**3. Intracranial pressure- waveform pathophysiology**

### **3.1 Waveform components**

*Advancement and New Understanding in Brain Injury*

recognition.

**2. History**

Sérgio Mascarenhas in 2012 [4].

(explained in detail below).

and clinical applications of ICPwf.

these pulses were related to ICP and CSF [6].

clusters of waveforms for different stages of pathology.

The information resulting from morphology will be treated in greater detail in this chapter, and today it is known that monitoring ICP is far over knowledge of a mean value, but also its trend over time, and the morphology of the pressure pulse

The history of ICPwf is centuries-old. For understanding, it is necessary to go back to the year 1783, after researcher Alexander Monro [1], who started studies of intracranial structures. His work was later completed by George Kellie [2], giving rise to the Monro-Kellie doctrine. This doctrine showed that the volume of intracranial components (blood, CSF and brain tissue) and the bone box that contains them is fixed. The volume of these components needs to be under balance, if there is an increase in one, the others need to compensate by reducing their volumes. Thus, intracranial hypertension (ICH) emerges when this compensation ceases to happen [3]. The stiffness of the skull was later challenged by the work of

Angelo Mosso, at the end of the 19th century, presented results showing the influence of brain activity on its blood flow. For the first time, it was possible to observe the brain pulses, through a system that captured these pulses and recorded them on paper. These figures can be seen in Zago's manuscript [5]. Many years later

Langfitt [7] brought an important contribution showing the mathematical hypothesis for the relationship between ICP and intracranial volume, making it easier to understand the importance of intracranial compliance (ICC=V/ P) in critical care. Marmarou [8] in 1975 added to the pressure-volume curve the information about the increase in the amplitude of ICPwf as the mean value of ICP increases, and demonstrated that ICPwf contains unique information on intracranial contents, this data has already proven useful in several diseases such as stroke, hydrocephalus, idiopathic intracranial hypertension and brain injuries. It is important for gathering information on cerebrovascular hemodynamics and also of the cerebrospinal compensatory system. In 1983, Cardoso [9] showed that with the increase in ICP, in addition to the increase in the amplitude of its pulse, there was also a change in its configuration, as morphology became pyramidal with an increase in amplitude in the middle region of the pulse. Cardoso also shows the ICPwf configuration: P1 - systolic peak, P2 - tidal wave and P3 - venous return

Hu [10], understanding the possibility of using ICPwf as information to aid in diagnosis, created an algorithm called MOCAIP (Morphological Clustering and Analysis of Continuous Intracranial Pressure). This software is able to turn the waveform into numbers to facilitate the interpretation of the medical team. Nucci [11], in 2016, presented results of a software to calculate ICPwf parameters and

Ballestero [12] and Bollela [13], in 2017, presented studies with hydrocephalus and meningitis respectively, that showed the applicability of a new noninvasive sensor to monitor the ICPwf, in the Ballestero study the ICPwf was analyzed through the relationship between the amplitude of the P2 and P1 pulses.

ICPwf is an important information, increasingly disseminated among physicians. New methods and analyses facilitate the use of this parameter, which is useful and disseminating over clinical institutions. The next chapters will provide more details

**2**

ICP is determined by the intracranial components volumes, as the brain tissue, the vascular or cerebral blood flow (CBF) and cerebrospinal fluid (CSF) [14, 15], and relations between them in a semi-rigid skull box, the Monroe-Kellie doctrine. Each cardiac beat corresponds to an ICP waveform composed of three peaks; arterial pulsation- P1, cerebral venous flow, secondary to autoregulation-derived cyclic fluctuations of arterial blood volume, reflecting intracranial compliance- P2, and the aortic valve closure- P3 (**Figure 1a**).

These cardiac-derived pulsatile signals are overlapped in time domain with the respiratory cycle, with influence in the cerebral venous pulsation by means of intrathoracic pressure generated by breathing, disclosed as slow waves [16] (**Figure 1b**). Moreover, ventilation plays a direct and remarkable role over CBF [17]. Thus, ICP is influenced by many physiological factors from extra and intracranial compartments. Moreover, factors as age, body posture, time of day as well as the clinical condition also are considerable variables, although in absence of disturbances, mean ICP is kept mostly within a range between 7 and 15 mmHg for adults, 3 and 6 mmHg in children, and between 1.5 and 6 mmHg in term infants [18].

**Figure 1.**

*(a) One single arterial pulse transmitted to the intracranial compartment, with three peaks observed; systolic peak (P1), tidal peak (P2) and aortic valve closure peak (P3). (b) Respiratory slow waves overlapping cardiac intracranial pulses spectrum (from Hall et al. [16]).*

There is an existing volume of reserve in the brain which is around 60–80 mL in young persons and approximately 100–140 mL in geriatric population, because of ongoing cerebral atrophy with age. However, in normal conditions and for short time observations, the brain volume is typically static, with mean ICP varying mainly according to the CBF and the balance between production and absorption or outflow of the CSF. The relation observed between these intracranial components is named intracranial compliance (ICC). Compensatory mechanisms exist to maintain intracranial volume homeostasis by extrusion of the CSF or venous blood, in order to preserve ICC, otherwise, these efforts may be insufficient in pathological conditions (i.e. traumatic brain injury) with intracranial hypertension (ICH) and ICC impairment producing primary or secondary brain tissue damage [19, 20].

Langfitt et al. characterized the transmission of pressure across the intracranial compartments as the intracranial elastance curve, observing an exponential behavior between ICP and intracranial volume [21], from a stable ICP vs. volume relation until

**Figure 2.**

*(a) Langfitt curve representing volume x ICP exponential behavior with A- normal ICC, B- intracranial buffering capacity begins to exhaust and C- ICC impaired with rapid ICP elevation (from Canac et al. [18]) (b) representation of altered ICP curve with ICC impairment.*

when a change in volume of any component will result in a commensurate change in ICP (**Figure 2a**). When ICP raises and compromises ICC, an inversion in ICP peaks relations may be observed [9], with ICH transmitted to the venous and ventricular compartments, affecting the buffering mechanisms (**Figure 2b**).

When mean ICP is elevated, the vascular (cardiac) waveform amplitude increases while the respiratory waveform amplitude decreases, associated with changes in the relationship between peaks P1, P2, and P3 [19, 22]. Different waves morphologies could reflect the residual compensatory capacity of the brain, since changes in the ICP wave shape are informative on an incoming or established alteration of the intracranial system (**Figure 3**) [11].

#### **Figure 3.**

*A - Normal, if the first peak (P1) exceeds the other two; B - potentially pathological, if the tidal peak (P2) equals or slightly exceeds the systolic one (P1) and the dicrotic peak equals or is slightly inferior to P1; class C - likely pathological, if the tidal and the dicrotic peaks exceed the first one; D and E- pathological, if the tidal and the dicrotic peaks surmount the first one or if the shape of the curve is so rounded as not to permit the identification of the three peaks (from Nucci et al. [11]).*

#### **3.2 Slow waves**

Additionally to all that was explained above, further phenomena in the observance of ICP waveforms may occur with high importance on alerting the neurophysician to initiate ICP control measures on an urgent basis. These phenomena were named slow waves by Lundberg et al., typically described as A, B and C waves (**Figure 4**). The A waves are denoted as plateau waves or vasogenic waves occurring during very high ICP (>50 mmHg), the B waves are short-duration elevations in ICP (1 to 2 per minute) with variable pressure levels up to 30–50 mmHg. C waves are more frequent (about 4–8 waves per minute) elevations of mean ICP (up to about 30 mmHg). A waves are clearly severe and with elevated risk of poor prognosis, whereas the clinical implication of the B waves is a research question that remains to be determined, since they are non-specific

**5**

**Figure 4.**

*Lundberg A, B and C waves (from Hirzallah et al. [23]).*

*Intracranial Pressure Waveform: History, Fundamentals and Applications in Brain Injuries*

*DOI: http://dx.doi.org/10.5772/intechopen.94077*

*Intracranial Pressure Waveform: History, Fundamentals and Applications in Brain Injuries DOI: http://dx.doi.org/10.5772/intechopen.94077*

**Figure 4.** *Lundberg A, B and C waves (from Hirzallah et al. [23]).*

*Advancement and New Understanding in Brain Injury*

when a change in volume of any component will result in a commensurate change in ICP (**Figure 2a**). When ICP raises and compromises ICC, an inversion in ICP peaks relations may be observed [9], with ICH transmitted to the venous and ventricular

*(a) Langfitt curve representing volume x ICP exponential behavior with A- normal ICC, B- intracranial buffering capacity begins to exhaust and C- ICC impaired with rapid ICP elevation (from Canac et al. [18])* 

When mean ICP is elevated, the vascular (cardiac) waveform amplitude increases while the respiratory waveform amplitude decreases, associated with changes in the relationship between peaks P1, P2, and P3 [19, 22]. Different waves morphologies could reflect the residual compensatory capacity of the brain, since changes in the ICP wave shape are informative on an incoming or established

Additionally to all that was explained above, further phenomena in the observance of ICP waveforms may occur with high importance on alerting the neurophysician to initiate ICP control measures on an urgent basis. These phenomena were named slow waves by Lundberg et al., typically described as A, B and C waves (**Figure 4**). The A waves are denoted as plateau waves or vasogenic waves occurring during very high ICP (>50 mmHg), the B waves are short-duration elevations in ICP (1 to 2 per minute) with variable pressure levels up to 30–50 mmHg. C waves are more frequent (about 4–8 waves per minute) elevations of mean ICP (up to about 30 mmHg). A waves are clearly severe and with elevated risk of poor prognosis, whereas the clinical implication of the B waves is a research question that remains to be determined, since they are non-specific

*A - Normal, if the first peak (P1) exceeds the other two; B - potentially pathological, if the tidal peak (P2) equals or slightly exceeds the systolic one (P1) and the dicrotic peak equals or is slightly inferior to P1; class C - likely pathological, if the tidal and the dicrotic peaks exceed the first one; D and E- pathological, if the tidal and the dicrotic peaks surmount the first one or if the shape of the curve is so rounded as not to permit the* 

compartments, affecting the buffering mechanisms (**Figure 2b**).

alteration of the intracranial system (**Figure 3**) [11].

*identification of the three peaks (from Nucci et al. [11]).*

*(b) representation of altered ICP curve with ICC impairment.*

**4**

**3.2 Slow waves**

**Figure 3.**

**Figure 2.**

indicators of diminished compliance and can also be present in patients with normal ICP [24]. Finally, C waves are products of cardiac and respiratory cycles interactions.
