Figure 25.1. The volume tolerance curve, formerly called the compliance curve.

The compliance curve was used to describe volume variation over pressure variation; as the curve is exponential, the compliance varies along it.

Three sectors are distinguished:

• Initial: almost horizontal. This is the compensating phase because increasing volume produces minimal changes in ICP, showing the effectiveness of compensating mechanisms.
  
• Intermediate: (decompensating phase) is the inflection and shows the transition between the two sectors. It corresponds to variable values of ICP (depending on the speed of onset) between 20 and 25 mmHg. This value must be considered as a warning sign because ICP will increase dramatically at higher values.
  
• Final: almost vertical (cerebral tamponing phase). The increasing volume generates rapid ICP increments because the compensation mechanisms can no longer counteract it. This phase corresponds to ICP values of around 50-60 mmHg, where only systolic flow (ICP=DAP) remains.

These variations in pressure and volume behaviour are determined by intracranial compliance, which is defined as the relationship between volume variations and pressure variations ((∆V/∆P). It is high initially and frankly decreases above 20 mmHg. Its normal range is 0.15 to 0.5 ml/mmHg. Many authors argue that compliance should be referred to as “pseudocompliance” because the intracranial volume is constant. They prefer to refer to it as a volume tolerance curve, referring to the displaced volume more than to the volume variation. Compliance is not homogeneous: it is greater in the supratentorium compartment (80%) than in the infratentorium (20%), in which the compliance curve is displaced to the left, indicating its lower tolerance to volume increments. Some authors prefer to refer to this property as as elastance and not compliance, which would be a more physiological definition, because the brain has a constant volume. Elastance is the opposite of the compliance, i.e., the pressure variations that must be generated to displace a certain volume.

The other important concept is that the compensating system is time-dependent. This means that the slower the volume load, the greater the system’s tolerance, ensuing in a lower pressure to a higher volume. This explains why slow-growing tumours can occupy intracranial space, whereas even a slight, sudden increase in ICP with a much smaller volume will generate a much higher pressure. Between this two extremes lie all kinds of intermediate situations, and the physician will need to consider the time factor when making decisions.

So, in short, the phasic state or transitory state of the intracranial system, according to Marmorou’s model, is described by the compliance curve or elastance. The system works with a non-ideal response with a variable compliance, the pressure/volume ratio is exponential and time-dependent.

25.2 Compliance

There are two ways to measure compliance with the compliance test:

• PVR (Miller): when injecting 1 ml/second it’s known that the ICP should be <4 mmHg.
  
• PVI: it’s index of pressure/volume of Marmorou.

This is the volume (normally >20 ml) needed to increase ICP 10 fold.

Commonly used in the 1980s, these indices are now rarely applied but serve to understand the logarithmic relationship between pressure and volume: the higher the volume, the better the compliance and therefore the more tolerant the system to volume loads.

25.3 ICP Waves

ICP waves refer to the study of cerebral pulse curve and periodic waves.

25.3.1 Cerebral Pulse Curve

Another way to understand the compliance curve is to study the cerebral pulse curve, i.e., the ICP instantaneous curve. It normally presents three consecutive peaks, (P1, P2 and P3). The first positive deflection, P1 (percussion wave), corresponds to the arterial pulse wave and represents the arrival of blood to the intracranial cavity. The second wave, P2 (volume wave), is considered a reflex of intracranial elastance. The meaning of the third wave, P3 (dicrotic wave), is still unknown. Normally, the amplitude of P1 is higher than that of P2; however, in situations of greater elastance or decreased compliance, P2 increases in relation to P1. The magnitude of this change is a measure of intracranial compliance, constituting the so-called compliance auto-test.

When we have a space occupying lesion, the arterial pulse constitutes a real volume load. From cerebral pulse wave analysis we can infer in what sector of the compliance curve we are. The normal pulse wave amplitude is 3 mmHg. A high amplitude (10 or 15 mmHg) pulse wave indicates a volume load in the ascending slope of the compliance curve.

25.3.2 Periodic Waves

In the classic description, following Lundberg who described ICP waves (A, B, C) which bear his name, Lundberg A waves, or plateau waves, are the most important from a pathologic point of view. According to its description they were ominous, with duration between 5 and 20 minutes, with an amplitude >50 mmHg, reaching values of 100 mmHg. B Lundberg waves last between 2 and 5 minutes, with an amplitude >20 mmHg, reaching 50 mmHg. Their clinical meaning is less accurate than A waves, but are warning signs that show a decrease in intracranial compliance. Type C waves, (Hering Traube), are of short duration, with low amplitude (<20 mmHg) and show arterial curves; their clinical meaning is unknown. Our current notion about ICP periodic waves follows the concept of Lemaire, which introduced the globalized concept of periodic events separated according to frequency range and taking the B waves as the centre, then subdividing them into infra B, B and ultra B, according to how it’s established (Table 25.1).

Table 25.1. Periodic wave classification.

To detect this type of waves it is important to count with slow ICP recordings. The usual display on most monitors, although they provide a good recording and visualization of the cerebral pulse curve, don’t permit these events to be observed. In these conditions, the existence of periodic waves may be sometimes suspected from spontaneous changes in ICP values above the treatment threshold and should prompt doubt about its treatment. What must be emphasized is that as long as the elevation in ICP is not excessive, we must always wait 15 to 20 minutes before starting to treat an increase in ICP so as to avoid unnecessary treatment of reversible ICP elevation caused by these periodic waves.

The phenomenon of periodic waves is essentially a physiological event, as has been demonstrated by transfontanel recording in normal neonates. It is generally of vasogenic origin, emerging from the normal vasomotricity of normal circulation and that of the brain circulation in particular. The most pathological forms would be given by the higher amplitude and slower frequency waves (infra B), which typically show: 1) a sharp drop compliance in all cases; and 2) conservation, but not always, of the autoregulating pressure. Detailed study of the chronobiology that initiates a wave of this type is essential for determining its mechanisms. With simultaneous multimodal monitoring and multichannel recording it is possible to determine whether it corresponds to cerebral autoregulating events that normally originate the wave or to a phenomenon of autoregulation loss.

25.4 Factors Which the ICP Depends on

In summary, ICP depends on the following factors: CSF production; CSF flow resistance; venous sinus pressure; and compliance. The first three are balance factors and determine basal ICP. The fourth is the compliance factor. Its behaviour shows with the other variables the volume, i.e., the change magnitude and the time variable, determining ICP by volume load.

For example, head-injured patients with normal ICP have alterations in the balance factors, mainly in the intravascular compartment. At the same time, subarachnoid hemorrhage with normal ICP also has great alterations in balance factors, but mainly the resistance to CSF flow.

25.5 Intracranial Hypertension Compensating Mechanisms

Due to the inextensibility of the cranial enclosure, compensations before elevation of ICP imply displacement of the intracranial structures to tolerate volume loads.

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