J. P. Muizelaar

ICP and PVI with Blood Pressure Alterations and Relation with CBF Autoregulation

Brain compliance is the ability of the cranial contents to accommodate an extra amount of volume (e.g., hematoma, CSF, increased cerebral blood volume, CBV) without much increase in ICP. PVI is a measure of brain compliance and is the calculated volume (in milliliters) required to raise ICP by a factor of 10 (Marmarou et al. 1978). It is thought to be a reflection of the vascular component of the intracranial compartment (Lofgren et al. 1973; Shapiro et al. 1980), also after head injury (Marmarou et al. 1973). Changes in blood pressure or CPP have a major influence upon the intracranial blood vessels, particularly arterioles, the extent and the direction of this influence being in turn dependent on whether autoregulation is (still) operative or not. Thus, several authors, using pentobarbit-alanesthetized animals, found that PVI or some other measure of brain compliance did not change with changes in CPP within the range of autoregulation (Avezaath et al. 1980; Leech and Miller 1974; Takagi et al. 1980). Outside the range of autoregulation, brain compliance or PVI became inversely related to changes in CPP in these and other studies (Avezaath et al. 1980; Gray and Rosner 1987; Leech and Miller 1974). However, Gray and Rosner found that within the limits of autoregulation PVI and CPP were related in a linear fashion, with increasing blood pressure being reflected by a rise in PVI (Gray and Rosner 1987). But, this relationship was marked only in cats anesthetized with methohexital and hardly present with pentobarbital anesthesia. They concluded that pentobarbital, because of its own major vasoconstrictory effect, blunted the responses of cerebral blood vessels to changes in CPP and therefore obscured the relationship between PVI and CPP (Gray and Rosner 1987). In the present paper responses of ICP and PVI to changes in blood pressure were investigated in severely head injured patients in whom anesthesia is not necessary at all. Moreover, in some of these patients autoregulation is intact, while in others it is absent (though, for unknown reasons) (Muizelaar et al. 1984).

Cerebral Blood Volume in Acute Head Injury: Relationship to CBF and ICP

Uncontrollable high ICP due to brain swelling is the single most important factor determining mortality from severe head injury [6, 7]. Yet, it is uncertain what the exact cause of posttraumatic brain swelling is, and no satisfying treatment for this problem exists. Theoretically, brain swelling may be caused by increased brain water content (edema), or by cerebrovascular engorgement with increased cerebral blood volume (CBV). While brain edema has been extensively studied both experimentally and clinically, relationships between cerebrovascular status and ICP have so far mostly been studied by cerebral blood flow (CBF) measurements [8]. However, it has become clear that CBF and CBV are not linearly related [3, 9], especially under pathologic conditions, and thus, CBF measurements alone may not be sufficient to fully comprehend the vascular contribution to raised ICP. To date, only scant data on posttraumatic CBV have been reported [4]. This may at least in part be due to the fact that thus far, no practical method for measuring CBV in humans has been available. Although measures of CBV can be reliably obtained by PET or SPECT, these techniques are difficult to implement in critically ill and unstable patients, additional equipment is required, and necessary transportation of the patients may interfere with acute treatment.

Cerebral Vasoconstriction is Not Maintained with Prolonged Hyperventilation

It is generally accepted that hyperventilation reduces ICP by reducing cerebral blood volume (CBV) through constriction of the pial and cerebral arterioles. As CO2 readily crosses the blood-brain barrier, a decreased PaCO2 is immediately reflected in a reduced PCO2 in interstitial brain fluid. This, in turn, leads to a reduction in H+ concentration in the vicinity of the cerebral blood vessels. Because the H+ ion is one of the most potent relaxants of smooth muscles of cerebral arterioles, a reduction in its concentration will lead to rapid vasoconstriction. Thus, vasoconstriction is not dependent on low CO2 and can be maintained only if the increased perivascular pH can be maintained (Kontos et al. 1977; Wahl et al. 1970). It has been shown, however, that pH in blood and cerebrospinal fluid (CSF) returns to normal during prolonged hyperventilation, despite sustained hypocapnia (Christensen 1974; Levasseur et al. 1979; McDowall and Harper 1968). The purpose of the present investigation was to examine whether the return to normal pH during prolonged hyperventilation would be accompanied by vasorelaxation.

Blood Pressure and ICP Dynamics in Severe Head Injury: Relation With CBF Autoregulation

There is controversy about the optimal blood pressure management in severely head-injured patients. Traditionally, high arterial blood pressure has been thought to break down the blood-brain barrier and cause cerebral edema, and therefore, antihypertensive therapy has been advocated [6]. However, when CBF is reduced, as is frequently the case in the first 24 hours, this procedure carries the risk of provoking cerebral ischemia by decreasing CPP, especially since AVDO2 is usually still high in this period [2]. Thus, maintaining adequate CPP may be more important than control of ICP per se. It has also been suggested that maintaining slightly elevated CPP, if necessary even by pharmacologically induced arterial hypertension, would prevent ICP “plateau” waves or even reduce ICP by autoregulatory vasoconstriction [9].

Relation Between CBF, ICP and PVI in Severely Head Injured Children

Bruce et al. (1979; 1981) and Obrist et al. (1979; 1984) have drawn attention to the correlation between elevated ICP and hyperemia, occurring more often in children. According to these authors, the increased cerebral blood volume (CBV) which, they propose accompanies the increased CBF, is the chief cause of high ICP. The exceptional results obtained by Bruce et al. (1979; 1981) were ascribed specifically to the generous use of hyperventilation to decrease CBF and CBV, resulting in control of ICP. On the other hand, the use of mannitol to control ICP in children was discouraged, as this agent had been found to increase CBF in a number of head injured patients in the past.