The document details the regulation of respiration, highlighting the neural and chemical controls involved in maintaining arterial blood gas levels. It explains the mechanisms of voluntary and automatic control of breathing, the roles of various respiratory centers in the medulla and pons, and the reflex actions that influence respiratory patterns. Additionally, it discusses the effects of different receptors on respiration and the impact of chemical changes in blood on respiratory regulation.

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.

34. Factors affecting 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.