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Brain perfusion is peculiar, reflecting the specificity of the brain in the human body. Brain metabolic function depends strictly on oxygen and glucose, yet it is not able to store them, meaning that all the energy must be supplied through blood flow, which must be tightly controlled to avoid hypoperfusion and ultimately ischemia.
Despite representing just 2% of the total body weight, the brain receives 15% of the cardiac output, resulting in a cerebral blood flow (CBF) of about 50 mL/100 g every minute. This is an average value between the flow received by the grey matter (70 mL/100 g every minute) and the flow received by the white matter (20 mL/100 g every minute). Such a discrepancy is due to the different metabolic activity of the two tissues. In fact, although glial cells make up almost half the weight of the brain, because of their low metabolic rate, their energy consumption is only 10% of the total energy used by the brain itself. On the other hand, neurons require a high amount of energy and nutrients to keep their membrane potential and to ensure the synaptic activity, explaining why the perfusion they receive is so high.
As mentioned previously the brain has no significant storage capacity; therefore CBF is tightly coupled with cerebral metabolism and oxygen extraction. This may be expressed by the equation:
in which
CMRO 2 is the cerebral metabolic rate for oxygen, an index of cerebral metabolism. In normal conditions, this value is 3.2 mL of O 2 /100 mL of blood
AVDO 2 is the arteriovenous difference of oxygen. This parameter is an index of oxygen extraction and normally is about 6.5 mL of O 2 /100 mL of blood
To gain a better understanding of the problem, we can use a simple mathematic model to describe the regulation of the CBF. In this kind of model, CBF is determined by the relationship shown in Eq. (2.2) :
in which
MAP is the mean arterial blood pressure ( Fig. 2.1 ).
ICP is the intracranial pressure, which has a great influence on the back pressure of the intracranial venous system because the brain sits in a closed cavity where the increase of pressure may cause the venous system to collapse.
CPP is the cerebral perfusion pressure.
CVR is the cerebrovascular resistance defined by the diameter and length of blood vessels and by the blood viscosity.
This simple formula shows how, through its determinants, CBF may be affected by many physiological or pathological conditions, both systemic and intracranial.
The brain has a strong tendency to keep the AVDO 2 constant. To reach this target the cerebral circulation acts by increasing or reducing CVR in response to the modifications of MAP (pressure autoregulation), blood viscosity (viscosity autoregulation), and cerebral activity (flow metabolism coupling).
The brain circulation is able to maintain constant the CBF within a wide range of variation of MAP by modifying the diameter of the cerebral vessels, increasing or decreasing CVR. As shown in Fig. 2.2 , CBF is guaranteed between 50 and 150 mm Hg. Outside these limits the CBF varies according to the variation of MAP. The precise mechanism of this regulation has not been explained yet and will not be discussed in this work.
Blood viscosity is determined by many factors including hematocrit, plasma viscosity, erythrocyte and platelet aggregation and erythrocyte deformability. Blood rheology affects the blood flow, and hematocrit is the main determinant.
Since blood viscosity is inversely proportional to CBF, a decrease in hematocrit from 25% to 35% leads to an increase of 30% in CBF as result of vasodilatation. This autoregulation is kept until a hematocrit of 19% and further hemodilution does not increase CBF for the exhaustion of this compensatory vasodilatation.
Since the end of the last two centuries, it has been well known that CBF depends on brain activity and metabolism. The AVDO 2 tends to increase with higher brain activity, and this tendency is compensated by the reduction of CBR, leading to a higher CBF. Again the mechanism between these regulations is complex and not yet completely understood.
Many other factors participate in regulation of CBF:
metabolic mediators
chemical
PaCO 2 : has a powerful vasoconstrictor effect on brain vessels. Within a physiological range, for each kPa increase of CO 2 in arterial blood, there is a reduction of 15 mL/100 g every minute in CBF
PaO 2 : in physiological conditions PaO 2 does not affect CsBF. However, when PaO 2 falls below 50 mm Hg, there is a quick rise in the CBF growth
temperature: hyperthermia affects CBF, increasing it by 6%–7% for every 1°C. Hypothermia has the opposite effect
neural control
circulatory peptides
Besides all the possible physiological changes in CBF, this parameter takes on a great importance in pathological conditions as well. For instance, patients with intracranial disease that causes an increase in intracranial pressure are particularly susceptible to a decrease in CBF, possibly leading to ischemia. In this case, monitoring may be crucial in avoiding secondary ischemic lesions.
The perfect CBF monitoring method should have great temporal resolution to quickly detect ischemia and induce a clinical intervention to avoid it. Furthermore, it should be noninvasive, cheap, repeatable, inexpensive, and portable.
Unfortunately, a technology including all these features is not available yet, and there is still a need to accept some compromise.
Currently, available CBF monitoring techniques may be divided into direct techniques (CBF is directly measured) and indirect techniques (CBF is derived as a result of calculation from its determinants) ( Table 2.1 ).
Noninvasive or minimally invasive | Invasive | |
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Direct |
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Indirect |
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