Neurosurgery notes/Trauma/Management of trauma/Non surgical/Hyperventilation (HPV)

Hyperventilation (HPV)

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Non surgical

General

  • Normal ventilation is currently the goal for severe TBI patients in the absence of cerebral herniation and normal partial pressure of carbon dioxide in arterial blood (PaCO2) ranges from 35-45 mm Hg.
  • In ventilated patients: Regulate PaCO2 levels through
    • Rate
    • Tidal volume

Intra-arterial carbon dioxide (PaCO2) is the most potent cerebrovascular vasodilator

  • Under normal conditions, PaCO2 is the most powerful determinant of cerebral blood flow (CBF) and, between a range of 20 mm Hg and 80 mm Hg, CBF is linearly responsive to PaCO2.

Mechanism

  • Changes in pH caused by the rapid diffusion of CO2 across the BBB.
  • Hyperventilation (HPV) lowers ICP by reducing PaCO2 which causes cerebral vasoconstriction, thus reducing the cerebral (intracranial) blood volume (CBV).
  • HPV → Acute alkalosis increases protein binding of calcium (decreases ionized Ca++ ) → Patient may develope ionized hypocalcemia with tetany (despite normal total [Ca])

❌ Hyperventilation (HPV) is to be used in moderation only in specific situations

  • HPV → Vasoconstriction → lowers cerebral blood flow (CBF) → focal ischemia in areas with preserved cerebral autoregulation as a result of shunting.
    • However, ischemia does not necessarily follow as the O2 extraction fraction (OEF) may also increase
  • HPV only to PaCO2 = 30–35mm Hg
    • CBF in severe head trauma patients is already about half of normal during the first 24 hrs after injury (typically <30 cc/100 g/min during the first 8 hours, and may be< 20 during the first 4 hours in patients with the worst injuries).
      • In one study, the use of HPV to PaCO2 = 30mm Hg within 8–14 hrs of severe head injury did not impair global cerebral metabolism, but focal changes were not studied.
      • Hyperventilation to PaCO2 < 30mm Hg further reduces CBF, but does not consistently reduce ICP and may cause loss of cerebral autoregulation.
        • If carefully monitored, there may be occasion to use this.
        • There are no studies showing any improvement in outcome with aggressive HPV (PaCO2 ≤25mm Hg) which can cause diffuse cerebral ischemia.
  • Reducing PaCO2 from 35 to 29mm Hg
    • Lowers ICP 25–30% in most patients.
    • Onset of action: ≤30 seconds.
    • Peak effect at ≈ 8 mins.
    • Duration of effect is occasionally as short as 15–20 mins.
    • Effect may be blunted by 1 hour (based on patients with intracranial tumours), after which it is difficult to return to normocarbia without rebound elevation of ICP.
      • HPV must be weaned slowly.
  • Prophylactic hyperventilation (PaCO2 ≤25mm Hg or 3.33kPa) is not recommended
    • This further reduces CBF but does not necessarily reduce ICP

Monitor

  • Monitor oxygen delivery via
    • Jugular venous oxygen saturation (SjO2) or
    • Brain tissue O2 partial pressure (BtpO2) measurements

Indications

  • HPV for brief periods (minutes) at the following times
    • Signs of transtentorial herniation/Intracranial hypertensionᵃ OR
        1. Pupillary dilatation (unilateral or bilateral)
        1. Asymmetric pupillary reaction to light
        1. Decerebrate or decorticate posturing (usually contralateral to blownᵇ pupil)
        1. Progressive deterioration of the neurologic exam not attributable to extracranial factors
      • ᵃItem 1-3 represent clinical signs of herniation. The most convincing clinical evidence of IC-HTN is the witnessed evolution of 1 or more of these signs. IC-HTN may produce a bulging fontanelle in an infant.
      • ᵇ”blown pupil”: fixed & dilated pupil
    • Progressive neurologic deterioration not attributable to extracranial causes
  • HPV for longer periods: when there is documented IC-HTN unresponsive to sedation, paralytics, CSF drainage (when available), and osmotic diuretics
  • HPV may be appropriate for IC-HTN resulting primarily from hyperaemia

Caveats for hyperventilation

  • Avoid during the first 5 days after head injury if possible (especially first 24 hrs)- Muizelaar 1991 et al
  • Do not use prophylactically: Has worse outcomes
    • Note: prophylactic HPV = no clinical signs of IC-HTN and where IC-HTN unresponsive to other measures has not been documented by ICP monitoring
  • If documented IC-HTN is unresponsive to other measures, hyperventilate only to PaCO2 =30– 35mm Hg
  • If prolonged HPV to PaCO2 of 25–30mm Hg is deemed necessary, consider monitoring SjVO2, AVdO2, or CBF to rule out cerebral ischemia
  • Do not reduce PaCO2 < 25mm Hg (except for very brief periods of a few minutes)
  • If HPV is used, jugular venous oxygen saturation (SjVO2) or PbtO2 should be measured to monitor brain O2 delivery

Evidence

  • See Muizelaar 1991
    • Only randomised trial looking at role of hyperventilation on outcome in severe TBI
    • Most influential study to date indicating that prolonged hyperventilation should be avoided in severe TBI
    • Looked at normo-ventilation, hyperventilation, and hyperventilation plus tomomethamine (introduced to see whether any effect of loss of CSF buffer during hyperventilation)
    • Single centre RCT, n = 113, Class II evidence
    • Primary outcome – GOS at 3, 6, 12 months
    • Stratified by severity of injury by GCS motor score (1-3 and 4-5)
    • Conclusions:
      • Prophylactic hyperventilation is harmful in patients with motor score 4-5
      • Harmful effects of hyperventilation could be overcome by THAM

Critique

  • Hyperventilation → vasoconstrict due to low pCO2 → lower ICP by lowering CBF (which can cause ischaemia)
  • Influential study that shows prolonged prophylactic hyperventilation to be harmful
  • Weaknesses:
    • Lack of blinding
    • 86% patients did not have raised ICP on admission (so hyperventilation truly prophylactic)
    • No power calculation - data may thus be insufficient to determine whether hyperventilation harmful or not (Shierhout and Roberts, 2000)