The document summarizes the neural control of breathing. It discusses how breathing is regulated by central neuronal networks in the brainstem and spinal cord to meet metabolic demands. The central neurons in the medulla and pons form the basic respiratory center that produces and controls respiration. These centers integrate input from higher brain areas, mechanoreceptors, and peripheral chemoreceptors. They regulate breathing frequency and tidal volume through motor neurons that control respiratory muscles. Chemical control of breathing also occurs through central and peripheral chemoreceptors that sense changes in blood gases like oxygen and carbon dioxide to modulate ventilation.

1. Dr . Nahid Sherbini
Consultant IM &Pulmonary
KFH ,Medina ,Saudi Arabia

2. Breathing is controlled by the central
neuronal network to meet the metabolic
demands of the body
– Neural
– Chemical

3. Keep arterial levels of O2 & CO2 constant.
Match perfusion by pulmonary blood
flow with ventilation of the lungs with
overall metabolic demand.

4. Control of Breathing
Central neurons determine minute
ventilation (VE) by regulating tidal
volume (VT) and breathing
frequency (f).
VE = VT x f

5. Definition:
A collection of functionally similar neurons
that help to regulate the respiratory
movement.

6.  Higher respiratory center: cortex,
hypothalamus & limbic system.
Medulla & Pons :
Basic respiratory center: produce and
control the respiration.
 Spinal cord: motor neurons.

7. Affect rate and depth of ventilation
Influenced by:
• higher brain centers
• peripheral mechanoreceptors
• peripheral & central chemoreceptors

9. Voluntary breathing center
Cerebral cortex.
Automatic (involuntary) breathing center
– Medulla
– Pons

10. CAN BYPASS LOWER CENTERS.
SPEECH,SINGING,COUGHING, BREATH
HOLDING .

11.  Voluntarily – speaking, blowing, whistling, pushing,
defecation.
 Voluntary control is bilateral – cannot contract half of
diaphragm or larynx.
 Descend via pyramidal tracts.
 Destroy voluntary control without losing involuntary
control can be.. i.e. stroke

12. To larynx and bronchi
To respiratory muscles
Nucleus parabrachialis
medialis (part of PRG)
Dorsal respiratory group
– nucleus of the solitary tract
Pons
Medulla
Ventral respiratory group
- Nucleus ambiguus
- Nucleus retroambigualis
PRG = pontine respiratory group

13.  Rhythmicity center:
• Controls automatic
breathing.
• Interacting neurons
that fire either during
inspiration
(I neurons) or
expiration
(E neurons).

14.  I neurons located primarily in dorsal respiratory
group (DRG):
• Regulate activity of phrenic nerve.
 E neurons located in ventral respiratory group
(VRG):
• Passive process.
 Activity of E neurons inhibit I neurons.
• Rhythmicity of I and E neurons may be due to
pacemaker neurons

15. Inspiratory
Muscles
Expiratory
Muscles
Inspiratory
Neurons
Expiratory
Neurons
• This implies that each group exhibits “self-inhibition” – they can switch
themselves off.
• Stops breathing getting stuck in inspiration or expiration.

16.  Apneustic center (lower pons) – to
promote Inspiration.
Pneumotaxic center (upper pons)
– inhibits apneustic center & inhibits
inspiration
-helps control the rate and pattern of
breathing.

17. Pons
Medulla
Cuts off
Produces apneustic
effect – long,
powerful inspirations
Stops breathing since
no automated output
to respiratory system
– cause of death

18. DRG
VRG
pons
medulla
Neural Control
of Breathing –
Respiratory
neurons

19. Neural Control
of Breathing –
The efferent
pathway
Phrenic n.
muscle supply
autonomic

20. DECENDING BULBOSPINAL FIBRES
ARE IN THE VENTRAL AND LATERAL
COLUMNS.
RESP NEURONS ARE IN VENTRAL Horn
EXP NEURONS -VENTROMEDIAL
INSP NEURONS- LATERAL

21. ASCENDING SPINORETICULAR FIBRES
CARRY PROPRIOCEPTIVE INPUTS TO
STIMULATE RESP CENTRE.
BILAT CERVICAL CORDOTOMY
LEADS TO RESPIRATORY
DYSFUNCTION (SLEEP APNEA).

22.  Diaphragm controlled directly by  motor
neurons – “C3,4 & 5 keeps the diaphragm alive”.
 Motor neurons take turns to stimulate different
groups of muscle fibres active to minimise
fatigue.
 Due to poor supply of muscle spindles , control
comes from DRG &VRG.
And this explains why rare to feel fatigue in
diaphragm.

23.  Larynx movements are synchronized with breathing.
 Superior and recurrent laryngeal nerves are branches of
vagus nerve.
Expiration – vocal cords together.
Inspiration – vocal cords apart.
 Automatic rhythm that we can override consciously.
 Opera singers try and maximise control of breathing
using these muscles.

24.  Control of breathing affected profoundly by
vagus nerves (Cranial Nerve X).
 Two of these run down either side of neck and
torso, near trachea.
 Regulate receptors which are most involved in
respiration:
• Slowly-adapting pulmonary stretch receptors (PSR’s)
• Rapidly-adapting (irritant) receptors (RAR’s)
• C-fibre receptors (J receptors)

25. Paintel et al (1970) :
Propose J receptors function TO LIMIT
EXERCISE WHEN INTERSTITIAL
PRESSURE INCREASES(J REFLEX)
MECHANISM:
INHIBITION OF RESP MOTOR
NEURONS.

26. •+ when pulmonary caps are
engorged or pulmonary edema.
create a feeling of dyspnea

27.  UNMYELINATED NERVE ENDINGS .
 RESPONSIBLE FOR BRONCHOSPASM
IN ASTHMA.
 INCREASED TRACHEOBRONCHIAL
SECRETIONS.
 MEDIATORS:
HISTAMINE, PROSTAGLANDINS ,
BRADYKININ.

28.  Herring-Breuer Inflation reflex
• stretch receptors located in wall of airways
• + when stretched at tidal volumes > 1500 ml
• inhibits the DRG
Inflation
Apnoea
Phrenic nerve activity
Lung volume
Safety threshold that
triggers reflex

29. Airway Receptors:
Slowly adapting (stretch - ends
inspiration)
Rapidly adapting (irritants -
cough)
Bronchial c-fiber (vascular
congestion - bronchoconstriction)
Parenchymal c-fiber (irritants -
bronchoconstriction)
Xth n.
Reflex Control of
Breathing –
Neural receptors
afferents

30. EXPT ANIMAL STUDIES
Rapid shallow breathing pattern in
response to bronchospasm is mediated
through vagal afferents.

31. MECHANORECEPTORS - SENSE
CHANGES IN LENGTH ,TENSION AND
MOVEMENT.
ASCENDING TRACTS IN ANTERIOR
COLUMN OF SPINAL CORD TO RESP
CENTRE IN MEDULLA.

32. SENSE CHANGES IN MSL LENGTH.
INTERCOSTALS > DIAPHRAGM .
REFLEX CONTRACTION OF MUSCLE IN
RESPONSE TO STRETCH.
INCREASE VENTILATION IN EARLY
STAGES OF EXERCISE.

33. SENSE DEGREE OF CHEST WALL
MOVT.
INFLUENCE THE LEVEL & TIMING OF
RESP ACTIVITY.

34.  Neural control
 Beta receptors causing dilatation
 Parasympathetic-muscarinic receptors causing
constriction
 NANC nerves (non-adrenergic, non-cholinergic)
○ Inhibitory release VIP and NO  bronchodilitation
○ Stimulatory  bronchoconstriction, mucous
secretion, vascular hyperpermeability, cough,
vasodilation “neurogenic inflammation”.

35. Local factors
• histamine binds to H1 receptors-constriction
• histamine binds to H2 receptors-dilation
• slow reactive substance of anaphylaxsis-
constriction-allergic response to pollen
• Prostaglandins E series- dilation
• Prostaglandins F series- constriction

37.  Monitor changes in
blood PC02, P02, and
pH.
 Central:
• Medulla.
 Peripheral:
• Carotid and aortic
bodies.
 Control breathing
indirectly.

39. RESPONSE TO HYPERCAPNIA
• 20-50% CAROTID BODIES
• 50-80% CENTRAL CHEMORECEPTORS

40. CO2, H+
Control of
Breathing by
Central
chemoreceptors
Central
chemoreceptors
major regulators of
breathing
CO2, H+
Central
chemoreceptors
Resp
neurons
VE

41. Carotid
body
O2
Chemical
Control of
Breathing –
Peripheral
chemoreceptors
IXth n.
CO2
pH
~10% contribution
to breathing

42. CO2 tension in blood
(mm Hg)
35 40 45
VE
5
50
(L/min)
quiet breathing
hypercapnia
CO2 drives ventilation

43. CO2 tension in blood
(mm Hg)
35 40 45
VE
5
50
(L/min)
Hypoxia is a weak ventilatory
stimulus
blood pO2 =
100 mmHg
blood pO2 =
50 mmHg

44. Are not stimulated directly by changes in
arterial PC02.
H20 + C02 H2C03 H+
Stimulated by rise in [H+] of arterial blood.
• Increased [H+] stimulates peripheral
chemoreceptors.

45.  NO CHANGE
CAROTID BODY
ACTIVITY TILL
PaO2 < 75mmHg.
 VENTILATION
MARKEDLY
INCREASED When
PaO2<50mmHg

46. RAPID PHASE- RAPID INCREASE IN VE
WITHIN SECONDS DUE TO
ACIDIFICATION OF CSF.
SLOWER PHASE- DUE TO BUILDUP OF
H+ IONS IN MEDULLARY
INTERSTITIUM.
CHRONIC HYPERCAPNIA- WEAKER
EFFECT DUE TO RENAL RETENTION
OF HCO3 WHICH REDUCES THE H+.

47. VENTILATORY RESPONSE TO ALV O2
 CO2 POTENTIATES
VENTILATORY
RESPONSE TO
HYPOXEMIA .
 BOTH HYPOXEMIC
AND HYPERCAPNIC
RESPONSES
DECREASE WITH
AGEING AND
EXERCISE
TRAINING.

48. Normal level of HCO3- = 25 mEq/L
Metabolic acidosis (low HCO3-) will
stimulate ventilation (regardless of CO2
levels).
Metabolic alkalosis (high HCO3-) will
depress ventilation (regardless of CO2
levels) .

49. EFFECT OF PaCO2 & pH ON
VENTILATION

51. SENSATION OF DYSPNEA WHEN
INCREASED RESP EFFORT DUE TO
“LENGTH- TENSION
INAPPROPRTATENESS”
REMOVAL OF FLUID RESTORES THE
END EXP MSL FIBRE LENGTH
RESTORES THE LENTH TENSION
RELATIONSHIP RELIEF.

52. SV & CO decreased
Coronary blood flow decreased
Repolarization of heart impaired
Oxyhemoglobin affinity increased
Cerebral blood flow decreased
Skeletal muscle spasm & tetany
Serum potassium decreased
• (common thread in most of above is hypocapnic
alkalosis)

53. Effect of brain edema
• depression or inactivation of respiratory centers
Effect of Anesthesia/Narcotics
• respiratory depression
 sodium pentobarbital
 morphine

54. BILATERAL CAROTID BODY
RESECTION
CAROTID ENDARTERECTOMY
REDUCES VE.
30% DECREASE IN RESPONSE TO
HYPERCAPNIA.

55. 59Y FEMALE COPD,CVA ( OLD)
CAROTID ENDARTERECTOMY 1YR
ELECTIVE CE (R) DONE
PREOP ABG ON R/A- 7.43/50/48/31
DAY 3 EXTUBATED O2 3L/MIN
DAY5: SOMNOLENT AND CONFUSED
ABG- 7.28/62/69/31
BiPAP INITIATED IMPROVED
ABG-7.38/72/54/36

56. COPD WITH HYPERCAPNIA &
WORSENING RESP ACIDOSIS FULL
OXYGEN THERAPY
• LOSS OF HYPOXIC DRIVE
• WORSENING V/Q MISMATCH
PHYSIOLOGIC DEAD SPACE
• CO2 CARRYING CAPACITY AS
OXYGENATION OF Hb IMPROVES
( HALDANE EFFECT)

57. PERIODIC BREATHING PATTERN WITH
CENTRAL APNEAS.
Causes
1. BILATERAL SUPRAMEDULLARY
LESION
2. CARDIAC FAILURE
3. HIGH ALTITUDE
4. SLEEP

58.  Response to hypoxia and
hypercapnia.
 Response to
MECHANORECEPTORS
Pa O2 AND PaCO2 BY 4-8 mmHg

59. HYPOTONIA OF UPPER AIRWAY-
OBSTR SLEEP APNEA.
HYPOTONIA OF SKELETAL& RESP
MUSCLES- (Ventilation DEPENDS ON
DIAPHRAGM)

60. PHASE I - IMMED VE WITHIN
SECONDS,NEURAL IMPULSES MSL
SPINDLES, JOINT PROPRIOCEPTORS .
PHASE II- WITHIN 20-30 SEC VENOUS
BLD FROM MSL,SLOW VE(
VENTILATION LAGS BEHIND CO2).

61. PHASE III - PULM GAS EXCHANGE
MATCHES THE METAB RATE TO
MAINTAIN STABLE O2, CO2, PH.
PHASE IV - BEGINS AT ANAOERBIC
THRESHOLD, O2 CONSUMTION> O2
DELIVERY AND LACTIC ACID
ACCUMULATES.

62. VENTILATORY RESPONSE TO EXERCISE