Neurosurgery notes/Trauma/Head Trauma general/Normal head trauma/CO2 reactivity

CO2 reactivity

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Normal head trauma
  • CO2 reactivity is the process by which PaCO2 affects CBF → cerebral vasculature.
  • Within the normal range of PaCO2 between 20 and 60 mmHg, every 1 mmHg fluctuation results in 2% to 3% change in CBF.
    • Hypercarbia (hypoventilation) → Vasodilation → increased CBF
    • Hypocarbia (hyperventilation) → Vasorestriction → decrease CBF
    • Mediated through changes in pH of the perivascular space via carbonic anhydrase,
      • This forms the basis of the acetazolamide challenge
        • Technique
          • Acetazolamide 1 g IV
        • Normal response:
          • Acetazolamide → inhibits CA → reduce H+ and HCO3- production → dec. pH → Vasodilation and augmentation of CBF to 30 – 60% over 10– 15 minutes.
        • Abnormal response
          • A failure to vasodilate in response to acetazolamide implies maximal vasodilation, usually resulting from chronic ischaemia.
  • Hyperaemia and metabolic acidosis in CSF
    • Are associated with the acute phase of TBI
    • Occur in the first 24 hours
  • Patients with persistent loss of CO2 reactivity risk high mortality or severe neurological compromise.
    • While CO2 reactivity causes changes in both CBF and AVDO2 (Arterio-jugular differences of oxygen)
      • Autoregulation affects CBF with AVDO2 maintained relatively constant.
  • Hyperventilation and control of PaCO2 are important therapeutic interventions in the management of raised ICP,
    • However this requires cerebral oxygenation monitoring to ensure that excessive arterial vasoconstriction does not inflict ischaemia.