Control of Respiration Respiratory centre as an integrator of inputs from chemoreceptors, other receptors and higher centres Exercise Chemoreceptors: Peripheral (respond to changes in O 2, CO 2 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  PCO 2  pH  PO 2 Peripheral: carotid bodies (aortic bodies) respond to:  PaCO 2  pH  PaO 2 respond to:  PCO 2 Central chemoreceptors: brain stem: near 3rd ventricle (cerebrospinal fluid) near respiratory centre PaCO 2 PcsfCO 2

For PCO 2, changes are sensed by: Peripheral chemoreceptors 20% rapid response Central chemoreceptors 80% somewhat slower + CO 2 + H 2 O  H 2 CO 3  H + + HCO 3 actually sensed  PaCO 2   ventilation  PaCO 2   ventilation Ventilation (L / min) PaCO 2 (mmHg)

Ventilation (L / min) PCO 2 (mmHg) 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 PO 2 : hypoxia — C

Ventilatory Response to CO 2 1. Response occurs at normal PaCO 2 2. At very high PaCO 2 (80 mmHg) CO 2 itself acts as respiratory depressant 3. Tolerance occurs Cont...

Tolerance to  PCO 2 : Most CO 2 response due to central chemoreceptors within brain side of blood brain barrier close to cerebrospinal fluid CO 2  H 2 CO 3  H + + HCO 3 Local pH regulation takes place over 1  3 days; cells lining 3rd ventricle can secrete HCO 3 +

O 2 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 O 2 i.e. PaO 2 not O 2 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 CO 2  PO 2  ventilation until PO 2 falls to  60mmHg 2. A high PO 2 does not inhibit ventilation 3. If PCO 2 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  PCO 2

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 Reflexes Afferent sensory input Brainstem medulla Irritation: Cough – sensory endings in wall of extrapulmonary respiratory tracts vagus Irritation: Sneeze – sensory endings in nose & upper pharnyx cranial nerveV Deep inspiration followed by Forced expiration against closed glottis  intrathoracic pressure Sudden glottic opening Forced expiration (nose) Rapid expulsion air at high speed through mouth (cough) Clears irritant