Control of Respiration

• Respiratory centre as an integrator of inputs from chemoreceptors, other receptors and higher centres

• Exercise

• Chemoreceptors: Peripheral (respond to changes in O2, CO2 and pH

• Inputs from other receptors

• Outputs to respiratory muscles and muscles of upper airway

Regulation of Ventilation

Inputs

• higher centres

• chemoreceptors

• “visual receptors”

Brain stem

Integrator

neural control

Respiratory centres

Outputs

• muscles of respiration rate & depth

• smooth mucle airways

• muscels upper airways (esp to during inspiration)

Higher centres:• voluntary control• speech• emotions: anxiety, shock• exercise

(joint position sense?)

Chemoreceptors

PCO2

pH

PO2

Peripheral:carotid bodies (aortic bodies)

respond to:

PaCO2

pH

PaO2 respond to:

PCO2

Central chemoreceptors:brain stem: near 3rd ventricle (cerebrospinal fluid)near respiratory centre

PaCO2 PcsfCO2

For PCO2, changes are sensed by:Peripheral

chemoreceptors20%

rapid response

Central chemoreceptors

80%somewhat slower

+

CO2 + H2O H2CO3 H+ + HCO3

actually sensed

PaCO2 ventilation

PaCO2 ventilation

Ve

nti

lati

on

(L

/ m

in)

PaCO2 (mmHg)

20 40 60

Ve

nti

lati

on

(L

/ m

in)

PCO2 (mmHg)20 40 60

C sensitivity

B sensitivity

Factors which affect slope of relationship:• gender, ethnic origin• sleep (slow wave sleep) — B• respiratory depressants — B

alcohol, barbiturate, anaesthetics, narcotics(unconsciousness)

• low PO2: hypoxia — C

Ventilatory Response to CO2

1. Response occurs at normal PaCO2

2. At very high PaCO2 (80 mmHg)

CO2 itself acts as respiratory depressant

3. Tolerance occurs

Cont...

Tolerance to PCO2:

• Most CO2 response due to central chemoreceptors within brain side of blood brain barrier close to cerebrospinal fluid

CO2 H2CO3 H+ + HCO3

• Local pH regulation

takes place over 13 days; cells lining 3rd ventricle can secrete HCO3

+

O2 response via carotid bodies (aortic body)

•small (2 mg) collections of neural tissue at

bifurcation of common carotid artery

• very high blood flow (equivalent of 2L/100g/min cf 54 ml/100g/min brain)

probably respond to dissolved O2

i.e. PaO2 not O2 content

response impaired in anemia, CO poisoning

• response present if blood flow or

blood pressure e.g. shock

• response caused also by cyanide

carotid body receptors activated by: nicotine

Response to hypoxia

1. Under normal circumstances

i.e. normal CO2

PO2 ventilation until PO2 falls to

60mmHg

2. A high PO2 does not inhibit ventilation

3. If PCO2 is high

that sensitivity to hypoxia

4. Tolerance does not occur

pH

• mainly sensed peripherally

• H+ doesn’t cross blood brain barrier well

• response to 7.3 – 7.5

pH ventilation

mild response cf PCO2

Visceral Receptors• Visceral reflexes that affect ventilation

cough, sneeze

vomit

• Stretch receptors in lung

Hering – Breuer reflex:

inflate lungs – stretch receptors detect stretch

respiratory centre to stop inspiration

Cough & Sneeze ReflexesAfferent sensory input Brainstem

medullaIrritation: Cough – sensory endings

in wall of extrapulmonary

respiratory tractsvagus

Irritation: Sneeze – sensory endings in nose & upper

pharnyxcranial nerveV

Deep inspiration followed by

Forced expiration against closed

glottis intrathoracic

pressureSudden glottic

opening

Forced expiration(nose)

Rapid expulsion air at high speed through mouth

(cough)

Clears irritant