CEREBRAL BLOOD FLOW
Cerebral blood flow (CBF) varies with metabolic activity. There are a variety of methods available to directly measure CBF. These methods include: positron emission tomography, xenon enhanced computed tomography, single photon emission computed tomography, and computed tomography perfusion scans. These methods do not lend them-selves to bedside monitoring of CBF. Blood f low studies confirm that regional CBF parallels meta-bolic activity and can vary from 10–300 mL/100 g/ min. For example, motor activity of a limb is associ-ated with a rapid increase in regional CBF of the cor-responding motor cortex. Similarly, visual activity is associated with an increase in regional CBF of the corresponding occipital visual cortex.
Although total CBF averages 50 mL/100 g/min, flow in gray matter is about 80 mL/100 g/min, whereas that in white matter is estimated to be 20 mL/ 100 g/min. Total CBF in adults averages 750 mL/min (15% to 20% of cardiac output). Flow rates below 20–25 mL/100 g/min are usually associated with cerebral impairment, as evidenced by slowing on the electroencephalogram (EEG). CBF rates between 15 and 20 mL/100 g/min typically produce a flat (isoelectric) EEG, whereas rates below 10 mL/ 100 g/min are usually associated with irreversible brain damage.
Indirect measures are often used to estimate the adequacy of CBF and brain tissue oxygen delivery in clinical settings. These methods include:
· The velocity of CBF can be measured using transcranial Doppler (TCD);. An ultrasound probe (2 mHz, pulse wave Doppler) is placed in the temporal area above thezygomatic arch, which allows insonation of the middle cerebral artery. Normal velocity in the middle cerebral artery is approximately 55 cm/ sec. Velocities greater than 120 cm/sec can indicate cerebral artery vasospasm following subarachnoid hemorrhage or hyperemic blood flow. Comparison between the velocities in the extracranial internal carotid artery and the middle cerebral artery (the Lindegaard ratio) can distinguish between these conditions. Middle cerebral artery velocity three times that of the velocity measured in the extracranial internal carotid artery more likely reflects cerebral artery vasospasm.
· Near infrared spectroscopy was discussed eariler. Decreased saturation is associated with impaired cerebral oxygen delivery, although near infrared spectroscopy primarily reflects cerebral venous oxygen saturation.
· Brain tissue oximetry measures the oxygen tension in brain tissue through placement of a bolt with a Clark electrode oxygen sensor. Brain tissue CO2 tension can also be measured using a similarly placed infrared sensor. Normal brain tissue oxygen tension varies from 20–50 mm Hg. Brain tissue oxygen tensions less than 20 mm Hg warrant interventions, and values less than 10 mm Hg are indicative of brain ischemia.
· Intracerebral microdialysis can be used to measure changes in brain tissue chemistry that are indicative of ischemia and/or brain injury. Microdialysis can be used to measure cerebral lactate, neurotransmitters, markers of inflammation, and glucose concentration. Increases in the ratio of lactate/pyruvate have been associated with cerebral ischemia.
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