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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5783_Библиотеки_им_академика_М_И_Перельмана.pdf
Chapter 21
Transcranial Doppler Ultrasound
Pulsatility Index: Utility andClinical
Interpretation
OscarM.Pinillos, CamiloN.Rodríguez, andRyanHakimi
Key Points
1. Physical examination of a critically ill patient with acute primary or secondary
neurological injury is often insufcient for medical decision making. Transcranial
Doppler/transcranial color coded sonography (TCD/TCCS) is a useful physiologic tool allowing one to individualize the management of each patient to optimize cerebral hemodynamics.
2. Pulsatility index (PI) is calculated by subtracting the peak systolic velocity
(PSV) from the end diastolic ow velocity (EDV) and dividing the difference by
the mean ow velocity (MVF); [PI=(PSV−EDV)/MVF].
3. Pulsatility Index is dependent on multiple variables including cerebrovascular
resistance (CVR).
4. Despite the correlative value of PI obtained from TCD/TCCS, the external ven-
tricular drain remains the gold standard in the measurement of intracranial pressure (ICP).
O. M. Pinillos
Intensive Care Medicine, Clinica de Occidente, Cali, Colombia
Neurointensive Care section - AMCI, Bogotá, Colombia
C. N. Rodríguez (
Intensive Care Medicine, Hospital Nacional Prof. Dr. A. Posadas, University of Buenos Aires
(UBA), Neurointensive Care Section - ESICM, Neurointensive Care Section - AMCI,
Neurointensive Care Committee - FEPIMCTI, Member of ESNCH, Buenos Aires, Argentina
e-mail: camilo.rodriguez@nesccco.com
R. Hakimi
Department of Medicine (Neurology), USC School of Medicine-Greenville,
Greenville, SC, USA
Neuro ICU, TCD Services, Prisma Health-Upstate, Greenville, SC, USA
American Society of Neuroimaging (ASN), Minneapolis, MN, USA
C. N. Rodríguez et al. (eds.), Neurosonology in Critical Care,
https://doi.org/10.1007/978-3-030-81419-9_21
*)
357© Springer Nature Switzerland AG 2022
358
O. M. Pinillos et al.
5. The absolute numerical value of the PI is less valuable than the PI trend in a
given patient when assessing ICP.
6. The PI numerically reects changes in the morphology of the TCD/TCCS wave-
form, which is dependent on cerebral perfusion pressure and changes in CVR.
21.1 Introduction
Obtaining a comprehensive medical history and performing a thorough neurological examination is always the rst step in assessing patients with acute neurological
injury. However, critically ill neurological patients often require sedation or analgesia limiting their clinical examination.
During the course of a neurocritical care patient’s ICU stay, there are frequent
uctuations in a given patient’s ICP and cerebral hemodynamics (PSV, MFV, EDV,
etc.) which represent the evolution of the acute neurological injury. These factors
are important in assessing and mitigating the extent of secondary brain injury and
its severity and duration and clinically correlate with the patient’s ultimate outcome.
Transcranial Doppler ultrasonography (TCD) and transcranial color-coded Duplex
sonography (TCCS) are non-invasive, bedside, portable tools for the assessment of
cerebral hemodynamics (Table 21.1) and detection of focal stenosis, arterial occlusion, monitoring the treatment effect of intravenous tissue plasminogen activator and
assessment of vasomotor reactivity. These instruments display spectral waveforms
that represent the depth, direction, and intensity of the blood ow through the intracranial vasculature. Although these instruments do not measure blood ow directly, the
parameters they do calculate do correlate with cerebral blood ow (CBF) [1].
In the past, TCD machines were only able to display a spectral waveform. The
operator was left to deduce which vessel was being insonated by attempting to
obtain the same waveform or an inverted version of the same waveform using a
variety of different approaches, termed windows, at different depths. With the addition of power motion–mode Doppler (PMD), sonographers are able to obtain the
spectral waveform as well as knowing the depth of the insonated vessel, the direction of ow relative to the probe and the intensity of the signal.
TCD and TCCS are bedside, non-invasive monitoring tool which provide “real
time” clinical information about changes in cerebral perfusion based on cerebral
hemodynamics derived from the spectral Doppler waveform. The Pulsatility index
Table 21.1 Transcranial
Doppler ultrasonography
parameters [1]
PSV (peak systolic velocity)
EDV (end diastolic velocity)
MFV (mean ow velocity)=1/3 PSV+2/3 EDV
Pulsatility index=(PSV−EDV)/MFV
Resistivity index=(PSV−EDV)/PSV
Lindegaard ratio=(MFV of middle cerebral artery)/MFV
of ipsilateral extracranial internal carotid artery
Courtesy Hakimi etal. [1]
21 Transcranial Doppler Ultrasound Pulsatility Index: Utility andClinical Interpretation
359
(PI) [Gosling’s Index] is the most commonly used measure of the pulsatility of
TCD/TCCS waveforms.
21.2 TCD/TCCS: Interpretation ofPulsatility Index (PI)
Conventional TCD is a “blind” technique wherein the location of the intracranial
vessels is ascertained based on depth, direction, and waveform morphology. In contrast, TCCS offers a non-invasive means of evaluating cerebral blood ow (CBF)
hemodynamics (ow velocities and indices) in the intracranial arterial and venous
vasculature with color and spectral Doppler as well as structural imaging of the
brain [2, 3].
Optimization of CBF and oxygen delivery are the key goals of neurologic management of patients with traumatic brain injury. Historically, this has been monitored by measuring ICP and monitoring cerebral perfusion pressure (CPP). However,
this model is inadequate because some patients have poor neurologic outcomes
despite appropriate management of these two parameters. Among non-invasive
modalities, TCD is the most accurate tool for measuring brain perfusion at the bedside [33].
The brain’s cerebral perfusion is maintained in both systole and diastole, as
shown by the systolic and diastolic component of the TCD waveform. In contrast,
the hand is perfused only in systole, as shown by a radial arterial line waveform.
This difference is caused by the marked difference in resistance, with the brain
being a low-resistance system and the hand being a high-resistance system, as well
as the higher energy requirements of the brain compared with the hand. Therefore,
the adequacy of CBF can be assessed by evaluating the diastolic component of the
TCD waveform and ensuring that its amplitude is approximately half of the peak
systolic amplitude. If it is less, the clinician can:
(a) Increase the patient’s blood pressure using IV uids, vasopressors, or by giving
a blood transfusion
(b) Decrease the PaCO
by increasing the respiratory rate on the ventilator (with
2
intubated patients) or increasing the patient’s sedation
(c) Reducing the patient’s ICP by cerebrospinal uid diversion, increasing seda-
tion, or treating the patient’s fever, among other means (Fig.21.1)
TCD can non-invasively monitor cerebral perfusion by the diastolic component
of the spectral waveform (EDV). Left panel shows high-resistance waveforms with
EDV (CBF) is not static. The cardiac cycle, through systolic blood pressure increase,
causes regular variations in blood ow into the brain that are synchronous with the
heart. The brain is contained in a rigid vault. Therefore, these pulsations in ow and
pressure are transferred into brain tissue, intracranial blood volume, and cerebrospinal uid (CSF) [4].
In the brain, these variations are due to the variation in arterial blood pressure
(ABP) over the cardiac cycle (beat by beat), known as cardiac pulsatility. However,
360
Fig. 21.1 TCD can non-invasively monitor cerebral perfusion by assessing the diastolic component of the spectral waveform (EDV). Left panel shows high resistance waveforms with EDV less
than 50% of the PSV.The patient then had an external ventricular drain placed (right panel) and
the pulsatility indices normalized resulting in an increase in the diastolic component of the waveform such that the EDV is greater than 50% of the PSV. (Courtesy Hakimi etal. [1])
O. M. Pinillos et al.
there are other pulsatile variations, such as respiratory and vasomotor induced oscillations, which affect pressure and ow over time but have less of an effect than
cardiac cycle-induced variations.
Variations in cardiac output (through preload, contractility, and afterload) have
two distinct effects on intracranial hemodynamics (brain pulsatility):
1. Variations in brain arterial blood pressure
[Pressure pulsation]
2. Variations in brain blood ow.
[Flow Pulsation]
When we approach the interpretation and measurement of brain pulsatility via
PI, we should consider: (Figs.21.2, 21.3, and 21.4) [4].
1. The intracranial pressure (ICP) monitoring is used to measure pressure pulsatil-
ity and requires placement of a pressure sensor within the brain. Pressure-based
measure of brain pulsatility.
[Measure of Pressure Pulsatility]
2. TCD/TCCS measures the velocity of CBF and displays it as a spectral wave-
form, where the net ow can be determined by the area under the curve.
[Measure of Flow Pulsatility]
It is important to consider that PI obtained with TCD/TCCS is derived from
blood ow velocity pulsatility (arterial/venous ow), which correlates with the
pressure pulsatility (ICP) obtained with invasive intracranial pressure monitoring,
but is not necessarily a linear correlation.
Envelope
Spectra
elocity)
C.N.Rodriguez 2019
P1
a
b
a
C.N.Rodriguez 2019
b
21 Transcranial Doppler Ultrasound Pulsatility Index: Utility andClinical Interpretation
PSV (Peak systolic velocity)
EDV
(End-distolic v
MFV
(Mean flow velocity)
361
Fig. 21.2 ICP and TCD/TCCS normal waveforms: TCD/TCCS spectral Doppler waveform with
its pulsatile component (PSV, EDV, and MFV) to calculate the transcranial Pulsatility Index (PI)
which represents the ow pulsatility. (Blue line): Envelope wave
Normal Compliance
Pattern
P2
P3
P1
Low Resistance
Pattern
PSV
EDV
Fig. 21.3 Relationship between ICP waveform and spectral Doppler waveform. (a) Pressure pulsatility: ICP waveform obtained via invasive monitoring with normal compliance pattern (P1>P2).
(b) Flow pulsatility: spectral Doppler waveform with a low resistance pattern (High EDV and low
PSV). When these two sets of waveforms are obtained, one would expect a low or normal PI (pulsatility index)
P2
P1
Low
Compliance
Pattern
P1
High Resistance
Pattern
PSV
MFV
EDV
Fig. 21.4 Relationship between ICP waveform and Spectral Doppler waveform. (a) Pressure pulsatility: ICP waveform from invasive monitoring with low compliance pattern (P2>P1). (b) Flow
pulsatility: Spectral Doppler waveform with a high resistance pattern (low EDV, low MFV and
high PSV). When these two sets of waveforms are obtained, one would expect a high PI (pulsatility index)
362
()
VP
TCD/TCCS are valuable tools when integrated with other clinical information in
the proper clinical context (Figs.21.3 and 21.4).
O. M. Pinillos et al.
21.2.1 Brain Compliance
Compliance is the relationship between intracranial volumes and pressure. It is the
property of the brain to maintain a stable ICP, despite variations in intracranial volumes (Eq. (21.1))
• Δ V: Variations in volume
• Δ P: Variations in pressure
This compliance is comprised of four main components:
1. Brain tissue compliance
2. Arterial compliance
3. Venous compliance
4. CSF compliance
Intracranial compliance is assumed to decrease primarily with increased
ICP. Decreased compliance with elevated ICP (initially, before compliance is
exhausted and brain impedance overcomes pulsatile blood ow) leads to increased
pressure pulsatility.
Transfer of pulsations through either the venous system or CSF is another way in
which intracranial pulsatility can also be affected manifesting as a change in either
pressure (brain compression) or ow pulsatility (hypoperfusion). Such is the case
with venous congestion from sino-venoocclusive disease, extracranial cervical
venous stenosis or thrombosis, elevated right atrial pressure, or blockage of CSF
outow pathways (obstructive hydrocephalus) [5].
Pressure pulsatility serves as a sensitive indicator of intracranial compliance. The
increase in intracranial pulsatility in obstructive hydrocephalus is most commonly
due to raised ICP from ventriculomegaly leading to brain compression (increase
brain impedance). However, intracranial compliance also depends on changes in
pulse pressure, which depends on changes in cerebral blood volume (CBV) which
in turn depends on the presence or absence of preserved cerebral autoregulation.
We can consider two clinical scenarios:
Ccompliance
=∆ ∆
/
(21.1)
1. A high compliance system:
A large increase in volume will only result in small increase in pressure.
2. A low compliance system:
A small increase in volume can lead to a signicant pressure rise.
Artery Pulsatility index (PI)
)0
21 Transcranial Doppler Ultrasound Pulsatility Index: Utility andClinical Interpretation
363
21.2.2 TCD/TCCS: Cerebral Hemodynamics
TCD/TCCS provides two clinically important measures:
1. Mean blood ow velocity (MFV): a measure of the integrity of cerebral perfusion
2. Pulsatility index (PI): an estimate of cerebrovascular resistance and intracranial
compliance [6]
Prevention and treatment of secondary injury are the goals of bedside multimodal monitoring. TCD/TCCS measures systolic, mean, and diastolic CBF velocities and calculates the pulsatility index (PI) from basal intracranial arteries (circle of
Willis) allowing for the interpretation of the cerebral hemodynamic behavior in real
time. However, the clinical interpretation of the waveform morphology with careful
attention to the changes in PSV and EDV is most important as it allows for precision
medicine (Fig.21.4).
Pulsatility index describes quantitative and qualitative changes in the morphology of the TCD/TCCS waveform resulting from cerebral perfusion pressure and
cerebrovascular impedance changes [9, 10].
The normal value of pulsatility index, in the most of the arterial territories, is
<1.2.(0.6–1.2). However, in the Ophthalmic artery, the PI is higher as it is an “externalized” intracranial vessel demonstrating a high-resistance spectral pattern [8, 11]
(Table21.2).
Some features to remember when interpreting PI:
(a) Consider that the PI is not affected by the angle of insonation [16].
(b) Consider that PI should be interpreted by taking into account variations by sex,
age, and ethnicity [15, 17, 18].
(c) PI is dependent on both pulsatility and mean ow velocity (cerebral perfusion).
Therefore, an increase in PI may not be strictly related to an increase in pulsatility (decrease intracranial compliance). Rather, it may be related to a decrease in
MFV (decreased CBF) [4].
Table 21.2 TCD/TCCS PI values [12–15]
Anterior cerebral artery (ACA) 0.71–1.04
Middle cerebral artery (MCA
Posterior cerebral artery (PCA) 0.70–1.02
Basilar artery (BA) 0.60–1.03
Vertebral artery (VA) 0.60–1.07
Ophthalmic artery (OA) >1.2
.76–1.08
364
Determinants of CBF
C.N.Rodriguez 2019
O. M. Pinillos et al.
21.3 Pulsatility Index (PI): Cerebrovascular
Resistance (CVR)
The regulation of CBF depends on the interplay between three interconnected components: [19] (Fig.21.5).
1. Arterial Blood Pressure (ABP)
Systemic blood pressure supplied and the presence or absence cerebral
autoregulation
2. Intracranial Pressure (ICP)
Volume of brain tissue, cerebral blood volume, and cerebral spinal uid volume
3. Cerebrovascular Resistance (CVR)
Diameter of arteriole and/or capillary vessels
In acute neurologic injury, the PI has been shown to be directly related to the
distal CVR.Thus, greater PI usually means higher CVR.However, this positive correlation is not seen in two clinical scenarios; namely hypercapnia which causes a
decrease in both CVR and PI, and during reductions in CPP with intact cerebral
autoregulation (such as systemic hemorrhagic shock) which results in a decrease in
CVR, but an increase in PI (Figs.21.6 and 21.7) [20–22].
21.4 Pulsatility Index (PI): Intracranial Pressure (ICP)
Elevated ICP is the nal common pathway of any space-occupying lesion. ICP
essentially consists of three components, driven by different patho-physiological
mechanisms [23]:
1. Inow and volume of arterial blood/venous blood outow
[Blood volume]
2. CSF circulation
[CSF volume]
ABP CVR ICP
Artery
Fig. 21.5 Determinants of CBF: (ABP) arterial blood pressure (arteries); (CVR) cerebrovascular
resistance (arterioles, capillaries, bridging veins), and (ICP) intracranial pressure
Arteriole CapillaryBridging
vein
Sagittal sinus
21 Transcranial Doppler Ultrasound Pulsatility Index: Utility andClinical Interpretation
365
Hypercapnia
[ ↑ PaCO
Vasodilation
CBF
↑
CVR
↓
PI
↓
ba
]
2
C.N.Rodriguez 2019 C.N.Rodriguez 2019
CPP
↓
Preserved
CAR
Vasodilation
CBF
↑
CVR
↓
CPP
↑
PI
↑
Fig. 21.6 (a) Effect of hypercapnia: vasodilation on CBF, CVR and PI. (b) Effect of decrease CPP
on CBF, CVR, CPP and PI
Heart (Pump) Considerations
Contractility Starling’s Law
Pre-load Ventricular filling
Post-load Ventricular emptying ←→Ventricular filling
Heart Rate
Cardiac Rhythm
ABP (Content) Considerations
Heart Contractility Effects CO
Preload Effects SV → Effects CO
Afterload Ventricular emptying
Heart rate
Cardiac Rhythm
Effects SV → Effects CO
Effects SV → Effects CO
Effects SV → Effects CO
Effect diastolic phase of the cardiac cycle
Ventricular filling
Effects SV → Affects CO
↑SVR effects SV → Effects CO
↓SVR (inflammation) → Vasoplegia → Low ABP
Effects diastolic phase of the cardiac cycle
Ventricular Filling
Affects SV → Effects CO
Cardiac
Pulsatility
CPP
PI
Brain
Pulsatility
PI
Fig. 21.7 Transcranial Pulsatility Index: Inuenced by Cardiovascular factors. ABP arterial blood
pressure, SV stroke volume, SVR systemic vascular resistance, CO cardiac output, PI pulsatility
index, ↓ low/decrease, ↑ high/increase
3. Brain parenchyma
[Parenchymal volume]
An increase in one component must cause a proportional decrease in the others
(Monro-Kellie Doctrine).
When there is an ICP increase, the following changes occur in this order:
1. CSF moves from the intracranial compartment to the spinal canal
2. An increase venous outow from the cerebral veins
3. Decrease in cerebral arterial inow (in extreme cases)
One should consider:
1. These compensation mechanisms are temporarily effective.
366
CPPMAP ICP= –
O. M. Pinillos et al.
2. ICP is compartmentalized and not evenly distributed throughout the skull.
Therefore, the ICP in the posterior fossa may be quite different than the right
middle cranial fossa.
The Guidelines for the Management of Severe Trauma Brain Injury (TBI) [24]
recommend ICP monitoring:
1. All salvageable patients with a severe TBI (GCS 3-8 after resuscitation) and an
abnormal head computed tomography (CT) scan. A brain CT-scan is deemed
abnormal when there is a presence of:
1.1 Hematomas
1.2 Contusions
1.3 Swelling
1.4 Herniation
1.5 Compressed basal cisterns
2. In patients with severe TBI with a normal head CT, ICP monitoring is warranted
if two or more of the following features are noted on admission:
2.1 Age over 40years
2.2 Unilateral or bilateral motor posturing
2.3 Systolic blood pressure (BP) <90mm Hg
3. Other clinical situations supporting the need for ICP monitoring are often based
on local practice. The indications for an ICP monitor remain debated in several
circumstances [25].
3.1 Intracranial hemorrhage
3.2 Coma
3.3 Cerebral edema
3.4 Hydrocephalus
3.5 Hepatic encephalopathy
3.6 Acute ischemic stroke
Elevated ICP is an important cause of secondary brain injury, and its severity and
duration have been correlated with poor outcomes. Intracranial hypertension (a surrogate for poor intracranial compliance) is the most common and harmful complication in the progression of acute neurological injury [26–28]. Therefore, it is
important to monitor ICP and to assess the effect of various medical and surgical
therapies.
Brain oxygen delivery and CPP optimization has assumed a central role in the
real-time treatments of neurocritical care patients (Eq. (21.2)).
(21.2)
• CPP: Cerebral perfusion pressure
• MAP: Mean arterial pressure
• ICP: Intracranial pressure