisms:
• Neural control
• Chemical control
Neural control :Voluntary
Automatic
Reflex control
Voluntary control
• Respiration can be controlled voluntarily to some extent
because all the muscles concerned with respiration are
voluntary.
• The center for voluntary control is motor cortex which
send impulses through corticospinal tract to the
respiratory motor neurons.
• Voluntary hyperventilation and voluntary apnea are
possible
• The point at which breathing can no longer be
voluntarily inhibited is called breaking point.
• Normally it is 40 seconds
Reason : During apnea there is increase in
Pco2,increase in H+ and decrease in Po2.
Presentation of respiration and reflex associated with it
Automatic control
• Automatic centre for control of respiration are
located in the pons and medulla.
• These centers are located bilaterally
• Nerve fibers mediating inspiration converge on
phrenic motor neurons(C3,4,5) and external
intercostal neurons in spinal cord.
• The fibres concerned with expiration converge on
spinal cord motor neuron that supply expiratory
muscles mainly internal intercostal muscles.
• The motor neurons to expiratory muscles are
inhibited when those supplying the inspiratory
muscles are activated through reciprocal innervation.
MEDULLARY CENTERS
• Rhythmic respiration is initiated by small group of
pacemaker cells in the pre-Bontziger complex on
both sides of medulla oblangata.
• These neurons can discharge spontaneously and are
responsible for the rhythmicity of respiration.
• Medulla also contain dorsal respiratory group and
ventral respiratory group.
DORSAL RESPIRATORY GROUP(DRG)
• DRG is located in and near the nucleus of tractus
solitarius(NTS).
• It is made up of inspiratory neurons which are
controlled by pacemaker cells in the Pre-Botziger
complex.
• They are active during inspiration.
• They receive impulses from lungs, chemoreceptors
and baro-receptors through vagus.
VENTRAL RESPIRATORY GROUP
• It is located in the ventrolateral part of medulla.
• It extends through nucleus ambiguus and nucleus
retro-ambiguus.
• It contains inspiratory and expiratory neurons.
• Expiratory neurons inhibit inspiratory neurons during
expiration.
Inspiratory ramp signal
• Pattern of action potential produced by the
respiratory center is called inspiratory ramp signal
• Initially there is a latent period then the intensity
of action potential increases and then decreases
followed by a latent period.
• The cycle is repeated and normally the duration of
one cycle is 4-5 seconds.
• The impulses pass to the inspiratory muscles and
produce inspiration
PONTINE CENTERS
• Rhythmic discharge of medullary neurons are
modified by neurons of pons and afferents coming
from the receptors in airways and lungs through
vagus.
• In the upper part of pons there is a pair of
respiratory centres called pneumotaxic centre.
• Pneumotaxic centers has inhibitory effect on I
neurons.
• When this area is stimulated ,I neurons are inhibited
and duration of IRS is reduced.
• Rate of respiration is increased and filling volume
will be decreased; respiration becomes shallow and
rapid.
• Lower part of pons contain another set of neurons
called apneustic center which is tonically active.
• It has excitatory effect on I neurons .
• Stimulation of these center increases duration of
IRS producing sustained contraction of inspiratory
muscles with expiratory gasps in between(apneusis).
Genesis of respiration
Genesis of inspiration:
• Apneustic center activates the inspiratory centre.
• Inspiratory center discharges over pathways in the
spinal cord to C3,4,5 and T1,2 and inspiration starts.
Genesis of expiration:
• Inspiratory neurons in the medulla send excitatory
impulses to pneumotaxic center which inturn inhibit
the apneustic center.
• Pulomonary stretch receptors in lungs get stimulated
during inspiration also send inhibitory impulses via
vagus nerve to the apneustic center.
• Pneumotaxic center stimulates expiratory neuron in
medulla which reciprocally inhibits the inspiratory
center.
• As a result inspiratory center stops discharging and
expiration follows.
• When the activity of inspiratory neurons are
increased the rate and depth of inspiration is also
increased.
Presentation of respiration and reflex associated with it
Presentation of respiration and reflex associated with it
Reflex control of respiration
Receptors are classified into :
• Receptors inside respiratory system
• Receptors outside respiratory system
Receptors inside respiratory centers:
• Stretch receptors
• Pulmonary irritant receptors
Stretch receptors
Hering –Breuer Reflexes:
Hering Breuer Inflation reflexes
• When there is increase in the tidal volume greater
than 1L,stretch receptors of lungs are stimulated .
• There is increased rate
of afferent impulses
passing through the
vagus to the inspiratory
centre and this leads to
inhibition of inspiratory
muscles
• This reflex operates
only when the tidal
volume exceeds 1-1.5 L
Hering Breuer Deflation reflex
• This reflex operates when there is excessive
deflation of lungs.
• Here there is stimulation of inspiration to bring back
the lung volume to normal.
Importance:
• It functions as an important feedback mechanism
and contribute to rhythmicity of respiration in NB
babies.
Irritant receptors.
• Pulmonary irritant receptors are found in airway
epithelial cells.
Stimulation of these receptors produce:
• Bronchoconstriction
• Hyperventilation
• Cough, sneezing etc
Cough reflex:
• This is a protective reflex .
• Stimulation of irritant receptors of larynx, trachea
and bigger bronchi produces cough.
Sneezing reflex:
• Stimulation of irritant receptors of nasal cavity and
upper airways produces sneezing.
• Sneezing is forced expiration against open glottis.
J reflex
• ‘J’ receptors are juxta-capillary receptors which are
present on the wall of the alveoli and have close
contact with the pulmonary capillaries.
• Stimulation of the ‘J’ receptors produces a reflex
response, which is characterized by apnea,
hyperventilation, bradycardia, hypotension and
weakness of skeletal muscles.
• Conditions when ‘J’ receptors are
stimulated :
• i. Pulmonary congestion
• ii. Pulmonary edema
• iii. Pneumonia
• iv. Over inflation of lungs
Receptors outside respiratory system
Those which stimulate respiration:
• Proprioceptors
• Nociceptors
• Thermoreceptors
• Emotions
Those which inhibit respiration:
• Baroreceptors
• Visceroceptors.
Proprioceptors
• These are receptors in muscles, tendons and joints.
• Stimulation of these receptors reflexly stimulates
I neurons which will increase ventilation at the
start of exercise .
•Nociceptors:
• These are pain receptors which when stimulated
stimulate the respiratory center.
• CHEMORECEPTORS:
• Acidosis and hypoxia stimulate chemoreceptors.
• THERMORECEPTORS:
• Thermoreceptors present in the hypothalamus are
stimulated when there is increase in body temperature
as in fever ,exercise.
• EMOTIONAL STIMULI
• Emotional stimuli produces impulses from hypothalamus
,limbic system which stimulate respiratory centre.
Those which inhibit Respiration:
Baroreceptors:
Increase in blood pressure stimulates baroreceptors
leading to inhibition of respiration.
Visceroceptors:
In visceral reflexes like vomiting, swallowing,
deglutition, there is reflex inhibition of respiration.
Factors affecting respiration
CHEMICAL REGULATION OF
RESPIRATION
• Changes in pO2,pCO2 and H+ concentration acts on
the respiratory centers in the medulla through a
set of receptors called as chemo receptors.
• Chemoreceptors are classified into:
 Central chemoreceptors
 Peripheral chemoreceptors.
Central chemoreceptors
• These are a set of neurons located on either side of
medulla near the exit of IX and X cranial nerves
• These can sense changes in H+ concentration in the
brain interstitial fluid.
• Central chemoreceptors are surrounded by brain
extracellular fluid.
• Blood brain barrier and blood CSF barrier are
easily crossed by carbondioxide.
• Whenever there is hypercapnia CO2 enters brain
tissue and CSF, where it is hydrated to form
H2CO3.
• This splits to form H+ and HCO3-.
• Increase in H+ concentration is only the direct
stimulant for central chemoreceptors.
• CO2 has only indirect action.
• Lack of oxygen does not have significant effect on
the central chemoreceptors
• Stimulation from central
chemoreceptors go to the
inspiratory center(DRG) and
stimulate respiration.
• Central chemoreceptors are
inhibited by anaesthesia,
cyanosis ,during sleep etc.
Presentation of respiration and reflex associated with it
Peripheral chemoreceptors
• These are carotid body and aortic body.
• These are neurovascular structures
Location:
• Carotid body is located at the bifurcation of common
carotid artery.
• Aortic bodies are located in the arch of aorta.
Presentation of respiration and reflex associated with it
Innervation of peripheral
chemoreceptors.
• Carotid body is supplied by a branch of ninth cranial
nerve(sinus nerve).
• Sensory impulses from carotid body are carried
through this nerve.
• Aortic body is supplied by a branch of vagus
nerve.(aortic nerve)
• Sinus nerve and aortic nerve together referred as
sino-aortic nerve.
• PCR contains two types of cells surrounded by
fenestrated sinusoidal capillaries.
• Type I cell/glomus cells
• Type II cells/Glial cells / supporting cells.
Type I cell or glomus cells.
• They contain dense granules with dopamine.
• They are in close association with afferent nerve
fibres of ninth cranial nerves.
Type II cells/glial cells or supporting cells.
• These cells surround 4-6 glomus cells .
• Function : Protection and support of glomus cells.
Mechanism of action of PCR
• Reduction in partial pressure of oxygen is the
most potent stimulus for PCR.
• If the arterial pO2 falls below 60 mm of Hg, the
peripheral chemoreceptors are strongly
stimulated which inturn will stimulate the
respiratory center .
• This leads to increase in rate and depth of
respiration which brings blood pO2 to normal
• In the absence of PCR, severe hypoxia depress
respiration by a direct inhibitory action on
respiratory centres.
Factors affecting PCR
Decrease in arterial pO2.
• Vascular stasis as in circulatory shock(stagnant
hypoxia).
• The PCR responds only to reduction in dissolved
oxygen in the blood.
• In anemic hypoxia and carbon-monoxide poisoning
there is no stimulation of respiration through PCR
Decrease in pCO2
• Peripheral chemoreceptors are also sensitive to
increased pCO2.
• Increased pCO2 stimulates peripheral chemo
receptors which inturn stimulates resp centre
• Increase in carbon dioxide washout until arterial
pCO2 becomes normal.
Effect of H+ concentration
Acidosis stimulates respiratory center and causes
hyperventilation
Alkalosis depress respiratory center and causes
hypoventilation.
Mediated by peripheral chemoreceptors.
NOTE : Action of CO2 on respiration is increased by
Hypoxia .
• Decreased by sleep, hypothermia and anaesthesia.
Presentation of respiration and reflex associated with it
ABNORMALITIES
Respiratory center depression:
• Causes : Old age
• Anesthetics.
Periodic breathing : Consists of alternating waxing
and waning of respiration or alternate hyperpnea and
apnea.
• It may be normal or abnormal.
Types of periodic breathing
• 1.Voluntary hyperventilation
• Hyperventilation in normal subject is followed by a
period of apnea which in turn is followed by a few
shallow breaths and then another period of apnea
followed again by few breaths.
• This cycles lasts for some time before normal
breathing is resumed.
2.Cheyne-stokes respiration
• Seen in both physiological and pathological conditions
• Regular alternating period of hyperventilation and
apnea are seen.
Physiological causes:
• Deep sleep
• Infants
• High altitude
Pathological causes:
• Congestive cardiac failure
• Raised ICT, Uremia and morphine poisoning.
3.Biot’s breathing
• This type of breathing is always pathological.
• Irregular periods of apnea and hyperventilation.
• Changes are abrupt.
Causes : Meningitis
Medullary lesions.

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Presentation of respiration and reflex associated with it

  • 2. REGULATION OF RESPIRATION • The main function of respiratory system is to maintain Pco2 ,Po2 and pH of arterial blood constant by adjusting ventilation. • Spontaneous respiration is produced by rhythmic discharges from the brain to the motor neurons that innervate respiratory muscles.
  • 3. • Respiration is regulated by two mechanisms: • Neural control • Chemical control Neural control :Voluntary Automatic Reflex control
  • 4. Voluntary control • Respiration can be controlled voluntarily to some extent because all the muscles concerned with respiration are voluntary. • The center for voluntary control is motor cortex which send impulses through corticospinal tract to the respiratory motor neurons. • Voluntary hyperventilation and voluntary apnea are possible
  • 5. • The point at which breathing can no longer be voluntarily inhibited is called breaking point. • Normally it is 40 seconds Reason : During apnea there is increase in Pco2,increase in H+ and decrease in Po2.
  • 7. Automatic control • Automatic centre for control of respiration are located in the pons and medulla. • These centers are located bilaterally • Nerve fibers mediating inspiration converge on phrenic motor neurons(C3,4,5) and external intercostal neurons in spinal cord.
  • 8. • The fibres concerned with expiration converge on spinal cord motor neuron that supply expiratory muscles mainly internal intercostal muscles. • The motor neurons to expiratory muscles are inhibited when those supplying the inspiratory muscles are activated through reciprocal innervation.
  • 9. MEDULLARY CENTERS • Rhythmic respiration is initiated by small group of pacemaker cells in the pre-Bontziger complex on both sides of medulla oblangata. • These neurons can discharge spontaneously and are responsible for the rhythmicity of respiration. • Medulla also contain dorsal respiratory group and ventral respiratory group.
  • 10. DORSAL RESPIRATORY GROUP(DRG) • DRG is located in and near the nucleus of tractus solitarius(NTS). • It is made up of inspiratory neurons which are controlled by pacemaker cells in the Pre-Botziger complex. • They are active during inspiration. • They receive impulses from lungs, chemoreceptors and baro-receptors through vagus.
  • 11. VENTRAL RESPIRATORY GROUP • It is located in the ventrolateral part of medulla. • It extends through nucleus ambiguus and nucleus retro-ambiguus. • It contains inspiratory and expiratory neurons. • Expiratory neurons inhibit inspiratory neurons during expiration.
  • 12. Inspiratory ramp signal • Pattern of action potential produced by the respiratory center is called inspiratory ramp signal • Initially there is a latent period then the intensity of action potential increases and then decreases followed by a latent period.
  • 13. • The cycle is repeated and normally the duration of one cycle is 4-5 seconds. • The impulses pass to the inspiratory muscles and produce inspiration
  • 14. PONTINE CENTERS • Rhythmic discharge of medullary neurons are modified by neurons of pons and afferents coming from the receptors in airways and lungs through vagus. • In the upper part of pons there is a pair of respiratory centres called pneumotaxic centre.
  • 15. • Pneumotaxic centers has inhibitory effect on I neurons. • When this area is stimulated ,I neurons are inhibited and duration of IRS is reduced. • Rate of respiration is increased and filling volume will be decreased; respiration becomes shallow and rapid.
  • 16. • Lower part of pons contain another set of neurons called apneustic center which is tonically active. • It has excitatory effect on I neurons . • Stimulation of these center increases duration of IRS producing sustained contraction of inspiratory muscles with expiratory gasps in between(apneusis).
  • 17. Genesis of respiration Genesis of inspiration: • Apneustic center activates the inspiratory centre. • Inspiratory center discharges over pathways in the spinal cord to C3,4,5 and T1,2 and inspiration starts.
  • 18. Genesis of expiration: • Inspiratory neurons in the medulla send excitatory impulses to pneumotaxic center which inturn inhibit the apneustic center. • Pulomonary stretch receptors in lungs get stimulated during inspiration also send inhibitory impulses via vagus nerve to the apneustic center.
  • 19. • Pneumotaxic center stimulates expiratory neuron in medulla which reciprocally inhibits the inspiratory center. • As a result inspiratory center stops discharging and expiration follows. • When the activity of inspiratory neurons are increased the rate and depth of inspiration is also increased.
  • 22. Reflex control of respiration Receptors are classified into : • Receptors inside respiratory system • Receptors outside respiratory system Receptors inside respiratory centers: • Stretch receptors • Pulmonary irritant receptors
  • 23. Stretch receptors Hering –Breuer Reflexes: Hering Breuer Inflation reflexes • When there is increase in the tidal volume greater than 1L,stretch receptors of lungs are stimulated .
  • 24. • There is increased rate of afferent impulses passing through the vagus to the inspiratory centre and this leads to inhibition of inspiratory muscles • This reflex operates only when the tidal volume exceeds 1-1.5 L
  • 25. Hering Breuer Deflation reflex • This reflex operates when there is excessive deflation of lungs. • Here there is stimulation of inspiration to bring back the lung volume to normal. Importance: • It functions as an important feedback mechanism and contribute to rhythmicity of respiration in NB babies.
  • 26. Irritant receptors. • Pulmonary irritant receptors are found in airway epithelial cells. Stimulation of these receptors produce: • Bronchoconstriction • Hyperventilation • Cough, sneezing etc
  • 27. Cough reflex: • This is a protective reflex . • Stimulation of irritant receptors of larynx, trachea and bigger bronchi produces cough. Sneezing reflex: • Stimulation of irritant receptors of nasal cavity and upper airways produces sneezing. • Sneezing is forced expiration against open glottis.
  • 28. J reflex • ‘J’ receptors are juxta-capillary receptors which are present on the wall of the alveoli and have close contact with the pulmonary capillaries. • Stimulation of the ‘J’ receptors produces a reflex response, which is characterized by apnea, hyperventilation, bradycardia, hypotension and weakness of skeletal muscles.
  • 29. • Conditions when ‘J’ receptors are stimulated : • i. Pulmonary congestion • ii. Pulmonary edema • iii. Pneumonia • iv. Over inflation of lungs
  • 30. Receptors outside respiratory system Those which stimulate respiration: • Proprioceptors • Nociceptors • Thermoreceptors • Emotions Those which inhibit respiration: • Baroreceptors • Visceroceptors.
  • 31. Proprioceptors • These are receptors in muscles, tendons and joints. • Stimulation of these receptors reflexly stimulates I neurons which will increase ventilation at the start of exercise . •Nociceptors: • These are pain receptors which when stimulated stimulate the respiratory center.
  • 32. • CHEMORECEPTORS: • Acidosis and hypoxia stimulate chemoreceptors. • THERMORECEPTORS: • Thermoreceptors present in the hypothalamus are stimulated when there is increase in body temperature as in fever ,exercise. • EMOTIONAL STIMULI • Emotional stimuli produces impulses from hypothalamus ,limbic system which stimulate respiratory centre.
  • 33. Those which inhibit Respiration: Baroreceptors: Increase in blood pressure stimulates baroreceptors leading to inhibition of respiration. Visceroceptors: In visceral reflexes like vomiting, swallowing, deglutition, there is reflex inhibition of respiration.
  • 35. CHEMICAL REGULATION OF RESPIRATION • Changes in pO2,pCO2 and H+ concentration acts on the respiratory centers in the medulla through a set of receptors called as chemo receptors. • Chemoreceptors are classified into:  Central chemoreceptors  Peripheral chemoreceptors.
  • 36. Central chemoreceptors • These are a set of neurons located on either side of medulla near the exit of IX and X cranial nerves • These can sense changes in H+ concentration in the brain interstitial fluid. • Central chemoreceptors are surrounded by brain extracellular fluid.
  • 37. • Blood brain barrier and blood CSF barrier are easily crossed by carbondioxide. • Whenever there is hypercapnia CO2 enters brain tissue and CSF, where it is hydrated to form H2CO3. • This splits to form H+ and HCO3-.
  • 38. • Increase in H+ concentration is only the direct stimulant for central chemoreceptors. • CO2 has only indirect action. • Lack of oxygen does not have significant effect on the central chemoreceptors
  • 39. • Stimulation from central chemoreceptors go to the inspiratory center(DRG) and stimulate respiration. • Central chemoreceptors are inhibited by anaesthesia, cyanosis ,during sleep etc.
  • 41. Peripheral chemoreceptors • These are carotid body and aortic body. • These are neurovascular structures Location: • Carotid body is located at the bifurcation of common carotid artery. • Aortic bodies are located in the arch of aorta.
  • 43. Innervation of peripheral chemoreceptors. • Carotid body is supplied by a branch of ninth cranial nerve(sinus nerve). • Sensory impulses from carotid body are carried through this nerve. • Aortic body is supplied by a branch of vagus nerve.(aortic nerve)
  • 44. • Sinus nerve and aortic nerve together referred as sino-aortic nerve. • PCR contains two types of cells surrounded by fenestrated sinusoidal capillaries. • Type I cell/glomus cells • Type II cells/Glial cells / supporting cells.
  • 45. Type I cell or glomus cells. • They contain dense granules with dopamine. • They are in close association with afferent nerve fibres of ninth cranial nerves. Type II cells/glial cells or supporting cells. • These cells surround 4-6 glomus cells . • Function : Protection and support of glomus cells.
  • 46. Mechanism of action of PCR • Reduction in partial pressure of oxygen is the most potent stimulus for PCR. • If the arterial pO2 falls below 60 mm of Hg, the peripheral chemoreceptors are strongly stimulated which inturn will stimulate the respiratory center .
  • 47. • This leads to increase in rate and depth of respiration which brings blood pO2 to normal • In the absence of PCR, severe hypoxia depress respiration by a direct inhibitory action on respiratory centres.
  • 48. Factors affecting PCR Decrease in arterial pO2. • Vascular stasis as in circulatory shock(stagnant hypoxia). • The PCR responds only to reduction in dissolved oxygen in the blood. • In anemic hypoxia and carbon-monoxide poisoning there is no stimulation of respiration through PCR
  • 49. Decrease in pCO2 • Peripheral chemoreceptors are also sensitive to increased pCO2. • Increased pCO2 stimulates peripheral chemo receptors which inturn stimulates resp centre • Increase in carbon dioxide washout until arterial pCO2 becomes normal.
  • 50. Effect of H+ concentration Acidosis stimulates respiratory center and causes hyperventilation Alkalosis depress respiratory center and causes hypoventilation. Mediated by peripheral chemoreceptors. NOTE : Action of CO2 on respiration is increased by Hypoxia . • Decreased by sleep, hypothermia and anaesthesia.
  • 52. ABNORMALITIES Respiratory center depression: • Causes : Old age • Anesthetics. Periodic breathing : Consists of alternating waxing and waning of respiration or alternate hyperpnea and apnea. • It may be normal or abnormal.
  • 53. Types of periodic breathing • 1.Voluntary hyperventilation • Hyperventilation in normal subject is followed by a period of apnea which in turn is followed by a few shallow breaths and then another period of apnea followed again by few breaths. • This cycles lasts for some time before normal breathing is resumed.
  • 54. 2.Cheyne-stokes respiration • Seen in both physiological and pathological conditions • Regular alternating period of hyperventilation and apnea are seen. Physiological causes: • Deep sleep • Infants • High altitude Pathological causes: • Congestive cardiac failure • Raised ICT, Uremia and morphine poisoning.
  • 55. 3.Biot’s breathing • This type of breathing is always pathological. • Irregular periods of apnea and hyperventilation. • Changes are abrupt. Causes : Meningitis Medullary lesions.