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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5783_Библиотеки_им_академика_М_И_Перельмана.pdf
X
- •Foreword
- •Acknowledgments
- •Contents
- •Contributors
- •1.2 How Is Critical Care Humanized?
- •References
- •2.1 Introduction
- •1.2.2 Communication
- •1.2.5 Post-ICU Syndrome
- •1.2.6 Humanized Infrastructure
- •1.2.7 End-of-Life Care
- •2.2 Which Patients Should Undergo ICP Monitoring?
- •2.5.2.3 CSF Drainage
- •2.5.2.4 Osmotherapy
- •2.5.2.5 Ventilation
- •2.5.2.6 CPP Augmentation
- •2.5.2.7 Metabolic Suppression
- •2.5.2.8 Pharmacologic Suppression
- •2.5.2.9 Temperature Modulation
- •2.5.2.10 Decompressive Craniectomy
- •2.7.1.1 Pressure Reactivity Index (PRx)
- •2.7.1.2 Multimodality Monitoring
- •2.8 Conclusion
- •Algorithm
- •References
- •3.1 Introduction
- •3.2 Intracerebral Hemorrhage (ICH)
- •3.3 ICH: Presenting Symptoms
- •3.5.1 Blood Hypertension
- •3.5.2 Other Risk Factors
- •3.6 ICH: Pathophysiology
- •3.7 ICH: Initial Management
- •3.7.1 Airway: Intubation
- •3.7.3 ICH: Imaging
- •3.7.4 ICH: Grading Scales
- •3.7.5 Fluid Management
- •3.7.6 Follow-Up Imaging
- •3.7.7 Blood Pressure Management
- •3.7.9 ICP Monitoring
- •3.7.10 Surgical Considerations
- •3.7.13 ICH: Venous Thromboembolism Prophylaxis
- •3.7.14 ICH: Seizure Management
- •3.8 ICH: Medical Complications
- •3.8.1 Glycemic Management
- •3.8.3 Disposition
- •3.9 Conclusion
- •Algorithm
- •Appendix: Direct Oral Anticoagulant Reversal
- •Reversal Strategies
- •References
- •4.1 Introduction
- •4.2.1 Hemodynamic Management
- •4.2.2 Hormonal Replacement Therapy
- •4.2.3 Respiratory Management
- •4.3 Cardiopulmonary Resuscitation (CPR)
- •4.4 Conclusion
- •Algorithm
- •References
- •5.1 Introduction
- •5.2.1 Vasoactive Agents
- •5.2.1.1 Vasodilators (Table 5.1)
- •Calcium Channel Blockers
- •Nimodipine
- •Nicardipine
- •Other Vasodilators
- •Magnesium
- •3-Hydroxy-3-Methyl-Glutaryl-CoA (HMG-CoA) Reductase Inhibitors (Statins)
- •Nitroprusside
- •Endothelin-1 Antagonists
- •Hydralazine
- •Phosphodiesterase Inhibitors
- •Papaverine
- •Norepinephrine
- •Epinephrine
- •Dopamine (DA)
- •Phenylephrine
- •Vasopressin
- •Neuromonitoring
- •5.2.2.1 Benzodiazepines
- •5.2.2.2 Barbiturates
- •5.2.2.3 Opioids
- •5.2.2.4 Anticonvulsant Medications
- •5.2.2.5 Other Sedatives/Anesthetics
- •5.2.3 Hemodynamic Agents
- •5.4 Conclusion
- •Algorithm
- •References
- •6.1 Introduction
- •6.2.3 Ultrasound Behaviour at Acoustic Boundaries
- •6.3 Pulse-Echo Principles (B-Mode Techniques)
- •6.4 Transducers
- •6.5 Artefacts
- •6.6 Doppler Principles
- •6.6.1 Pulsed Wave Doppler
- •6.6.2 Duplex Scanning
- •6.6.3 Colour Flow Imaging (CFI)
- •6.7.2 Flow Changes
- •6.7.3 Cerebrovascular Resistance
- •6.8 Transcranial Colour-Coded Duplex Sonography (TCCS)
- •6.9 Ultrasound Safety
- •6.10 Conclusion
- •References
- •7.1 Introduction
- •Mesencephalic Plane
- •7.2.1.2 Diencephalic Plane (Thalamic Plane)
- •6.6.4 Power Doppler Imaging (PDI)
- •6.7 Transcranial Doppler Ultrasound (TCD)
- •6.7.1 Velocity Measurement
- •7.2.1.3 Ventricular Plane (Cella Media)
- •7.2.1.4 Upper Pons Plane
- •7.2.1.5 Lower Pons Plane
- •7.2.2 Transforaminal Window
- •7.3.1.2 Anterior Circulation
- •Carotid System
- •Anterior Cerebral Artery
- •Anterior Communicating Antery
- •7.3.1.3 Posterior Circulation
- •Vertebrobasilar System
- •Posterior Communicating Artery
- •Posterior Cerebral Arteries
- •7.5 Cerebral Circulation: Anatomical Variations
- •7.5.1.1 Anterior Circulation
- •Most Common Variations [28]
- •7.5.1.2 Posterior Circulation
- •Most Common Variants [28]
- •7.6.1.1 Deep Middle Cerebral Vein (DMCV)
- •7.6.1.2 Basal Vein (of Rosenthal)
- •7.6.1.3 Great Cerebral Vein (of Galen)
- •7.6.2.1 Sphenoparietal Sinus
- •7.6.2.2 Superior Petrosal Sinus
- •7.6.2.3 Inferior Petrosal Sinus
- •7.6.2.4 Cavernous Sinus
- •7.6.2.5 Transverse Sinus
- •7.6.2.6 Straight Sinus
- •7.7 Conclusion
- •Algorithm
- •References
- •8.1 Introduction
- •8.2 Cerebral Blood Flow Measures
- •8.3 Transcranial Doppler (TCD/TCCS)
- •8.4.1 Cerebral Autoregulation (CA)
- •8.4.2 CO2 Vasoreactivity
- •8.6.2 TCD/TCCS: Use After Traumatic Brain Injury (TBI)
- •8.7 Conclusion
- •References
- •9.1 Introduction
- •9.3 TCD Hemodynamic Parameters: Variations by Sex
- •9.4 TCD Hemodynamic Parameters: Variations by Age
- •9.5 TCD Hemodynamic Parameters: Variations by Laterally
- •9.7 TCD Normal Values: Latin American Population Sample
- •9.8 TCD Hemodynamic Parameters: Altitude
- •9.10 Conclusion
- •References
- •10.1 Introduction
- •10.2 TCD/TCCS: Acoustic Windows
- •10.2.1.1 Technique
- •10.2.2.1 Technique
- •10.2.3.1 Technique
- •10.2.4.1 Technique
- •10.2.5.1 Technique
- •10.4.1 Decompressive Craniectomy
- •10.4.2 Patient’s Position
- •10.5 TCD/TCCS: Contrast-Enhanced
- •10.6 Conclusion
- •Algorithm
- •References
- •11.1 Introduction
- •11.2 Basic Methods
- •11.2.1 Flow Velocities
- •11.2.2 Pulsatility Index (PI)
- •11.3 Advanced Methods
- •11.3.2 TAU (Cerebrovascular Time Constant)
- •11.3.4 Autoregulation
- •11.4.1 Traumatic Brain Injury
- •11.4.2 Aneurysmal Subarachnoid Hemorrhage
- •11.4.3 Stroke
- •11.4.4 Other Clinical Scenarios
- •11.5 Conclusion
- •Algorithm
- •References
- •12.1 Introduction
- •12.2 TCD: Spectral Wave
- •12.4 TCD: Clinical Utility
- •12.6 TCD: Technique
- •12.6.2 Transtemporal Acoustic Window
- •12.6.2.1 Anterior Circulation
- •Middle Cerebral Artery (MCA)
- •12.6.2.2 Posterior Circulation
- •Posterior Cerebral Artery (PCA)
- •12.6.3 Submandibular Acoustic Window
- •12.6.3.1 Internal Carotid Artery (ICA—Extracranial Portion)
- •12.6.4 Transoccipital Acoustic Window
- •12.6.4.1 Posterior Circulation
- •12.6.5 Transorbital Acoustic Window
- •12.6.6.2 Pulsatility Index
- •12.7.1 High-Velocity Pattern
- •12.7.2 Low-Velocity Pattern
- •12.7.3 High Resistance Pattern
- •12.7.4 Cerebral Circulatory Arrest Pattern
- •12.8 TCD: Other Clinical Uses
- •12.8.1.1 Cerebral Vascular Reactivity
- •12.9 TCD: Limitations
- •12.10 Conclusion
- •Algorithm
- •References
- •13.1 Introduction
- •13.2 Acoustic Windows
- •13.3 2D-Guided TCD Monitoring
- •13.6 Conclusion
- •Algorithm
- •References
- •14.1 Introduction
- •14.2 TCCS: Anatomical Aspects
- •14.3.1 Anterior Circulation
- •14.3.1.1 Carotid System
- •14.3.2 Posterior Circulation
- •14.3.2.1 Vertebro-Basilar System
- •14.5 TCCS: Examiner Considerations
- •14.6 TCCS: Acoustic Windows
- •14.7 TCCS: Examination Protocol
- •14.7.1.1 Considerations
- •Doppler: (Convention)
- •14.7.2 Transtemporal Acoustic Window Examination (Coronal Planes)
- •14.7.3 Transoccipital (Transnuchal/Transforaminal) Acoustic Window Examination
- •14.7.4 Submandibular Acoustic Window Examination
- •14.7.5 Transorbital Acoustic Window Examination
- •14.7.6 Frontal Bone Window Examination
- •14.8 TCCS Protocol: Clinical Applications
- •14.9 TCCS Protocol: Hemodynamic Parameters
- •14.10 TCCS Protocol: Limitations
- •14.10.1 Limitations
- •14.10.1.1 Acoustic Windows
- •Transtemporal Acoustic Window
- •Suboccipital Acoustic Window
- •14.10.1.2 Middle-Line Shift Measurement
- •14.11 Conclusion
- •Algorithm
- •References
- •15.1 Introduction
- •15.2 Clinical Applications
- •15.2.1 Intracranial Stenosis
- •15.2.2 Cerebral Vasospasm
- •15.2.3 Cerebral Veins
- •15.3 Conclusion
- •References
- •16.1 Introduction
- •16.3.1 Autoregulation Index (ARI)
- •16.3.2 Mean Flow Velocity Index (Mx)
- •16.5 Conclusion
- •References
- •17.1 Introduction
- •17.2.1 Cerebrovascular Resistance (CVR)
- •17.2.2 Cerebral Autoregulation
- •17.2.4 Carbon Dioxide Reactivity
- •17.3.2 Collateral Flow
- •17.3.3 Elastic Reservoir (“Windkessel Effect”)
- •17.4 TCD: Waveform Interpretation
- •17.4.1 TCD Waveforms
- •17.5.1 Aneurysmal Subarachnoid Hemorrhage
- •17.5.2 Increased ICP
- •17.6 Conclusion
- •References
- •18.1 Introduction
- •18.3.1 Subarachnoid Hemorrhage (SAH)
- •18.3.1.1 Cerebral Autoregulation (CA)
- •18.3.1.2 Intraparenchymal Cerebral Oxygen Monitoring
- •18.3.1.3 Cerebral Blood Flow
- •18.3.1.4 Electrophysiology
- •Seizure Detection
- •18.3.1.5 Cerebral Metabolism
- •18.3.2 Intracerebral Hemorrhage (ICH)
- •18.3.2.1 Intraparenchymal Cerebral Oxygen Monitoring
- •18.3.2.3 Electrophysiology
- •18.3.3 Traumatic Brain Injury (TBI)
- •18.3.3.2 Cerebral Autoregulation
- •18.3.3.3 Intraparenchymal Cerebral Oxygen Monitoring
- •18.3.3.4 Cerebral Blood Flow
- •18.3.3.5 Electrophysiology
- •18.3.3.6 Cerebral Metabolism
- •18.3.4 Acute Ischemic Stroke (AIS)
- •18.3.4.1 Cerebral Blood Flow
- •18.3.4.2 Electrophysiology
- •18.3.5.1 Cerebral Blood Flow
- •18.4 Conclusion
- •References
- •19.1 Introduction
- •19.2 Cerebral Blood Haemodynamic Measurements
- •19.3 Cerebral Blood Flow (CBF): Physiology Principles
- •19.4 Vasoreactivity Determining: Methods
- •19.6 Technical Tips
- •19.7 Vasoreactivity: Clinical Importance
- •19.8 Conclusion
- •References
- •20.1 Introduction
- •20.5.4.1 Experimental Endotoxemia
- •20.6 Conclusion
- •Appendix
- •Methods
- •Group 1: Graphic Methods
- •“Beat-by-Beat Method”
- •Method Described by Aaslid
- •Group 2: Multiparameter or Impedance Methods [14]
- •References
- •21.1 Introduction
- •21.2.1 Brain Compliance
- •21.2.2 TCD/TCCS: Cerebral Hemodynamics
- •21.4 Pulsatility Index (PI): Intracranial Pressure (ICP)
- •21.5.1 Cardiovascular Factors
- •21.5.2 Cerebrovascular Factors
- •21.5.3 Cardiopulmonary Factors
- •21.5.4 Metabolism Factors
- •21.5.5 Vascular Factors
- •21.5.6 Other Factors
- •21.6 Conclusion
- •Algorithm
- •References
- •22.1 Introduction
- •22.2 Aneurysmal Subarachnoid Hemorrhage (aSAH)
- •22.3 Cerebral Vasospasm After aSAH
- •22.5.1 TCD/TCCS: Examination Protocol
- •22.5.1.1 Transtemporal Window
- •22.5.1.2 Orbital Window
- •22.5.1.3 Suboccipital/Transforaminal Window
- •22.5.1.4 Submandibular Window
- •22.7 Conclusion
- •Algorithm
- •References
- •23.1 Introduction
- •23.3.1 Premise
- •23.3.3 Limitations
- •23.4.1 Technical Requirements
- •23.4.3 Limitations
- •23.6 Future Directions
- •23.7 Conclusion
- •Algorithm
- •References
- •24.1 Introduction
- •24.2.1 Vasospasm
- •24.2.2 Vasospasm Diagnostic Criteria
- •24.3 TCD/TCCS: Cerebral Vasoreactivity
- •24.4 TCD/TCCS: Intraoperative Monitoring
- •24.7 Conclusion
- •References
- •25.1 Introduction
- •25.4 CAD: Diagnosis
- •25.6 Pupil: Ultrasound Examination
- •25.11 Conclusion
- •Algorithm
- •References
- •26.1 Introduction
- •26.2 Optimal Settings
- •26.2.1 Probe Types
- •26.2.2 Frequencies
- •26.2.3 Focus
- •26.2.4 Depth
- •26.2.5 Pulse Repetition Frequency (PRF)
- •26.2.6 Frame Rate
- •26.2.8 Freeze
- •26.2.9 Cine Loop
- •26.2.10 Smoothing (Interpolation), Interlacing, Correlation
- •26.2.11 Postprocessing
- •26.2.12 Resolution
- •26.2.13 Doppler-Technique
- •26.2.14 PW-Doppler (Pulsed-Wave Doppler)
- •26.2.15 Color Duplex
- •26.3 Indications
- •26.4.1.2 Morphological Differences
- •26.4.1.3 Flow Differences
- •26.4.1.4 Compression
- •26.5 B-Mode Examination
- •26.5.1 Dilation
- •26.5.2 Intima-Media Thickness (IMT)
- •26.5.3 Plaque Analysis
- •26.5.3.1 Location
- •26.5.3.3 Maximal Thickness
- •26.5.3.4 Surface
- •26.5.3.5 Echogenicity
- •26.5.4 B-Flow Imaging
- •26.6.1 Color Doppler Imaging (CDI)
- •26.6.2 Power Doppler Imaging (PDI)
- •26.7.1 Stenosis Measurement
- •26.7.1.1 Diameter Stenosis
- •26.7.1.2 Area Stenosis
- •26.7.1.3 Residual Luminal Diameter
- •26.7.2 Occlusion
- •26.7.3 Subtotal Stenosis: (>95% Stenosis)
- •26.7.4 Long Segment Stenosis
- •26.8 Doppler Spectrum
- •26.10 Contrast Enhanced Ultrasound (CEU)
- •26.11.1 Common Carotid Artery
- •26.11.2 Internal Carotid Artery
- •26.11.2.1 Stenosis
- •26.11.2.2 Dissection
- •26.11.2.3 Occlusion
- •26.11.2.4 Subtotal Occlusion: (95–99% Stenosis)
- •26.11.2.5 Multiple (Tandem) Stenosis
- •26.11.2.6 Long Segment Stenosis
- •26.11.3 External Carotid Artery (ECA)
- •26.11.3.1 Occlusion
- •26.13 Negative Report
- •26.14 Conclusion
- •Algorithm
- •References
- •27.1 Introduction
- •27.2 Anatomy: Vertebrobasilar System
- •27.3 Vertebrobasilar Circulation: Ultrasound Examination
- •27.4 TCD: Aneurysmal Subarachnoid Hemorrhage
- •27.4.1 Delayed Cerebral Ischemia
- •27.4.2 Vasospasm
- •27.5 TCD: Vertebrobasilar Dissection
- •27.6 TCD: Intracranial Stenosis
- •27.7 TCD: Microembolus Detection
- •27.9 Subclavian Steal Syndrome
- •27.10 TCD: Multimodal Monitoring
- •27.11 TCD: Traumatic Brain Injury
- •27.12 TCD: Brain Death Determination
- •27.13 Conclusion
- •References
- •28.1 Introduction
- •28.2 Cerebral Venous System: Anatomy
- •28.3 vTCCS: Ultrasound Investigation Technique
- •28.4 CVST: Venous Ultrasound Findings

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The interaction between the prole of the waveform and the total parallel resistance of stenotic and/or collateral vessel is rather intricate [34, 45]. The waveform
changes when the pulsatile wave travels through an arterial narrowing with signicant ow resistance. This reduces the sensitivity of the pulsatility index (PI)
(Eq.17.5). Its sensitivity is again augmented when PI is normalized by dividing the
observed PI by a reference PI (PI
culated as PI/PI
.
ref
). The pulsatility transmission index can be cal-
ref
PI PSV EDVMFV=
(17.5)
17.4 TCD: Waveform Interpretation
The feasibility of using TCD technology to measure CBFV in the basal arteries of
the brain’s anterior circulation was rst demonstrated in the early 1980s in 50
healthy subjects [41, 47]. It was then proposed that TCD could be used to monitor
vasospasm in aSAH and cerebrovascular disease, when using a Doppler operating
at a lower range (1–2 MHz). Instruments operating at higher ranges (typically
5–10MHz) were used to evaluate extracranial vessels, and they do not penetrate the
skull. Before this, ultrasound technology had been used to examine CBF, but only
intraoperatively during craniotomies.
TCD technology has been used in the clinical evaluation of cerebral autoregulatory reserve, and different indices have been proposed to study cerebral hemodynamics. The indices include those that are “static,” which require articially
increasing or decreasing blood pressure using intravenous vasopressors or vasodilators in steady-state conditions (static cerebral autoregulation), and those that are
“dynamic,” which measure the cerebrovascular hemodynamic response to interventions such as changes in arterial CO
transient carotid occlusion (e.g., autoregulatory index, transient hyperemic response
ratio). The third category has been created to describe more advanced methods,
wherein CBFV calculated from TCD is used to derive a third variable (e.g., noninvasive ICP, critical closing pressure).
Current practices in the neurocritical care unit do not routinely include maneuvers to challenge the injured brain to measure its autoregulatory response, mainly
because that type of testing may require the patient to be cooperative (e.g., squatting) or because the safety remains debatable (e.g., carotid compression). It has
been proposed that cerebral autoregulation be estimated by measuring it from
spontaneous variations of MAP [48]. Transform function analysis is a mathematical representation in frequency domain of a system between input and output data
and has emerged as a technology suiting this purpose. The effect of oscillations in
/pH, rapid pneumatic thigh cuff deation, or
2

17 Neuro-ICU: Cerebral Hemodynamics and Transcranial Doppler (TCD/TCCS…
307
MAP over CBFV can be studied by recording a series of times as input and output
of the system. This has been done in a range of frequencies, and it is attained by
employing a Fast Fourier Transformation (FFT) [49]. Typically, oscillation frequencies are separated into three bands: low (<0.07 Hz), intermediate
(0.07–0.3Hz), and high (>0.3Hz), although the limits vary among authors [47].
The behavior of the system interprets cerebral autoregulation as a high-pass lter
based on three parameters: coherence, gain, and phase shift [48]. At high frequencies, (1) the oscillations of CBFV follow those of ABP, so coherence (which is
simply a correlation coefcient within dened frequency range) is high; (2) these
parameters oscillate almost synchronously, so the phase lag between them is near
zero degrees (low phase shift); and (3) the ABP oscillations are transmitted
undampened to the output (CBFV), so gain (amplitude) is usually >1. The opposite occurs toward the low-frequency band, with low coherence and gain and
higher phase shift values. That is the way cerebral autoregulation is believed to
exert its effect in the lower band of frequencies. This type of response is expected
from a physiologic point of view, as vascular tone takes a few seconds to adjust to
changes in ABP.To apply transform function analysis, researchers have proposed
using CBFV and ABP time series monitoring for at least 10minutes. Module of
coherence varies between 0 and 1, from good to impaired cerebral autoregulation.
Phase shift varies between 0 and 90 degrees, from nonexistent to effective cerebral autoregulation. Lower gain means adequate cerebral autoregulation and
higher gain means poor cerebral autoregulation.
Currently available software uses proprietary algorithms to obtain different indices. Such numbers can be altered from physiologic changes (e.g., vessel caliber) but
also by FFT size (number of points used), FFT length (time), FFT transformation
overlap (%), transmitted ultrasound frequency (MHz), high-pass lter settings (Hz),
and recording time (minutes). Standard settings have not been universally agreed
upon. Nonetheless, cerebral autoregulation studies with TCD always rely on the
assumption that MCA diameter does not change during the monitoring time.
Another consideration to keep in mind is that CBF is measured in units of ml/
min/100 g, whereas TCD technology provides CBF velocity (CBFV) in units of
cm/s. There is a positive correlation between the absolute increase in CBF obtained
by regional CBF with single-photon emission computed tomography and the
increase in CBF velocity by TCD after acetazolamide administration (modest correlation r=0.63, p<0.01) [50, 51]. These results suggest that TCD combined with
acetazolamide test may be used in clinical situations to assess cerebral
vasoreactivity.
The major advantages of TCD are that it is noninvasive, has remarkable temporal
resolution (~5ms), and is highly reproducible (~5% variability). Some have called
TCD “a stethoscope for the brain.” Disadvantages include the lack of temporal window in up to 10% of patients and the fact that continuous monitoring of TCD is very
sensitive to movement.

308
L. L. P. Mejia et al.
17.4.1 TCD Waveforms
The spectral waveform of blood ow velocity can be used to evaluate resistance to
the ow. High-resistance vascular beds are characterized by a waveform with a
sharp upstroke accompanied by a relatively abrupt waning in velocity immediately
after peak systole with low end-diastolic velocity. Low-resistance waveforms are
characterized by a steadier upstroke, a more gradual decline, and a higher enddiastolic velocity. The cerebral vascular bed is a low-resistance bed. Changes in the
resistance, as detected by spectral waveform analysis, can be secondary to local
stenosis or to the effects of proximal or distal disease within the insonated vascular
bed [52].
The TCD waveform of ow is represented by blood ow velocity over time during the cardiac cycle. The sonographer must recognize a waveform pattern visually
by its appearance on the screen as well as by the sound of the ow signal.
Sonographers must annotate the machine settings, including (1) transducer and
sample volume (gate) positioning, (2) ow direction, (3) angle of insonation, (4)
scale settings, and (5) sweep speed. Then, the different components of the cardiac
cycle are identied, namely, (1) beginning of systole, (2) peak velocity during systole, (3) dicrotic notch (signifying the closure of the aortic valve), (4) end-diastolic
velocity, and (5) shape and magnitude of ow deceleration during the cardiac cycle.
The crucial aspects to waveform presentation are the identication of the following components: (1) early systolic upstroke (slow, sharp, or delayed); (2) late systolic and diastolic deceleration (uninterrupted, stepwise, or smoothed); (3) waveform
shape (at, sharpened, or dampened); (4) systolic—diastolic velocity difference
(ow pulsatility); and (5) other components of the Doppler spectra (embolism,
bruit, narrowing, etc.). Normal waveforms exhibit sharp systolic ow acceleration
and stepwise deceleration with positive end-diastolic ow. Additionally, enddiastolic ow velocity falls between 20% and 50% of the peak systolic velocity
values (low resistance). Finally, at the level of the ICA bifurcation, a bidirectional
signal with simultaneous sharp systolic upstrokes and similar stepwise deceleration
in both ow directions denotes low-resistance ow patterns.
The ow velocity in a blood vessel is roughly parabolic in shape, with the fastest
velocity in the center of the vessel. Consequently, the Doppler spectrum represents
a distribution of velocities that requires mathematical calculations to derive useful
velocity values. Normally, a power spectrum distribution is produced from segments of about 2–5seconds using an FFT, and maximum or mean velocity is calculated from the maximum or intensity-weighted mean, respectively [53] (Fig.17.1).
Modern TCD ultrasonographic instruments that are currently available use
computer- based statistical pattern recognition systems developed for the analysis of
the spectral waveforms. The various indices obtained from such wave analysis are
as follows:
Systolic Acceleration RateSAR
()
Height
=
Rise time

()
Mean time
()
17 Neuro-ICU: Cerebral Hemodynamics and Transcranial Doppler (TCD/TCCS…
Area under spectral
waveform
Height
Systolic
Mean time
Decay timeRise time
Fig. 17.1 An example of the feature extraction from the spectral waveform of the middle cerebral artery
309
Diastolic
Pulsatility Index of Gosling and KingPI
llocity EndDiastolic velocity
Peak systolic ve
Resistivity Index of PourcellotRI
Peak systolic velocity
Systolic Diastolic Ratio SDR
/
Rise Decay Time Ratio RDTR
/
Rise Mean Time Ratio RMTR
/
Blood Volume Rate
The Lindergaard Ratio LR
Peak systolic velocity
−−
−−−EndDiastolic velocity
Peak systolic velocity
=
()
()
()
Area under spectral waveform
=
()
−
EndDi
=
=
Mean time
MCAvelocity
=
ICAvelocity
=
=
aastolic velocity
Rise time
Decay time
Rise time
mean time

310
L. L. P. Mejia et al.
If the gain settings are correct, the envelope outlines the waveform shape after
the peak systolic rise, the ow deceleration, and the proportion of the end-diastolic
ow component. These computer-based pattern recognition approaches have been
developed to analyze TCD signals by detecting the boundary edge (envelope or follower) of spectral waveform using the Sobel edge detection algorithm [54].
Gosling’s pulsatility index (PI) and the Pourcelot resistivity index (RI) give an
estimation of cerebral perfusion pressure, pulsatility of arterial blood pressure,
downstream resistance in cerebral circulation, and compliance of cerebral vessels.
The PI reference range is between 0.5 and 1.19 [55]. In the presence of proximal
stenosis or occlusion, the PI may be <0.5 due to arteriolar vasodilation distally;
conversely, a distal occlusion or constriction increases the PI to >1.19 secondary to
increased resistance distally [56]. A PI >1.17 correlates with the presence of silent
brain damage on magnetic resonance imaging (MRI) (e.g., microvascular disease)
in patients with chronic systemic hypertension [57]. Conversely, despite an elevated
PI in young people free of chronic systemic hypertension (PI=1.2), a high pulsatility waveform in the MCA indicates normal patency of its proximal segment.
PI is regarded by many as an often misleading or imprecise reection of the true
resistance, as it has limitations. Critical closing pressure is the internal pressure at
which the blood vessel collapses and closes completely. Cerebral perfusion pressure
(CCP) is the principal determinant of PI.Consequently, some experts argue that PI
has no distinctive physiologic meaning by itself [58]. Michel and Zernikow [58]
concluded that the use of PI as a measure of resistance in autoregulated circuits
should be abandoned because the autoregulation models that use PI do not uniformly match experimentally induced changes in vascular resistance.
A Pourcelot RI > 0.8 suggests increased distal resistance [59] or abnormally
decreased cerebral perfusion pressure. Elevated RI in different intracranial pathologies that result in increased ICP is comparable to that of an abnormal PI.Nonetheless,
the RI is less sensitive to ICP variations than is PI [60].
The Lindegaard ratio (LR) tends to increase in relation to the degree of vasospasm. Normal reference range is from 1.1 to 2.3 and in the absence of vasospasm
is <3 [61].
In patients with irregular heart rhythm (extrasystole, atrial brillation, etc.), the
end-diastolic velocities may fall below 30% of peak systole. This decrease also
affects estimation of ow resistance (increased values of PI calculated with envelope tracings) from the averaged values of 2–5cycles. A single cycle may be selected
for manual measurements. Prolonged pauses between cardiac cycles may lead to
lower end-diastolic velocities that excessively underestimate the velocity and overestimate the PI.In those cases, a manual measurement of the highest velocity cycle
is recommended instead, a practical but inaccurate solution.
Various efforts to examine the use of TCD ultrasound for the assessment of intracranial arterial ow velocity have been published [29, 30, 34, 62–64]. The common
techniques used are simply to measure the values of the peak systolic, peak diastolic, and mean ow velocity from FFT Doppler spectra at selected depths.
Nonetheless, the standard deviation of normal values is wide. Physiologic variability in parameters such as blood pressure, cardiac output, peripheral resistance, and

17 Neuro-ICU: Cerebral Hemodynamics and Transcranial Doppler (TCD/TCCS…
arterial compliance lead to high intra-individual variation in peak systolic ow in
the MCA (91.0±16.9cm/s), peak diastolic ow (44.3±9.5cm/s), and average
mean velocity (57.7±11.5cm/s) [63] and can result in diagnostic errors. It is difcult with this approach to objectively classify in quantitative terms those spectral
features that are associated with varying degrees of stenosis in the intracranial arteries. The use of a more quantitative and objective approach to analyzing Doppler
spectral waveforms and classifying the varying degree of stenosis in the intracranial
arteries is thus highly desirable.
311
17.5 Transcranial Flow Velocity Monitoring
inNeurocritical Care
In this section, we are limiting our discussion to those conditions in which TCD has
been applied: (1) daily monitoring of CBFV during aSAH-induced vasospasm, (2)
imminent brain death, and (3) MCA blood ow during increased ICP.In the following chapters, each of these applications will be described in detail. In this section,
we focus on the physiology of the waveform interpretation.
17.5.1 Aneurysmal Subarachnoid Hemorrhage
Delayed cerebral ischemia after aSAH is a major cause of morbidity and mortality.
Frequently, the presenting sign is a neurologic decit, which may be detected too
late to reverse. TCD ultrasonography is used to guide clinical decision-making in
regard to additional diagnostic evaluation and therapeutic interventions. When performed in isolation, the contribution of TCD to improving patient outcome has not
been established. Nevertheless, TCD has become a regularly used tool in neurocritical care and perioperative settings. A specic condition called hyperemia will produce a unique pattern of high-velocity–low-resistance waveforms in one or several
arteries, whereas the remainder of the vessels will have normal velocities and PIs.
This phenomenon can be seen in hyperdynamic states after aSAH and must not be
confused with vasospasm [61]. When the CBFV is elevated but the LR is lower than
3, the elevation is considered to be caused by hyperemia. An LR>6 indicates severe
vasospasm [61, 65–67], and LR>3 denotes mild to moderate vasospasm. A modied LR (mLR; basilar artery mean CBFV divided by left or right extracranial vertebral artery mean CBFV) has also been proposed for evaluation of posterior
circulation vasospasm. mLR=2–2.49 indicates possible vasospasm; mLR=2.5–2.99
suggests moderate vasospasm; and mLR >3 signies severe vasospasm. A CBFV
variation of more than 14% with TCD side-to-side is considered abnormal; most
individuals (95%) will not have day-to-day variation of mean CBFV of more than
10cm/s [68, 69].
In patients with severe vasospasm, the use of a large sample volume (gate) may
produce a simultaneous display of waveforms detected at different arterial segments

312
L. L. P. Mejia et al.
a
b
Fig. 17.2 Vasospasm. Panel A. Transcranial Doppler waveform from the left middle cerebral
artery in a patient on day 3 after aneurysmal subarachnoid hemorrhage shows a mean velocity of
90cm/s. Panel B. Transcranial Doppler waveform from the left middle cerebral artery in the same
patient from Panel A on day 11 shows a mean velocity of 240cm/s (diastolic notch is still present)
(i.e., terminal ICA, proximal M1, or adjacent segments with different patency). The
highest velocities in waveform are often considered to be the site of maximum vasospasm (Fig.17.2). However, a mirror artifact and/or hyperemia must be excluded by
using the LR.The signal-to-noise ratio appears to be optimized (i.e., no noise in the
background).
17.5.2 Increased ICP
A ow signal above baseline that shows sharp systolic upstrokes followed by sharp
deceleration represents an increased ow resistance. Elevated PI and RI have been
observed in patients with increased ICP (Fig.17.3). The Doppler signal shows a
sharpened waveform secondary to a fast ow deceleration. Also, a waveform above
baseline that exhibits a signicant diastolic ow likely suggests that some ow is

17 Neuro-ICU: Cerebral Hemodynamics and Transcranial Doppler (TCD/TCCS…
313
a
Fig. 17.3 Increased intracranial pressure. Panel A. Transcranial Doppler waveform from a lowresistance vessel exhibiting continuous forward ow throughout both systole and diastole. Panel
B. Transcranial Doppler waveform from a vessel with high resistance caused by elevated intracranial pressure shows a sharp systolic upstroke, a narrow peak in systole, and less ow in diastole
b
directed to a vascular bed with a lower resistance. This can happen in patients with
TBI because different brain areas may sustain various degrees of disturbed autoregulation or unequal distribution of ICP and mass effect.
No irrefutable, close relationship between ICP and mean MCA ow velocity or the
shape of the ow waveform has been demonstrated. Nevertheless, some general statements can be made regarding the MCA ow signal alterations after ICP elevation. For
instance, in TBI, ow velocity increases immediately after the injury onset and lasts for
several days or even weeks. However, ICP is not markedly elevated during this period.
When ICP increases sharply, a hyperperfusion prole (i.e., high velocities, decrease of
pulsatility) appears initially but rapidly evolves to an increasingly pulsatile, high-resistance ow prole, and nally to a reversed ow of the blood volume. PI is intrinsically
related to ICP.A PI variation of 2.4% is reected by a 1mmHg change in ICP in the
same direction [70]. Indeed, several studies have proposed a strong correlation between
PI and ICP, independent of the type of intracranial pathology [59, 60, 71].
Unfortunately, correlation-based approaches are not able to measure absolute
ICP accurately enough for TCD ultrasonography to be used in clinical treatment
planning. Yet, one study found that the noninvasive ICP measurement technique
based on two-depth TCD ultrasound had a better diagnostic reliability in neurological patients than the optic nerve sheath diameter ultrasonography when expressed
by the sensitivity and specicity for detecting elevated ICP >14.7mmHg. Another
study showed that changes of ICP in time domain during plateau waves are replicated by noninvasive ICP methods with strong correlations. In addition, the methods offered high performance for detecting intracranial hypertension [72].
17.5.3 Impending Brain Death: Progression toBrain Death
An oscillating or reverberating ow spectrum represents two waveforms (above and
below the baseline) with an extremely high resistance to ow. Flow signals above
baseline appear as sharp spikes, and a rushed ow deceleration to zero corresponds

314
b
a
L. L. P. Mejia et al.
with the time of the aortic valve closure and absence of positive end-diastolic ow.
The same blood volume bounces back its direction during the entire diastole, generating the sign of ow reverberation or oscillation. An exceptionally high resistance to ow impedes brain perfusion. This waveform typically is observed in
patients who have developed substantial cerebral edema with progression to cerebral circulatory arrest. When reverberating ow is found in all intracranial basal
arteries, it accurately predicts the absence of brain perfusion in nuclear CBF studies.
Hemodynamically, this waveform indicates that all blood that registered through the
sample volume toward the brain in systole was pushed out of the distal vasculature
in diastole as a result of no ow traveling to brain parenchyma (Fig.17.4).
Fig. 17.4 Impending brain death. Panel A. Transcranial Doppler waveform of oscillating ow. A
sharp forward ow is present in systole with reversal of ow in diastole. Panel B. Transcranial
Doppler waveform of a systolic spike. There is brief forward ow during systole and no ow during diastole. Both waveforms are consistent with brain death

17 Neuro-ICU: Cerebral Hemodynamics and Transcranial Doppler (TCD/TCCS…
315
17.6 Conclusion
TCD is an imperfect technique. As such, several technical and interpretative aspects
must be considered to obtain a dependable TCD exam. Nevertheless, TCD ultrasound is capable of following dynamic cerebrovascular processes noninvasively.
Daily or continuous monitoring of ow velocities and proles can help clinicians to
recognize trends or pattern changes that alert them to deterioration and the need for
a therapeutic response in the care of neurocritically ill patients.
References
1. Alpers BJ, Berry RG, Paddison RM.Anatomical studies of the circle of Willis in normal brain.
AMA Arch Neurol Psychiatry. 1959;81(4):409–18.
2. Lehrer HZ.Relative calibre of the cervical internal carotid artery. Normal variation with the
circle of Willis. Brain. 1968;91(2):339–48.
3. Sorteberg W, Lindegaard KF, Rootwelt K, Dahl A, Russell D, Nyberg-Hansen R, et al.
Blood velocity and regional blood ow in dened cerebral artery systems. Acta Neurochir.
1989;97(1–2):47–52.
4. Knowlton FP, Starling EH.The inuence of variations in temperature and blood-pressure on
the performance of the isolated mammalian heart. J Physiol. 1912;44(3):206–19.
5. Grifths DJ. Steady uid ow through veins and collapsible tubes. Med Biol Eng.
1971;9(6):597–602.
6. Skalak R, Keller SR, Secomb TW. Mechanics of blood ow. J Biomech Eng.
1981;103(2):102–15.
7. Brower RW, Noordergraaf A.Pressure-ow characteristics of collapsible tubes: a reconcilia-
tion of seemingly contradictory results. Ann Biomed Eng. 1973;1(3):333–55.
8. Stromberg DD, Fox JR.Pressures in the pial arterial microcirculation of the cat during changes
in systemic arterial blood pressure. Circ Res. 1972;31(2):229–39.
9. Czosnyka M, Smielewski P, Kirkpatrick P, Laing RJ, Menon D, Pickard JD.Continuous assess-
ment of the cerebral vasomotor reactivity in head injury. Neurosurgery. 1997;41(1):11–7. discussion 7–9
10. Rivera-Lara L, Zorrilla-Vaca A, Geocadin RG, Healy RJ, Ziai W, Mirski MA. Cerebral
autoregulation-oriented therapy at the bedside: a comprehensive review. Anesthesiology.
2017;126(6):1187–99.
11. Lassen NA. Cerebral blood ow and oxygen consumption in man. Physiol Rev.
1959;39(2):183–238.
12. Budohoski KP, Czosnyka M, Smielewski P, Varsos GV, Kasprowicz M, Brady KM, et al.
Cerebral autoregulation after subarachnoid hemorrhage: comparison of three methods. J Cereb
Blood Flow Metab. 2013;33(3):449–56.
13. Fog M.Autoregulation of cerebral blood ow and its abolition by local hypoxia and-or trauma.
Scand J Clin Lab Invest Suppl. 1968;102:V:B.
14. Strandgaard S, Paulson OB.Cerebral autoregulation. Stroke. 1984;15(3):413–6.
15. Halpern W, Osol G.Inuence of transmural pressure of myogenic responses of isolated cere-
bral arteries of the rat. Ann Biomed Eng. 1985;13(3–4):287–93.
16. Symon L, Held K, Dorsch NW.A study of regional autoregulation in the cerebral circulation
to increased perfusion pressure in normocapnia and hypercapnia. Stroke. 1973;4(2):139–47.
17. Winn HR, Rubio R, Berne RM.Brain adenosine production in the rat during 60 seconds of
ischemia. Circ Res. 1979;45(4):486–92.
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