The Monroe-Kelley doctrine is the basis for understanding intracranial pressure-volume interactions. It states that an increase in the volume of one intracranial compartment must be compensated by a decrease in the volume of one or more of the other compartments, so that the total volume remains fixed. The intracranial compartments include intracellular space, extracellular space, cerebral blood volume, and the cerebrospinal fluid volume. The normal range for intracranial pressure is zero to 10 mmHg. The threshold for treatment of increased intracranial pressure is generally accepted to be 20 mmHg or greater.
An intracranial mass lesion or brain swelling forces cerebrospinal fluid out of the intracranial compartment, resulting in obliteration of the ventricular system and basal cisterns with no initial rise in intracranial pressure. A non-contrast head CT scan will readily demonstrate these changes ( Fig 1). If there are further increases in the volume of the lesion or swelling, intracranial pressure begins to rise in an exponential fashion ( Fig... . . . .2). Cerebral perfusion pressure is defined as the difference between the mean arterial pressure and the intracranial pressure. It represents the pressure gradient that drives cerebral blood flow. Cerebral ischemia is the most important secondary injury occurring in patients with elevated intracranial pressure. Therefore maintenance of a suitable cerebral perfusion pressure is considered by many experts to be of equal or greater importance than strict control of intracranial pressure. The current consensus for cerebral perfusion pressure management is that a minimum pressure of 70 mmHg should be maintained (Bullockefa/ 1996).
Fig. 1 Non-contrast head CT scan of a severely head-injured patient. A large right frontal hemorrhagic contusion is present with shifting of the midline structures. Additional hallmarks of elevated intracranial pressure are present, including effacement of the basal cisterns, marked right frontal lobe cerebral edema, effacement of the right lateral ventricle, and obliteration of the right temporal horn of the lateral ventricle.
Fig. 2 Idealized intracranial pressure-volume curve. Point A represents the position of a normal brain on the compliance curve. Point B represents an increase in the intracranial volume which has been partially compensated for by the decrease in cerebrospinal fluid and contraction of the cerebral blood volume. Point C represents a further increase in the intracranial volume. In this region of the curve no further compensation is possible and pressure begins to rise exponentially. Cerebral perfusion pressure may drop below the critical levels necessary to maintain neuronal metabolism and result in 'secondary ischemic injury'.
Autoregulation is the mechanism by which cerebral blood flow is maintained constant despite variations in cerebral perfusion pressure. Autoregulation of flow occurs by dilatation and constriction of the cerebral vessels and subsequent changes in cerebrovascular resistance. Stimuli for autoregulation include mechanical changes in pressure or chemical changes in the local concentration of metabolic products, for example oxygen tension, partial pressure of carbon dioxide, increased potassium, and fluctuations in local pH. Functionally, autoregulation serves to maintain homeostasis. It buffers changes in pressure and maintains precise control of the delivery of oxygen and nutrients to match the metabolic needs of local tissues (Fig 3). Autoregulation is frequently perturbed to varying degrees in cases of severe head injury and other processes with marked elevations in intracranial pressure. In these situations, the cerebral vessels become pressure passive. The cerebral vascular bed loses its ability to compensate for decreases in cerebral perfusion pressure with arterial vasodilatation; thus hypoperfusion and ischemia result. Conversely, when there is loss of autoregulation in a hypertensive patient, cerebral blood flow exceeds the metabolic requirements, resulting in hyperemia. Additionally, in a pressure-passive vascular bed, cerebral blood volume increases in direct proportion to the cerebral perfusion pressure because of vasodilatation ( Fig.S). Hypertensive therapy in patients with disrupted autoregulation can result in further elevations of intracranial pressure.
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Fig. 3 Idealized autoregulation curve. Curve A represents intact autoregulation. Constant cerebral blood flow is maintained over a wide range of perfusion pressures. Curve B represents complete loss of autoregulation. In this case the cerebral vessels are pressure passive, and cerebral perfusion pressure is directly proportional to cerebral blood flow and cerebral blood volume. Consequently, patients with disturbed autoregulation are caught in a delicate balance between adequate cerebral perfusion pressure and avoidance of increased intracranial pressure from vasodilatation. Curve C represents partial loss of autoregulation. In this case the brain is vulnerable to hypotension, but maintains autoregulation at higher pressures. Increases in cerebral perfusion pressure may result in decreased intracranial pressure through vasoconstriction and contraction of the cerebral blood volume.
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