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Control of Respiration

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

yvonne-buckner
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Control of Respiration

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  1. 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

  2. Regulation of Ventilation neural control • Inputs • higher centres • chemoreceptors • “visual receptors” • Outputs • muscles of respiration rate & depth • smooth mucle airways • muscels upper airways (esp to  during inspiration) Brain stem Integrator Respiratory centres • Higher centres: • voluntary control • speech • emotions: anxiety, shock • exercise • (joint position sense?)

  3. Chemoreceptors  PCO2  pH  PO2 respond to:  PaCO2  pH  PaO2 Peripheral: carotid bodies (aortic bodies) Central chemoreceptors: brain stem: near 3rd ventricle (cerebrospinal fluid) near respiratory centre respond to:  PCO2 PaCO2 PcsfCO2

  4. For PCO2, changes are sensed by: Peripheral chemoreceptors 20% rapid response Central chemoreceptors 80% somewhat slower + CO2 + H2O  H2CO3  H+ + HCO3 actually sensed  PaCO2   ventilation  PaCO2   ventilation Ventilation (L / min) 20 40 60 PaCO2 (mmHg)

  5. C  sensitivity B  sensitivity Ventilation (L / min) 20 40 60 PCO2 (mmHg) • 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

  6. 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...

  7. 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 13 days; cells lining 3rd ventricle can secrete HCO3

  8. 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

  9. 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

  10. pH • mainly sensed peripherally • H+doesn’t cross blood brain barrier well • response to 7.3 – 7.5 •  pH   ventilation • mild response cf  PCO2

  11. 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

  12. 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 (nose) Forced expiration against closed glottis  intrathoracic pressure Clears irritant Rapid expulsion air at high speed through mouth (cough) Sudden glottic opening

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