Intracranial Pressure

Explain the control of intra-cranial pressure

Normal ICP is ≤13mmHg, with some rhythmic variation occurring on the transduced waveform:

• P1 is the first peak, and represents arterial pulsation
• P2 is the second peak, and represents intracranial compliance
  If P2>P1, this is suggestive of poor intracranial compliance
• P3 is the third peak, and is a dicrotic wave representing valve closure

In addition, a second set of Lundberg waves are described:

• A waves are pathological, and consist of square-wave plateaus up to 50mmHg lasting 5-20 minutes. They are suggestive of herniation, and are always pathological.
• B waves are variable spikes in ICP at 30-120 second intervals, suggestive of cerebral vasospasm
• C waves are oscillations that occur 4-8 times per minute, and are a benign phenomena occurring with respiratory and blood pressure variations

Raised intracranial pressure may cause focal ischaemia when ICP >20mmHg, and global ischaemia when the ICP >50mmHg:

Monroe Kellie Doctrine

This states that:

• The skull is a rigid container of a fixed volume, containing approximately 8 parts brain, 1 part blood, and 1 part CSF
• As it has negligible elastance, any increase in volume of one substance must be met with a decrease in volume of another or a rise in ICP
  • Elastance is technically correct as we are discussing a change in pressure for a given change in volume
    Compliance is a change in volume for a given change in pressure.

Physiological Responses to an Increase in ICP

• Displacement of CSF into the spinal subarachnoid space
• Compression of vascular bed
• Increased CSF reabsorption

• The Cushing reflex may occur in brainstem herniation
  This is a triad of hypertension, bradycardia, and irregular respiration secondary to SNS activation, and is a reflexive response to medullary ischaemia.
  • Hypertension
    To improve CPP.
  • Bradycardia
    Due to a baroreceptor response.
  • Irregular respiration
    Due to respiratory centre dysfunction.

Physiological Basis of Treatment

Treatment can be classified as per the Monroe Kellie doctrine:

Brain

• Osmotic agents such as mannitol and hypertonic saline
  Increase plasma osmolality and expand blood volume, creating an osmotic gradient between brain parenchyma and blood with a resulting reduction in brain oedema and ICP.
• Timely evacuation of mass lesions and intracranial haemorrhage

CSF

• External Ventricular Drain
  Facilitates removal of CSF.

Blood

• Reducing cerebral metabolic rate
  Results in reduced blood flow due to flow-metabolism coupling. May be achieved with:
  • CNS depressants such as propofol, benzodiazepines, or barbiturates
    Have several beneficial effects:
  • Depress cerebral metabolism which reduces oxygen requirements
  • Reduce seizure risk, which is detrimental because it greatly increases cerebral O₂ demand and impairs venous return
  • Improves ventilator dyssynchrony, limiting coughing and bearing down, and subsequent rises in ICP
  • Avoid hyperthermia
    Causes a reduction in cerebral metabolism and risk of seizures.
  • Prevention of hypoxia or hypercapnea
    Hypoxia and hypercapnea both cause vasodilatation, with a subsequent increase in cerebral blood volume, blood flow, and ICP.
    • Aim low-normal CO₂
      Causes vasoconstriction and a subsequent reduction in cerebral blood flow and blood volume. This leads to:
      • Reduction in ICP
      • Reduction in cerebral oxygen delivery
        Consequently, a low-normal ETCO₂ target is used to avoid tissue hypoxia.

References

1. Kam P, Power I. Principles of Physiology for the Anaesthetist. 3rd Ed. Hodder Education. 2012.
2. Cross ME, Plunkett EVE. Physics, Pharmacology, and Physiology for Anaesthetists: Key Concepts for the FRCA. 2nd Ed. Cambridge University Press. 2014.
3. Stocchetti N, Maas AI. Traumatic intracranial hypertension. N Engl J Med. 2014 May 29;370(22):2121-30.
4. Barrett KE, Barman SM, Boitano S, Brooks HL. Ganong's Review of Medical Physiology. 24th Ed. McGraw Hill. 2012.