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- •Preface
- •Contents
- •Contributors
- •Resolution
- •Axial Resolution
- •Lateral Resolution
- •Elevational Resolution
- •Temporal Resolution
- •The Resolution—Penetration Interplay
- •Sound Waves
- •Ultrasound
- •Pulsed Ultrasound
- •The Range Equation
- •Ultrasound Image Formation
- •Time Gain Compensation
- •M-Mode Imaging
- •The Doppler Principle
- •Doppler Imaging
- •Continuous Wave (CW) Doppler
- •Pulsed Wave (PW) Doppler
- •Color Flow (CF) Doppler
- •Tissue Doppler Imaging (TDI)
- •Pulsed Wave TDI
- •Color TDI
- •Tissue Harmonics Imaging (THI)
- •Probe Selection
- •Curved Linear Array Transducers
- •Linear Array Transducers
- •Phased Array Transducers
- •Ultrasound Artifacts (See Chap. 3)
- •Space/Time Artifacts
- •Refraction
- •Mirror Image
- •Reverberation
- •Bayonet
- •Edge
- •Attenuation Artifacts
- •Shadowing
- •Enhancement
- •Doppler Artifacts
- •Aliasing
- •References
- •Probe Selection
- •Harmonic Imaging
- •Imaging Modes
- •Color Doppler
- •Spectral Doppler
- •Tissue Doppler
- •References
- •3: Ultrasound Artifacts
- •Reverberation Artifacts
- •Comet-Tail Artifact
- •Ring-Down Artifact
- •Mirror Image Artifacts
- •Shadowing Artifact
- •Enhancement Artifact
- •Side-Lobe Artifacts
- •Refraction Artifacts
- •References
- •References
- •Parasternal Long Axis (PLAX)
- •External Surface Anatomy
- •Sonographic Anatomy
- •Imaging Tips
- •External Surface Anatomy
- •Sonographic Anatomy
- •Imaging Tips
- •External Anatomy
- •Sonographic Anatomy
- •Imaging Tip
- •Parasternal Short Axis (PSAX)
- •External Anatomy
- •Sonographic Anatomy
- •Scanning Tips
- •Suprasternal/Supraclavicular View
- •External Anatomy
- •Sonographic Anatomy
- •Imaging Tips
- •6: Transthoracic M-Mode Echocardiography
- •Imaging Tips
- •Apical: A4C, A5C, A2C, A3C
- •Apical Four-Chamber View (A4C)
- •External Anatomy
- •Sonographic Anatomy
- •Scanning Tips
- •Apical Five-Chamber View (A5C)
- •External Anatomy
- •Sonographic Anatomy
- •Scanning Tips
- •Apical Two-Chamber View (A2C)
- •External Anatomy
- •Sonographic Anatomy
- •Scanning Tips
- •Apical Three-Chamber View (A3C)
- •External Anatomy
- •Sonographic Anatomy
- •Scanning Tips
- •Subcostal: SC4, SC Long Access, IVC
- •Subcostal Four-Chamber View (SC4)
- •External Anatomy
- •Sonographic Anatomy
- •Scanning Tips
- •Subcostal Long Axis IVC
- •External Anatomy
- •Sonographic Anatomy
- •M-Mode Echocardiography
- •Left Ventricular (LV) Function
- •Right Ventricular (RV) Systolic Function
- •Cardiac Valves
- •Pericardial Tamponade
- •Inferior Vena Cava (IVC) Collapsibility
- •References
- •7: Transthoracic Doppler Echocardiography
- •General Approach
- •Spectral Broadening
- •Pulse Repetition Frequency
- •Pulmonary Venous Flow (Diastolic Function)
- •Hepatic Vein Flow
- •Pulse-Wave/CW Doppler (Aorta Flows)
- •References
- •8: Transesophageal Echocardiography: Insertion, Manipulation, Risks, Complications
- •Indications
- •Post Cardiac Surgery
- •Acute Cardiopulmonary Disease
- •Hypovolemia, Fluid Responsiveness
- •Endocarditis
- •Aortic Pathology
- •Insertion
- •Manipulation
- •References
- •2D Transesophageal Imaging
- •References
- •Ultrasound Assumptions
- •Reverberation Artifact
- •Side-Lobe Artifact
- •Intravascular Devices
- •3D Ultrasound
- •Stitch Artifact
- •Right Atrium: Crista Terminalis, Eustachian Valve, Chiari Network
- •Right Ventricle-Moderator Band
- •Left Ventricle: Fibroelastoma Versus Lambl’s Excrescence
- •References
- •11: LV Systolic Function
- •Structural Anatomy
- •Left Ventricular Hypertrophy
- •LV Function: Linear Measurements
- •EPSS Method
- •Caution
- •LV Function: Ejection Fraction
- •EF (Simpson’s Biplane) Method
- •Cautions
- •LV Function: Cardiac Output
- •Regional Wall Motion Abnormalities
- •Methods
- •Strain
- •Strain Methods
- •Cautions
- •References
- •Ultrasonic Enhancement Agents (UEAs)
- •M-Mode
- •Mitral Annular Plane Systolic Excursion
- •dP/dt
- •Tissue Doppler Imaging (TDI)
- •Systolic Mitral Annular Velocity (s′)
- •References
- •13: The Right Ventricle
- •The Right Ventricle
- •Right Ventricular-Focused View
- •Semi-Quantitative Right Ventricular Assessment
- •Interventricular Septum
- •Right Ventricular Dimensions
- •Right Ventricular Wall Thickness
- •Right Ventricular Area/Volume
- •Regional Systolic Functional Assessment
- •TAPSE (Tricuspid Annulus Plane Systolic Excursion)
- •Tricuspid Annular Systolic Velocity (Right Ventricular S′)
- •Global Systolic Functional Assessment
- •Right Ventricular Fractional Area Change
- •Right-Sided Hemodynamics
- •Right Ventricular-Pulmonary Artery Coupling
- •Right Ventricular Diastolic Function
- •Right Ventricular Strain
- •Conclusion
- •References
- •Left Atrium
- •Technical Considerations
- •Left Atrial Function
- •Atrial Septum
- •Right Atrium
- •References
- •15: Left Ventricular Diastolic Function
- •Introduction
- •Diastole
- •Isovolumic Relaxation
- •Early Diastolic Filling
- •Diastasis
- •Late Diastolic Filling
- •Diastolic Function Assessment
- •Normal Pattern (Grade 0)
- •LV Relaxation Abnormality Pattern (Grade 1)
- •Pseudonormalization Pattern (Grade 2)
- •Restrictive Pattern (Grade 3)
- •Mitral Annular Motion Velocity
- •Left Atrial Volume Index (LAVI)
- •Tricuspid Regurgitation (TR) Jet Peak Velocity
- •Pulmonary Vein Flow
- •ASE Recommendation 2009
- •ASE Recommendation 2016
- •References
- •16: Cardiomyopathies
- •Dilated Cardiomyopathy
- •Hypertrophic Cardiomyopathy
- •Restrictive Cardiomyopathies
- •Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia (ARVC/D)
- •Stress-Induced Cardiomyopathy
- •Takotsubo Cardiomyopathy
- •Neurogenic Stress Cardiomyopathy
- •Cirrhotic Cardiomyopathy
- •Noncompaction Cardiomyopathy
- •Septic Cardiomyopathy
- •References
- •17: Aortic Stenosis
- •Introduction
- •Anatomic Evaluation
- •Hemodynamic Evaluation
- •References
- •Aortic Regurgitation
- •Doppler Findings
- •Vena Contracta (VC)
- •Jet Width/Area
- •Proximal Flow Convergence
- •Pressure Half-Time (PHT)
- •Pulmonary Regurgitation
- •Color Flow Doppler Findings: Jet Width, Jet Area, Jet Length, Vena Contracta
- •References
- •Mitral Stenosis
- •Etiologies
- •Planimetry
- •Continuity Equation
- •Pressure Half-Time
- •Deceleration Time
- •Mean Pressure Gradient
- •Tricuspid Stenosis
- •Etiology
- •Planimetry
- •Continuity Equation
- •Pressure Gradients
- •Pressure Half-Time
- •Consequences
- •References
- •Causes
- •Primary Causes
- •Secondary Causes
- •Jet Area
- •Vena Contracta
- •Jet Density
- •Pressure Half-Time
- •References
- •The Bernoulli Equation
- •Intracardiac Pressures
- •Left Atrial Pressure
- •Left Ventricular End-Diastolic Pressure
- •Right Ventricular Systolic Pressure
- •Case
- •References
- •22: Prosthetic Valves
- •General Imaging Principles
- •2D Imaging
- •3D Imaging
- •Doppler Evaluation
- •Case 1
- •2D Evaluation
- •Doppler Evaluation
- •Prosthetic Aortic Valve Dysfunction: Stenosis
- •Case 2
- •Prosthetic Aortic Valve Dysfunction: Regurgitation
- •Case 3
- •Case 4
- •Prosthetic Mitral Valve Dysfunction: Stenosis
- •Case 5
- •Prosthetic Mitral Valve Dysfunction: Regurgitation
- •Case 6
- •Prosthetic Valve Endocarditis
- •Case 7
- •Prosthetic Valve Thrombosis
- •Mechanical Valve Thrombosis
- •Case 8
- •Bioprosthetic Valve Thrombosis
- •Case 9
- •References
- •23: Infective Endocarditis
- •Introduction
- •Diagnosis
- •Echocardiographic Assessment
- •Left-Sided Endocarditis
- •Right-Sided Endocarditis
- •Prosthetic Valve Endocarditis
- •References
- •24: Cardiac Tamponade
- •Clinical Criteria
- •Cardiac Chamber Collapse
- •Inferior Vena Cava Plethora
- •Spectral Doppler Flow Variation
- •References
- •25: Ultrasound-Guided Pericardiocentesis
- •Background
- •Transthoracic Echocardiogram
- •Inferior Vena Cava Plethora
- •Right Heart Chamber Systolic/Diastolic Collapse
- •Doppler Flow Velocity Changes
- •Complications
- •References
- •Pathophysiology
- •Echocardiographic Diagnosis
- •Evolving Evidence
- •Two-Dimensional Evaluation
- •Septal Motion
- •Other 2D Findings
- •Doppler Evaluation
- •Hepatic Vein Pulse-Wave Doppler
- •References
- •Introduction
- •Normal Anatomical Variants
- •Right Atrium
- •Crista Terminalis
- •Eustachian Valve
- •Thebesian Valve
- •Chiari Network
- •Coronary Sinus
- •Persistent Left Superior Vena Cava (PLSVC)
- •Patent Foramen Ovale (PFO)
- •Atrial Septal Aneurysm
- •Left Atrium
- •Left Atrial Appendage
- •Atrial Suture Line After Cardiac Transplant
- •Right Ventricle
- •Moderator Band
- •Left Ventricle
- •False Tendons
- •Extracardiac Spaces
- •Pericardial Space
- •Sinuses
- •Exogenous Devices
- •Benign Masses
- •Myxoma
- •Fibroelastomas
- •Lambl’s Excrescences
- •Reverberations
- •Mirror Image
- •Side Lobe
- •Acoustic Shadowing
- •Conclusion
- •References
- •28: Left Ventricular Thrombus Part 1
- •Introduction
- •Etiology
- •Diagnosis
- •Echocardiography Technique
- •Contrast-Enhanced Echocardiography
- •Clinical Implications
- •References
- •29: Left Ventricular Thrombus Part 2
- •LV Thrombus Recognition: Sonographic Features
- •References
- •30: Left Atrial Thrombus
- •Etiology
- •Diagnosis
- •Clinical Implications
- •References
- •31: Right-Sided Thrombus
- •Introduction
- •Etiology
- •Diagnosis
- •Clinical Implications
- •Evolving Evidence
- •References
- •Introduction
- •Aortic Dissection
- •Abdominal Aortic Aneurysm
- •Aortic Thrombus
- •Image Acquisition
- •Pitfalls
- •References
- •33: Adult Congenital Heart Disease
- •Problems Causing Increased Pulmonary Blood Flow
- •Patent Ductus Arteriosus (PDA)
- •Atrial Septal Defect (ASD)/Patent Foramen Ovale (PFO) (Unrepaired/Repaired)
- •Problems Causing Decreased Pulmonary Blood Flow
- •Ebstein’s Malformation (Unrepaired)
- •Bicuspid Aortic Valve
- •Summary
- •References
- •Further Reading
- •Scanning Technique
- •Transudative Versus Exudative Fluid
- •Malignant Fluid
- •Empyema
- •References
- •Introduction
- •Background
- •Technique
- •Conclusion
- •References
- •36: Pulmonary Edema
- •Cardiogenic Vs. Noncardiogenic
- •Lung Zones/Locations
- •References
- •References
- •38: Diaphragm
- •Introduction
- •Measurement
- •Caveats
- •Diaphragm Thickening
- •Measurement
- •Caveats
- •Diaphragm Excursion
- •Measurement
- •Caveats
- •Measurement
- •Caveats
- •References
- •Introduction
- •Thoracentesis Technique
- •Tube Thoracostomy Technique
- •Manometry
- •Procedural Complications
- •Subpleural Mass Biopsy
- •Conclusion
- •References
- •40: Ultrasound During Intubation
- •Evidence
- •Limitations
- •References
- •41: Transcutaneous Laryngeal Ultrasonography: Vocal Fold Ultrasound
- •Introduction
- •Vocal Fold Motion Abnormalities
- •Paradoxical Vocal Cord Motion Disorder
- •References
- •Concept
- •Indications
- •Limitations
- •Views
- •The Hepatorenal Recess (Morrison’s Pouch)
- •The Splenorenal Recess
- •The Pericardial Space
- •The Pelvis
- •Pathologic Findings
- •References
- •Indications
- •Limitations
- •Bladder Ultrasound
- •Bladder Volume
- •Urinary Catheters
- •Hydronephrosis
- •Pitfalls
- •Renal Blood Flow
- •References
- •Stomach
- •Liver
- •Biliary System
- •Diagnostic Applications
- •Stomach
- •Liver
- •Biliary System
- •Paracentesis
- •Technique
- •Blakemore/Minnesota Tubes
- •Gastrostomy Tube
- •References

Assessment ofLeft Ventricular
Systolic Function inPatients
withDicult or Poor Acoustic
Windows
BrandonM.Wiley
12
Patient Positioning andAlternative
Acoustic Windows
The optimization of patient positioning is the initial approach for improving visualization of the
left ventricle. The parasternal and apical windows are usually optimized by placing the patient
in the left lateral decubitus position with the left
arm raised to expand the intercostal spaces.
Intubated, postsurgical, or other intensive care
patients with limited mobility can be slightly
tilted into a left lateral decubitus position by
using pillows placed under the right shoulder and
thorax (Fig. 12.1). The subcostal imaging window is a simple and high-yield view that is optimized with the patient supine and the knees bent
to relax the abdominal muscles (Video 12.1). In
spontaneously breathing patients, apical imaging
may be improved withheld expiration. Whereas
subcostal imaging is optimized with forceful
inspiration.
In addition to patient repositioning and respiratory control, the use of alternative acoustic windows may be valuable in patients with challenging
imaging. For example, in patients with moderate
to large left pleural effusions and nondiagnostic
transthoracic echocardiograms using traditional
acoustic windows, the left posterior thoracic window has been shown to provide improved visualization of the left ventricle [1, 2]. In patients with
left ventricular assist devices (LVAD), the right
transhepatic view has been shown to improve the
delineation of right and left ventricular systolic
function [3].
Supplementary Information The online version contains supplementary material available at https://doi.
org/10.1007/978- 3- 031- 80038- 2_12.
B. M. Wiley (*)
Keck School of Medicine, University of Southern
California, Los Angeles, CA, USA
e-mail: brandon.wiley@med.usc.edu
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2025
M. J. Lanspa, A. T. Levinson (eds.), Echocardiography and Ultrasonography in the ICU,
Respiratory Medicine, https://doi.org/10.1007/978-3-031-80038-2_12
149

150
ab
B. M. Wiley
Fig. 12.1 Patient positioning improves acoustic window (Video 12.1). (a) This hospitalized ICU patient is
imaged in the supine position and the resulting parasternal long- axis view is poor which precludes assessment of LV function. (b) The same patient is now
Ultrasonic Enhancement Agents (UEAs)
turned onto the left-side by placing towels under the
right shoulder and thorax. This repositioning signicantly improves the acoustic window providing adequate endocardial border denition for LV function
assessment
dence of transient back pain associated with
Denity that spontaneously resolves. The most
serious potential complication is an anaphylac-
Ultrasonic enhancement agents (UEAs), previously termed ultrasound contrast agents, are
composed of microbubbles that contain inert
high-molecular weight gas. These microbubbles
are smaller than red blood cells which allow them
to pass through the pulmonary circulation. UEAs
undergo volumetric oscillation when exposed to
an ultrasound eld and as a result, opacify the
blood pool during echocardiography which provides a strong contrast to the myocardium and
improves endocardial denition (Fig. 12.2).
Three commercially available UEAs in the
United States are approved for left ventricular
opacication (LVO) (Table12.1).
In practice, these agents are given intravenously either diluted in normal saline or as a tiny
bolus with a saline ush (Table 12.1). Dilution
and slow infusion of UEAs help avoid attenuation of the LV cavity. Additionally, B-mode
imaging with UEAs should be performed using
harmonic imaging at a low mechanical index
(MI<0.3) which prevents the destruction of the
microbubbles.
UEAs are safe and large studies have not
shown increased mortality in a variety of patient
populations [4]. The most common side effects of
UEA appear to be headaches. There is a low inci-
toid reaction which occurs at a rate of about 1in
10,000 [4]. The contraindications for each UEA
are listed in Table 12.1. Notably, in 2021, the
Food and Drug Administration removed hypersensitivity to blood and blood products as a contraindication for the use of Optison. Additionally,
studies have demonstrated safety in patients with
LVADs and those supported by extracorporal
membrane oxygenation (ECMO) [5, 6]. These
agents can also be used in patients with right-toleft intracardiac shunts and in those patients with
pulmonary hypertension. Finally, the American
Society of Echocardiography states that UEAassisted echocardiography “should not be withheld on the basis of any particular diagnosis or
comorbidity” in ICU or emergency room patients
with technically difcult imaging [4].
Clinical studies have shown that the use of
ultrasound enhancement agents greatly reduces
the number of suboptimal or nondiagnostic transthoracic echocardiograms (Video 12.2) [7]. In
addition to improved endocardial border delineation, LVO has been demonstrated to yield more
accurate and reproducible measurement of left
ventricular size and systolic function [8]. The
American Society of Echocardiography and the
European Association of Echocardiography rec-

ab
12 Assessment ofLeft Ventricular Systolic Function inPatients withDicult or Poor Acoustic Windows
151
c
Fig. 12.2 Echocardiogram with ultrasound enhancement
agent (UEA) (Video 12.2). Example of improvement in
endocardial border delineation with UEA. (a) and (c) are
apical 4-chamber and apical 2-chamber views without
Table 12.1
Ultrasound enhancement agents (UEAs)
Brand
name Manufacturer Important points Contraindications
Lumason Bracco Diagnostics
Denity Lantheus Medical
Optison GE Healthcare
Ultrasound enhancement agents approved for clinical use in the United States
• Requires refrigeration prior to use
• Requires mechanical agitation prior to use
• Given as 0.5mL bolus with slow saline
ush
Imaging
• Stored as dry powder
• Requires manual agitation prior to use
• Given as infusion diluted with normal
saline
• Requires refrigeration prior to use
• Requires resuspension prior to use
• Given as infusion diluted with normal
saline
d
UEA. (b) and (d) are the same views after the addition of
intravenous UEA.The UEA imaging is performed with
low mechanical index (MI 0.16). (Note the left ventricle is
on the left in image a and b)
Allergy to sulfur
hexauoride
Allergy to perutren
Allergy to perutren
ommend that ultrasound enhancement agents
should be used to improve left ventricular endocardial visualization when ≥2 contiguous wall
segments are not seen, to increase accuracy of LV
ejection fraction or to increase the physician con-
dence in the interpretation of LV size and function [8, 9].
The ability of ultrasound enhancement agents
to improve LV visualization is of particular
importance in the intensive care unit where a sig-

152
B. M. Wiley
nicant percentage of patients have suboptimal
or difcult acoustic windows (Fig.12.1, Video
12.2). A study of 632 consecutive patients (180
ICU patients) with technically difcult echocardiograms showed that the greatest benet of
UEAs was in ICU patients where nondiagnostic
studies decreased from 16.7% to 0.5% and
technically difcult studies decreased from
82.7% to 13.8%. The use of ultrasound enhancement agents averted the need for a transesophageal echocardiogram in 16.7% of the medical
ICU patients and 31.4% of the surgical ICU
patients. In addition, 9% of the medical ICU
patients and 25.5% of the surgical ICU patients
had a change in their medication regimen (hemodynamically active medications or anticoagulation) as a result of the ultrasound enhancement
agent [10]. These ndings were supported by a
larger study that retrospectively analyzed
1,538,864 patients who underwent transthoracic
echocardiography in an ICU setting [11]. Only
3.3% of these critically ill patients had an echocardiogram with an UEA.However, after multivariate adjustment, those patients who underwent
TTE with UEAs were statistically more likely to
have a change in inotropic therapy, vasopressor
therapy, and anticoagulant therapy. Additionally,
patients who underwent TTE with UEA had a
10% shorter ICU length of stay and were less
likely to undergo additional TTE or TEE studies.
M-Mode
Motion mode (M-mode) ultrasound demonstrates
a line of motion over time. Although this onedimensional mode of imaging has limitations, it
provides simple and reproducible parameters for
assessing LV systolic function when endocardial
denition by 2D echocardiography is suboptimal.
annulus toward the apex during LV systole. This
displacement distance is a measure of longitudinal
shortening of the LV cavity and correlates with LV
systolic function [12]. MAPSE can be assessed at
the septal, anterior, lateral, or inferolateral aspects
of the mitral annulus. The measurement is highly
angle-dependent and therefore must be performed
using the apical acoustic window to ensure parallel
alignment of the M-mode cursor with the LV
walls. The average systolic excursion distance varies between 12 and 15mm and is typically lowest
at the anterior and septal points [13, 14]. In general, MAPSE >10mm is associated with normal
systolic function (LVEF≥ 55%), and a value of
<8mm is associated with abnormal systolic function (LVEF<50%) (Fig.12.3) [13]. A large study
using the average of septal and lateral MAPSE
found that normal LVEF corresponded to ≥13mm
in men (sensitivity 92%, specicity 85%) and
≥11 mm (sensitivity 92%, specicity 72%) in
women [14]. A reduced MAPSE of <6mm (sensitivity 73–100%, specicity 99–100%), regardless
of gender, was associated with severely reduced
LV systolic function (ejection fraction ≤30%)
[14].
It is important to note that MAPSE, like ejection fraction, is pre—and afterload dependent.
MAPSE reects global LV longitudinal systolic
function but does not reect regional wall motion
abnormalities. The correlation of MAPSE with
ejection fraction is best in patients with normal or
dilated cardiomyopathies and may be limited in
the presence of severe LV hypertrophy or the
elderly. The reduced LV longitudinal function in
elderly or severely hypertrophied ventricles may
be compensated for by augmentation of radial
and circumferential contraction [13, 15].
Additionally, signicant mitral annular calcication may reduce LV longitudinal annular motion
in the presence of normal LVEF.
Mitral Annular Plane Systolic Excursion
Mitral annular plane systolic excursion (MAPSE),
also referred to as atrioventricular plane displacement (AVPD), describes the descent of the mitral
E-Point toSeptal Separation
The mitral valve E point-to-septal separation
(EPSS) is the distance between the interventricular septum and the anterior leaet of the mitral
valve during early diastole. This parameter is

ab
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12 Assessment ofLeft Ventricular Systolic Function inPatients withDicult or Poor Acoustic Windows
153
Fig. 12.3 M-Mode mitral annular plane systolic excursion (MAPSE). MAPSE is the measurement of mitral
annular apical displacement during systole and reects
longitudinal shortening of the ventricle. This measurement is typically performed using the septal or lateral
aspect of the mitral annulus. The M-mode cursor is placed
on the mitral annulus and aligned in parallel to the left
Fig. 12.4 M-Mode mitral valve E-point septal separation (EPSS). The normal M-mode prole of the mitral
valve includes opening of the leaets in early diastole
(E-point) followed by atrial contraction (A-point) and
then valve closure during systole (C-point). (a) The tracing of normal- sized left ventricle with normal systolic
function. There is brisk excursion of the mitral valve
ventricular wall. The measurement is made from the diastolic nadir of the M-mode tracing to the peak at endsystole. (a) Normal left ventricular systolic function,
MAPSE 15mm (measured on septal aspect of annulus).
(b) Dilated cardiomyopathy with severely reduced systolic function, MAPSE 5mm (measured on lateral aspect
of annulus). (LV left ventricle)
anterior leaet during early diastole and as a result the
distance between the tip of the anterior leaet and ventricular septum is small (EPSS <7mm, yellow bars). (b)
The tracing from a patient with a dilated cardiomyopathy and severely reduced left ventricular systolic function. The EPSS distance is markedly increased (25mm,
red line)
assessed using the parasternal long-axis view
with the M-mode cursor perpendicular to the
interventricular septum and directed through the
tip of the anterior leaet of the mitral valve.
Normal LV size and systolic function are associated with a small EPSS distance (0–5mm) due to
the brisk early diastolic excursion of the mitral
leaets which causes the anterior leaet to contact, or nearly contact, the interventricular septum
(Fig.12.4). The EPSS distance increases progressively with worsening LV systolic dysfunction
and dilation. An EPSS >7–8mm is a highly sensitive threshold for the presence of LV systolic
dysfunction [16, 17].
It is important to note that EPSS is not valid in
patients with prosthetic mitral valves.
Overestimation of left ventricular systolic function can occur when a small EPSS distance is the

154
B. M. Wiley
result of asymmetric septal hypertrophy or in the
presence of severe mitral regurgitation. Severe
aortic regurgitation or restricted excursion of the
mitral leaets due to intrinsic valvular disease
can cause a large EPSS that may lead to an underestimation of LVEF.The presence of atrial brillation may cause beat-to-beat variability in EPSS
which can confound its association with LV systolic function.
Pulse Wave andContinuous Wave
Doppler Echocardiography
Pulse wave Doppler echocardiography and continuous wave Doppler echocardiography measure the velocity of red blood cells and provide a
beat-to-beat assessment of cardiac hemodynamics that correlate well with invasive measures.
Stroke Volume andCardiac Output
Pulse wave (PW) Doppler echocardiography provides a noninvasive measurement of forward ow
which can be used to calculate stroke volume and
cardiac output. PW Doppler-derived stroke volume is calculated using the left ventricular outow (LVOT) velocity-time integral (VTI) and the
LVOT cross-sectional surface area (CSA) [18].
The LVOT VTI is measured through PW Doppler
interrogation of systolic ow in the LVOT. The
assessment is performed using the apical vechamber or three-chamber acoustic window
which enables the PW Doppler sample volume to
be placed in LVOT, just proximal to the aortic
valve annulus, with the angle of interrogation
aligned parallel to the ow. The LVOT systolic
PW Doppler spectral envelop should demonstrate
laminar ow and therefore appear smooth with a
discrete band of velocities. The LVOT systolic
PW Doppler signal should also include the closure click of the aortic valve. Tracing area under
the LVOT systolic PW Doppler signal yields the
LVOT VTI or systolic stroke distance (the distance the red blood cells travel during systole).
LVOT VTI is directly proportional to stroke volume with normal values of 17–24cm [19]. The
2
LVOT CSA=πr
since it is assumed to be circular and unchanging during systole [18]. The
radius (r) is derived from the LVOT diameter
(normal 2.1±2.2cm) which is measured in the
parasternal long-axis view at the same level the
PW Doppler sample volume was placed for the
LVOT VTI [20]. The nal calculation of LV
stroke volume is a product of LVOT VTI (cm)
and LVOT CSA (cm2) which yields a volume
(cm3=mL) [18]. The LV stroke volume is multiplied by the heart rate to provide the cardiac output (Fig.12.5).
The PW Doppler-derived stroke volume and
cardiac output correlate well with invasively
derived measurements in critically ill patients
[21, 22]. PW Doppler-derived stroke volume
index correlates with shock severity and
improves risk stratication for in-hospital mortality [23]. It is important to note that the LVOT
diameter is a xed parameter whereas the LVOT
VTI is variable and therefore the change in
LVOT VTI can be used to monitor dynamic
hemodynamics and assess relative changes in
stroke volume [24]. For example, the likelihood
of uid responsiveness can be evaluated by simply using the percentage change in LVOT VTI
elicited by uid challenge or passive leg raise
[25]. Furthermore, LVOT VTI has been shown
to be a powerful predictor of hospital mortality
in patients with cardiogenic shock [26].
The LVOT diameter (d) requires special attention since the value is squared
(CSA = π(d/2)
2
) which magnies any error in
measurement. Therefore, the LVOT diameter
should be measured using a focused, zoomed
view to maximize accuracy. The PW Doppler
sample volume interrogation angle must be parallel to LVOT ow (apical ve-chamber or threechamber view) to avoid underestimation of stroke
volume. Overestimation of the LVOT VTI and
calculated stroke volume can occur in the presence of abnormal ow acceleration or turbulence
in the LVOT caused by the systolic anterior
motion of the mitral valve or subaortic stenosis. It
is important to average several [1, 2, 27] PW
Doppler LVOT VTI signals in patients with irregular rhythms to account for beat-to-beat variation
in stroke volume. It is important to note that low

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Fig. 12.5 Example of PW Doppler LV stroke volume and
cardiac output calculation. (a) The systolic ow in the LVOT
is interrogated by PW Doppler. The sample volume is placed
in the LVOT just proximal to the aliasing of color Doppler
caused by turbulence and ow acceleration through the aortic
valve. (b) The PW Doppler signal of LVOT systolic ow
should be smooth, reecting laminar ow, with a discrete
band of red blood cell velocities (orange arrow). The closure
click of the aortic valve should be visible (blue arrow).
LV stroke volume may not reect primary LV
systolic dysfunction and instead be the result of
reduced LV preload caused by right ventricular
failure, obstructive shock, hemorrhagic shock, or
reduced forward ow due to severe mitral
regurgitation.
dP/dt
Continuous wave (CW) Doppler echocardiography can be utilized to evaluate the rate of pressure rise in the LV during isovolumic contraction.
This rate of pressure rise (dP/dt) is a marker of
LV contractility that is less affected by loading
conditions [28]. Normal LV systolic function is
characterized by a short isovolumic contraction
period with the concomitant rapid increase in LV
pressure. The isovolumic contraction period pro-
Tracing the area under the curve of the signal yields the
LVOT VTI (22cm). (c) The LVOT diameter (2.20cm) is
measured just at the annulus of the aortic valve using a
zoomed view. SV is approximated using the volume of a cylinder. The base of the cylinder is the CSA of the LVOT.The
height of the cylinder is the LVOT VTI. (PW pulse wave, LV
left ventricle, LVOT left ventricular outow tract, VTI velocity time integral, SV stroke volume, CSA cross-sectional surface area, HR heart rate)
longs and the rise of LV pressure is attenuated
with progressive worsening of LV contractility.
The CW Doppler-derived dP/dt is calculated by
measuring the time interval between the mitral
regurgitant velocity at 1 and 3m/s. This method
has been shown to correlate well with catheterderived invasive measurements of dP/dt [29, 30].
Normal LV contractility is associated with a dP/
dt > 1200 mmHg/s (steep pressure/time slope)
and severe LV systolic dysfunction is associated
with dP/dt<800mmHg/s [28] (Fig.12.6).
The accuracy of dP/dt evaluation by Doppler
echocardiography is angle-dependent and accurate
measurements require a parallel alignment of the
CW Doppler cursor with early systolic mitral regurgitation signal. An increased CW Doppler cursor
intercept angle will result in an underestimation of
dP/dt. The feasibility of dP/dt measurements is limited with inadequate mitral regurgitation or in the

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B. M. Wiley
Fig. 12.6 dP/dt (rate of pressure rise). This illustrates
the calculation of dP/dt using the CW Doppler tracing of
mitral regurgitation in a patient with an ischemic cardiomyopathy and severely reduced LV systolic function.
The red dashed line represents the time interval (Δt)
required for an increase in mitral regurgitation velocity
from 1 to 3m/s. The mitral regurgitation velocity is a
presence of an eccentric regurgitant jet that precludes parallel alignment of the CW Doppler cursor
during the target time interval.
Tissue Doppler Imaging (TDI)
TDI measures the velocity of the myocardium in
contrast to conventional PW and CW Doppler
which measure the velocities of red blood cells.
TDI can be performed using both pulsed wave
(PW-TDI) and color modes. PW-TDI measures
the peak velocity and the color-TDI mode measures the mean velocity. TDI provides a sensitive
assessment of regional systolic and diastolic
myocardial mechanics [31].
Systolic Mitral Annular Velocity (s′)
The TDI-derived systolic mitral annular velocity (s′ or sm) is analogous to MAPSE, an indicator of LV systolic longitudinal function. The s′
surrogate for the change in LV pressure since the left
atrial pressure is relatively stable during early systole.
As LV contractility worsens, the rate of rise of LV pressure is attenuated and the time interval (Δt) prolongs.
Normal LV contractility is associated with a dP/
dt>1200mmHg and severe LV systolic dysfunction is
associated with a dP/dt<800mmHg
velocity is measured using PW-TDI with the
sample volume placed at the medial or lateral
aspects of the mitral annulus in the apical fourchamber view. The s′ measurement is angledependent and the PW-TDI cursor must be
parallel to the apical descent of the mitral annular plane. The peak s′ velocity has been correlated to LV ejection fraction and dP/dt [32]. The
mean s′ velocity is 8.9cm/s in healthy controls
with the septal s′ velocity usually lower than
that of the lateral [33]. Additionally, the mean s′
velocity decreases with age [33]. An s′ value
<8cm/s has a sensitivity of 86% and specicity
of 93% for mild to moderately reduced LV systolic function (LVEF 30–50%). An s′<6cm/s
has a sensitivity of 92% and specicity of 84%
for severely reduced LV systolic function (LVEF
<30%) [34] (Fig.12.7).
It is important to note that TDI interrogates
myocardial velocity and as a result, it can be
affected by tethering and translational forces
which may mask regional hypokinesis. The presence of a mitral prosthesis or signicant mitral

12 Assessment ofLeft Ventricular Systolic Function inPatients withDicult or Poor Acoustic Windows
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Fig. 12.7 TDI mitral annular systolic velocity (s′). TDI
mitral annular systolic velocity provides a measure of
myocardial velocity. The s′ velocity, similar to MAPSE, is
a measure of LV systolic longitudinal function. The measurement is the peak positive velocity during systole and
can be made using the medial (s
) or lateral (sl) aspect of
m
annular calcication precludes the correlation of
s′ velocity with LV systolic function.
Cardiac Cycle Time Intervals
andMyocardial Performance Index
The myocardial performance index (Tei index) is a
parameter that enables the assessment of global LV
function [35]. Tei index is performed by using
Doppler echocardiography (conventional PW or
TDI-PW) to dene cardiac cycle time intervals and
is founded in the principle that LV dysfunction is
characterized by prolongation of LV isovolumetric
contraction and isovolumetric relaxation with concomitant shortening of the LV ejection time.
TDI-PW is the simplest method for calculating the
Tei index in patients with challenging acoustic windows since the entire cardiac cycle time can be captured using a single view of the medial or lateral
aspect of the mitral annulus in the apical fourchamber window [36] (Fig.12.8). Additionally, the
TDI-PW method simultaneously provides the
medial s′ velocity parameter for LV systolic func-
the mitral annulus. (a) This patient with acute decompensated had left ventricular ejection fraction of 15% and a s′
velocity of 3cm/s. (b) The s′ velocity of 10cm/s correlated with normal left ventricular systolic function and
ejection fraction of 65%. (TDI tissue Doppler imaging,
MAPSE mitral annular plane systolic excursion)
tion assessment. The measurement of the Tei index
using conventional PW Doppler requires imaging
of both the mitral inow pattern and LVOT systolic
ow signal [35]. The Tei index has been shown to
be highly reproducible and independent of blood
pressure, heart rate, and mitral regurgitation [35].
Normal mean LV Tei index is >0.40 and studies
have correlated increased values with worse clinical outcomes in patients with congestive heart failure, acute myocardial infarction, and transcatheter
aortic valve replacement [35–39]. It is important to
note that the myocardial performance index can
also be used to assess right ventricular function.
The evaluation of right ventricular index of myocardial performance (RIMP) is analogous to the
PW-TDI left ventricular method but uses the lateral
aspect of the tricuspid annulus (normal RIMP
PW-TDI is >0.54) [40].
The application of the Tei index is limited in
patients with variable rhythms (atrial brillation
or signicant ectopy). The assessment is precluded in patients with signicant intraventricular dyssynchrony, paced rhythms, and prosthetic
mitral valves.

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Fig. 12.8 Tissue Doppler imaging—Tei index (myocardial performance index). (a) The Tei index can be assessed
using Tissue Doppler imaging (TDI) of the medial annulus of the mitral valve. This patient has normal LV diastolic and systolic function with short IVCT and IVRT
intervals. The Tei index in this patient is 0.39 (normal
<0.40). Note that the s′ velocity is also normal (10cm/s).
Summary Points
• Delineation of left ventricular systolic function using traditional 2D-echocardiography
can prove challenging in critically ill patients
due to poor acoustic windows.
• Ultrasound enhancement agents improve
visualization of the endocardium and have
been demonstrated to be effective at salvaging
technically challenging or nondiagnostic
echocardiograms in the intensive care unit.
• Pulse wave Doppler-derived stroke volume
and cardiac output are key parameters that
correlate well with invasive measurements in
critically ill patients.
– LVOT VTI can be monitored to assess
dynamic changes in hemodynamics.
(b) This is a 25-year-old patient with a dilated cardiomyopathy and severe LV systolic dysfunction. The isovolumetric contraction and relaxation times are prolonged.
The Tei index in this patient is 0.63. Note the s′ velocity is
also reduced at 6.8cm/s. (IVCT isovolumetric contraction
time, IVRT isovolumetric relaxation time, LV left
ventricle)
– dP/dt>1200mmHg/s correlates with nor-
mal LV systolic function.
– dP/dt < 800 mmHg/s correlates with
severely reduced LV systolic function.
• Tissue Doppler mitral annular systolic
velocity (s′) correlates with LV systolic
function.
– s′ >8 correlates with normal LV systolic
function.
– s′<6 has high sensitivity and specicity
for severely reduced LV systolic
function.
• Myocardial performance index (Tei index) is a
parameter that assesses global LV function.
– Tei index <0.40 is associated with normal
LV systolic function.
• Mitral annular plane systolic excursion
(MAPSE) is an M-mode parameter that correlates with LV systolic function.
– MAPSE >10mm is associated with normal
LV systolic function.
– MAPSE <6mm is associated with severely
reduced LV systolic function (LVEF <30%).
• Pulse wave Doppler-derived dP/dt is a measure of LV contractility that correlates with
invasive measurements.
Questions
1. A 45-year-old male with no prior medical history presents to the cardiac intensive care unit
after undergoing emergent percutaneous
intervention for acute ST-elevation myocardial infarction. He is tachycardiac (heart rate
114) with a blood pressure of 95/65mmHg.
What is his cardiac index if his body surface
area is 2.2m2?
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