Cerebral Ischemia And CBF Measuring

Afza.Malik GDA

Nursing Care of Cerebral Ischemia

Cerebral Ischemia And CBF Measuring

Cerebral Ischemia, Cellular Changes During Ischemia , First Blood Flow Study CBF

Cerebral Ischemia

    Cerebral ischemia is defined as inadequate blood flow to the brain to meet metabolic and nutritional needs of the brain tissue ( Edvinsson , MacKenzie , & McCulloch, 1993). 

    The severity of ischemia depends on the severity and duration of the reduction in cerebral blood flow (CBF) adversely affecting various functional and metabolic processes as CBF decreases ( Heiss & Rosner, 1983). 

    The brain stores no oxygen and little glucose, and is thus dependent on a constant supply of oxygen and glucose from the blood.

    Cerebral ischemia may be focal or global, depending on whether a part of the brain or the entire brain is ischemic. Focal cerebral ischemia occurs when a major cerebral artery becomes occluded or constricted from arterial spasm, emboli, or thrombosis. 

    Global. ischemia occurs from an overall decrease in CBF, for example after cardiac arrest. Global oxygen deprivation of the brain may also occur as a result of asphyxia, anemia, hypoxia, or near drowning. 

    Nurses are responsible for identifying individuals at risk for focal or global cerebral ischemia. Nursing assessment of early symptoms of cerebral ischemia can allow for intervention and minimize the prob ability of permanent damage.

Cellular Changes During Ischemia 

    Spielmeyer first described "ischemic cell change in 1922, ( Spielmeyer , 1922), and Brierley presented the time course for neuronal change during a low flow state and provided evidence of the threshold for cerebral anoxic ischemia (Brierley, Brown, & Meldrum, 1971; Chiang, Kowada , Ames, Wright, & Majno , 1968. He observed and described in further detail the process of ischemic cell change (Brierley, 1973).

    With the initial decrease in blood flow, oxygen, and/or glucose to the brain , the contour of cells, the nucleus, and nucleolus remain un- changed. There is disruption of mitochondria and an increase in the astrocyte processes sur- rounding the neurons.

    As the nucleus continues to shrink and the cytoplasm becomes more amorphous, incrustations begin to form comes increasingly homogeneous, astrocytes proliferate and lipid phagocytes form in preparation for removal of the now "ghost cell." 

    As the flow lowers and the mitochondria fail, energy sources change from an aerobic to an anaerobic pathway, with a corresponding increase in lactic acid production , metabolic derangement, and loss of ion and transmitter homeostasis. 

    If this process continues unchecked, there will be inadequate energy to maintain the sodium potassium pump across the cell membrane (Jones et al., 1981). Researchers have increasingly detailed the process in an attempt to identify and improve the brain's tolerance to recover from an ischemic challenge.

First Blood Flow Study CBF

    Servetus, in the 16th century, first presented the idea that blood flowed through the lungs; he was burned at the stake for his efforts. William Harvey (1578-1657) supported Servetus findings by describing the flow of blood through the body. 

    Nearly 200 years later, oxygen was discovered by Priestley, and Steele and Lavoisier made the connection that oxygen contributed to the production of "hear" or energy. 

    Adolf Fick, in 1870, defined blood flow as the quantity of a substance, such as oxygen, that is taken up by a specific organ over a unit of time (Fick, 1870; Obrist, 2001). The first "measures" of CBF involved direct and indirect observations of intracranial vessels (Roy & Sherrington, 1890). 

    It was not until 1945, when Kety and Schmidt applied the Fick principle to diffusible gas, nitrous oxide, that one was able to estimate cerebral blood flow ( Kety , 1950; Kery & Schmidt, 1948).

    Kety was the first person to measure global CBF in humans using vascular transit time. The technique was modified by Lassen and Ingvar when Xe-133, a highly diffusible gas, was injected into the internal carotid artery (Lassen & Ingvar, 1972). 

    Multiple extracranial detectors traced the transit time of the radiation from the Xe-133 as it flowed through the brain, providing focal CBF measures. Diffusible tracers are now combined with tomographic reconstruction such as computed tomography, PET, or magnetic resonance imaging (MRI), to calculate vascular transit time. 

    For example, stable xenon-enhanced CT scanning measures CBF via conventional scanner interfaced with computer hardware and software and directs the delivery of xenon gas transit throughout brain regions. 

    Serial CT scans are conducted during the inhalation of a gas mixture containing 30% xenon, 30% to 60% oxygen, and room air. The serial images are stored and regional flows are calculated. 

    CBF is also estimated from measurement of cerebral blood volume. One way to estimate cerebral blood volume is using a gradient-echo planar system on MR systems. The dynamic contrast-enhanced susceptibility- weighted perfusion imaging technique involved giving a bolus of paramagnetic contrast material ( ie ., gadolinium). 

    The contrast media is traced and the amount of signal attenuation is proportional to the cerebral blood volume. With a series of multi-slice measurements, one may generate a time-density curve, and the area under the curve provides an index of relative blood volume (Grandin, 2003). Similar techniques are adapted to CT scanners with the capability for rapid sequential scanning.

    The threshold for irreversible brain damage from cerebral ischemia is generally defined as below 20 ml/100 g of tissue/minute (Jones et al., 1981; Yonas, Sekhar, Johnson, & Gur, 1989). CBF below this level alters the functioning of the mitochondria to produce energy.

     Studies show that the threshold for irreversible brain damage are volume and time dependent. Global brain ischemia that is sustained for longer than 4 to 5 minutes will result in permanent brain damage (Brierley, Meldrum, & Brown, 1973). 

    The majority of studies show that above 23 ml/ 100 g/minute, little impairment occurs; how-ever, below 20 ml/100g/minute symptoms of neurologic impairment develop (Branston, Symon, Crockard , & Pasztor , 1974). 

    Below 18-20 ml/100g/minute evidence of diminished electrical activity by evoked potentials or electroencephalogram occurs (Sundt, Sharbrough , Anderson, & Michenfelder , 1974). Below 15 ml/100 g/minute is considered to be a threshold for synaptic transmission ( Astrup , Siesjo , & Symon, 1981). 

    In addition, factors including temperature, drug administration, and individual variation contribute to the complexity of defining this threshold. Recent work focuses on methods that "noninvasively" detect, track changes in, or treat cerebral ischemia.

    The determination and prediction of cerebral ischemia is only as good as the technique used to detect low flow states. Absolute CBF of the cerebral vessels combined with a marker of tissue response would provide the ultimate information in the evaluation of cerebral ischemia. However, the perfect technique is not yet available.

    Future directions in cerebral ischemia include the development of noninvasive techniques to measure regional blood flow that have increased sensitivity and resolution. 

    As techniques become increasingly more portable and useable, there will be a translation from the radiology department to application by nurses in the community or at the bedside to assess, predict, and identify patients at risk for cerebral ischemia.

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