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138
EF
V=−
()
J. N. Wilkinson and F. Mohammed
LV Function: Ejection Fraction
The most common method of assessing LV systolic function is the ejection fraction (EF) from
the biplane method of disks. This method measures LV systolic and diastolic volumes in two
different planes. Utilizing the apical fourchamber view and apical two-chamber views, the
endocardial borders are traced, then the cavity is
divided into approximately 20 discs. The EF is
calculated by taking the difference of LVEDV
and LVESV, divided by the LVEDV.
Normal EF values are presented in Table11.1,
although as with all values in Table 11.1, it is
important to remember that these ranges constitute a continuum rather than a discrete threshold
between normal and abnormal. Reference values
also vary with age [1]. It is important to remember the clinical context when interpreting
EF.Ejection fraction is affected by preload and
afterload, as well as by vasoactive medications. A
patient who has an EF of 52% while on high
doses of vasopressors may have abnormal contractility. Similarly, a patient who has an EF of
75% in the setting of low preload may decrease
their EF substantially upon receipt of intravenous
uid. A patient’s ejection fraction may change
over the course of hours or days in response to
critical illness or treatment [8]. These frequent
changes imply three conclusions especially relevant for the critically ill: (1) EF is not always the
best marker of intrinsic cardiac function, (2)
assessing ventricular function may require alternative methods, and (3) repeated measurements
may be needed to track changes in EF.
Patients with high ejection fractions
(>70–75%) are classied as hyperdynamic.
These patients are often tachycardic, and often
hypovolemic. When interpreting these images, it
is important not to conate tachycardia with
hyperdynamic contractility—it is easy to do so
when assessing qualitatively. Ejection fraction
does not always correspond to stroke volume or
cardiac output. In the setting of hyperdynamic
hypovolemia, a patient may have very high EF
with a low stroke volume. In the setting of dilated
LVEDVLVESV LVED
/
cardiomyopathy or dilated ischemic heart disease, a patient may have a relatively preserved
stroke volume despite having a profoundly low
EF.The use of EF also requires adequate image
quality to measure LVEDA and LVESA.
EF (Simpson’s Biplane) Method
• Perform the following in BOTH the apical
two-chamber and four-chamber views.
• Trace the endocardial borders of the LV,
excluding any sub-valvular apparatus/papillary muscles.
• Ensure the axis line is placed as perpendicular
to the LV cavity as possible, running from the
LV apex to the base.
• Record one series in LV diastole.
• Record another in LV systole.
Cautions
• When performing any Simpson’s biplane
measurements for EF, axis measurements
should be as identical as possible between the
A4c and A2c views (<10% difference). Large
differences may highlight off-axis views, or
measurements performed that were not truly
perpendicular to the LV cavity.
• If the views are foreshortened, then EF measurements may be over-estimated.
LV Function: Cardiac Output
Ironically, stroke volume is typically not measured using volumetric assessments, as minor
errors in image acquisition and tracing can lead
to inaccurate measurement. The preferred method
of calculating stroke volume is the product of the
left ventricular outow tract (LVOT)
cross- sectional area and the velocity time integral
(VTI) of blood ow exiting the LVOT during systole. This method is also used in the continuity
equation calculation for valve areas among other
applications (see Chap. 17) [9]. The LVOT diameter is measured from an apical ve-chamber
Ar=
π
2
11 LV Systolic Function
139
view. The diameter is measured from the inner
edge of the septal myocardium to the inner edge
of the anterior mitral leaet in mid-systole. The
diameter is measured approximately 0.3–1.0cm
from the aortic valve orice (Fig. 11.10). The
diameter should be parallel to the aortic valve,
and perpendicular to the outow tract walls. The
cross-sectional area is calculated from the LVOT
diameter as:
where the radius, r, is one-half the diameter.
The second component of the calculation of
stroke volume is the velocity time integral from
the apical ve-chamber or apical long-axis
(three-chamber) view. This waveform is obtained
by placing the sample gate of a pulsed wave
Doppler proximal to the aortic valve, ideally the
same distance as where the LVOT diameter was
measured. The angle of the jet should be aligned
LVOT Diameter
Cardiac Index
π
=
2
to be parallel to the ultrasound. The operator
should adjust the baseline, scale, and sweep
speed to optimize the waveform for measurement. The waveform should demonstrate laminar
ow with a bright narrow band and a black interior, with a well-dened peak. The waveform is
traced using the modal velocity (the middle of the
dense signal, Fig. 11.11), not the black-white
edge (Fig.11.12). The imaging software should
calculate the area above the curve or the integral.
The integral of velocity and time is distance,
therefore the VTI is reported in cm. The VTI can
be thought of as the average distance blood travels through the LVOT during systole. Multiplying
the VTI with the LVOT cross-sectional area
yields the stroke volume in cubic centimeters or
milliliters. Multiplying the stroke volume by the
heart rate will yield cardiac output in milliliters.
Dividing the cardiac output by body surface area
will yield a cardiac index.
2
××
LVOT VTI
Body Surface Area
1000
L
1
mL
× Heart Rate
Fig. 11.10 Measurement
of the diameter of the left
ventricular outow tract
in mid systole, 0.3–1.0
cm from the aortic valve
orice. Calipers can be
seen. A normal
measurement is around
2cm
140
Fig. 11.11 An apical
5-chamber view. Pulsed
wave doppler is placed
into the LVOT, proximal
to the aortic valve, at the
point the LVOT was
measured. The correct
mid part of the dense
black waveform is
traced, using the modal
velocity
Fig. 11.12 An apical
5-chamber view. Pulsed
wave doppler is placed
into the LVOT, proximal
to the aortic valve, at the
point the LVOT was
measured. The incorrect
black/white edge of the
trace has been measured
here
J. N. Wilkinson and F. Mohammed
There are multiple potential errors that may
arise when measuring the stroke volume. The
LVOT diameter is an imperfect measurement for
the LVOT cross-sectional area, as the LVOT is not
truly circular. Additionally, any minor imprecision
in the measurement of the LVOT will be squared
and multiplied. When performing serial measurements of cardiac output, it is unnecessary to measure the LVOT diameter multiple times, as each
time will introduce unnecessary variation. As many
decisions in critical care rely on relative changes in
stroke volume or cardiac output rather than absolute measurements, many intensivists may forgo
the measurement of the LVOT diameter altogether,
instead of assessing changes in LVOT VTI and/or
heart rate. Additional errors can occur when the
pulsed wave Doppler is not aligned with the outow jet. The greater the angle, θ, between the true
jet and the ultrasound beam, the greater the inaccuracy in measuring velocity. Measured velocity is
the true velocity multiplied by cosineθ. One could
correct this error by dividing the velocity by
11 LV Systolic Function
141
cosineθ, but this introduces another potential error
in measuring θ. In practice, it is preferred to not
attempt correction but to attempt to align the jet so
θ is <15°, which would mean the measured jet is
>97% of the true jet. For repeated measurements of
stroke volume, consistency is essential. Changing
the angle of the probe will affect the measurement
of stroke volume. Arrhythmia is another potential
source of inaccuracy. If the VTI is not representative of the average VTI or the heart rate, the cardiac
output will be inaccurate. One should not select the
VTI occurring in relationship to a premature ventricular complex. In the setting of atrial brillation,
one may take an average of several consecutive cardiac cycles to estimate stroke volume or cardiac
output. Respiratory variation will also affect cardiac output, as it may affect preload. Measuring
cardiac output from a VTI at end-inspiration may
be substantially different from one measured at
end-expiration. Severe aortic insufciency will
also result in inaccuracy. The VTI will measure
blood exiting the ventricle, but will not account for
blood reentering the ventricle, thus overestimating
cardiac output. In such a case, it may be preferable
to either calculate the regurgitant fraction, if possible (see Chap. 18) or to calculate stroke volume
from another area of the heart, such as mitral inow
or right-sided cardiac output.
Regional Wall Motion Abnormalities
The left ventricle is divided into segments.
Although 16- and 18-segment models exist, the
17-segment model is the most commonly used
(Fig. 11.13, regional abnormalities in contractile
function). This model correlates with the segments
used in other imaging modalities. The base and
mid-chamber are each divided into six segments:
anteroseptal, anterior, anterolateral, inferolateral,
inferior, and inferoseptal, while the apex is divided
into ve segments: anterior, lateral, inferior, septal,
and apical. The standard assessment of these segments is visual estimation, although newer technologies such as strain (see below) may quantify
function with greater reproducibility and accuracy.
Regional wall motion abnormality is an indicator
of ischemic heart disease, but it may also be present
in other conditions, including myocarditis, stress
cardiomyopathy, and septic cardiomyopathy.
When assessing each segment, it is important to
evaluate wall thickening rather than wall movement. Translation of diseased myocardium may still
occur when that region is tethered to an adjacent
segment or when the entire heart is displaced during
the cardiac cycle. Each segment should be assessed
in multiple views. The short- axis view, when
scanned from base to apex, will image all segments
RCA
LAD
CX
Fig. 11.13 Coronary artery territories associated with anatomical areas of the heart
RCA or CX
LAD or CX
RCA or LAD
142
J. N. Wilkinson and F. Mohammed
of the heart. The parasternal or apical long axis will
image the anteroseptal and inferolateral walls. The
apical four-chamber will image the anterolateral
and inferoseptal walls, and the apical two-chamber
will image the anterior and inferior walls.
Each segment is assigned a wall motion score
based on the visualized thickening of the myocardium. Normokinesis should thicken ≥5 mm or
>40%; Hypokinesis should thicken 2–4mm or
10–40%; Akinesis should thicken 0–1 mm or
<10%; and dyskinesis is akinesis with expansion
of the segment during systole. These scores are
graded 1–4 from normokinesis to akinesis for
each segment. The wall motion score is the sum
of all these scores. The wall motion score index is
the sum of these scores divided by the number of
visualized segments. Although global assessments are useful, regional wall motion assessments are more useful when they are correlated
with coronary artery territories (Fig.11.14). As
mentioned above, regional wall motion abnormalities may occur in the absence of coronary
Fig. 11.14 Detailed anatomical area descriptions of the transthoracic echo views
()
()
/e
∆∆ ∆
ε
=
11 LV Systolic Function
143
artery disease. Bundle branch block, other conduction delays, and right or left ventricular pacing may result in abnormal regional wall motion.
Right ventricular pressure or volume overload
may also result in abnormal septal motion.
Methods
• Obtain the following views
– Parasternal Short-axis view
– Apical four-chamber view
– Apical two-chamber view
– Parasternal long-axis view
Strain instantaneous lengthbaselinelengthbaseline l
ε
=−
Strain rate is the rate at which deformity
occurs.
//timemyocardial velocity
Strain may represent different axes of contraction. Radial strain represents the thickening of
the myocardium in the short axis. Circumferential
strain represents the shortening of the short axis
during systole, and longitudinal strain represents
the myocardial shortening from base to apex.
During systole, the ventricular wall contracts,
resulting in a negative longitudinal strain value.
Discussion of strain can be confusing, as a
change from −15% to −20% is described as an
improvement in strain, and the literature is
inconsistent with describing this change as an
increase or a decrease in strain. Strain is typically assessed using specialized software that
employs frame- by- frame tracking of unique
speckle “ngerprints” within the myocardium.
The method of assessment is semi-automated.
The operator typically selects an appropriate
image and traces the myocardium. The software
will track the tracing throughout the cardiac
cycle (Fig. 11.15, Video 11.2, Strain). Strain
imaging requires high- quality images and high
gradient baseline length
• Assess wall thickening during systole
– Normal: >40%, ≥5mm
– Hypokinetic: 10–40%
– Akinetic: <10%
– Dyskinetic: Akinesis and expansion during
systole
Strain
Strain is a newer assessment of ventricular function that measures the amount of deformation in
a region of the myocardium. Strain is the percent
change in length relative to its baseline.
ength
frame rates (40–90Hz). For global longitudinal
strain, the apical four- chamber, apical twochamber, and apical long- axis (three-chamber)
are all measured, and the software will create a
composite 17-segment ventricle, with strain values for each region as well as a global value. The
role of strain imaging is well established in conventional echocardiography, as it may detect
subtle dysfunction that is otherwise missed in
conventional assessment. Strain may herald
changes in cardiac function well before it is
reected by changes in EF.Strain is inuenced
by preload (it increases as LV size increases) and
afterload (decreases as blood pressure rises)
[10]. Strain rate may be less dependent on load
than strain. One potential application of strain is
that it may be less preload or afterload dependent than ejection fraction, and global longitudinal strain might identify patients with septic
cardiomyopathy that might otherwise be missed
[11]. Despite this, the role of strain in critical
care is still evolving, with insufcient evidence
at present to justify its routine application in the
critically ill. Normal reference values may
depend on the software version and vendor.
Healthy persons may have a global longitudinal
strain of around −20%.
144
Fig. 11.15 Strain measurement of the LV cavity
J. N. Wilkinson and F. Mohammed
Strain Methods
• Strain measurement method may be software-
dependent
• Normal longitudinal systolic strain
– − 16% to −22% with values closer to 0
being abnormal
• Normal resting longitudinal strain rate
– 1.0/s (s) to 1.4/s
Global Longitudinal Strain measurement can
detect:
– Left ventricular Hypertrophy
– Degree of cardiotoxicity
– Ischemic heart disease
– Regional strain
– Chamber function
– Diastolic dysfunction
– Valve disease
– Atrial Fibrillation risk
– Pulmonary hypertension
Cautions
– When regional tracking is suboptimal in more
than two myocardial segments in a single view,
the calculation of GLS should be avoided.
– Intervendor and intersoftware variability exist,
therefore the serial assessment of GLS in individual patients should be performed using the
same vendor’s equipment and the same
software.
(a) Measuring LVOT diameter parallel to the
aortic valve during each assessment of cardiac output.
(b) Ensuring that the pulsed wave Doppler is
aligned <15° from the outow jet during
each assessment of cardiac output.
(c) Measuring velocity time integral tracings at
end-expiration for each assessment of cardiac output.
(d) Selecting velocity time integral tracings dur-
ing periods without arrhythmia for each
assessment of cardiac output.
11 LV Systolic Function
145
Questions
1. A 67-year-old male presents to the intensive
care unit in septic shock for communityacquired pneumonia. Prior to admission, he
had complained of 3 days of dyspnea and
1day of pleurisy. He is receiving mechanical
ventilation, norepinephrine, and epinephrine.
A troponin-I level is measured at 3.2ng/mL
(normal range<0.04ng/mL). An echocardiogram is performed (Video 11.3). Which of the
following is most correct?
A. The patient has global hypokinesis from
septic cardiomyopathy.
B. The patient has takotsubo cardiomyopa-
thy with apical ballooning and compensatory basal hyperkinesis.
C. Vasopressors may worsen contractility in
this setting.
D. The patient is experiencing a myocardial
infarction in the circumex distribution.
Answer: C.Vasopressors may sometimes
worsen contractility in this setting. This
patient has septic cardiomyopathy with
regional wall motion abnormality: a hypokinetic inferoseptal wall. The pathophysiology
of septic cardiomyopathy is complicated. One
proposed mechanism for dysfunction is circulating endogenous or exogenous catecholamines. In some cases, additional vasopressors
can worsen function [8]. A is incorrect.
Although septic cardiomyopathy can present
with global hypokinesis, this patient is demonstrating a normokinetic anterolateral wall.
B is incorrect. Although septic cardiomyopathy and stress cardiomyopathy may have similar pathophysiology, the reason this answer is
incorrect is because the takotsubo pattern
describes a specic type of stress cardiomyopathy with apical ballooning and basal
hyperkinesis (Video 11.4) not seen here. D is
incorrect. Myocardial infarction is a possible
complication of septic shock, but this distribution of regional wall motion abnormality
demonstrates inferoseptal hypokinesis, consistent with right coronary or left anterior
descending coronary distribution. The circumex is more likely to perfuse the anterolateral wall. Troponin elevation and regional
wall motion abnormalities in the absence of
coronary artery disease are common ndings
in septic shock.
2. A 17-year-old male presents to the emergency
department in hemorrhagic shock after a
motor vehicle collision. Massive transfusion
protocol is initiated. The heart rate is
124beats/min. Blood pressure is 68/44mmHg.
An echocardiogram is performed to measure
cardiac output. The velocity time integral
from this image is measured at 60 cm
(Fig.11.16). The LVOT diameter is measured
at 1.95cm. Which of the following is true:
A. The cardiac output is 22.2L/min.
B. The VTI is an underestimate because the
ultrasound angle of insonation is not
aligned with the LVOT jet.
C. The cardiac output is high because of
severe aortic insufciency.
D. The VTI is high because its corresponding
cross-sectional area is severely reduced.
Answer: D. The VTI is high because its
corresponding cross-sectional area is severely
reduced. This patient has dynamic outow
obstruction. The Doppler waveform is very
high because the ventricular cross-sectional
area is extremely small during mid—to late
systole. The image reveals that the sample
gate is positioned mid-chamber rather than at
the LVOT.The late-peaking waveform is suggestive of dynamic outow obstruction. A is
incorrect. Although the calculation of cardiac
output from the numbers provided yields an
answer of 22.2L/min, the VTI is not the VTI
of the LVOT, but of the LV mid-ventricle,
which has a different cross-sectional area, and
is likely much smaller than 1cm
2
during systole. B is incorrect. Although the ultrasound
angle is not aligned with the outow jet, the
sample gate is also not positioned in the
LVOT.C is incorrect. There is no evidence of
severe aortic insufciency in the provided
image, although this image is not useful to
ascertain the presence or absence of aortic
insufciency. Cardiac output may be overestimated in the setting of aortic insufciency, as
the calculation for cardiac output from VTI
does not typically account for the regurgitant
146
J. N. Wilkinson and F. Mohammed
Fig. 11.16 Question 2 LVOT VTi measurement
volume. In such a case, the cardiac output
would be lower than calculated. Regardless,
aortic insufciency would not explain the
Doppler pattern seen in this patient.
3. A 58-year-old woman presents to the emergency department in cardiogenic shock after
an out-of-hospital arrest with the return of
spontaneous circulation. The patient continues to have frequent premature ventricular
complexes. The ICU team monitors her status
with serial echocardiography. Which of the
following may worsen accuracy for repeated
measures calculation of cardiac output:
A. Measuring LVOT diameter parallel to the
aortic valve during each assessment of
cardiac output.
B. Ensuring that the pulsed wave Doppler
is aligned <15° from the outflow jet
during each assessment of cardiac
output.
C. Measuring velocity time integral tracings
at end-expiration for each assessment of
cardiac output.
D. Selecting velocity time integral tracings
during periods without arrhythmia for
each assessment of cardiac output.
Answer: A. Measuring LVOT diameter
parallel to the aortic valve during each assessment of cardiac output. LVOT diameter is not
expected to change during these assessments,
but the potential imprecision in measuring the
LVOT can result in signicant errors. For
example, a measurement of 20 mm versus
19mm results in an 11% difference in cardiac
output. When making serial measurements,
consistency is important. It is reasonable to
use a single high-quality measurement of
LVOT diameter for repeated assessments of
stroke volume. All the other answers will
improve the accuracy of the cardiac output.
11 LV Systolic Function
147
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