1. The document describes the automatic respiratory control system, including both nervous and chemical regulation of breathing. 2. The nervous control involves afferent nerves that transmit sensory information to respiratory centers in the brainstem, which then send efferent signals to respiratory muscles via motor nerves. 3. Chemical control involves central and peripheral chemoreceptors that detect levels of oxygen, carbon dioxide, and hydrogen ions in the blood and stimulate breathing as needed to maintain homeostasis.

1. AUTOMATIC RESPIRATORY CONTROL

2. RESPIRATION
Process by which cells in the body use oxygen and
produce carbon dioxide, exchanging these gases with the
atmosphere
Efficient respiration also requires many functions of the
cardiovascular and central nervous system

3. REGULATORY MECHANISM OF BREATHING
NERVOUS
CHEMICAL

4. NERVOUS CONTROL
AFFERENT
NERVES
RESPIRATORY
CENTERS
EFFERENT
NERVES
Medullary and pontine
centers collects
sensory information
about the level of
oxygen and carbon
dioxide in the blood
and determines the
signals to be sent to
the respiratory muscles
The nucleus of the
tractus solitarius is the
sensory termination of
both the vagal and the
glossopharyngeal
nerves, which transmit
sensory signals into the
respiratory center
from
(1) peripheral
chemoreceptors,
(2) baroreceptors,
(3) several types of
receptors in the lungs.
Phrenic nerve fibers:
supplies diaphragm
The intercostal nerve
fibers: supplies
intercostal muscles.

6. Sensory
(receptors)
Central
controller
(brain and
centers of
respiration)
Effectors
(muscles)

7. Location of respiratory centers and units
centers
medullary
pontine
Pulmonary
recpeptor

8. Medullary centers
 a. Inspiratory Area - DRG - dorsal respiratory group neurons
 b. Expiratory Area - VRG - ventral respiratory group neurons
 a. Pneumotaxic Center - located in upper pons (“off switch”)
 b. Apneustic Center - located in lower pons (prevents turn-off)
 a. pulmonary stretch receptors (Hering-Breuer reflex)
 b. other receptors
Pontine centers
Pulmonary receptor

9. Dorsal Respiratory Group of Neurons
 Located within the nucleus of Tractus Solitarius which in itself is the sensory
termination of Vagus and Glossopharyngeal nerves.
 Basic rhythm of respiration is generated here.
 It generates the Inspiratory Ramp Signal to the inspiratory muscles like
diaphragm.
 This causes an inspiration which begins weakly & increases steadily in a ramp
manner for 2 seconds & then ceases abruptly for the next 3 seconds to allow
elastic recoil of lungs & chest wall to cause expiration.
 This ramp pattern causes a steady increase in the volume of lungs rather than
inspiratory gasps

10. Ventral Respiratory Group of Neurons
 Located anterior and lateral to the dorsal group.
 Present within Nucleus Ambiguus & Nucleus Retroambiguus
 Totally inactive during normal quiet respiration.
 Important in providing powerful expiratory signals to the abdominal muscles
during heavy exercise.

12. Pneumotaxic Centre
 Located dorsally in the Nucleus Parabrachialis of upper pons.
 Controls the switch-off point of the inspiratory ramp, thus controlling the
duration of filling phase of the lung cycle.
 It limits the inspiration.
 Thus, it secondarily increases the respiratory rate

13. Apneustic Centre
 Located in the lower part of pons.
 Sends signals to the dorsal group to retard the switch-off of the inspiratory
ramp signal.
 Thus, it increases the inspiratory time.
 Operates in association with the pneumotaxic centre to control the intensity
of inspiration.

15. Respiratory regulation

17. Motor cortex (exercise) - vasodilation
Amygdala (defensive) - vasodilation
Cerebellum (posture changes) - vasoconstriction

18. Role of higher centers
In addition to simple changing the dgree of ventilation, it
causes unusual aspect such as gasping
Medulla respond by adjusting speed and depth of respiration
Muscles
Higher brain centers such as hypothalamus can inhibit or stimulate
medulla
Medulla oblongata

19. Chemical control of ventilation
 The ultimate goal of respiration is to maintain proper concentrations of O2,
CO2 and H+ ions in the tissues.
 All these are involved in the chemical control of ventilation.
 These chemicals ultimately affect the respiratory centres & thus control the
ventilation.

20.  Chemoreceptor
Central Peripheral

21. Central chemoreceptor
 CO2 and H+ ions are involved.
 These act upon the chemosensitive area of the respiratory centre directly.
 O2 has virtually no effect on the respiratory centre itself.

22. Chemosensitive Area of the Respiratory
Center
 Located bilaterally beneath the ventral surface of medulla.
 Highly sensitive to changes in the blood PCO2 or Hydrogen ion concentration
 It excites the other portions of the respiratory centre

23. Response of the Chemosensitive Neurons
to Hydrogen Ions: The Primary Stimulus
 Hydrogen ions are the most important direct stimulus for these neurons.
 But, Hydrogen ions don’t easily cross the blood-brain barrier.
 So changes in blood concentration of hydrogen ions have less effect in
stimulating the chemosensitive neurons than do changes in CO2.
 CO2 acts secondarily on these neurons by changing the hydrogen ion
concentration.

24. Effect of Blood Carbondioxide to
Stimulate the Chemosensitive Area
 CO2 has a very potent indirect effect on the chemosensitive area.
 CO2 passes easily through the blood brain barrier.
 CO2 reacts with H2O to form hydrogen ions in the CSF & interstitial fluid of
medulla.
 Thus more H+ ions are paradoxically released into the respiratory
chemosensitive area when blood CO2 rises than when blood hydrogen ion
concentration rises.
 Blood CO2 concentration has a more potent acute effect, but a weak chronic
effect on controlling ventilatory drive. This is because of the readjustment by
kidneys (by increasing blood bicarbonate which enters CSF & binds with the H+
ions), which bring back the hydrogen ion concentration to normal.

26.  is very sensitive to increase in H+
concentration.
H+ cannot cross the blood brain barrier
and blood cerebrospinal fluid barrier.
On the other hand if CO2 increases in
the blood as it is a gas it can cross both
the barrier easily and after entering the
brain it combines with water to form
carbonic acid.
As carbonic acid is unstable, it
immediately dissociates into hydrogen
and bicarbonate ions.
H2CO3  H+ + HCO3-
The H+ now stimulates the central
chemoreceptors, which stimulates dorsal
group of respiratory center (inspiratory
group) and increase rate and force of
breathing.
Chemosensitive Area

27. Peripheral Chemoreceptor System
 Includes the chemoreceptors in carotid bodies and aortic bodies.
 Carotid bodies are located bilterally at the bifurcation of the common
carotids of the two sides. Their afferents pass through the Glossopharyngeal
nerves.
 Aortic bodies are located along the arch of aorta. Their afferents pass through
the Vagi of the two sides.
 Both afferents reach the dorsal respiratory centre.
 The “Glomus cells” in these bodies function as the chemoreceptors.
 These are stimulated by a fall in blood O2 concentration, particularly when
PO2 falls from 60 mmHg down to 30 mmHg. This is the range in which
hemoglobin O2 saturation decreases rapidly.

28. Location

30. Effect of CO2 & hydrogen ion concentration
on peripheral chemoreceptors
 Peripheral chemoreceptors are also stimulated by a rise in blood CO2 and
hydrogen ion concentration.
 This is very minute in comparison to their direct effect on central
chemoreceptors.
 But, the effect of CO2 on peripheral chemoreceptors is 5 times as rapid as on
central chemoreceptors. This might be important at the onset of exercise.

33. Classification of mechanoreceptors
Situated in the
mucous of
bronchi and
bronchioles
Pulmonary/ irritant
Situated on
the wall of
bronchi and
bronchioles
stretch
Present on the
wall of alveoli
and close
association with
pulmonary
capillary
juxtacapillary

34. Effect of Pulmonary Stretch Receptors:
The Hering- Breuer Inflation Reflex
 Mediated through the Stretch Receptors located in the muscular portions of
the walls of bronchi & bronchioles.
 These stretch receptors transmit signals through the vagi into the dorsal
respiratory group of neurons when the lungs are overstretched, leading to
switching-off of the inspiratory ramp.
 This reflex is activated at a tidal volume of > 1.5 litre.
 It thus acts as a protective mechanism in preventing excessive lung inflation.
 It also leads to an increase in respiratory rate.

35. Hering-Breuer reflex

36.  THE HERING BREUER INFLATION REFLEX :- When it restrict the
inspiration and limit the overstretching of lung tissue
 Reverse of it is called as THE HERING BREUER DEFLATION REFLEX :-
Occur during expiration
 During expiration stretching of lung is absent, deflation occur

38. The Effect of Irritant Receptors
 Irritant receptors :
a) Located in epithelium of trachea, bronchi &
bronchioles.
b) Cause coughing & sneezing.
c) Also cause bronchial constriction in asthma &
emphysema.

39. The Effect of J-Receptors
 J- Receptors :
a) Located in alveolar walls in juxtaposition to pulmonary capillaries.
b) Stimulated when pulmonary capillaries are engorged with blood or in
pulmonary edema, CHF (chronic heart failure).
c) Their excitation leads to a feeling of dyspnea.

40. Effect of Golgi tendon organs
 These occur in series arrangement within the ventilatory muscles, particularly
the intercostal muscles.
 When the lungs are full & the chest wall is stretched, these receptors send
signals to the brainstem that inhibit further inspiration.

41. Propioceptor
 Proprioceptors are the receptors which give response to the change in the
position of different parts of the body.
 This receptors are situated in joints, muscles and tendons. They get
stimulated during exercise and sends impulses to the cerebral cortex.
 Cerebral cortex in turn by activating medullary respiratory centres causes
hyperventilation.

42. Thermoreceptors
 Thermoreceptors give response to change in the body temperature.
 They are cutaneous receptors namely cold and warmth
 When this receptors get stimulated they send signals to cerebral cortex
 Cerebral cortex in turn stimulates respiratory centres and causes
hyperventilation

43. Pain receptors
 Pain receptors give response to pain stimulus.
 Like other receptors this receptors also send impulses to the cerebral cortex.
 Cerebral cortex in turn stimulates the respiratory centers ad causes
hyperventilation.

44. Respiratory muscle
Diaphragm (Phrenic nerve (C3 - C5) and sensory supply by phrenic
nerve to central tendon and lower 6 or 7 intercostal nerve to
peripheral parts
Ext.intercostal (by intercostal
nerves Th1-Th11)
Int.intercostal
by intercostal nerves
Th1-Th11
Sternocleidomastoid (accessory nerve. It supplies
only motor fibres. The cervical plexus supplies
sensation, including proprioception, via
the ventral primary rami of C2 and C3. )
Scalneus
C4-C6

45. Reflexes
Cough reflex
Sneezing reflex
Deglutition reflex

46. Cough reflex
 This is a protective reflex caused by irritation of parts of the respiratory tract
beyond nose like larynx, trachea and bronchi.
 Irritation of any of this part causes stimulation of vagus nerve and cough
occurs.
 Cough begins with deep inspiration followed by forceful expiration with
closed glottis.
 So the intrapleural pressure rises above 100 mm Hg.
 Then, glottis is suddenly opened with explosive outflow of air at a higher
velocity. So the irritants may be expelled out of the respiratory tract.

47. Sneezing reflex
 It is also a protective reflex which occurs due to the irritation of nasal mucus
membrane.
 During irritation of nasal mucus membrane, the olfactory receptors and
trigeminal nerve endings present in the nasal mucosa are stimulated leading
to sneezing.
 Sneezing starts with deep inspiration, followed by forceful expiratory effort
with opened glottis and the irritants are expelled out of the respiratory tract.

48. Deglutition reflex
 During swallowing of the food, the respiration is arrested for a while.
 Temporary arrest of the respiration is called apnea and apnea which occurs
during swallowing called swallowing apnea or deglutition apnea.
 This prevents entry of the food particles into the respiratory tract.

49. The Phenomenon of Acclimatization
 It’s the phenomenon whereby one can withstand lower concentrations of
atmospheric O2 when chronically exposed to such an atmosphere.
 Found in mountain climbers who climb the mountains over a period of days.
 Reason: Within 2 to 3 days the respiratory centre in the brain stem loses 4/5th
of its sensitivity to changes in arterial PCO2 and hydrogen ion concentration.
Thus the high ventilatory blow-off of CO2 that can depress ventilation, fails to
do so. Thus, the low O2 concentration can drive the respiratory system to a
much higher level of ventilation than under acute settings.

50. CONTROL OF VENTILATION DURING
EXERCISE
 In strenous exercise O2 consumption & CO2 production can increase as much
as 20-fold.
 But, the alveolar ventilation increases almost exactly in step, and thus, the
arterial PO2, PCO2 & pH remain almost exactly normal.

51. Factors causing Increased Ventilation in
Exercise
 Contrary to expectations, PCO2, PO2 & pH don’t have a role to play in
stepping up the ventilation during exercise, because their levels don’t change
significantly during exercise.
 The brain, while transmitting motor signals to the muscles, also transmits
collateral impulses into the brain stem to excite the respiratory centre,
analogous to the vasomotor centre to increase the arterial BP during exercise.
 During exercise, the body movements excite the muscle & joint
proprioceptors which transmit excitatory impulses to the respiratory centre,
thus increasing ventilation

52. Role of respiratory system in acid base
balance
Ventilatory Response to Acid-Base Changes
 Because the CO2-bicarbonate buffer system plays a significant role in
regulating pH, the lungs can alter arterial pH by changing arterial Pco2.
 Ventilation is increased in response to metabolic acidemia.
 Ventilation is decreased in response to metabolic alkalemia.

53. & Hb

54. Respiratory System
 2nd line of defense.
 Acts within min. maximal in 12-24 hrs.
 H2CO3 produced converted to CO2, and excreted by the lungs.
 Powerful, but works with volatile acids
 Exhalation of carbon dioxide.
 CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3
-
 Body pH can be adjusted by changing rate and depth of breathing

56. Acid-Base Imbalances
 pH< 7.35 acidosis
 pH > 7.45 alkalosis
 The body response to acid-base imbalance is called compensation
 May be complete if brought back within normal limits
 Partial compensation if range is still outside norms.

57. Respiratory Acidosis
 Carbonic acid excess caused by blood levels of CO2 above 45 mm Hg
 Hypercapnia – high levels of CO2 in blood
 Chronic conditions:
 Depression of respiratory center in brain that controls breathing rate – drugs or head
trauma
 Paralysis of respiratory or chest muscles
 Emphysema
 Acute conditions:
 Adult Respiratory Distress Syndrome
 Pulmonary edema
 Pneumothorax

58. Compensation for Respiratory Acidosis
 Kidneys eliminate hydrogen ion and retain bicarbonate ion
 Acute respiratory failure:
pH low, [HCO-
3] high normal, or slightly raised
 Chronic respiratory failure:
pH normal or low depending upon chronicity, [HCO-
3] raised

59. Signs and Symptoms of Respiratory
Acidosis
 Breathlessness
 Restlessness
 Lethargy and disorientation
 Tremors, convulsions, coma
 Respiratory rate rapid then gradually depressed
 Skin warm and flushed due to vasodilatation caused by excess CO2

61. Respiratory Alkalosis
 Carbonic acid deficit
 pCO2 less than 35 mm Hg (hypocapnea)
 Primary cause is hyperventilation
 Conditions that stimulate respiratory center:
 Hysterical over breathing (overrides normal respiratory control)
 Raised intracranial pressure - ICP (which stimulate respiratory centre)
 Hypoxia
 Pulmonary edema
 Lobar pneumonia
 Pulmonary collapse or fibrosis
 Excessive artificial ventilation

62. Compensation of Respiratory Alkalosis
 Compensatory fall in plasma [HCO-
3] tends to correct the pH
 Pco2 always reduced
 [HCO-
3] low normal or low
 pH raised (uncompensated or partly compensated) or normal (fully
compensated)