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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5783_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •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

16 Neurocritical Care Monitoring in ICU: Measurement of the Cerebral…
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TCD and subsequently Mx can assess this rather easily; values of Mx less than or
equal to 0 are representative of an intact autoregulatory reserve in which CBFV
actively responds to changes in CPP, whereas positive Mx trends state the opposite
[23], which provides an example of a patient with disturbed autoregulation, as
assessed with Mx.
However, the time-domain calculation of Mx itself does not rely entirely on noninvasive data collection to express autoregulatory reserve; once again, CPP is the
difference between ABP and ICP, making Mx somewhat dependent on ICP uctuations as a result. Lang etal. [11] attempted to attain Mx with two separate input
signals: CPP and ABP, the latter rendering the parameter to be quantiable with
non-invasive measures. Although possible to use, Mx determined from ABP is not
as sensitive as Mx determined from CPP [19]. Continuing the search for an entirely
non-invasive Mx function, Budohoski etal. [12] cited correlations between the systolic (Sx), diastolic (Dx), and mean (Mx) components of the CBFV waveform when
using the input signals of either ABP or CPP.Separate analyses yielded the same
result: Mx calculated with CPP is the superior predictor of functional patient outcome [1, 12].
16.4 TCD: Benets andLimitations
TCD/TCCS is an important tool to have in neurocritical care units. It is inexpensive,
portable, and relatively simple to use once trained in how to do so. TCD examinations are as accurate as MRI when assessing vascular pathology [9] and do not
require patients to be moved to imaging suites. Additionally, TCD devices can be
paired with clinical monitoring software such as ICM+ (Cambridge Enterprise,
Ltd.) to return pertinent information about a TBI patient’s state of cerebral autoregulation that cannot be gleaned from bedside monitors. Without TCD and dedicated analytical platforms such as ICM+, mortality and functional outcome could
not be determined on the basis of one or two functions (ARI is a more robust predictor of mortality than Mx is more sensitive to functional outcome [19, 23, 25]). The
benet of both ARI and Mx is that they assign scalar value to cerebral autoregulation to the “weighted spatial averages as seen from the aspect of the MCA” [26]
when employing the TCD monitoring technique.
Although there is a shortage of “autoregulation markers” [5], the above surrogates (ARI, Mx) can technically be monitored continuously, as their respective values can be repeatedly calculated over any specied time period during the patient’s
neuro-intensive care stay. Therefore, ARI and Mx can be reported in the same fashion as ABP and ICP.Despite this important point, TCD and thus its derived parameters are only intermittently afxed to the patients (<1 hour) due to the relative
“clumsiness” and potential disruptiveness of the instrument to routine nursing interventions (i.e., turning the patient, preparing the patient for an X-ray or scan, etc.).
TCD is primarily viewed as a research tool and is treated as an accessory to the
patient; for example, it is nearly impossible to retain a stable probe position if a

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L. A. Calviello and M. Czosnyka
patient is being re-positioned or examined, as nurses are not obligated to be vigilant
over the TCD recording session itself. TCD’s time dependence only permits clinicians to receive “snapshots” of cerebral hemodynamic activity [1]. Another drawback of TCD is its reliance on operator validity [10]; even experienced technicians
may not agree on the probe placement, depth of the MCA, etc. If the diameter of the
MCA were ever to be proven variant, the core of TCD monitoring technology and
thus its credibility would be undermined.
16.5 Conclusion
TCD monitoring is entirely non-invasive and allows unique insight into cerebral
hemodynamics, particularly through the MCA.The activity within the MCA is central to the brain’s ability to balance pressure and ow load demands that can be
altered by TBI.Although limited by time and technicalities related to its operation,
TCD remains a popular tool in neurocritical care centers due to its ability to provide
surrogate markers of cerebral autoregulation.
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26. Czosnyka M, Smielewski P, Lavinio A, Pickard JD, Panerai R.An assessment of dynamic
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Chapter 17
Neuro-ICU: Cerebral Hemodynamics
andTranscranial Doppler (TCD/TCCS)
Waveform Interpretation intheMost
Common Neurocritical Pathologies
L.LucianoPonceMejia, BahattinB.Ergin, andLucíaRivera Lara
Key Points
1. Adequate brain function requires sufcient, uninterrupted blood ow. Thus, fast-
acting mechanisms are needed to restore blood ow when it drops acutely.
Cerebrovascular reactivity is the ability of vascular smooth muscle to change
basal tone in response to variations in physiologic parameters, such as arterial
blood pressure (ABP), and metabolic factors, such as cerebral carbon dioxide
and oxygen levels.
2. The ow velocity decreases as it reaches small vessel branches. Local dimin-
ished vessel diameter (i.e., vasoconstriction) results in a dramatic acceleration in
blood ow velocity and a decrease in the pressure. This phenomenon is governed
by Bernoulli’s principle, described by Daniel Bernoulli in 1738.
3. Only around 50% of the population has a classic conguration of the circle of
Willis [1]. Stenotic segments are found in more than 25% of people [2]. When
the degree of proximal vessel stenosis in the ICA is severe, the blood ow is
largely dependent on the collateral vessels. Such collateral circulation tends to
be more effective within the circle of Willis because ECA-ICA anastomotic vessels are very small and narrow and therefore generate signicant resistance.
L. L. P. Mejia
Departments of Neurology, The Johns Hopkins University School of Medicine,
Baltimore, MD, USA
B. B. Ergin
Anesthesiology & Critical Care Medicine, The Johns Hopkins University School of
Medicine, Baltimore, MD, USA
e-mail: bergin1@jhmi.edu
L. Rivera Lara (
Department of Neurology, Anesthesiology and Critical Care Medicine, The Johns Hopkins
School of Medicine, Baltimore, MD, USA
e-mail: lriver14@jhmi.edu
C. N. Rodríguez et al. (eds.), Neurosonology in Critical Care,
https://doi.org/10.1007/978-3-030-81419-9_17
*)
299© Springer Nature Switzerland AG 2022

300
4. 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 end-diastolic 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.
5. The Lindegaard ratio (LR) tends to increase in relation to the degree of vaso-
spasm. Normal reference range is from 1.1 to 2.3 and in the absence of vasospasm is <3.
L. L. P. Mejia et al.
17.1 Introduction
Transcranial Doppler (TCD) has gained popularity among physicians because it is
a quick, inexpensive, and noninvasive way to evaluate blood ow in the basal cerebral arteries. The applications of TCD in the neurologically or neurosurgically critically ill patient include vasospasm screening in those with aneurysmal subarachnoid
hemorrhage (aSAH) or traumatic brain injury (TBI), detection of embolism after
transient ischemic attack or cerebrovascular accident, and evaluation of total cerebral circulatory arrest in those with brain death. TCD has also been used for estimating cerebral autoregulation and cerebrovascular reactivity and for detecting
abnormally high intracranial pressure (ICP).
Interpreting the ndings of TCD requires an understanding of cerebral hemodynamic principles. Cerebral hemodynamics is inuenced by a complicated interaction among various factors in critically ill patients, namely, (1) mean arterial blood
pressure (MAP), (2) ICP, (3) blood viscosity, (4) degree of proximal vessel stenosis,
(5) vessel caliber, (6) degree of collateral circulation, and (7) integrity of cerebral
autoregulation. In this chapter, we will review the physiology of cerebral hemodynamics and focus on TCD waveform interpretation.
17.2 Cerebral Blood Flow (CBF) andCerebral Perfusion
Pressure (CPP)
The CPP is equivalent to MAP minus the ICP. The drive to generate blood ow
through the cerebral arteries, branches, and capillaries is produced in the left ventricle and maintained by the elastic properties of the aorta and extracranial arteries
(common carotid artery [CCA] and internal carotid artery [ICA]), resulting in a
pulsatile forward pressure. Although the venous blood pressure cannot be

CVRCPP CBF= /
17 Neuro-ICU: Cerebral Hemodynamics and Transcranial Doppler (TCD/TCCS…
discounted, its hemodynamics are far more complex. Often the intracranial venous
pressure does not equal the central venous pressure, especially under pathological
conditions when an increase in the ICP leads to collapse of the vein wall and a
resulting change in ow resistance. Some authors have proposed to use instead of
the venous sinus blood pressure (vSBP) because the venous sinuses do not collapse
when the ICP rises above that of the vSBP [3]. Nevertheless, the veins that drain
into the cerebral sinuses (bridging veins) do collapse when ICP increases, isolating
the cerebral venous sinus pressure, an indication that vSBP matches ICP.
301
17.2.1 Cerebrovascular Resistance (CVR)
CVR is maintained mainly by small arteries, resistance vessels, capillaries, and
venules. It has been dened as in Eq.17.1. This special pressure–ow relationship
is known as Starling resistance, which was rst described in 1912 [4]. The ow in
collapsible systems that allows us to dene vSBP as equal to ICP has also been
described in detail [5–7]. Microinvasive methods show a signicant descent in pressure from distributing arteries (about 90mmHg) to the arterioles (<30mmHg) [8].
In 1838, using tubes of ne bore in a series of experiments, Jean Leonard Marie
Poiseuille (1797–1869) established that ow is inversely proportional to the length
of the tube and directly proportional to the pressure gradient and to the fourth power
of the tube diameter, the now famed Law of Poiseuille (Eq.17.2):
where ΔP is the pressure difference between the two ends, L is the length of tube
(vessel), μ is the dynamic viscosity (hematocrit), Q is the volumetric ow rate (ow
velocity), and R is the radius of the vessel. Notably, the radius of the cerebral vessels
decreases distally and changes according to physiologic and pathophysiologic
states. Consequently, the quantitative use of the Law of Poiseuille is limited. Also,
the blood viscosity is non-Newtonian because it is proportional to the velocity of
ow. One useful lesson deduced from the Law of Poiseuille is that a modest change
in vessel diameter induces a dramatic increase in ow resistance.
DPmLQ pR= 84.../.
(17.1)
(17.2)
17.2.2 Cerebral Autoregulation
Adequate brain function requires sufcient, uninterrupted blood ow. Thus, fastacting mechanisms are needed to restore blood ow when it drops acutely.
Cerebrovascular reactivity is the ability of vascular smooth muscle to change basal

302
L. L. P. Mejia et al.
tone in response to variations in physiologic parameters, such as arterial blood pressure, and metabolic factors, such as cerebral carbon dioxide and oxygen levels [9].
Cerebral autoregulation is one aspect of cerebrovascular reactivity that involves vascular tone changes in response to uctuations in arterial blood pressure [10]. The
rst studies of cerebral autoregulation showed that in a normal physiologic state,
CBF remains constant when MAP uctuates within 50–150mmHg margin [11].
Modern multimodal monitoring techniques of cerebral autoregulation and cerebrovascular reactivity have shown that the cerebral autoregulation plateau may be much
narrower. In a study of adults with acute subarachnoid hemorrhage, the cerebral
autoregulatory plateau was found to be 80–120mmHg [12]. Adjustments of CVR
are responsible for maintaining a constant CBF.Thus, CBF is not disturbed by modest degrees of stenosis or spasm of proximal vessels. The resistance vessels dilate
yielding a lower CVR, which in turn restores CBF [13]. Conversely, a sudden
increase in CPP (i.e., MAP) that threatens the integrity of the fragile cerebral capillaries results in rapid vasoconstriction of the proximal resistance vessels to avoid
high transmural pressures. Evidently, more complex and slow metabolic adaptations occur in response to abrupt changes in CPP in addition to the fast-myogenic
response [14–18].
17.2.3 Determination ofCerebrovascular Reactivity Via TCD
In a study of dogs, a 20–25mmHg change in systemic blood pressure produced only
a 2.5% change in diameter of the coronary arteries, thanks to their relative stiffness
[19]. Cerebral arteries have similar properties. A mean change in blood pressure of
30±16mmHg and a change in end-tidal CO2 (EtCO2) of 14±6mmHg resulted in
a mean diameter change in the large cerebral arteries (carotid, middle cerebral artery
[MCA], vertebral artery) of less than 4%, but the smaller arteries (anterior cerebral
artery, M2 segment of MCA) showed diameter changes as large as 29% to ETCO
changes and 21% to blood pressure changes [20, 21]. Hence, as the diameter of the
large vessels is relatively stable to changes in blood pressure and CO2, one can
assume that the CBF is proportional to the CBF velocity (CBFV). Such changes in
CBFV can be measured using TCD technology. Under this premise, CBFV approximates CBF [22]. Cerebrovascular reactivity can be calculated clinically, with the
most common methods being (1) dose-controlled CO2 inhalation, (2) acetazolamide
injection, and (3) breath-holding index [23–25].
17.2.4 Carbon Dioxide Reactivity
Changes in the partial pressure of CO2 (PCO2) cause changes in CVR because CO2
affects the degree of vasodilation of the smaller vessels responsible for regulating
CVR.However, the effect of PCO2 on basal cerebral artery diameter is insignicant.
2

()
17 Neuro-ICU: Cerebral Hemodynamics and Transcranial Doppler (TCD/TCCS…
303
By measuring EtCO2 in normal subjects, Markwalder etal. [26] established that
ow velocity in the MCA changes 3.4±0.5% per each mmHg change in EtCO2.
According to the Poiseuille equation, a change in ow resistance of 3–4% is attained
by approximately 1% change in vessel caliber in the resistance vessels.
Cerebrovascular reactivity in the neurocritical intensive care unit will be reviewed
extensively in a different chapter.
17.3 Physiology ofBlood Vessel Stenosis
The ow velocity decreases as it reaches small vessel branches. Local diminished
vessel diameter (i.e., vasoconstriction) results in a dramatic acceleration in blood
ow and a decrease in the pressure. This phenomenon is governed by Bernoulli’s
principle, described by Daniel Bernoulli in 1738. It states that pressure and velocity
in a moving uid have an inverse proportional relationship [27]. Energy is involved
in accelerating the uid. Energy is transformed from static energy, namely, pressure,
into kinetic energy during acceleration. Such transformation of energy is derived
from Bernoulli’s equation (Eq.17.3):
PP rV V
–½–=
21 221
DP
2
(17.3)
where ΔP is the pressure difference between the two points with velocities V1 and
V2, respectively, and ρ is the density of blood.
The energy is lost, or rather transformed, in turbulence distal to the stenosis.
Note that Bernoulli’s principle takes into consideration the density (viscosity) of the
blood. A higher viscosity (hematocrit) results in a higher ΔP. In the brain, there are
basically three pathological conditions that can affect blood ow acceleration: (1)
large- and mid-size stenosis due to atherosclerotic disease of the extra- and intracranial arteries, (2) vasospasm (i.e., subarachnoid hemorrhage), and (3) narrowed congenital communicating vessels in the circle of Willis (anterior and posterior
communicating arteries).
17.3.1 Evaluation ofIntracranial Stenosis by TCD
Using Doppler ultrasound technology to evaluate atherosclerotic disease resulting
in stenosis of the CCA bifurcation predates TCD [28]. The development of TCD
technology with a transorbital approach of the carotid siphon made possible the
evaluation of intracranial stenotic disease with an overall accuracy of 88%, a 95%
specicity, and a 73% sensitivity when compared to angiography [29]. The transtemporal and suboccipital approaches were later described with a correlation coefcient of 0.89 (p=0.0001) [30, 31]. A proposed model of unilateral carotid artery

304
L. L. P. Mejia et al.
stenosis suggests that for a severe unilateral stenosis of the right carotid artery, the
partial pressure of oxygen in the brain area at risk can be restored only if the corresponding cerebral resistance is signicantly decreased and if the circle of Willis is
complete [32]. Another report showed no preoperative difference in number of
intracerebral arteries with reverse ow between symptomatic and asymptomatic
patients with severe unilateral carotid stenosis. In contrast, pulsatility index, cerebrovascular reactivity, and ow acceleration on the side of stenosis were signicantly lower in symptomatic patients. After surgery, all TCD parameters improved
signicantly in both symptomatic and asymptomatic patients [33]. The Doppler
ndings showed increased ow velocity at the site of stenosis, a decrease in velocity
with a dampened waveform distally, and at least a 20–30mmHg pressure loss. This
phenomenon has a parabolic relationship. Stenotic atherosclerotic lesions have
obvious hemodynamic effects. The inverse correlation of low velocity obtained by
TCD as a function of lumen dimension has been reported in patients with intracranial artery disease when the measurements of diameter were corrected by angiography [34]. Such inverse correlation ndings appear to deviate less in atherosclerotic
disease than in vasospasm.
17.3.2 Collateral Flow
Only around 50% of the population has a classic conguration of the circle of
Willis [1]. Stenotic segments are found in more than 25% of people [2]. When the
degree of proximal vessel stenosis in the ICA is severe, the blood ow is largely
dependent on the collateral vessels. Such collateral circulation tends to be more
effective within the circle of Willis, because ECA-ICA anastomotic vessels are
very small and narrow and therefore generate signicant resistance. Variability in
the pressure of the various collateral connecting vessels (stumps) in the circle of
Willis has been reported to be high, ranging from as low as 10mmHg to almost
equating the systemic blood pressure [35]. The resistance to ow in a given collateral connection is determined by vessel diameter, length, and viscosity. The effect
of the circle of Willis conguration on cerebrovascular hemodynamics and the distribution of ow appears to be highly variable from individual to individual [36,
37]. Consequently, studying its inuence is very difcult [38–40]. One of the most
common noninvasive TCD techniques used to assess collateral ow within circle
segments uses carotid compression [41]. Because blood volume is directly proportional to ow velocity, common carotid compression measures its effect on blood
ow velocity in the ipsilateral posterior cerebral artery and contralateral anterior
cerebral artery. Thus, this test shows that the communicating arteries are open and
to what degree. The presence of chronic atherosclerotic lesion and its effect on ow
velocity in the circle of Willis has also been studied. Researchers have shown
increased, reversed, and crossover ow in the different compensating vessels ipsilateral and contralateral to the atherosclerotic lesion, sometimes greater than 1.5

CVP=∆ ∆/
17 Neuro-ICU: Cerebral Hemodynamics and Transcranial Doppler (TCD/TCCS…
305
times the velocity in the ipsilateral MCA when the extracranial ICA occlusion
reached about 90% [30, 34].
17.3.3 Elastic Reservoir (“Windkessel Effect”)
It is important to remember that the properties described so far (resistance, turbulence, etc.) and their effects on ow apply only to a model with a static pressure–
ow relationship. However, the pulsatile nature of the pressure in extra- and
intracranial vessels results in a dynamic pressure–ow relationship because these
vessels are elastic. The most important dynamic relationship is known as the
“Windkessel” effect. The Windkessel model described by Otto Frank [42, 43]
denes the hemodynamics of the arterial system in terms of resistance and compliance. It describes the aortic pressure decline during diastole but not entirely so during systole. Impedance was proposed as a third component of the Windkessel model.
The heart ejects blood intermittently; however, the ow is more continuous as the
blood pressure pulsates because the elasticity of the arterial system acts as a reservoir of the energy supplied during systole, thus making the system more efcient.
This model can then predict the classic shape of the ow waveform seen in a pulsatile system [42, 43]. Windkessel is roughly translated from German to English as
“air chamber,” drawing the analogy with the air chamber used in re engines in the
eighteenth century [44]. CBF waveforms obtained by TCD are consistent with lowresistance ow, which changes in pathological states. The Windkessel model is a
lumped model and therefore not appropriate for the evaluation of wave travel, but it
is a fair approximation of ventricular afterload.
Compliance (C) is the ability of a vessel to distend and increase volume with
increasing transmural pressure or the tendency to resist recoil toward its original
dimensions on application of a distending or compressing force. It is dened as
(Eq.17.4)
(17.4)
The following are scenarios in which the effect of compliance markedly affects
the ow velocity waveform. (1) Proximal stenosis resulting in a dampened velocity
waveform [34, 45]. The Windkessel effect produces a more smoothed waveform
because of the increased inow resistance. (2) Size and amount of arteriovenous
malformation feeders. Because arteriovenous malformations have high volume
stiffness and very low ow resistance, they result in a dampened waveform. (3)
Hypocapnia results in increased ow velocity pulsatility [26]. Low PCO2 leads to
vasoconstriction that increases resistance, revealing the Windkessel effect. (4)
Pathological ICP elevation also results in a very pulsatile waveform [46]. Two fac-
tors have been proposed to explain this phenomenon. First, the pulsatility of the
CPP increases with increasing ICP, and second, the total volume compliance
increases so that more blood is required in systole to ll the “Windkessel.”
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