3-Mar-16Control of Respiration1 Neural Mechanisms Chemical Mechanisms

May 8, 2023 Control of Respiration 1

Control of Respiration

Neural MechanismsChemical Mechanisms


Introduction

Function of respiration include– Regulation of alveolar ventilation

•Maintain constant supply of O2 to tissues– Normal 250 ml O2 /min– This can increase to 20 times during

exercise•To eliminate CO2 from the tissues•Thus PO2, PCO2, pH

– Maintained at constant values or nearly constant values


Introduction

Other functions of respiration include– Phonation, singing, laughing,

whistling etcIn all these

– Extremely complicated respiratory movements are performed

– Require coordinated control


Neural Control of Respiration

Two neural control mechanisms regulate respiration– One responsible

for voluntary control

– The other one for automatic control

Cerebral cortex

Pons & medulla

Spinal cord

Respiratory muscles

Corticospinal tract

Reticulospinal tract


Neural Control of Respiration

Voluntary control system – Located in

cerebral cortex– Send impulses to

respiratory muscles via• Corticospinal

tracts (CST)

Cerebral cortex

Pons & medulla

Spinal cord

Respiratory muscles

Corticospinal tract



Control Systems for Respiration

Automatic system– Located in pons

and medulla oblongata

– Efferent output from this system to respiratory muscles • Located in spinal

cord close to CST

Cerebral cortex

Pons & medulla

Spinal cord

Respiratory muscles

Corticospinal tract




Nerves serving inspiration converge in ventral horns– C3,4,5 (phrenic

nerve)– External intercostal

motor neurons Fibres concerned

with expiration– Converge on internal

intercostals motor neurons

Cerebral cortex

Pons & medulla

Spinal cord

Respiratory muscles

Corticospinal tract




Reciprocal activity– Motor neurons to

expiratory muscles• Inhibited when

those to inspiratory muscles are activated &vice versa

Cerebral cortex

Pons & medulla

Spinal cord

Respiratory muscles

Corticospinal tract



Breathing Pattern

During quite breathing

Inspiration is brought about by– Progressive

increase in activation of inspiratory muscles

End of inspiration associated with– Rapid decrease in

excitation

Inspira

tion

Expir

ation

2 sec 3 sec

Electrical activity (diaphragm)


Breathing Pattern

The progressive activation of inspiratory muscle cause– Lungs to fill at

constant rate until tidal vol reached

End of inspiration associated – Rapid decrease in

excitation of inspiratory muscles• Expiration occurs

Inspira

tion

Expir

ation

2 sec 3 sec

Electrical activity (diaphragm)


Respiratory Neurons

Two types of brainstem respiratory neurons

Inspiratory neurons (I-neurons)– Discharge during inspiration

Expiratory neurons(E-neurons)– Discharge during expiration

• During quite breathing – Remain silent

• Become active only when ventilation is increased


Respiratory Centers

IX

X

XI

XII

D R G

V R G

Vag

us,

glos

opha

ryng

eal

Pneumotaxic center

DRG

VRG

Apneustic center


Respiratory Centers

Composed of several groups of neurons– Located

bilaterally in •Medulla

oblongata•Pons

IX

X

XI

XII

D R G

V R G

Pneumotaxic center

Apneustic center


Respiratory Centers

Three major collection of neurons– Dorsal respiratory

group (DRG)– Ventral respiratory

group (DRG)– Pneumotaxic center– ? Apneustic center

IX

X

XI

XII

D R G

V R G

Apneustic center

Pneumotaxic center


Respiratory Centers

Dorsal respiratory group (DRG)– Located on the

dorsal portion of medulla• In or near the

Nucleus of Tractus Solitarius(NTS)

IX

X

XI

XII

D R G

V R G


Respiratory Centers

NTS– Sensory terminal

of vagus & glossopharyngeal• Transmit sensory

signals from– Peripheral

chemoreceptors– Baroreceptors– Receptors in the

lungs

IX

X

XI

XII

D R G

V R G


Respiratory Centers

DRG made up– Of I – neurons

• Some project monosynaptically to phrenic nerve motor neurons (MN)

– Cause inspiration

IX

X

XI

XII

D R G

V R G


Respiratory Centers

VRGLong column

extends through – Nucleus ambiguus– Nucleus

retroambiguus in the ventral medulla

IX

X

XI

XII

D R G

V R G


Respiratory Centers

VRG has both I & E neurons– E – neurons at its

rostral end– I-neurons at the mid

portion– E-neurons at its

caudal end• Some of these

neurons project to– Respiratory

motor neurons

IX

X

XI

XII

D R G

V R G


Generation of Breathing Pattern

Rhythmic respiratory pattern– Appear to be

initiated by the • Rhythmic

discharges of neurons in the medulla and pons

IX

X

XI

XII

D R G

V R G

A

D



Trans-section of brain– Below medulla

• Stops respiration– Above the pons

• Automatic breathing is still present

Neurons in medulla & pons– Responsible for

generating the rhythmic respiratory movements

IX

X

XI

XII

D R G

V R G

A

D



The actual mechanism responsible for – Rhythmic respiratory

discharge not known However,

– Group of pacemaker neurons have been identified• Pre-Böttzinger

Complex• Area between nucleus

ambiguus & lateral reticular nucleus

IX

X

XI

XII

D R G

V R G

A

D


Pontine & vagal Influence

The spontaneous rhythmic discharges of medullary neurons is modified by– Neurons in the

pons– Afferents in the

vagus from receptors in the airways and lungs

IX

X

XI

XII

D R G

V R G



Pneumotaxic center located in– Nucleus

parabrachialis in dorsal lateral pons

Contain both– I-neurons & E-neurons– Also contain neurons

that are active in both phases of respiration

IX

X

XI

XII

D R G

V R G

Pneumotaxic center



When this area is damaged – Respiration becomes

slower– Tidal volume greater

Pneumotaxic center may play a role– Switching

between inspiration & expiration

IX

X

XI

XII

D R G

V R G

Pneumotaxic center



Apneustic center– Situated in lower

pons Send signals to DRG

– Prevent “switching-off” of respiratory ramp (increase duration of inspiration)

– Lungs become completely filled with air

IX

X

XI

XII

D R G

V R G

Pneumotaxic center

Apneustic center



Apneustic center is inhibited by – Vagus & pneumotaxic

center Vagotomy &

destruction of pneumotaxic center causes– Prolonged period of

inspiration• Apneusis

IX

X

XI

XII

D R G

V R G

Pneumotaxic center

Apneustic center


Chemical Control

Pulmonary ventilation– Regulated to meet different levels of

metabolic demands• Supply O2 • Elimination of CO2

Achieved by feed back control of respiratory center activity– In response to chemical

composition of blood•PCO2, H+, PO2


Chemical Control

Types of receptors– Central chemo-receptors– Peripheral receptors– Others


Central Chemoreceptors

Chemosensitive neurons– Bilateral beneath

the ventral medulla

Sensitive to changes in PCO2 & H+

H+ only important direct stimulus

DRG

CO2 + H2O ⇌ H2CO3 ⇌ HCO3- +

H+

Chemosensitive neurons



H+ crosses the blood-brain –barrier (BBB) very poorly– Changes in H+ in

blood have less immediate effect on respiration

CO2 diffuse easily across BBB– It is then hydrated

and dissociates to H+

& HCO3-

DRG

CO2 + H2O ⇌ H2CO3 ⇌ HCO3- +

H+




An increase CSF CO2 causes chemoreceptors to stimulate respiration

A decrease CSF CO2 causes chemoreceptors to inhibit respiration

DRG

CO2 + H2O ⇌ H2CO3 ⇌ HCO3- +

H+



Peripheral Chemoreceptors Located in the carotid & aortic

bodiesThese receptors respond to

– Lowered arterial O2 tension– Rise in arterial CO2 tension– Increase in H+ conc in arterial

blood


Peripheral ChemoreceptorsArterial O2 tension

– Only site in the body that detect changes in O2 tension of body fluids

Peripheral chemoreceptors– Receive a lot of blood flow for

their size•2000 ml/100 gm/min (cf brain = 54

ml/100 gm/min)


Peripheral ChemoreceptorsThus they monitor–O2 tension rather than O2

content O2 cause by anaemia, methaemoglobin, CO poisoning– Do not stimulate peripheral

chemoreceptors


Peripheral ChemoreceptorsWhen PO2 falls below 60–80

mm Hg– There is an increase in rate of

discharge of fibers from the receptors to RC

– ↑Rate and depth of respiration– ↑Alveolar ventilation

•Elimination of CO2


Peripheral chemoreceptorsElimination of CO2

– Respiratory alkalosis • ↓H+ conc CSF• Inhibition of respiratory drive

Over the course of several days– Ionic pumps (pia matter, choroid

plexus)• Transfer HCO3

- from CSF to blood• CSF pH returns towards normal• Respiratory drive returns


Peripheral chemoreceptorsEffect of CO2 tensionElevation of CO2 tension also

– Stimulate peripheral chemoreceptors

– But most of effect of CO2 is on the central chemoreceptors


Peripheral chemoreceptorsEffect of H+ concentration↑in H+ conc

– Stimulate peripheral chemorecptors– Increase in ventilation

The increase in alveolar ventilation– ↓CO2 tension– pH return towards normal– Ventilatory drive tends to reduce


Other receptors

Pulmonary stretch receptors– Lie within the walls of airways

They are stimulated by– Inflation of the lung

Initiate inspiratory inhibition– Termination of inspiration– Hering – Breuer reflex


Other Receptors

Irritant receptors– Lie in large airways

• Between airway epithelial cells– Stimulated by

• Noxious gases, smoke, particulates in inhaled air

– Initiate reflex that stimulate• Coughing, bronchospasm, mucus secretion• Breath holding (apnoea)


Other Receptors

J-receptors– Juxta-capillary – Located in the pulmonary

interstitium at the level of pulmonary capillaries

– Stimulated by the distension of pulmonary capillaries•Caused by ventricular failure,

emboli, chemicals


Other Receptors

J-receptors– Initiate reflex that cause

• Rapid, shallow breathing, tachypnoeaNose & upper airway receptors

– Upper respiratory pathways contain receptors• Respond to mechanical, chemical stimuli

– Reflex initiated • Sneezing, coughing, bronchoconstriction


Other Receptors

Joint & muscle receptors– Impulses from moving limbs

• Are believed to be part of stimuli for ventilation – Early stages of exercises

Baroreceptors– A rise in BP cause

• Reflex hypoventilation– A fall in BP cause

• Reflex hyperventilation

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3-Mar-16Control of Respiration1 Neural Mechanisms Chemical Mechanisms