Nursing Care of Cerebral Ischemia
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.