Cerebral blood flow

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The cerebral blood flow (CBF from English Cerebral blood flow ) is a measure for the supply of the brain with blood in a certain time unit. Although the brain makes up only about 2% of the body mass of an adult, the cerebral blood flow represents about 15% of the cardiac output and is about 750 milliliters per minute. In order to do justice to size differences, the cerebral blood flow is usually given as the flow volume per 100 g of brain mass and minute with the unit ml / 100 g / min.

In contrast to the total cerebral blood flow, the regional cerebral blood flow (rCBF) is a measure of the blood flow to certain areas of the brain. By determining the rCBF, one can identify areas of the brain with more or less blood flow. The rCBF is also given in the unit ml / 100 g / min, the measured values ​​being strongly method-dependent.

Physiology and anatomy

The capillary bed of the brain consists of a tight network of communicating vessels. The total length of the capillaries in the human brain is about 640 kilometers. The intravascular pressure differential between the precapillary arterioles and the postcapillary venules is the most important regulator of blood flow through the capillaries. It is mainly determined by the position of the arterioles, which act as resistance vessels, the expansion of which leads to an increase in the microvascular capillary flow.

Under physiological conditions, there are differences between the cerebral blood flow in the gray and white matter of the brain. The gray matter, which has a capillary density about 4 times higher than the white matter, is supplied with about 90 ml / 100 g per minute. In contrast, the blood flow in white matter is only approx. 25 ml per 100 g of substance per minute. This results in a blood flow of 40 to 50 ml / 100 g / min for the entire brain.

Regulatory mechanisms

Autoregulation of cerebral blood flow

In order to ensure an adequate and even supply of blood and thus oxygen and nutrients to the brain , the cerebral blood flow is kept constant over a relatively wide range of blood pressure when the systemic blood pressure fluctuates .

It is determined by the mean systemic arterial pressure (MAP), the intracranial pressure (ICP) and the resistance of the cerebral vessels (cerebral vascular resistance (CVR)) and can be calculated using the following formula:

CBF = (MAP - ICP) / CVR

The difference between the mean arterial blood pressure (MAP) or the mean aortic pressure and the intracranial pressure (ICP) is also known as the cerebral perfusion pressure (CPP):

CPP = MAP - ICP

The main parameter in the regulation of the cerebral blood flow is the resistance of the cerebral vessels, which is regulated according to the mean arterial pressure. Via the so-called Bayliss effect , the arterioles narrow when the systemic blood pressure rises ( vasoconstriction ), while they widen when the blood pressure drops ( vasodilation ). In a healthy person, the body uses this mechanism, known as autoregulation , to keep the cerebral blood flow constant at a systemic blood pressure in the range between 50 and 150 mmHg.

In addition, the arterioles also react to the concentration of gases dissolved in the blood . An increased CO 2 partial pressure in the arterial blood at constant systemic blood pressure leads to an expansion of the cerebral vessels, which increases the cerebral blood flow. Conversely, the vessels react to a decrease in the CO 2 partial pressure with a constriction, which leads to an increase in the cerebral vascular resistance and thus a reduction in the cerebral blood flow. The oxygen partial pressure , on the other hand, has only a minor influence on the cerebral vascular resistance. Only when the pO2 value in the arterial blood is below 50 mmHg do the cerebral vessels react with an expansion, so that there is an increase in blood flow.

Furthermore, the sympathetic and parasympathetic innervation of the larger vessels as well as the reaction of the vascular muscles of the arterioles to endocrine and chemical factors ( pH , adenosine , potassium ) influence the vascular resistance.

Measurement

Global cerebral blood flow can be determined using Fick's principle , a method developed by neuroscientist Seymour S. Kety . The test person inhales nitrous oxide (N 2 O) in low concentration, the concentration of which is then determined in a blood sample taken from the internal jugular vein . By multiplying the CBF determined in this way by the respective concentration difference between arterial and venous blood, the metabolic rate of the brain for certain metabolites such as oxygen, carbon dioxide, glucose or lactate can also be determined. In 1988, Kety was awarded the NAS Award in the Neurosciences for establishing the method .

The blood flow in certain areas of the brain, known as regional cerebral blood flow (rCBF), can be measured using various imaging methods in the living organism in order to identify areas of the brain with poor blood supply. To determine the rCBF, positron emission tomography (PET), SPECT , xenon computed tomography , transcranial Doppler sonography and magnetic resonance tomography (MRT) are used. The rCBF is also given in the unit ml / 100 g / min, whereby the measured values ​​are strongly method-dependent, which is why method-specific reference values ​​are used.

Pathophysiology and dysregulation

If the systemic blood pressure is below 50 mmHg or above 150 mmHg, the autoregulation mechanism can no longer compensate for this by adapting the vessel diameter and the cerebral blood flow follows the central perfusion pressure (CPP) in a pressure-passively linear manner.

Too little blood flow ( ischemia ) leads to an insufficient supply of the brain with oxygen and nutrients. The brain can initially compensate for a reduction in blood flow by half through improved oxygen utilization. A short-term reduction to less than 20 ml per 100 g and minute already leads to reversible changes in the brain cells. If the blood flow rate drops to less than 15 ml per 100 g and minute, nerve cells will finally die within a few minutes to a few hours.

Excessive blood flow ( hyperemia ) to the brain can lead to an increase in intracranial pressure, which can damage the sensitive brain tissue. In the event of a massive acute excess of the regulatory limit of the systemic blood pressure above 150 mmHg, e.g. B. in a hypertensive crisis , there is a sharp increase in cerebral blood flow and central perfusion pressure (CPP) with a disruption of the blood-brain barrier . Cerebral edema can develop due to the leakage of plasma proteins from the blood vessels .

With persistent high blood pressure , the limits of autoregulatory adjustment shift upwards, as a result of which the body tries to adapt to the changed parameters. The autoregulation as a whole can also be disturbed by diabetes mellitus that has been poorly controlled over a longer period of time .

In the case of reversible cerebral vasoconstriction syndrome , there is a brief segmental arterial vasoconstriction, which causes a sudden reduction in blood flow in the affected areas. The main symptom is a sudden annihilating headache , which, depending on the affected brain region, can be accompanied by other neurological deficits.

See also

Individual evidence

  1. ^ DJ Begley DJ, MW Brightman: Structural and functional aspects of the blood-brain barrier. In: Prog Drug Res. (61) 2003, pp. 39-78.
  2. ↑ DM Hermann, T. Steiner, HC Diener: Vascular Neurology: Cerebral ischemias, hemorrhages and vascular dementia, Georg Thieme Verlag, 2010, p. 8
  3. ↑ Otto Detlev Creutzfeldt : General neurophysiology of the cerebral cortex. In: Otto Detlev Creutzfeldt (Ed.): Cortex cerebri. Springer Verlag, Berlin 1983, ISBN 3-540-12193-5 .
  4. ^ H. Ito, I. Kanno, H. Fukuda: Human cerebral circulation: positron emission tomography studies. In: Annals of nuclear medicine. Volume 19, Number 2, April 2005, pp. 65-74, ISSN  0914-7187 . PMID 15909484 .
  5. ↑ Reinhard Larsen: Anesthesia and intensive medicine in cardiac, thoracic and vascular surgery. (1st edition 1986) 5th edition. Springer, Berlin / Heidelberg / New York et al. 1999, ISBN 3-540-65024-5 , p. 445.
  6. ↑ Kandel ER , Schwartz, JH, Jessell, TM 2000. Principles of Neural Science, 4th ed., McGraw-Hill, New York. p.1305
  7. ↑ E. Kochs, HA Adams, C. Spies: Anaesthesiology. Georg Thieme Verlag, 2008, p. 264
  8. ↑ a b c E. Kochs, HA Adams, C. Spies: Anaesthesiology. Georg Thieme Verlag, 2008, p. 265
  9. ↑ SS Kety, CF Schmidt: The nitrous oxide method for the quantitative determination of cerebral blood flow in man; theory, procedure and normal values. In: The Journal of clinical investigation. Volume 27, Number 4, July 1948, pp. 476-483, ISSN  0021-9738 . doi : 10.1172 / JCI101994 . PMID 16695568 . PMC 439518 (free full text).
  10. ^ NAS Award in the Neurosciences from the National Academy of Sciences (nasonline.org); Retrieved December 25, 2014
  11. ↑ E. Kochs, HA Adams, C. Spies: Anaesthesiology. Georg Thieme Verlag, 2008, p. 263
  12. ^ Klaus Poeck, Werner Hacke: Neurology. 10th completely revised edition. Springer, Berlin 1998, ISBN 3-540-63028-7 .
  13. ↑ L. Edvinsson, ET MacKenzie, J. McCulloch: Cerebral Blood Flow and Metabolism . Raven, New York 1993, ISBN 0-88167-918-6 .
  14. ↑ Ducros A. Reversible cerebral vasoconstriction syndrome . In: The Lancet Neurology (11) 2012, pp. 906-917.