The numerical difference between ICP and mean BP within the cerebral vessels is termed cerebral perfusion pressure (CPP). Besides the aforementioned brain tissue shifts, which are discussed more fully in relation to coma and other clinical signs in Chap. 16, elevation in ICP that approaches the level of mean systemic BP eventually causes a widespread reduction in cerebral blood flow. In its most severe form, this results in global ischemia and produces brain death. Lesser degrees of raised ICP and reduced cerebral perfusion cause correspondingly less severe, but still widespread, cerebral infarction that is similar to what arises after cardiac arrest. In all circumstances, not only the severity but also the rapidity and duration of reduced cerebral perfusion, are the main determinants of the degree of cerebral damage. These are theoretical models that guide practice but are often found to be imprecise in clinical work.
Lundberg has been credited with recording and analyzing intraventricular pressures over long periods of time in patients with brain tumors. He found ICP to be subject to periodic spontaneous fluctuations, of which he described three types of pressure waves, designated as A, B, and C (Fig. 29-2). B-waves are ballistic waveforms that follows the blood pressure wave and are the result of blood entering the basal cerebral vessels (see below for further comments on B-waves). C-waves follow the respiratory cycle and are a complex result of several transmitted pressures from the thorax to the spinal fluid compartment.
Only the A-waves have proved to be entirely separable from arterial (B-waves) and respiratory (C-waves) pulsations and are of most clinical consequence. They consist of prolonged rhythmic wave-like elevations of ICP, up to 50 mm Hg, occurring every 15 to 30 min and lasting about 1 min, or of smaller but more protracted elevations. They are apparent only when the trend of ICP is monitored over many minutes or longer. These plateau waves, as they have come to be known, coincide with an increase in intracranial blood volume, presumably as a result of a temporary failure of cerebrovascular autoregulation. Rosner and Becker observed many years ago that plateau waves are sometimes preceded by a brief period of mild systemic hypotension. In their view, this slight hypotension induces cerebral vasodilatation in order to maintain normal blood flow. Upon recovery of the BP, the response in cerebrovascular tone is delayed, thereby allowing intracranial blood volume to accumulate in the dilated vascular bed, and raising ICP in the form of a plateau wave. In support of this explanation is the observation that a brief period of induced elevation of BP paradoxically restores the normal cerebrovascular tone and leads to an abrupt cessation of a plateau wave.
The configuration of the Lundberg B-waves, which are ballistic ICP waveforms corresponding to the inflow of blood into the cerebral vessels during systole, give some sense of cerebral dynamics. They have a dicrotic notch, just as the blood pressure wave, and the two small peaks, termed for convenience P1 and P2 (some have detected a P3), give an approximate indicator of cerebral compliance (or elastance), a higher P2 corresponding to less compliant intracranial contents (see insert top of Fig. 29-2).
The high rates of mortality and morbidity associated with acute cerebral mass lesions is in part related to uncontrolled elevations in ICP. As mentioned earlier, ICP in a resting and reclining adult is generally 3 to 7 mm Hg (lower when an individual is upright). For clinical trials and research, levels above 15 mm Hg are considered abnormal but are not in themselves hazardous; in fact, adequate cerebral perfusion can be maintained at an ICP of 40 mm Hg provided BP remains normal. A higher ICP or a lower BP may combine to reduce CPP and cause diffuse ischemic damage.
Causes of Raised ICP
In clinical practice, there are several mechanisms for elevated ICP: 1.