chemoreceptors

• Importance of Chemoreceptors: 

  • Control and modify ventilation on breath by breath basis, very quick 

  • Feedback input to RCC → alter intrinsic respiratory pattern  

  • To maintain PaCO2, PaO2 and pH within physiological limits regardless of activity 
• Peripheral Chemoreceptors: 

  • Located aortic arch & carotid body – first side blood reaches when blood is pumped out  

  • Sample surrounding arterial blood  

  • Sensitive to arterial hypoxaemia  

  – > 40% reductions in PaO2  

  – PaO2 8KPa or less  

  • ↑H+ content arterial blood  

  • Weakly sensitive to PaCO2 
• Central Chemoreceptors: 

  • Located ventral lateral surface of medulla bilaterally 

  • Bathed in CSF (cerebral spinal fluid) 

  • CSF PCO2 = arterial PCO2  

  • Sensitive to arterial hypercapnia – Specifically ↑ H+ ion concentraion  

  • Responsible for 70% of drive to breath  

  • Central chemoreceptors have ↑ sensitivity to 

  • CO2 with mild hypoxia and acidosis 
• CO2 Stimulation Central Chemoreceptors: 

  • CO2 diffuses across blood brain barrier  

  • CO2 combines with H2O in CSF  

  • This forms carbonic acid  

  • Carbonic acid disassociates to form bicarbonate and hydrogen ions  

  • CO2 + H2O --> H2CO3 --> HCO3 + H+  

  • H+ ↑ acidity ↓ pH of CSF  

  • ↓ pH CSF stimulates central chemoreceptors 
• Response of central chemoreceptors: 

  • Central chemoreceptors feedback to the RCC 

  • RCC stimulate effectors 

  • Increase rate & depth of ventilation 

  • Until CO2/pH levels are in normal range 

  • When CO2 is low rate & depth of ventilation is reduced to allow CO2/pH to normalise 
• Additional Actions of Chemoreceptors:  

  • Stimulate sympathetic activity  

  • Inhibit parasympathetic activity  

  • Increase arterial blood pressure 
• Chronic Hypercapnia: 

  • CO2 + H2O --> H2CO3 --> HCO3 + H+  

  • Transport of HCO3 across blood brain barrier to “buffer” CSF H+  

  • May take up to 3 days for full effect  

  • Effective buffering from the kidneys returns CSF pH to normal  

  • Reducing sensitivity of central chemoreceptors  

  • But arterial blood CO2 remains raised  

  • Blood pH remains acidotic
• What would happen if patient with COPD and hypercapnia is given high levels of therapeutic O? 

  It would make the patient worse 

   

  Elevated levels PaCO2: 

  • Secondary to  

  – Loss of hypoxic drive  

  – Increased V/Q mismatch due to reversal HPVC  

  – Haldane effect 
• Loss of Hypoxic Drive: 

  • COPD patients with chronic hypercapnia rely on peripheral chemoreceptors to sense arterial hypoxaemia  

  • If patient given high dose O2 arterial hypoxaemia reversed  

  • Only remaining drive to breathe is removed 
• Hypoxic pulmonary vasoconstriction: 

  • areas of poor ventilation leads to a decrease of gas exchange & hypoxia 

  • when PaO2 falls to 6Kpa/SaO2 low 80s hypoxia is sense by receptors in arterioles 

  • arterioles passing through area of poor ventilation constrict to minimise V/Q mismatch 

  • blood flow is redirected to area with good ventilation to facilitate gas exchange  

   
• Increased V/Q Mismatch: 

  • COPD patients have areas of lung destruction with poor ventilation → hypoxia  

  • V/Q mismatch  

  • Compensatory HVC occurs in those areas  

  • If COPD patient given high dose O2 hypoxia in good lung tissue is reversed  

  • Sensed by control centres so HPVC is also reversed  

  • Leading to perfusion of non-ventilated lung and increased V/Q mismatch 

   
• Haldane Effect: 

  • Haemoglobin (Hb) has strong affinity for O2 

  • O2 transported bound to Hb  

  • When low O2 e.g. COPD CO2 binds to Hb  

  • If give patient high dose O2 Hb breaks off from CO2 in preference to bind with O2  

  • CO2 dissolves in plasma  

  • Raising PaCO2