11-chemical control of breathing

8/3/2019 11-Chemical Control of Breathing

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Changes in the chemical

composition of blood



Impulses are transmitted via afferentsto the medullary respiratory centers .



The medullary respiratory

center receives information

about the body¶s needs for

gas exchange

The medullary respiratory

center receives information

about the body¶s needs for

gas exchange

Then it responds by sending

signals to the respiratory

muscles to adjust the rate

and depth of ventilation

Then it responds by sending

signals to the respiratory

muscles to adjust the rate

and depth of ventilation



The signals

which o ventilation

o PCO2 q PO2o H+

These factors operate through chemoreceptors



Chemoreceptors

Central Peripheral

Located in the medulla

in the vicinity of the

respiratory center

Known as carotid bodies

and aortic bodies located

at the bifurcation of thecommon carotid arteries

and in the arch of aorta



Sensory

nerve fiber

Carotid sinus

Carotid artery

Aortic arch

Sensory

nerve fiber

Carotid bodies

Aortic bodies

Heart



Changes in breathing pattern

Changes in PCO2 , PO2 and pH

Chemoreceptors

Medullary respiratory center

respiratory muscles

C h a n g e s i n P

C O 2 , P O 2 a n d p H

a r e c o r r e c t e d



R ole of PO2 in R espiration

PO2 mediates its effects

on respiration through

peripheral

chemoreceptors

PO2 mediates its effects

on respiration through

peripheral

chemoreceptors

peripheral

chemoreceptors

respond only when thearterial PO2 is

60 mm Hg

peripheral

chemoreceptors

respond only when thearterial PO2 is

60 mm Hg



R ole of PO2 in R espirationUp to PO2 60 mm Hg,

Hb is still 90%saturated

Up to PO2 60 mm Hg,

Hb is still 90%saturated

Abro

20 40 60 80 1000

PO2 mm Hg

100

80

60

40

20 P e r c e n t s a t u r a t i o n o f h e m o g l o b i n

Plateau

phase

Therefore peripheral

chemoreceptors serve as an

emergency mechanismin dangerously low

arterial PO2 states



Figure 13.36

Page 498

Arterial P O2 <60 mm Hg

Emergency

life-saving

mechanism

Medullary

respiratory

center

o Ventilation

oArterial P O2

Central

chemoreceptors

Peripheral

chemoreceptors

No

effect

on

Relieves



R ole of PO2 in R espiration

Sudden severe drop in PO2

(Below 20mmHg)

Sudden severe drop in PO2

(Below 20mmHg)

Depress the brain

causes loss of consciousness

and death in 4 min

Depress the brain

causes loss of consciousness

and death in 4 min



R ole of PO2 in R espirationperipheral chemoreceptors

respond to the PO2 of the blood,not the total O2 content

of the blood

peripheral chemoreceptors


of the blood

In conditions like CO poisoning and anemia, the

total O2 content of the blood can be reduced

but the arterial PO2 remains normal

Thus respiration is not stimulated although

the person may die from cellular O2 deprivation





of the blood



of the blood

In stagnant hypoxia, because of

vascular stasis the amount of O2 delivered

to receptors/ unit time is reduced

Thus respiration is stimulated by

O2 deficiency at receptors (& hence PO2)





of the blood



of the blood

In hitotoxic hypoxia, because of Cyanide

O2 delivered

to receptors is not utilized (not sensed)

Thus respiration is powerfully stimulated by

O2 deficiency



R ole of PCO2 in R espiration

o arterial PCO2

q arterial PCO2

o ventilation to

eliminate excess

CO2

q ventilation to

accumulate reduced

CO2

Any minor change in PCO2

brings appropriate changes in ventilation



R ole of PCO2 in R espiration

Arterial PCO2

is the most

important regulator of ventilation

under resting conditions

Arterial PCO2

is the most

important regulator of ventilation

under resting conditions

Arterial PCO2

is

monitored by central

chemoreceptors

Arterial PCO2

is

monitored by central

chemoreceptors

Central chemoreceptors

do not monitor CO2 itself but theyare sensitive to changes in CO2

induced [H+] in the ECF

Central chemoreceptors

do not monitor CO2 itself but theyare sensitive to changes in CO2

induced [H+] in the ECF



Figure 13.37

Page 501

Arterial P CO2 Relieves

o Brain ECF P CO2

o Brain ECF H+

Centralchemoreceptors

Medullary

respiratorycenter

o Ventilation

o Arterial P O2

Peripheralchemoreceptors

Weakly

(when

arterial

P CO2

>70-80

mm Hg)

Brain ECF



oVentilationq arterial PCO2

Central

chemoreceptors

CO2 + H2O

H2CO3

H+ + HCO3-

o Brain ECF PCO2

o Brain ECF [H+]

Medullary

respiratorycenter

o arterial PCO2

Peripheral

chemoreceptors

+

+ In brain ECF+



Breath holding

(voluntarily)

oArterial PCO2

Breathing

resumed

Stimulates

respiratory

centero [H+] in ECF

Voluntary control to

hold breath overridden



Excitatory inputs from

central chemoreceptors

stimulated by H+

generated by CO2

Inspiratory neurons

in DRG(rhythmically firing)

Phrenic nerve DiaphragmSpinal cord

Medulla

-

-

Voluntary breath holding from

center in cerebral cortex

++



PCO2 " 70 - 80 mm Hg

Depression of respiratory

center



Chronic lung disease

Hypoventilation

o PCO2PO2 60 mm Hg

Central

chemoreceptors

Peripheral

chemoreceptors

o ECF[H+]

oVentilation

+ +



Serious chronic lung disease

Hypoventilation

o PCO2 PO2 60 mm Hg

Central

chemoreceptors

no more affected

Peripheral

chemoreceptors

o ECF [H+

]

o Ventilation

H2CO3 = HCO3-

+ H

q ECF [H+]

In these cases O2 should be administered carefully as hypoxic

drive to ventilation is the only and prime stimulus

v



Non-CO2-H+ produced

by metabolic acidsis sensed by


Non-CO2-H+ produced

by metabolic acidsis sensed by


It is not sensed by


because it does not penetrate

Blood Brain Barrier

It is not sensed by


because it does not penetrate

Blood Brain Barrier



o arterial

non-CO2 ? H+A

peripheral

chemo-

receptors

R espiratory

center

o ventilation



Figure 13.38

Page 502

Acidosis Arterial non-CO2-H+

Peripheralchemoreceptors

Medullary

respiratorycenter

Centralchemoreceptors

Cannot penetrate

blood-brain barrier

No

effect

on

o Ventilation

q Arterial P CO2

q Arterial -CO2-H+

Relieves

11-chemical control of breathing

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