The brain requires a constant and significant supply of oxygen and glucose to function properly. Accordingly, it has a rich vascular supply and receives about 15% of total cardiac output. Additionally, the brain is responsible for 20% of the body’s total oxygen demand.2 The paired carotid and vertebral arteries (which fuse to form the basilar artery) ensure a constant flow of blood to the brain, or cerebral blood flow (CBF). Cerebral blood flow is controlled by a process termed autoregulation, in which the volume of the cerebral vasculature is tightly controlled to allow just enough blood to ensure adequate cerebral perfusion. This is important because too little blood flow fails to meet the brain’s oxygen and glucose demands, while too much can actually cause a rise in ICP. To support autoregulation, the cerebral vasculature is extremely sensitive to the concentration of carbon dioxide in the blood (partial pressure, or pCO2). Increased pCO2 (hypercapnia) results in vasodilation and increased CBF, and decreased pCO2 (hypocapnia) results in vasoconstriction of the cerebral vasculature and decreased CBF. The normal pCO2 is 35–45 mmHg. The vascular response to changes in pCO2 is nearly linear between values of 20–60 mmHg, and results in a change in the diameter of cerebral blood vessels by 2%–3%.2,3
Adequate CBF also depends on the cerebral perfusion pressure (CPP), the pressure of the blood flowing into the brain. CPP is unique because it is not related to blood pressure alone. Rather, it depends on the relationship between the mean arterial pressure (MAP) and intracranial pressure (Table 2). Normal MAP is between 70–110 mmHg. Normal ICP is between 7–15 mmHg, or about 10 mmHg. This means there is always some intracranial pressure. An adequate CPP is at least 70 mmHg. When cerebral perfusion pressure drops below 70 mmHg for sustained periods, cerebral hypoxia and ischemia occur. Under normal physiologic conditions, autoregulation ensures CPP is kept between 70–90 mmHg, which is enough to ensure adequate cerebral blood flow. Autoregulation occurs primarily via control of the cerebral vasculature.
The Monro-Kellie doctrine illustrates the relationship between intracranial pressure, the volume of cerebral spinal fluid, blood, brain tissue and cerebral perfusion pressure.4,5 As discussed earlier, the cranial vault is a closed, rigid, nonflexible container with a fixed volume. Located in it are the brain, CSF and blood (within the cerebrovascular system). ICP represents a balance of the pressures exerted by these cranial constituents. These components create a state of pressure-volume equilibrium, and an increase in the volume of any one of them will result in an increase in pressure. If the volume of any one of these constituents increases, there must be a decrease in the volume of one or more of the others, or ICP will increase. Increased ICP is defined as CSF pressure greater than 15 mmHg.6
There is a buffer system in place to compensate for any increase in one of the constituents. CSF can be shifted from the intracranial space into the spinal column, and to a lesser degree blood volume can be shifted out of the cerebral vasculature. So for an increase in, say, the volume of an expanding hematoma from an epidural bleed, CSF is shifted into the spinal column, and venous blood out of the cranium. These compensatory mechanisms maintain a normal ICP for any change in volume less than approximately 100–120 mL.6
Let’s put this into more practical terms. Inside your cranium are your brain, blood and CSF. Together, these things fill up the volume of your cranium and exert a certain amount of pressure, the ICP. As long as you are able to maintain an adequate MAP, CPP will be adequate, and your body will be able to force arterial blood into the cranium and perfuse your brain.
But say something happens to change this equilibrium. Maybe you hit your head, suffer an epidural hematoma and start bleeding into your brain. Maybe it’s an aneurysm. Maybe you have lung cancer, and it metastasizes to your brain and starts to grow. In all of these scenarios, we are introducing into the cranium a new constituent that is taking up space (because it has volume). Initially, an increase in ICP is prevented by CSF shifting out of the cranium and into the spinal cord. In addition, venous blood is shifted retrograde out of the cranium as well. When these compensatory mechanisms are depleted, ICP will start to rise as this new cranial constituent continues to take up space.
As ICP Rises
As ICP increases above 15 mmHg, numerous events occur that contribute to additional progressive, life-threatening increases.
Cerebral hypoxia, both local and global, can cause injury and eventual death to brain cells, resulting in cerebral edema. Cerebral edema compresses cerebral arteries, further decreasing cerebral perfusion. As cerebral perfusion is compromised, CO2 accumulation results in vasodilation, increasing ICP. When ICP reaches a point where CPP is compromised, autoregulation is lost, and further vasodilation of the cerebral vasculature occurs, further increasing ICP.
Even though the signs and symptoms of increasing intracranial pressure may seem overwhelmingly complicated, they tend to develop in a predictable pattern. The best indicator of rising ICP is a changing mental status. Early signs begin with disorientation (confusion), which progresses into irritability and then combativeness.