Cerebral blood flow

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Cerebral blood flow (CBF), is the blood supply to the brain in a given time.[1][broken citation] In an adult, CBF is typically 750 millilitres per minute or 15% of the cardiac output. This equates to an average perfusion of 50 to 54 millilitres of blood per 100 grams of brain tissue per minute.[2][3][4] CBF is tightly regulated to meet the brain's metabolic demands.[2][5] Too much blood (a condition known as hyperemia) can raise intracranial pressure (ICP), which can compress and damage delicate brain tissue. Too little blood flow (ischemia) results if blood flow to the brain is below 18 to 20 ml per 100 g per minute, and tissue death occurs if flow dips below 8 to 10 ml per 100 g per minute. In brain tissue, a biochemical cascade known as the ischemic cascade is triggered when the tissue becomes ischemic, potentially resulting in damage to and death of brain cells. Medical professionals must take steps to maintain proper CBF in patients who have conditions like shock, stroke, Cerebral edema, and traumatic brain injury.

Cerebral blood flow is determined by a number of factors, such as viscosity of blood, how dilated blood vessels are, and the net pressure of the flow of blood into the brain, known as cerebral perfusion pressure, which is determined by the body's blood pressure. Cerebral blood vessels are able to change the flow of blood through them by altering their diameters in a process called autoregulation; they constrict when systemic blood pressure is raised and dilate when it is lowered.[6] Arterioles also constrict and dilate in response to different chemical concentrations. For example, they dilate in response to higher levels of carbon dioxide in the blood and constrict to lower levels of carbon dioxide.[6]

For example, a normal arterial CO2 (paCO2) is 40 mm Hg, if the paCO2 dips to 30 mm Hg, this represents a 10 point decrease from normal. The CBF decreases by 1ml per 100g per min for each 1mm Hg decrease in paCO2, resulting in a new CBF of 40ml per 100g per minute (with normal being 50).

CBF is equal to the cerebral perfusion pressure (CPP) divided by the cerebrovascular resistance (CVR):[7]

CBF = CPP / CVR

Control of CBF is considered in terms of the factors affecting CPP and the factors affecting CVR. CVR is controlled by four major mechanisms:

  1. Metabolic control (or 'metabolic autoregulation')
  2. Pressure autoregulation
  3. Chemical control (by arterial pCO2 and pO2)
  4. Neural control

Functional magnetic resonance imaging and positron emission tomography are neuroimaging techniques that can both be used to measure CBF. These techniques are also used to measure regional CBF (rCBF) within a specific brain region. rCBF at one location can be measured over time by thermal diffusion[8]

Role of intracranial pressure[edit]

Increased intracranial pressure (ICP) causes decreased blood perfusion of brain cells by mainly two mechanisms:

See also[edit]

References[edit]

  1. ^ Tolias C and Sgouros S. 2006. "Initial Evaluation and Management of CNS Injury." Emedicine.com. Accessed January 4, 2007.
  2. ^ a b Orlando Regional Healthcare, Education and Development. 2004. "Overview of Adult Traumatic Brain Injuries." Accessed 2008-01-16.
  3. ^ Shepherd S. 2004. "Head Trauma." Emedicine.com. Shepherd S. 2004. "Head Trauma." Emedicine.com. Accessed January 4, 2007.
  4. ^ Walters, FJM. 1998. "Intracranial Pressure and Cerebral Blood Flow." Physiology. Issue 8, Article 4. Accessed January 4, 2007.
  5. ^ Singh J and Stock A. 2006. "Head Trauma." Emedicine.com. Accessed January 4, 2007.
  6. ^ a b Kandel E.R., Schwartz, J.H., Jessell, T.M. 2000. Principles of Neural Science, 4th ed., McGraw-Hill, New York. p.1305
  7. ^ AnaesthesiaUK. 2007. Cerebral Blood Flow (CBF). Accessed 2007-10-16.
  8. ^ P. Vajkoczy, H. Roth, P. Horn, T. Lucke, C. Thome, U. Hubner, G. T. Martin, C. Zappletal, E. Klar, L. Schilling, and P. Schmiedek, “Continuous monitoring of regional cerebral blood flow: experimental and clinical validation of a novel thermal diffusion microprobe,” J. Neurosurg., vol. 93, no. 2, pp. 265–274, Aug. 2000. [1]