One may be able to derive information from the shape of the ICP waveform. Whether this information on its own is useful, in terms of changing the way you manage the patient, is open to debate. For the CICM trainee, this chapter is of passing interest only; it is unlikely that we will ever see a bedside use for this. In terms of exam preparation, this topic can be safely ignored.
Increasing amplitude of the waveform suggests rising intracranial pressure
As the intracranial pressure rises, the amplitude of all waveforms increases. (conversely, as the ICP falls, the amplitude of these waveforms decreases. It has been shown that the drainage of CSF decreases the amplitude of all wave peaks, but the overall morphology of the waveform doesn't change (i.e. the P1 is still taller than P2, etc.)
Decreasing amplitude of the P1 waveform suggests decreased cerebral perfusion
The P1 waveform reflects the transmission of the arterial systolic pressure into the choroid plexus, and it can be used a surrogate representation of cerebral perfusion. If this waveform diminishes in absence of increasing intracranial pressure, it could be be interpreted as vasospasm. I suppose in this situation the P3 wave should also decrease in amplitude.
Increasing amplitude of the P2 waveform suggests decreased cerebral compliance
The P2 wave is vaguely correlated to cerebral compliance. It has been shown that manoeuvres which decrease the cerebral bulk (e.g.. hyperventilation) will decrease the amplitude of the P2 wave; conversely an increase in cerebral bulk (eg. worsening cerebral oedema) will cause the P2 wave to become more prominent.
Thus, a prominent P2 wave suggests that cerebral compliance is reduced, especially when it is in the presence of increased ICP.
In the absence of a raised ICP, this could be another sign of vasospasm (i.e. its not that the P2 has become prominent, but rather that the P1 has diminished in amplitude).
Flattening of ICP breathing variation occurs with increasing intracranial pressure
The normal respiratory pattern of ICP waveforms is blunted by rising ICP, so that the respiratory variation becomes more and more difficult to discern and it disappears altogether above an ICP of 50mmHg or so.
A waves, or "Plateau" waves, suggest intact cerebral blood flow autoregulation
Unlike the pulse waveforms or breathing waveforms, these are waves seen over several minutes.
There is an initial rapid rise in the ICP, which is followed by a sustained plateau (where the ridiculously high pressure is sustained), followed by a drop to a level which may even be below the original baseline.
What is happening here? It appears that this waveform correlates with a greatly increased cerebral blood volume. It has been suggested that this increase in ICP is the result of increased blood flow into the brain, which occurs in response to decreased cerebral perfusion. Given the inflexibility of the intracranial volume, this extra blood flow adds to the already high ICP (and this is the plateau). But however high the pressure flow still occurs, and the brain parenchyma then autoregulates its perfusion back to a normal level, with a correlated decrease in ICP to pre-plateau levels.
Is there evidence for this? Masuka et al (in 1979) demonstrated within a small case series that yes, in fact these A-waves are correlated with marked cerebral vasodilatation. Furthermore, later authors have remarked that these waves are suggestive of a positive outcome (after all, the ability to autoregulate your cerebral perfusion is a good ability to retain if you are severely head-injured).
Sinusoidal B-waves may be normal, and are a sign of intact cerebral bloodflow autoregulation
These waves occur at a rate of 0.5 to 2 per minute. So, they are somewhat less frequent then breathing waves, but more frequent than A-waves.
These seem to reflect oscillations of vascular smooth muscle tone inside the brain. There is some evidence that these waves correlated with cyclical changes in pial vessel diameter, and some authors have found that healthy volunteers have sinusoidal B-waves (albeit of a lower amplitude than the head injury patients).
Again, this is suggestive of an intact system of cerebral bloodflow autoregulation.
Ramp-like B-waves are produced by increases in PCO2
Ramp-like B waves are correlated to increases in PCO2 associated with snoring an sleep apnoea. Again, it is a cerebral vascular phenomenon (as PCO2 rises vasodilate cerebral vessels, the intracranial blood volume rises and thus the ICP increases). These can be viewed as normal, but they are not exactly productive when you are trying to manage somebody's head injury.