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10 Transcranial Doppler (TCD/TCCS) Approaches: Acoustic Windows
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neuroimaging of stroke: a comprehensive reference; 2017.
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the ICU.Neurocrit Care. 2019;33:115.
11. Yoshimura S, Koga M, Toyoda K, Mukai T, Hyun B-H, Naganuma M, et al. Frontal bone
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19. Bor-Seng-Shu E, de-Lima-Oliveira M, Nogueira RC, Almeida KJ, Paschoal EHA, Paschoal
FM Jr. Decompressive Craniectomy for traumatic brain injury: postoperative TCD cerebral
hemodynamic evaluation. Front Neurol. 2019;10:354.
20. Bor-Seng-Shu E, Paiva WS, Figueiredo EG, Fujimoto Y, de Andrade AF, Fonoff ET, et al.
Posttraumatic refractory intracranial hypertension and brain herniation syndrome: cerebral hemodynamic assessment before decompressive craniectomy. Biomed Res Int.
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J. Ca rr izosa
Chapter 11
Neurocritical Patient inICU: Transcranial
Doppler (TCD/TCCS) astheBrain
Stethoscope
ChiaraRobba andDaniloCardim
Key Points
1. Cerebral blood ow velocity
The spectral waveform derived from TCD is characterized by three components: peak systolic ow velocity (PSV), mean ow velocity (MFV), and enddiastolic velocity (EDV) values.
2. Pulsatility index
Pulsatility index (PI) can provide information about the downstream cerebral
vascular resistance and describe quantitative and qualitative changes in the morphology of the TCD waveform resulting from cerebral perfusion pressure changes.
3. Cerebral compliance
Cerebral compliance (C) is the ability of the brain to adapt to changes in vol-
ume inside the cranium in response to a change in pressure to avoid intracranial
hypertension.
4. Cerebrovascular time constant
The cerebrovascular time constant (TAU) is a non-invasive TCD-based index
indicating theoretically the time to establish a change in cerebral blood volume
after a sudden change in arterial blood pressure during one cardiac cycle.
C. Robba (*)
Department of Anaesthesia and Intensive Care, Ospedale Policlinico San Martino IRCCS,
IRCCS for Oncology, University of Genoa, Genoa, Italy
Deputy Neurointensive Care section - ESICM, Brussels, Belgium
e-mail: kiarobba@gmail.com
D. Cardim
Brain Physics Laboratory, Division of Neurosurgery, Department of Clinical Neurosciences,
Addenbrooke’s Hospital, University of Cambridge, Cambridge, UK
Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital
Dallas, Dallas, TX, USA
Department of Neurology and Neurotherapeutics, University of Texas Southwestern Medical
Center, Dallas, TX, USA
C. N. Rodríguez et al. (eds.), Neurosonology in Critical Care,
https://doi.org/10.1007/978-3-030-81419-9_11
195© Springer Nature Switzerland AG 2022
196
C. Robba and D. Cardim
5. Critical closing pressure
Critical Closing Pressure (CrCP) is described as the sum of intracranial pres-
sure (ICP) and vascular wall tension (WT). The latter represents the active vasomotor tone that alongside ICP determines the CrCP.Clinically, CrCP represents
a lower threshold of arterial blood pressure, below which the brain microvasculature collapses and cerebral blood ow (CBF) ceases.
6. Cerebral autoregulation
Cerebral blood ow autoregulation refers to the intrinsic ability of the brain
to maintain a stable CBF despite uctuations in cerebral perfusion pressure.
7. Non-invasive assessment of intracranial pressure
ICP evaluation is crucial in many neurological diseases, and it is commonly
measured through intraventricular or intraparenchymal catheters, but their invasive nature and related complications preclude their use in many conditions.
TCD waveform analysis has been widely investigated as a technique for noninvasive ICP (nICP) estimation.
11.1 Introduction
Transcranial Doppler ultrasonography (TCD)/TCCS has the potential to be used as
an alternative diagnostic tool for the assessment of cerebral hemodynamics rather
than costly and potentially risky investigations such as invasive ICP monitoring.
In the neurointensive care setting, the monitoring of TCD-derived indices may
provide an early detection of the onset of cerebrovascular derangements. The
knowledge of cerebrovascular dynamics can facilitate clinical management of cerebral pathologies, including traumatic brain injury (TBI), aneurysmal subarachnoid
hemorrhage (aSAH), intra- and extracranial arterial stenosis and occlusion, brain
death, cerebral infections, and hydrocephalus [1].
The aim of this chapter is to provide an overview of the basic and advanced
TCD-derived methods (Table11.1) and clinical applications of TCD in critically ill
Table 11.1 Basic and
advanced signals derived from
transcranial Doppler
ultrasonography
Basic signals Flow velocity
Pulsatility index
Advanced signals Autoregulation
CrCP
WT
C
, C
a
i
Tau
nCPP
nICP
Abbreviations: CrCP critical closing pressure, WT wall
tension of the cerebral vasculature, C
cerebral arterial bed, C
space, Ta u cerebrovascular time constant, nCPP non-invasive cerebral perfusion pressure, nICP non-invasive intracranial pressure
compliance of the intracranial
i
compliance of the
a
11 Neurocritical Patient in ICU: Transcranial Doppler (TCD/TCCS) as the Brain…
Table 11.2 Clinical applications of transcranial Doppler ultrasonography
Clinical Applications Role of TCD
TBI Non-invasive ICP and CPP estimation [7, 10]
Autoregulation [45, 46]
Compliance and cerebrovascular dynamics [49]
Prediction of neurological deterioration in the
emergency room
SAH (Aneurysms and
AVM)
Stroke Diagnosis and treatment of ischemic stroke [62–65]
Brain death Diagnosis of brain death [66]
Sickle cell disease Risk from a spectrum of brain injuries that include
Cerebral venous
thrombosis
Right to left cardiac shunt Evaluation of paradoxical embolism through right to
Peri-procedural/operative Autoregulation
Liver failure and hepatic
encephalopathy
Preeclampsia Assessment of autoregulation and FV as prognostic
Sepsis Assessing cerebral perfusion changes in septic patients
Abbreviations: AV M arteriovenous malformation, CPP cerebral perfusion pressure, FV cerebral
blood ow velocity, ICP intracranial pressure, SAH subarachnoid hemorrhage, TBI traumatic brain
injury, TCD transcranial Doppler ultrasonography
Vasospasm [55, 56, 66]
Autoregulation [58, 60]
subclinical infarction, acute stroke and hemorrhage
left cardiopulmonary shunts (e.g., patent foramen
ovale)
Non-invasive ICP and CPP
Non-invasive ICP estimation and prognosis for acute
liver failure
for preeclampsia
as risk of Sepsis-associated encephalopathy
Main
references
[50, 51]
[67]
[6]
[68]
[69–71]
[82]
[83]
197
patients in the neurointensive care setting (Table11.2), and to describe the utility of
TCD in the diagnosis and monitoring of cerebrovascular diseases as a “stethoscope
for the brain.”
11.2 Basic Methods
11.2.1 Flow Velocities
The spectral waveform derived from TCD/TCCS is characterized by three
components:
1. Peak systolic ow velocity (PSV),
2. Mean ow velocity (MFV), and
3. End-diastolic velocity (EDV) values (Fig.11.1).
198
Time
CBFV (cm/s)
90
FVs
80
70
FVd
60
50
Fig. 11.1 Representation of the TCD cerebral blood ow velocity (CBFV) waveform, presenting
a peak systolic and an end diastolic. (FVs=PSV); (FVd=EDV)
C. Robba and D. Cardim
PSV is predominantly dependent on the cardiac output, that is, systemic hemodynamics, rather than depicting cerebral hemodynamics.
The use of EDV as a relevant parameter is currently thriving in clinical practice,
especially in intensive care. Some authors have reported a reduction of CPP by rising ICP or by falling arterial blood pressure (ABP) in head-injured patients, which
resulted in a greater fall in diastolic ow velocity than other ow parameters [2].
TCD/TCCS cerebral blood ow velocities are commonly measured modalities in
clinical and experimental environments. Through analysis of TCD waveform, many
authors attempted to investigate the relationship between the cerebral blood ow
(CBF) and cerebrospinal uid (CSF) dynamics, proposing several mathematical
and hydrodynamic models derived mostly from ow velocity (FV), ABP, and intracranial pressure (ICP) signals as inputs [3, 4].
11.2.2 Pulsatility Index (PI)
Gosling’s pulsatility index (PI) can provide information about the downstream cerebral vascular resistance and describe quantitative and qualitative changes in the
morphology of the TCD/TCCS waveform resulting from cerebral perfusion pressure changes [5].
PI is calculated as the relationship between the difference of systolic ow velocity and diastolic ow velocity divided by mean ow velocity, and in normal conditions, it usually ranges from 0.5 to 1.19 [6]. Proximal stenosis or occlusion may
lower PI below 0.5 due to downstream arteriolar vasodilation, whereas distal occlusion or constriction may increase PI above 1.19 [7]. A PI less than 0.5 may also
indicate an arteriovenous malformation as the resistance in proximal vessels is
reduced due to continuous distal venous ow [8]. More recently, a larger study
including more than 350 healthy individuals has reported normative values for TCD
assessment of arteries in the circle of Willis [9]. Normal PI values have been reported
as 0.82±0.16 and 0.81±0.13 for distal and proximal middle cerebral artery (MCA),
()
–/
ICP (mmHg) ICP (mmHg)PI
PI
11 Neurocritical Patient in ICU: Transcranial Doppler (TCD/TCCS) as the Brain…
199
respectively. Being a ratio, PI is not affected by the angle of insonation and therefore
may be a sensitive parameter for early detection of intracranial hemodynamic
changes [9] (Eq.11.1).
PI PSV EDVMFV=
(11.1)
Mathematically, PI can be calculated as inversely proportional to CPP, directly
proportional to pulse amplitude of ABP, and nonlinearly proportional to the compliance of the arterial bed (Ca), heart rate (HR), and cerebrovascular resistance
(CVR) [5].
PI has been used for the assessment of distal CVR [10] as many experimental
and clinical studies have supported the concept that PI is a reection of the distal
CVR, attributing greater PI to higher CVR [8]. However, an experimental study
demonstrated that hypercapnia causes a decrease in both CVR and PI, whereas a
reduction in CPP with intact autoregulation induces a decrease in CVR but an
increase in PI [11].
PI has been also widely investigated as non-invasive estimator of ICP, as it has
been demonstrated that ICP and PI are positively correlated during increases of ICP
(Fig.11.2). However, the role of PI as non-invasive estimator of ICP can be controversial [12].
11.3 Advanced Methods
Several secondary advanced model-based methods for cerebral hemodynamics
assessment have been introduced.
60
50
40
30
20
4
3
2
60
50
40
30
1.4 1.6 1.8 2 2.2 2.4 2.6 2.8 3 3.2 3.4 3.6 3.8 4
Fig. 11.2 Plot showing the positive relationship between pulsatility index (PI) and intracranial
pressure (ICP) in traumatic brain injury
Time
200
ICP Amp (mmHg) ICP (mmHg)
Time
ab c
C. Robba and D. Cardim
11.3.1 Compliance ofArterial andCSF Compartments
Cerebral compliance (C) is the ability of the brain to adapt to changes in volume
inside the cranium in response to a change in pressure to avoid intracranial hypertension. This parameter includes the cerebrovascular arterial compliance (Ca),
which describes the change of arterial blood volume in response to change in arterial pressure, and the compliance of the cerebrospinal space (Ci), which refers to
changes of volume of the intracranial space in regards to changes in ICP [13].
TCD/TCCS allows a non-invasive estimation of cerebral arterial blood volume
(CaBV) [14] and enables the assessment of the relative changes in C
two parameters reect the relationship between pulsatile changes in ABP and CaBV
(Ca) and ICP and CaBV (Ci). This model is based on the mechanism of brain pulsatility that describes the physiological interactions of the intracranial compartments
undergoing volumetric changes during the cardiac cycle.
This method was widely described in patients with TBI during “plateau waves”
of ICP [13, 15] monitored using TCD.The origin of plateau waves includes intrinsic
cerebral vasodilatation, with a rise in cerebral blood volume and a rise in
ICP.Therefore, according to the “vasodilatory cascade” hypothesis, these changes
are associated with rapid increase in Ca caused by vasodilatation of cerebral resistive vessels during a wave and a reduction of Ci due to the decrease in cerebrospinal
compensatory reserve caused by the increase in cerebral blood volume [16, 17].
More recently, Kim etal. conrmed this relative inverse change in Ca and Ci in head
injury patients, illustrating that both compartmental compliances can be continuously monitored over a cardiac cycle [18].
The pulsatile component of ICP (Fig.11.3) and a clinical management guided by
cerebral compliance has been associated with outcome prediction in several contexts, including SAH, TBI, and normal pressure hydrocephalus [19].
and Ci. These
a
20
15
10
5
0
5
4
3
2
1
50
45
40
35
30
ICP (mmHg)
25
20
5
4
3
2
1
ICP Amp (mmHg)
Fig. 11.3 Amplitude of intracranial pressure (ICP Amp) in different clinical conditions: (a) B
waves of ICP; (b) increase in ICP during plateau wave; (c) increase in ICP during cerebral spinal
uid infusion test in patient with normal pressure hydrocephalus. In all cases, an increase in intracranial pressure is followed by an increase in ICP amplitude
45
40
35
30
25
20
ICP (mmHg)
15
10
6
5
4
3
2
1
ICP Amp (mmHg)
uC
()
11 Neurocritical Patient in ICU: Transcranial Doppler (TCD/TCCS) as the Brain…
201
11.3.2 TAU (Cerebrovascular Time Constant)
The cerebrovascular time constant (TAU) is a non-invasive TCD-based index indicating theoretically the time to establish a change in cerebral blood volume after a
sudden change in arterial blood pressure during one cardiac cycle [20] (Eq.11.2).
TAU is an analog to time constant and is calculated as a product of cerebral arterial compliance (Ca) and cerebrovascular resistance (CVR), expressed in time units
(seconds).
Ta
The dependence of TAU on hemodynamic and cerebrovascular parameters was
studied on 46 New Zealand rabbits undergoing hemodynamic manipulations. TAU
resulted to be inversely correlated with the changes in ABP (during arterial hypoand hypertension) and CPP (during intracranial hypertension). Specically, during
a decrease in CPP, Ca increased while CVR decreased. During hypercapnia, the
decrease in CVR was more pronounced than the increase in Ca, resulting in a total
decrease in Tau [20].
In normal subjects, where Ca and CVR were estimated using mathematical transformations of ABP and TCD, Tau was studied following cerebral blood ow velocity waveform changes in end-tidal CO2 (EtCO2). The time constant resulted to be
shortened with increasing EtCO2, while hypocapnia lengthened the time constant [21].
TAU was also studied in healthy volunteers and in patients with severe stenosis
of the internal carotid artery (ICA), and it was found to be signicantly shorter in
severe internal carotid artery stenosis [21] than in controls and that it correlated with
the degree of stenosis. Moreover, TAU was found to be signicantly decreased during vasospasm in SAH patients [22], and in particular, it was found to be shortened
on the side of the aneurysmal SAH before the vasospasm was identied by the clinical or conventional TCD signs of vasospasm.
In a recent study [23], TAU was assessed in patients with traumatic brain injury
(TBI) with and without intracranial hematomas (epidural, subdural, and multiple
hematomas). Tau was shorter in both groups in comparison with normal data, but in
patients with intracranial hematomas, the time constant was even shorter, indicating
a failure of autoregulation of cerebral capillary blood ow after severe TBI occurs.
=×
VR s
C
a
(11.2)
11.3.3 Critical Closing Pressure andWall Tension
Critical Closing Pressure (CrCP) was rst introduced by Burton’s model, and it is
described as the sum of ICP and vascular wall tension (WT) [24]. Wall tension
(WT) represents the active vasomotor tone that alongside intracranial pressure
determines the critical closing pressure. Clinically, CrCP represents a lower
202
()
()
()
C. Robba and D. Cardim
threshold of ABP, below which the brain microvasculature collapses and CBF
ceases [24].
CrCP can be assessed non-invasively using TCD/TCCS, by comparing the pulsatile waveforms of blood ow velocity and ABP, and given the association with the
vasomotor tone of small blood vessels (wall tension), CrCP can provide important
information regarding cerebral hemodynamics and changes in cerebral perfusion
pressure in several neurological conditions [25, 26]. The estimation of CrCP through
TCD has also been shown to be clinically useful for estimating changes in ICP noninvasively or for cerebrovascular tone assessment to direct therapies in patients at
risk to develop vasospasm after subarachnoid hemorrhage or hyperemia [27].
With TCD/TCCS, CrCP can be assessed non-invasively by comparing the pulsatile waveforms of CBFV and ABP [27–29] assuming a linear relationship between
these two parameters during one cardiac cycle. Alternatively, the fundamental harmonics of the pulse waveforms of ABP and CBFV can also be used [25, 30].
However, a limitation of all these methods consists in the possibility to obtain negative values of CrCP, which cannot be clinically and physiologically explained [31,
32]. Varsos etal. proposed a new method for estimating CrCP derived based on the
model of cerebrovascular impedance [26], eliminating the issue of rendering negative values (Eq.11.3).
CrCP ABP
=−
where CVR
=
ABP
FV
CVRHR
Here, CVR (mmHg/(cm/s)) represents cerebral vascular resistance, C
ABP
⋅⋅ ⋅
C 21
a
C
BV
a
C
=
a
a
1
2
π
1
mmHg
#
+
(11.3)
(cm/
a
mmHg) denotes compliance of the cerebral arterial bed (arteries and arterioles), and
HR is the heart rate given in beat/s. a1 represents the pulse amplitude of the rst
harmonic of the ABP waveform, and CaBV1 is the pulse amplitude of the rst harmonic of the cerebral arterial blood volume waveform (CaBV). The pulse amplitude
of the rst harmonics is determined with fast Fourier transformation.
Derived from CrCP and ABP, other indices, such as the diastolic closing margin
(DCM) of the brain microvasculature, can be obtained. Previous works have demonstrated that diastolic ABP (ABPd) below CrCP is associated with the loss of measurable CBFV during diastole [33], causing an acceleration of brain ischemia when
CPP decreases further. The difference in pressures between ABPd and CrCP (DCM)
represents the force that allows cerebral blood ow circulation during diastole.
When DCM is exhausted (≤0mmHg), vessels will collapse resulting in cessation of
cerebral blood ow [33, 34] (Eq.11.4).
DCMABP CrCP mmHg
=
–
d
(11.4)