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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

21 Transcranial Doppler Ultrasound Pulsatility Index: Utility andClinical Interpretation
367
Cerebral autoregulation (CA) is maintained through variable vascular resistance,
wherein the radius of small and large arteries change to maintain constant CBF, over
a wide range of CPP values and metabolic changes. Variation in minute ventilation
alters the PaCO2 which has a powerful hemodynamic effect in response to metabolic supply and demand (coupling).
Therefore, real-time simultaneous monitoring of ICP and MAP allows one to
make the best therapeutic decisions to individualize the patient’s CPP.Moreno etal.
(2000) describe the relationship between decrease CPP and increase in PI, suggesting a reduction of 1 unit in CPP results in an increase in 0.02 units in the PI [29].
Invasive ICP measurement modalities are considered the Gold Standard and are
widely used in neurocritical care populations [30]. However, this procedure has a
risk of life-threatening complications and has many contraindications related to
device placement and misplacement: principally infections, bleeding, and technical
failure [31–34].
Non-invasive ICP estimation would be helpful in clinical situations where the
risk-benet balance of invasive ICP monitoring is unclear or invasive ICP monitoring modalities are not immediately available or are contraindicated [35, 36].
Ideally, a non-invasive ICP monitor should be readily available at the bedside in
the ICU, inexpensive, accurate, and simple to use. Using Gosling’s pulsatility index,
TCD/TCCS, is a validated tool for estimating ICP in certain scenarios [37–40].
When trended, TCD/TCCS can be used to give a rough estimate for ICP (correlated PI to ICP in clinical practice) [29], but not as a surrogate for accurate invasive
ICP monitors. When ICP increases, the intracranial blood ow velocities change
(PSV increases and EDV decreases), while cerebral vessels narrow from external
pressure resulting in an increased resistance to CBF [35, 38, 41, 42].
The clinical correlation and interpretation of the PI depends of several factors:
[7, 9, 41, 43, 44].
1. Pulse amplitude of arterial blood pressure
2. Heart rate (HR)
3. CPP
4. PaCO
2
5. CV
6. Compliance of the arterial bed (Ca)
Non-invasive ICP, based on TCD/TCCS, had been estimated by different hemodynamic parameters proposal, such as Gosling’s pulsatility index (PI), Critical
Closing Pressure (CrCP), Optic Nerve Sheath Diameter (ONSD), pupillary light
reex (PLR), straight sinus systolic ow velocity (SSFV) [45], etc. However, none
of these methods seem to be accurate enough to be used as a replacement for invasive ICP measurement and, at present, TCD/TCCS is reserved for assessing changes
(ICP trends) of non-invasive ICP, rather than absolute ICP.
Other than PI, the mean ow index (Mx) (which is the correlation coefcient
between MFV and CPP) and systolic ow index (Sx) (which is the correlation coefcient between PSV and CPP) are useful parameters for assessing increased ICP
[46, 47].

368
Elevated right atrial pressure
O. M. Pinillos et al.
21.5 Transcranial Pulsatility Index (PI): Clinical Factors
toConsider
The performance and clinical interpretation of the pulsatility index depends on the
various physiological and pathophysiological conditions as well as the clinical context of each critical patient (Table21.3).
We recommend taking into account all cerebrovascular and systemic factors
when analyzing a given patient’s PI.Consider the following: (Fig.21.13).
21.5.1 Cardiovascular Factors
The cardiovascular status of the critical patient, with or without acute neurological
injury, depends on beat to beat changes in the following hemodynamic parameters:
1.1 CPP (pulsatility pressure)
1.2 CBF (pulsatility ow)
Therefore, the cardiac pulsatility induces real-time changes on the brain pulsatility, resulting in changes in PI (Fig.21.7) [4, 7, 9].
21.5.2 Cerebrovascular Factors
Except in extreme circumstances, during the primary or secondary injury, the brain
will adjust intracranial hemodynamic parameters (Table21.3) through intracranial
compliance changes (Monro-Kellie Doctrine) [48].
Table 21.3 Conditions that can modify TCD/TCCS Gosling’s pulsatility index (PI)
Decrease PI Increase PI
Hypercapnia (high PaCO2) Hypocapnia (low PaCO2)
Hyperemia Raised ICP
Vasospasm Hypothermia
Arteriovenous malformation Blood hyperviscosity
Rewarming following hypothermia Intracranial artery occlusion
Intracranial artery stenosis Hypovolemia
VA-ECMO (miss-interpretation) Bradycardia
V-A ECMO veno-arterial ECMO
Anemia Decrease CPP
Fever Cerebral circulatory arrest
High cardiac output Aortic regurgitation
Arterial hypertension Advanced age

21 Transcranial Doppler Ultrasound Pulsatility Index: Utility andClinical Interpretation
369
Brain
Parenchymal Volume
Venous System Considerations
Venous Outflow ↓Venous drainage → ↑ Venous pressure → ↑ swelling /
Arterial System Considerations
Arterial Inflow Preserved CA ←→Impaired CA
Cerebrospinal Fluid
CSF Volume Hydrocephalus
Considerations
Increased interstitial volume→ ↑ swelling / edema
treat with fluid restriction, avoiding free water administration,
and induction of hyperosmolar state with mannitol and
hypertonic saline
edema
Treat by removal of thromoses or possibly internal jugular
central venous catheters
↑↓ABP
↑↓Cardiac Output
Hyperemic ←→ Hypoperfusion
Considerations
production - Drainage disequillibrium
Drainage by EVD
Brain
Compliance
CPP
PI
PI
ICP
Fig. 21.8 Pulsatility index: inuenced by cerebrovascular factors. CSF cerebrospinal uid, EVD
external ventricular drain, CPP cerebral perfusion pressure, ICP intracranial pressure, ABP arterial
blood pressure, CA cerebral autoregulation, PI pulsatility index, ↓ low/decrease, ↑ high/increase,
↓↑ maybe increase or decrease
The brain pulsatility is the consequence of the interaction between these hemodynamic parameters and intracranial impedance, which will vary during the clinical
course of the brain injury (Fig.21.8).
21.5.3 Cardiopulmonary Factors
Maintenance of normal ICP through treatments aimed at affecting the intracranial
components which contribute to ICP is critical in patients with acute brain injury
(parenchymal volume, CSF volume, and blood volume) [48]. This includes ensuring appropriate venous outow, CSF diversion, modication of the parenchymal
volume by treatment of edema, and augmentation of the MAP, among others. These
factors must be taken into consideration when interpreting a given patient’s PI
(Fig.21.9) [5, 49, 50].
21.5.4 Metabolism Factors
Brain oxygenation and metabolism is the conuence of cardiovascular (O2 delivery)
and pulmonary systems (gas exchange– ventilation). In the clinical interpretation of
the PI, we should consider the following variables: [51, 52] (Fig.21.10).

370
O. M. Pinillos et al.
Pulmonary
Pulmonary
Hypertension
Cardiac Considerations
Pump Failure Left ventricular failure
Considerations
ARDS / Non-cardiogenic Pulmonary
Edema / COPD
Mechanical Ventilation Strategies
V
/ PEEP / PP / RR / I:E
T
(Tends)↑ELWI ←→ ↑PVPI (Tends)
↓Pulmonary compliance
Pulmonary hypertension
(Tends)↑ELWI ←→ ↑PVPI (Tends)
Right ventricular failure
High right
ventricular
pressure
Low
cerebral
venous
outflow
PI
Fig. 21.9 Transcranial pulsatility index: inuenced by cardiopulmonary factors. ARDS acute
respiratory distress syndrome, COPD chronic obstructive pulmonary disease, V
tidal volume, PP
T
prone position, RR respiratory rate, I:E inspiration: expiration relationship, EVLWI extra-vascular
lung water index, PVPI pulmonary vascular permeability index, PI pulsatility index, ↓ low/
decrease, ↑ high/increase
Oxygenation
O2 Delivery
Systemic
Inflammation
Ventilation
Hypercapnia
Hypocapnia
Considerations
ICP ← CPP → DO
→ CO → SpO
DO
2
↑ICP → ↓CPP → ↓DO
Cerebral perfusion pertubations
Cerebral autoregulations → Impaired
Low vasomotor reactivity
Considerations
Mechanical ventilation strategies
Low VT / PEER / RR
Preserved ← Cerebral autoregulations → Impaired
Mechanical ventilation strategies
High VT / PEER / RR
Preserved ← cerebral autoregulations → Impaired
2
→ Hb
2
→ Low P
2
btO2
(Hypoxia)
CVR CBFV
PI
Fig. 21.10 Metabolic factors which inuence PI.ICP intracranial pressure, CPP cerebral perfusion pressure, CO cardiac output, DO
ration, Hb hemoglobin, P
btO2
delivery of oxygen, SpO2 peripheral capillary oxygen satu-
2
brain tissue oxygen tensión, VT tidal volume, RR respiratory rate,
CVR cerebrovascular resistance, CBFV cerebral blood ow velocity, PI pulsatility index, ↓ low/
decrease, ↑ high/increase
21.5.5 Vascular Factors
The focal or segmental stenoses of intracranial vessels, whether due to intracranial
atherosclerosis, cerebral artery vasospasm, or vasculitis, inuence ICP and cerebral
perfusion. TCD/TCCS is a useful non-invasive tool in monitoring cerebral perfusion over time via MFV and PI.Although there is a lack of data in this arena, monitoring of trends in MFV and PI as vascular factors are manipulated, such as induced
hypertension, allows one to customize each patient’s treatments and hemodynamic
parameters [53–57] (Fig.21.11).

21 Transcranial Doppler Ultrasound Pulsatility Index: Utility andClinical Interpretation
Vascular Considerations
Vasospasm Alterations in cerebral vascular tone
Vasculitis Inflammation of Wall vessels
SAH / TBI
↑CBFV (MFV) ⇒↓ PI ⇒ Predictor
RCVS
↑CBFV (MFV)
Patchy ↑↓ CBFV
CVR
CBFV
PI
371
Fig. 21.11 The effect of vascular factors on PI.SAH subarachnoid hemorrhage, TBI traumatic
brain injury, RCVS reversible cerebral vasoconstriction syndrome, CBFV cerebral blood ow
velocity, MFV mean ow velocity, CVR cerebrovascular resistance, PI pulsatility index, ↓ low/
decrease, ↑ high/increase, ↓↑ maybe increase or decrease
Temperature
Blood viscosity
ECC
Considerations
Fever / Re-warming
↑Metabolism ↑Blood-brain barrier permeability
brain edema?
Increase CBFV
↑ PI
Hypothermia
↑Metabolism
↑CBFV ⇒ ↓ PI
Considerations
Anemia
↑Hematocrit ⇒ ↑ CBFV
↑↓ PI
Polycythemia
↑Hematocrit ⇒ ↓ CBFV
↑↓ PI
Considerations
VA-ECMO (Without IABP)
Non-pulsating circulation
Miss interpretation of the spectral doppler waveform
Cerebral Autoregulation?
Low cardiac pulsatility ⇒ Low brain pulsatility
(Damping of the velocity waveform)
↓ PI
RRT
Changes in the Cerebral compliance (Brain Edema)
Hypotension situations (↓MAP)
↓MAP and/or ↑ICP ⇒ ↑PI
Cerabral Autoregulation?
↑↓ CBFV
↑Hematocrit (After RRT)
Ultrafiltration ⇒ ↓ CBF
ICP
PI
CBFV
Fig. 21.12 Other systemic factors affecting PI.CBFV cerebral blood ow velocity, PI pulsatility
index, IABP intra-aortic blood pump, RRT renal replacement therapy, MAP mean arterial pressure, ICP intracranial pressure, CBF cerebral blood ow, ECC extracorporeal circulation, ↓ low/
decrease, ↑ high/increase, ↓↑ maybe increase or decrease
21.5.6 Other Factors
Other systemic factors that inuence cerebrovascular hemodynamics can affect
PI.These include fever, CNS infections, hypothermia, among others and are listed
in the table below [58–60] (Figs.21.12 and 21.13).

372
Extracorporeal circulation
O. M. Pinillos et al.
Brain Pulsatility
Neurological Injury
CARDIOVASCULAR
FACTORS
ABP= CO x SVR
ABP
CO
SVR
SV
HR
CPP
MAP
ICP
Hypothermia / Re-warming
Cardiac Pulsatility
SAP / DAP / MAP
Pre-Load
Cardiac Contractility
Post-Load
Systemic Inflammation
CO= SV x HR
Euvolemia
Bradycardia
Tachycardia
Cardiac Rhythm
CPP= MAP - ICP
ABP / CO / SVR
CO / SAP / DAP
Cerebral Factors
OTHER FACTORS
Anemia
Blood Hyperviscosity
Fever
Age / Ethnicity
CEREBRAL AUTOREGULATION
Spectral Doppler Waveform analysis
TCG/TCCS
Consider Acoustic
Window
CBF
PULSATILITY
INDEX
INTERPRETATION
KIP IN MIND
Clinical Context
Consider Tends of Values
Is a Complementary Tool
CEREBROVASCLUAR
FACTORS
Brain Parenchyma
[Brain volumen]
Venous Outflow / Arterial Inflow
[Cerebral blood volumen]
Cerebrospinal Fluid
[CSF volumen]
Brain Compliance
ICP
CVR
METABOLIC FACTORS
Brain O
2
PaO
2
VASCULAR FACTOR
Atherosclerotic Disease
Cerebral vasoreactivity
CARDIOPULMONARY
Elevated Right Atrial Pressure
Hypoxia
Hypocapnia
Hypercapnia
Vasculitis
Vasospasm
FACTORS
Fig. 21.13 Schema of clinical considerations in the pulsatility index interpretation. Transcranial
pulsatility index can be variable and affected by physiological as well as pathologic conditions.
ABP arterial blood pressure, CO cardiac output, SV stroke volume, CPP cerebral perfusión pressure, SVR systemic vascular resistance, HR heart rate, MAP mean arterial pressure, ICP intracranial pressure, CVR cerebrovascular resistance, SAP systolic arterial pressure, DAP diastolic
arterial pressure, CSF cerebrospinal uid, CBF cerebral blood ow
21.6 Conclusion
Although invasive monitoring is the gold standard, non-invasive monitoring should
be considered in certain clinical scenarios. TCD/TCCS, through Gosling’s pulsatility index, is a validated tool for estimating changes in ICP.TCD/TCCS can be used
to give a rough estimate for ICP (correlated PI to ICP in clinical practice), but not as
a surrogate for accurate invasive ICP monitors. The clinical correlation and interpretation of the Gosling’s pulsatility index depends on several factors.
During TCD/TCCS monitoring, it is important to consider the spectral Doppler
waveform. Cerebral perfusion is driven primarily by the diastolic component of the
TCD/TCCS waveform. Therefore, we recommend that the PI should be interpreted

INTENSIVE CARE UNIT (ICU)
yC
Follow-up
21 Transcranial Doppler Ultrasound Pulsatility Index: Utility andClinical Interpretation
373
in conjunction with the spectral Doppler waveform morphology noting qualitative
and quantitative changes.
Absolute ICP measurements based on TCD/TCCS have been estimated by various
methods. However, none of these methods seem to be accurate enough to be used as
a replacement for invasive ICP measurement and, at present, TCD/TCCS is reserved
for assessing changes (ICP trends) of non-invasive ICP, rather than absolute ICP.
Algorithm
EMERGENCY DEPARTMENT (ED)
Clinical Status of the Patient
ABCD
Level of Consciousness (GCS)
Bilateral Pupilar Reactivity?
Hemodynamic Stability?
Oxygenation?
DIAGNOSIS
Subarachnoid Hemorrhage (SAH) Status Epilepticus / NCSE
Acute Ischemic Stroke (AIS)CNS Infection
Acute Liver Failure (ALF)Post-Cardiac Arrest
Traumatic Brain Injury (TBI)
MULTIMODAL MONITORING (MMM)
Invasive Non-Invasive
btO
•
P
2
SjvO
•
2
•
ICP SSEPs
CMD
•
Brain-CT Scanand/or MRI
Intracerebral Hemorrhage (ICH)
•
cEEG–QEEG
NIRS
•
•
TCD / TCCS
•
INVASIVE ICP MONITORING
[Contraindicated or Not Available]
Transcranial Color Coded duplex Sonography (TCCS)
MLS PULSATILITY INDEX (PI) ONSD PLR
a) Increased ICP?
b) Cerebral Compliance variations?
c) Brain Pulsatility variations?
FACTORS TO CONSIDER CLINICAL INTERPRETATION
1. Cardiovascular
2. Cerebrovascular Main Syndrome / Disease (Clinical Information)
3. Cardiopulmonar
4. Metabolism Spectral Doppler Waveform Analysis
5. Vascular Consider Tends of Hemodynamic values
6. Others Remember it is a Complementary Tool
Transcranial Doppler (TCD)
NON-INVASIVE ICP ESTIMATION
KEEP IN MIND
linical Context (Clinical Evolution)
Real-Time Therapeutic Decisions &
SE status epilepticus, NCSE non-convulsive status epilepticus, CNS central nervous system, PRL
pupillary light reex, MLS middle-line shift, SSEPs somatosensory evoked potentials, ABCD airway, breathing, circulation, disability, SjvO
jugular bulb venous oxygen saturation, PbtO2 brain
2
tissue oxygen tensión, MRI magnetic resonance imaging, ←→ inter-related, CMD cerebral
microdialysis

374
O. M. Pinillos et al.
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