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8 Transcranial Doppler (TCD/TCCS) and Cerebral Blood Flow: Applications…
151
8.4.1 Cerebral Autoregulation (CA)
Cerebral autoregulation (CA) is dened as the ability of the cerebrovascular system
to maintain relative constant CBF despite changes in cerebral perfusion pressure
[17]. Thus, cerebral autoregulation is dened as a pressure phenomenon. The majority of autoregulatory control occurs at the level of the cerebral arterioles. Arterioles
will constrict and dilate in response to increases and decreases in cerebral perfusion
pressure, respectively, to maintain constant CBF between a cerebral perfusion pressure (CPP) of 50–150mmHg [18]. CBF outside of these ranges becomes dependent
upon the perfusion pressure. A signicant proportion of vascular resistance, however, is also mediated at the level of the small arteries. Alterations in sympathetic
tone of these pial arteries can shift the autoregulatory curve upward or downward
[19] (Fig.8.3).
The theoretical mechanisms by which CBF is maintained over a wide range of
perfusion pressures are quite extensive and beyond the scope of this review. Briey,
however, hypothesized mechanisms can be grouped into myogenic, metabolic, and
neurogenic categories. The myogenic theory postulates that smooth muscle cells of
the arteries and arterioles constrict or dilate in response to changes in transmural
pressure generated across the vessel wall [20]. This may be mediated through alterations in the position of the actin-myosin laments in these smooth muscles [21].
Passive
collapse
75
50
25
Cerebral Blood Flow (ml/100 g/min)
25
Vasodiatory
Cascade Zone
50 75 75
VASCULARCALIBER
Cerebral Perfusion Pressure (mm Hg)
Zone of Normal
Autoregulation
100125 150
Autoregulation
Breakthrough Zone
60
40
ICP (mm Hg)
20
Fig. 8.3 Dark line representing the autoregulatory curve. Note CBF matches CPP at the extremes
of the curve. The lighter line represents cerebral blood volume and the above vessels refer to the
state of patency at varying cerebral perfusion pressures. (Rose and Mayer [18])
152
The metabolic theory postulates that local changes in cerebral blood ow release a
variety of substances that both affect vessel diameter and couple ow with metabolism [22]. The neurogenic theory suggests that small intrinsic nerves may be responsible for changes in CBF [23].
E. M. Manno and F. Sorond
8.4.2 CO2 Vasoreactivity
Unlike cerebral autoregulation which is a pressure phenomenon, CO2 vasoreactivity
is a metabolic phenomenon. There is a direct increase in CBF with increasing PaCO2
[24, 25]. The response curve of CBF to Pa CO2 is sigmoidal with the CBF response
attening below 15–20mmHg and above 100mmHg (Fig.8.3). PaCO2 will freely
diffuse across the blood–brain barrier; however, changes in CBF are mediated through
changes in cerebral spinal uid (CSF) hydrogen ion concentration. These changes,
however, are short-lived as the choroid plexus of the brain will equilibrate and buffer
these changes over a few hours [26] returning CBF to its baseline level. Cerebrovascular
reserve is a terminology that is used to dene the amount of ow during maximal
arteriolar dilation. It is described as a percentage of maximal dilation [27].
8.5 TCD/TCCS: Assessment ofCerebral Autoregulation
andCO
Vasoreactivity
2
The assessment of cerebral autoregulation and CO2 vasoreactivity requires continuous monitoring of TCD/TCCS ow velocities during manipulations of blood pressure and CO2, respectively. Technically, this is achieved through the use of a head
holder that locks down the probes during insonation of bilateral ow velocities in
the vessels of interest.
Cerebral autoregulation can be evaluated under dynamic or static conditions.
Dynamic testing involves an induced drop in blood pressure or spontaneous blood
pressure oscillations during continuous TCD monitoring. Induced changes are often
performed during rapid deation of thigh blood pressure cuffs. The abrupt drop in
blood pressure leads to a mirrored drop in TCD ow velocities. In patients with poor
autoregulation, TCD ow velocities will parallel a slow return in blood pressure. In
patients with intact autoregulation, TCD/TCCS ow velocities will return to baseline immediately and will precede improvements in blood pressure. A similar type
of response called a transient hyperemic response to carotid compression can also
be employed [28]. In practice, however, these tests are rarely utilized in the intensive care unit.
Static autoregulation is measured using pharmacologic manipulation of blood
pressure during continuous TCD monitoring. It is calculated as a percentage change
in cerebrovascular reserve (CVR) / a percent change in CPP x 100. CVR is dened
8 Transcranial Doppler (TCD/TCCS) and Cerebral Blood Flow: Applications…
as CPP /mean TCD velocities Using this method, autoregulation is expressed as a
percentage with 100% signifying intact autoregulation [29, 30].
CO2 vasoreactivity can similarly be addressed while measuring continuous TCD
ow velocities during manipulation of PCO2. This can be achieved through breath
holding or changes in inspired pCO2. Acetazolamide can similarly be used, but concerns have been raised using this pharmacology since acetazolamide may directly
affect middle cerebral artery (MCA) diameter during testing and may complicate
the calculation of changes in CBF [31].
153
8.6 TCD/TCCS: Use intheNeurological Critical Care Unit
8.6.1 TCD/TCCS: Use inSubarachnoid Hemorrhage
TCD can be used in the neuro ICU for a variety of neurological processes. It is most
commonly used to detect the development of cerebral vasospasm after subarachnoid
hemorrhage. Cerebral vasospasm is a self-limited vasculopathy that develops
4–14days after subarachnoid hemorrhage. Pathologically, the basal cerebral arteries develop a T-cell inltrate, collagen remodeling, and smooth muscle proliferation
[32]. This can potentially lead to vessel narrowing and cerebral ischemia. Vasospasm
appears to be a reaction to the amount and location of subarachnoid blood as rst
described by Fisher [33] and later veried by Kistler [34].
Prior to the development of TCD, vasospasm could only be detected through the
use of cerebral angiography. Aaslid was able to demonstrate, however, a good correlation between MCA ow velocities and actual vessel luminal diameter as measured by angiography. Mean MCA ow velocities greater than 120cm/s represented
mild narrowing, while ow velocities greater than 200cm/sec represented severe
narrowing [1].
While TCD ow velocities can correlate with vessel narrowing, using TCD to
predict which patients will develop subsequent cerebral ischemia has been more
problematic. Initial studies suggested that absolute or rapid increases in ow velocities were indicative of impending neurological decits [35, 36]. However, subsequent studies could not reproduce these ndings [37].
The reasons for this discrepancy in ndings may be technical. TCD ow velocities need to be corrected for a variety of physiological parameters [38] but in practice rarely are. In an attempt to differentiate increased blood ow from vessel
narrowing, Lindegaard developed a ratio of ow velocities from the extracranial
carotid artery to the MCA.Elevated ow velocities in the MCA not matched in the
extracranial internal carotid artery (ICA) would suggest vessel narrowing, while
similar changes would suggest hyperemia [39]. Similar ratios have been developed
for the posterior circulation [40]. Disturbances in cerebral autoregulation after subarachnoid hemorrhage can lead to a misinterpretation of TCD ow velocities.
Manipulations of blood volume and blood pressure commonly employed for
154
E. M. Manno and F. Sorond
treatment of cerebral vasospasm can directly affect TCD ow velocities in patients
with disturbed autoregulation [30]. Measurements of cerebral vascular reserve in
patients with vessel narrowing may prove to be predictive of which patients are at
risk for developing ischemic decits [41].
Finally, the premise that vessel narrowing is the source of cerebral ischemia after
subarachnoid hemorrhage may be inaccurate. Recent speculations have suggested
that the hemoglobin released into the subarachnoid space binds spinal uid nitrous
oxide which is needed for vasomotor coupling of metabolism to CBF [42].
Rabinstein reported that most cerebral infarcts after subarachnoid hemorrhage
occurred in vascular territories unaffected by vessel narrowing [43]. Similarly, the
results of the Conscious-2 trial a randomized study of an endothelin receptor antagonist reported signicant improvement in vessel narrowing after subarachnoid hemorrhage with no effect on ischemic decits or outcome [44].
8.6.2 TCD/TCCS: Use After Traumatic Brain Injury (TBI)
TCD/TCCS has been used to facilitate management in the intensive care unit [45].
TCD use after TBI can be utilized to estimate intracranial pressure (ICP), determine
the status of cerebral autoregulation, and determine if cerebral vasospasm.
Changes in TCD waveforms have been documented with increases in ICP.Loss
of distal compliance leads to an increased pulsatility index. Continued increases
lead to loss of diastolic ow velocities. At extreme levels, systolic spikes and loss of
TCD waveforms are noted [46]. Pulsatility indexes have been correlated with ICP
in a variety of cerebral conditions; however, attempts to dene ICP based on TCD/
TCCS waveform analysis have fallen short [47].
While TCD/TCCS waveforms as yet cannot be used to replace ICP, monitoring
increases in pulsatility indexes can be used to potentially identify expanding lesions,
focal or global increases in ICP, and decreases in CPP.Continuous TCD monitoring
has noted an increase in pulsatility indexes in head trauma patients at their CPP
dropped below 70mmHg, thus potentially providing a warning for inadequate perfusion [48]. Flow velocities below 35cm/sec suggesting decreased CBF after head
trauma have been associated with poor outcomes [48, 49]. Similarly, loss of cerebral
autoregulation is common after head trauma and has been associated with worse
outcomes. Identifying these disturbances early in the post-traumatic course may
allow for individualized therapies [50, 51].
Traumatic subarachnoid hemorrhage is common, and cerebral vasospasm can
develop in similar patterns as detected after aneurysmal subarachnoid hemorrhage.
Cerebral vasospasm after head trauma has been identied as a predictor of poor
outcome [52], and medical maneuvers designed to increase CBF can potentially be
employed. Interestingly, posterior circulation vasospasm is more common after
traumatic subarachnoid hemorrhage [53].
8 Transcranial Doppler (TCD/TCCS) and Cerebral Blood Flow: Applications…
155
8.6.3 TCD/TCCS: Conrmation ofBrain Death
TCD can be utilized as a conrmatory test to assess for the absence of CBF in
patients that have met criteria for brain death. The portability of TCD allows for the
assessment of hemodynamically unstable patients that may not tolerate transfer outside of the intensive care unit. TCD use as a conrmation test has been reported to
shorten the time of diagnosis.
Several patterns of waveforms have been described to indicate the absence of
effective perfusion. These include small systolic spikes, oscillating ow, and loss of
signal which had previously been isolated [54]. If vessels have not been previously
insonated, the absence of signal cannot be utilized since in about 10% of patients’
vessels cannot be insonated through the temporal bone. Sensitivity increases with
the number of vessels which can be isolated. A lower false-positive rate has been
reported when using a transorbital approach [55].
A recent meta-analysis conrmed the diagnostic accuracy or TCD conrmation
of brain death, and most countries accept TCD as an ancillary test to conrm brain
death [56]. Consensus guidelines for the determination of circulatory arrest have
been proposed by the World Federation of Neurology [57]. Despite this, Canada,
Australia, and New Zealand prefer other methods for conrmation [58].
8.6.4 TCD/TCCS: Use inIntracerebral Hemorrhage
TCD use after intracerebral hemorrhage traditionally had limited value. Poorer outcomes have been noted in patients with disturbed cerebral autoregulation and CO2
vasoreactivity [59]. Differences in the middle cerebral artery pulsatility indexes
may suggest side-to-side differentials in ICP.
Newer sonographic techniques have been used in the ICU to evaluate intracerebral hemorrhages. Transcranial color-coded sonography has identied spontaneous
hemorrhages [60]. Transcranial duplex sonography has identied midline shift after
intracerebral hemorrhage and has been utilized to predict outcome after hemorrhage
[61, 62].
8.6.5 TCD/TCCS: Other Uses intheIntensive Care Unit
A variety of information can be gathered during routine TCD evaluation. Evidence
for midline shift or a different location of a vessel previously insonated can suggest
the development of a mass lesion. High-intensity transient signals (HITS) suggest
recurrent emboli which can be detected during transient ischemic attack evaluation
156
E. M. Manno and F. Sorond
or post-carotid endarterectomy [63]. Reversal or patency of vessels can be evaluated
using TCD after bypass operations. Changes in vascular resistance can signify a
local mass lesion or decreased perfusion. All may point to the need for additional
imaging. More recently, increased continuous MCA ow velocities were noted during episodes of non-convulsive status epilepticus [64].
8.7 Conclusion
TCD/TCCS has gained increasing acceptance and use due to its many advantages of
ease of use and access, cost, portability, and reliability. By measuring ow velocities, both cerebral and CO2 vasoreactivity can be assessed providing valuable information to the neurological status of the patient. TCD, while unable to predict with
condence which patients will develop ischemic complications after subarachnoid
hemorrhage, is quite useful in identifying that cerebral vasospasm is developing.
Subsequently, this can focus neurological assessments and treatments. It is a useful
tool in several circumstances for conrming brain death in the hemodynamically
unstable patient. Newer sonographic techniques have been developed that will offer
promising new insights into both the pathogenesis and prognosis of a number of
acute neurological conditions.
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Part III
Neurosonology: Neurocritical Care Patient