Changes in the chemical composition of blood

Impulses are transmitted via afferents to the medullary respiratory centers .

Thenmedullary respiratory The it responds by sending center receives respiratory signals to the information about the bodys needs for muscles to adjust the rate and depth of ventilation gas exchange

The signals which o ventilation

o PCO2

o H+

q PO2

These factors operate through chemoreceptors

Chemoreceptors

Central

Peripheral Known as carotid bodies and aortic bodies located at the bifurcation of the common carotid arteries and in the arch of aorta

Located in the medulla in the vicinity of the respiratory center

Sensory nerve fiber Carotid sinus

Sensory nerve fiber

Carotid bodies

Carotid artery

Aortic bodies

Aortic arch

Heart

Changes in PCO2 , PO2 and pH are corrected

Changes in PCO2 , PO2 and pH Chemoreceptors Medullary respiratory center respiratory muscles Changes in breathing pattern

Role of PO2 in Respiration

PO2 mediates its effects on respiration through peripheral chemoreceptors peripheral chemoreceptors respond only when the arterial PO2 is 60 mm Hg

Role of PO2 in Respiration Up to PO 60 mm Hg,

2

Hb is still 90% saturated

100 Pe rcent saturation of hemoglobin

Therefore peripheral Plateau 60 phase chemoreceptors serve as an 40 emergency mechanism in dangerously low 20 arterial PO2 states
0 20 40 60 80 100 Abro PO 2 mm Hg

80

Figure 13.36<60 mm Hg Arterial P Page 498 Emergency

O2

Relieves

life-saving mechanism

No effect on

Peripheral chemoreceptors

Medullary respiratory center

Central chemoreceptors

o Ventilation

oArterial PO2

Role of PO2 in Respiration

Sudden severe drop in PO2

(Below 20mmHg)

Depress the brain causes loss of consciousness and death in 4 min

Roleperipheral chemoreceptors of PO2 in Respiration

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

Roleperipheral chemoreceptors of PO2 in Respiration

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

Roleperipheral chemoreceptors of PO2 in Respiration

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

Any PCO2 in in PCO2 Role of minor changeRespiration brings appropriate changes in ventilation

o arterial PCO2

o ventilation to eliminate excess CO2 q ventilation to accumulate reduced CO2

q arterial PCO2

Role of PCO2 in Respiration

Central chemoreceptors Arterial PCOPCO2 ismost Arterial 2 is the do not monitor CO2 itself but they important regulator of ventilation monitored by central are sensitive to changes in CO2 under resting conditions chemoreceptors induced [H+] in the ECF

Arterial PCO2

Relieves

Figure 13.37 Page 501

(when arterial PCO2 >70-80 mm Hg)
Brain ECF

o Brain ECF PCO2

o Brain ECF H+ Weakly

Peripheral chemoreceptors

Medullary respiratory center

Central chemoreceptors

o Ventilation o Arterial PO2

o arterial PCO2

o Brain ECF PCO2

CO2 + H2O

H2CO3

o Brain ECF [H+]

H+ + HCO3 -

+
Peripheral chemoreceptors

+ +
Central chemoreceptors Medullary respiratory center

In brain ECF

q arterial PCO2

o Ventilation

Breathing resumed

Breath holding (voluntarily)

Voluntary control to hold breath overridden

o Arterial PCO2

Stimulates respiratory center

o [H+] in ECF

Voluntary breath holding from center in cerebral cortex Excitatory inputs from central chemoreceptors stimulated by H+ generated by CO2

Inspiratory neurons in DRG (rhythmically firing) Medulla

Spinal cord

++
Phrenic nerve Diaphragm

PCO2 " 70 - 80 mm Hg

Depression of respiratory center

Chronic lung disease Hypoventilation o PCO2 o ECF[H+]

+ +
PO2 60 mm Hg

Central chemoreceptors

Peripheral chemoreceptors

o Ventilation

Serious chronic lung disease Hypoventilation o PCO2 H2CO3 = HCO3 - + H o ECF [H+]
Central chemoreceptors no more affected

PO2 60 mm Hg

q ECF [H+]

Peripheral chemoreceptors o Ventilation

In these cases O2 should be administered carefully as hypoxic drive to ventilation is the only and prime stimulus

Non-CO2-H+ produced by metabolic acids is sensed by peripheral chemoreceptors

It is not sensed by central chemoreceptors because it does not penetrate Blood Brain Barrier

o ventilation

o arterial non-CO2 ? H+A

Respiratory center

peripheral chemoreceptors

Relieves

Figure 13.38 Page 502

Peripheral chemoreceptors

Acidosis

Arterial non-CO2-H+

Cannot penetrate blood-brain barrier

Medullary respiratory center o Ventilation q Arterial PCO2

No effect on

Central chemoreceptors

q Arterial -CO2-H+