REGULATION

OF
RESPIRATION.

Dr Arpana Hazarika
 OBJECTIVES
■ Introduction.
■ Neural Regulation.
■ Automatic control.
■ Afferent impulses to respiratory centre.
■ Chemical regulation.
■ Chemoreceptors.
■ Effect of pO2, pCO2 & H+ ion conc on respiration.
■ Applied aspects.
Friday, June 17, 2016
 INTRODUCTION.
■ The normal rate of respiration in
adults is 12-18/min,
■ Tidal volume of approx. 500 ml.
■ Adjusted to the requirements of
the body.
■ Spontaneous respiration -
rhythmic discharge of motor
neurons that innervate the
respiratory muscles.

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 CONTROL MECHANISMS.
■ Automatic control as
an involuntary
function.
■ Located in medullary
& pontine centres.
■ Functional
significance – breath
without conscious
effort as in sleep.

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 CONTROL MECHANISMS.
■ Voluntary control.
■ Located in cerebral
cortex.
■ Functional
significance – facilitate
acts like talking, singing,
swimming, laughing,
breath holding &
hyperventilation.

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 FUNCTIONS OF RESPIRATORY
CENTRES.
■ Genesis of normal
respiratory
spontaneous rhythm.
■ Control rate & depth
of respiration.

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 REGULATION.
■ Neural
■ Automatic control.
■ Afferent impulses to respiratory centre.

■ Chemical.
■ Chemoreceptors
■ Effect of Po2, Pco2 &pH.

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 AUTOMATIC CONTROL.
■ Medullary respiratory
centres.
■ Pontine respiratory
centre.
■ Reticular activating
system.

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 MEDULLARY RESPIRATORY
CENTRES.
■ Dorsal respiratory
group of neurons.
■ Ventral respiratory
group of neurons.

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 DORSAL RESPIRATORY GROUP OF
NEURONS..
■ NTS (Nucleus of Tractus
Solitarius)
■ I neurons – Discharge
during inspiration only.

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 CENTRAL INSPIRATORY
ACTIVITY NEURONS.(RΑ)
■ Central inspiratory
activity neurons.(Rα)
■ Inspiratory pump.
■ Ramp signal.
■ Inspiratory off-switch
(IOS) neurons.
■ Terminate inspiratory
Ramp.
■ Integrator neurons.
(Rβ)
■ Friday, June 17, 2016
Other neurons.(P
 INTEGRATOR NEURONS. (RΒ)
■ Excitatory inputs. ■ Inhibitory inputs.
■ Cerebral cortex. ■ Apneustic centre.

■ Pneumotaxic

centre.
■ Vagal afferents

from stretch
receptors.

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 VENTRAL RESPIRATORY GROUP
OF NEURONS.
■ Caudal part or nucleus
Retroambigualis
(NRA)
■ E neurons
■ Bulbospinal expiratory
Premotor neurons.
■ Intermediate part.
■ I neurons.
■ N. Parambigualis
■ Most Rostral part.
(NRF)
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■ neurons)
 VENTRAL RESPIRATORY GROUP
OF NEURONS.
■ Interactions of I & E ■ Reciprocal
neurons. innervations.
■ Role of VRG
neurons.
■ Totally inactive in
quiet breathing.
■ Active during forceful
respiration.
■ Example -- During
exercise
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 PONTINE RESPIRATORY
CENTRE.
■ Apneustic Centre (APN)
■ Inhibitory neurons
bilaterally in pons.
■ APN – Integrator –
■ IOS
Prevent switch off of ramp
■ from CIA
Increases depth &
■ duration
– Apneusis.
Normally kept inhibited by
vagus
Friday, & Pneumotaxic centre
June 17, 2016
 PONTINE RESPIRATORY
CENTRE.
■ Pneumotaxic centre.
(PNC)
■ In N. Parabrachialis in
upper pons.
■ Excite integrator N &
inhibits Apneustic C.
■ Increases rate of
breathing.
■ So Rhythm by DRG, rate &
depth controlled by
APN,PNC.
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 RETICULAR ACTIVATING
SYSTEM.
■ Increases respiratory
drive.
■ During sleep – RAS
activity decreases –
respiratory drive
decreases – alveolar
ventilation decreases
– raise Pco2.

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 AFFERENT IMPULSES TO
RESPIRATORY CENTRE.
■ From higher centre.
■ From non-chemical receptors.
■ From chemical receptors.

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The respiratory centers generate the respiratory
rhythm and execute their effects through the efferent
Nerves supplying the respiratory muscle .The activity
Of the respiratory centre is in turn influenced by the
Afferent impulses from the lung and various parts of
the body.These affrent impulses guide the respiratory
centre to regulate their activity so as to serve number
Of purposes
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1.To cope up with 02 demand of the body and
wash out CO2 from the body
2.To regulate H+ ion concentration
3.To maintain appropriate 02 tension of
blood
4.To help maintain the normal body
temperature
Various afferent impulse to the respiratory centre
1.Afferent impulses from the higher centres
2.Afferent impulses from non chemical receptor
3.Afferent impulses from chemical receptor
 FROM HIGHER CENTRE.
■ Voluntary control ■ Limbic control
system. system.
■ Controlled by ■ Limbic system –
Neocortex pontomedullary
■ Bypasses medullary respiratory neurons.
respiratory centres & ■ So alter during pain &
project directly to spinal emotional stimuli.
respiratory neurons.
■ For talking, singing,
swimming &
breath holding.
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vVoluntary control system
Normally breathing is an involuntary effort and
goes on automatically .However the respiratory
muscles are typical skeletal muscle
And can also be controlled voluntarily.The
voluntary control of respiration is mediated by
pathway which originates from
neocortex,bypass the medullary respiratory
centres to project directly to spinal respiratory
neurons.The voluntary control is exercised
Breath Holding or Voluntary apnoea
Breathing can be stopped voluntarily for about
50 to 60sec.But after this time the chemical
drive overdrive the voluntary inhibition and the
Person has uncontrollable desire to breathe and
untimely breathing is resumed
involuntarily.That is why it is impossible to
commit suicide by holding the breath
voluntarily.The decrease in arterial Pco2 and
And increase in arterial pCO2 seem to be the
chief cause of breadth holding
VOLUNTARY HYPERVENTILLATION
Voluntary hyperventilation can only be done for
Sometime
2.LIMBIC CONTROL SYSTEM
Pain and emotional stimuli influence the rate
and depth of breathing.It indicates the presence
Of afferents from limbic system to the
pontomedullary respiratory neuron
 FROM NON-CHEMICAL RECEPTORS.
■ From Pulmonary stretch receptors (Hering-
Breuer Reflex)
■ From J-Receptors.
■ From Irritant receptors in the respiratory
tract.
■ From Proprioceptors..
■ From Chest wall stretch receptors.
■ From Baroceptors.
■ From Thermoceptors.
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Friday, June 17, 2016
 FROM PULMONARY STRETCH RECEPTORS
(HERING-BREUER REFLEX)
■ Lung inflation –
stimulation of
stretch receptors in
bronchi & bronchioles
– vagi –
pontomedullary
respiratory centers –
inhibit respiration.
■ Only when TV > 1-
1.5L
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 FROM J-RECEPTORS.
■ Indian physiologist A.S ■ Stimulation causes
Paintal 1954. apnoea,
■ Juxtapulmonary capillary hyperventilation,
receptors.
bradycardia ,
(unmyelinated vagal
■ afferents) hypotension &
Sensitive to increase in
weakness of skeletal
content of interstitial fluid muscles.
between capillary
endothelium & alveolar
epithelium.

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 FROM IRRITANT RECEPTORS IN
THE RESPIRATORY TRACT.
■ Cough reflex.
■ Sneezing reflex.
■ Hering-Breuer
deflation reflex.
■ Reflex tachypnoea &
bronchoconstriction.
■ Deglutition reflex.

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 FROM PROPRIOCEPTORS.

■ Stimulate inspiratory neurons – increase rate &

depth of respiration.

■ Increases ventilation during exercise.

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 FROM CHEST WALL STRETCH
RECEPTORS.
■ In muscle spindles of
intercostal muscles
■ Co-ordinate breathing
during change in posture
& during speech.
■ Intercostal to intercostal
reflex.
■ Intercostal to Phrenic
reflex.

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 FROM BAROCEPTORS.
■ Raise BP – stimulate
Baroreceptors in
carotid sinus & aortic
arch.
■ Inhibition of
respiration.

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 FROM THERMOCEPTORS.
■ 2 types, warm & cold.
■ Warm receptors – via
somatic afferent
nerves – cerebral
cortex –
hyperventilation.
(Heat loss mechanism)
■ E.g. Panting in Dogs.

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 FROM CHEMICAL RECEPTORS.
CHEMORECEPTORS.
■ Peripheral
■ Central.
■ Pulmonary & Myocardial.

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 PERIPHERAL CHEMORECEPTORS.
■ Location - carotid bodies &
aortic bodies.
■ Structure.
■ Capsule – surrounding
bodies.
■ Sinusoidal large capillaries
below capsule
■ Epithelial cells – type I
(Glomus cells) like
chromaffin cells contains
catecholamine.
■ Type II (Glial cells).

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PERIPHERAL CHEMORECEPTORS.
■ Mechanism
■ Less Po2 – decreases
activity of K channels –
decrease K efflux –
depolarization of glomus
cells – open L-type ca
channels – Ca influx –
release neurotransmitter
& stimulate afferent
nerve.

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 FACTORS STIMULATING
■ O2 tension V o2 ■ Functions
content. ■ Carotid bodies
■ Elevated Pco2 increases both rate &
■ H+ conc. depth, aortic bodies
■ Hyperkalemia. only rate of
respiration.
■ Asphyxia.

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 CENTRAL CHEMORECEPTORS.
■ Location – beneath ■ Mechanism.
ventral surface of ■ Co2 crosses BBB – in
medulla. CSF
■ Innervations – ■ co2 + H2O – H2CO3
project directly to ■ H2CO3 ------H+
respiratory centres HCO3
deeper to central
■ H+ ion stimulate
chemoreceptors.
central
chemoreceptors.
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 PULMONARY & MYOCARDIAL
CHEMORECEPTORS.
■ Location – pulmonary &
coronary blood vessels.
■ Innervations – by
Vagus
■ (X) nerve.
■ Characteristics &
effects.
■ Caused by injection of
veratridine or nicotine
Causes – bradycardia,
hypotension, apnoea
followed by tachypnoea.
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Friday, June 17, 2016
 EFFECT OF PO2, PCO2 & H+ ION
CONC ON RESPIRATION.

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 EFFECT OF HYPOXIA
■ Normal arterial Po2 is
100 mm Hg. Decrease
in Po2 causes
Hypoxic Hypoxia.
■ A decrease in arterial
Po2
■ Po2 100-60mm Hg. –
breaking effect of CO2.
■ Po2 below 60 mm Hg.

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 EFFECT OF HYPERCAPNIA.
■ Normal pco2 – 40 mm Hg.
■ Effect of Hypercapnia.
■ Co2 Narcosis when PCO2 >
50 mmHg.
■ Leads to depress CNS,
Respiratory centre,
headache, confusion,
convulsion, coma & Death.

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 EFFECT OF ARTERIAL pH
■ Increase H+ ion conc.
■ Primary pulmonary
(metabolic
acidosis)- leads to hypoventilation
hyperventilation. In causes respiratory
DKA, renal failure, acidosis.
severe exercise. ■ Primary pulmonary
■ Decrease H+ ion conc. Hyperventilation
(metabolic alkalosis) causes respiratory
alkalosis.

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 EFFECT OF HYPERVENTILATION.

■ Hypoventilation.

■ Apnoea.

■ Periodic breathing

(chynes-stokes

breathing)
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 EFFECT OF SLEEP ON
RESPIRATION.

■ Apnoea for brief

period (10 sec)

■ Sleep apnoea

syndrome.

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Thank
You