Intracranial hypertension may result from a wide variety of surgical and medical conditions. The association between elevated ICP and the potential for devastating brain stem herniation has been recognized for centuries. Because the skull is essentially a closed container, its contents have only limited compressibility. The intracranial contents are composed of three compartments: (1) the brain and interstitial fluid, which comprise approximately 80 percent of the intracranial space; (2) intravascular blood, which accounts for 10 percent of intracranial space; and (3) the CSF (in the ventricles and subarachnoid space), which comprises the final 10 percent. In order to maintain physiological ICP, an increase in volume of one compartment must lead to a compensatory decrease in the volume of
another compartment. As an example, diffuse cerebral edema causes an increase in the parenchymal and interstitial compartment that necessitates a compensatory decrease in the amount of blood or CSF (or both) in the intracranial space. Similarly, an increase in the CSF compartment (hydrocephalus) must lead to a decrease in the parenchymal or blood compartments.
The body is able to regulate and modify the diameter of brain arterial vasculature to maintain a relatively constant amount of blood flow over a range of systemic blood pressures that vary among patients (...Fig 2.6.-7.). This regulatory mechanism, termed autoregulation, allows the brain to regulate the flow of blood to meet its metabolic needs. Under normal conditions, the cerebral blood flow ranges between 50 and 60 ml per 100 gm brain per minute (approximately 700 to 850 ml blood/min for the whole brain)^ and accounts for about 20 percent of the total cardiac output. In patients with chronic hypertension, the graph is shifted to the right (see Fig.; 2.6:7. ). The cerebral vasculature is innervated by cholinergic-, noradrenergic-, and neuropeptide-containing neurons; however, it is unlikely that these neurotransmitters contribute significantly to autoregulation, although they certainly contribute to cerebral blood flow. The control of autoregulation more likely arises from the intrinsic sensitivity of the vascular smooth muscle cells to tension across the vessel wall. Additionally, hydrogen ions also have effects on the vessels, and increases in their concentration result in dilatation. The precise role of the mechanisms involved in cerebral vasculature autoregulation under all conditions remains unclear.
Many of the diseases or syndromes that increase ICP do so by causing cerebral edema (...TabJ.e. ..„2.6Z5 ). The pathophysiology of cerebral edema is based on one (or more) of three causes (...I§bJie,...26z6) ). In vasogenic edema, an increase in capillary permeability occurs through the widening of tight junctions and increases in pinocytotic vesicles at the level of the blood-brain barrier. Because a disruption of the blood-brain barrier occurs with this disorder, MRI and CT studies administered with contrast typically demonstrate brain parenchymal enhancement. In cytotoxic edema, a swelling of the neurons, glia, and endothelial cells of the brain is present. Cytotoxic edema occurs in the setting of a decreased energy supply to brain cells (i.e., hypoxia) or osmotic disequilibrium (i.e., dialysis disequilibrium). The third type of cerebral edema occurs with hydrocephalus and results in an increase in interstitial fluid in the periventricular region. Through this mechanism, hydrocephalus raises ICP by increasing CSF volume and causing periventricular cerebral edema.
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Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...