Contents

Contents
1. Physics in Ultrasonography ................................................................................................. 03
2. Lung Ultrasound - Basics ...................................................................................................... 10
3. Summarizing Lung USG ....................................................................................................... 20
4. Echocardiography – Basics .................................................................................................. 22
5. Focussed Assessment with Sonography in Trauma (FAST)....................................... 29
6. Ultrasonographic assessment of Inferior Vena Cava (IVC) ........................................ 37
7. Cranial Ultrasound ................................................................................................................... 43
8. Cases ............................................................................................................................................ 55
9. Predicting and measuring fluid responsiveness with echocardiography ........... 64
10. Echocardiography Atlas ....................................................................................................... 77
11. Echocardiographic Calculations ....................................................................................... 90

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 Contributors
Contributors
Dr Neeraj Agarwal
Dr Parveen Bharadwaj
Dr Vikas Bansal
Dr Ashish Simaly
Dr Veena
Dr Amit Vij
Dr Neil Castellino
Dr Nilay Chaudhry
Dr Ashwin Arora
Dr Anuj Khatri
Dr Neeraj
Dr Satender Mittal
Dr Sameer Punia
Dr Bharat Mehra
Dr Ravi
Dr Vinamra
Dr Mukul

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CHAPTER 1
Physics in Ultrasonography

1. WHY DO I NEED TO LEARN h>dZ^KhE

Beginners in any course are often tempted to skip the basic principles of physics, understanding its
basis; but initially concentrate on the practice & skills.
Although this appears acceptable, we will soon find it becomes difficult to cope with image
optimization which is the most essential step in critical care ultrasound as you will guide your
diagnostic & therapeutic treatment strategies based on it. It helps us understand the limitations of
my equipment & is vital to understand artifacts with their potential correction. So, in short without
understanding basics, we may be able to acquire a skill but we will not be able to master it.

2. WHAT IS ULTRASOUND?

Sound with a frequency above 20,000 Hz is termed ultrasound. Diagnostic ultrasound utilizes a
frequency range of 2–20 MHz (1 MHz = 106 Hz).

3.PROPERTIES OF SOUND WAVE

x Frequency=number of cycles per second (Hz=1/s)
x Wavelength=length of one complete cycle (measurable distance)
x Velocity of sound is constant for a given medium (330 meters/s in air; 1500 meters/s in water)
x Velocity=Frequency X Wavelength
x Sound travels through tissues, causing molecules to vibrate
x Human hearing: 20 Hz to 20,000 Hz
x Ultrasound: >20,000 Hz
x Diagnostic ultrasound: 1 MHz to >20 MHz

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 x Most ŽŵŵŽŶůLJƵƐĞĚ&ƌĞƋƵĞŶĐŝƐŝŶCritical Care: 2.5-10 MHz

4. UNDERSTANDING FREQUENCY & ITS IMPORTANCE

V = frequency (f) X wavelength (λ)
x However, this velocity is relatively constant in soft tissue at 1540 m/s, and so wavelength is
inversely proportional to frequency, ie λ α 1/f.
x So if V is constant, then…..if frequency increases, wavelength must decrease…..which means
that with increased frequency, the distance the sound waves travel decreases (i.e. less
penetration into tissue)
x In simple terms, more the frequency, we can see superficial structures better with good
resolution like a linear probe (8-12Hz) for vascular access.
x The scanning applications for a High Frequency Transducer include;
Superficial blood vessels, Breasts, Testes, Thyroid, Nerves, Superficial skin lumps, Lung

x The scanning applications for a Low Frequency Transducer include:

Abdomen – liver, spleen, kidney, gall bladder, bladder; Aorta; Obstetrics; Focused Assessment
using Sonography for Trauma (FAST) scan; Lung, Muscle Biofeedback

5. HOW IS IMAGE PRODUCED IN USG SCREEN?

A source of alternating current makes the piezoelectric crystals in transducers to vibrate at high
frequency producing ultrasound waves. This wave is then transmitted to the patient through a
conductive gel. These sound waves go through structures underneath the transducer and
information is relayed back as reflected sound waves.
A transducer acts as a generator of ultrasound waves for only 1% of the time and acts as a
microphone to listen to the incoming waves for the rest 99% of the time. These echoed waves
than cause the crystals in transducer to vibrate. These vibrations than generates an electrical
current; which is then presented as the grayscale you see on the ultrasound screen
Higher frequency produces more waves in a given time, thereby increasing the resolution (ability
to discriminate between 2 separate structures along the axial plane).

6. WHAT DO WE SEE ?
Images formed by properties of the returning echoes: Depth and Direction
Depth - distance from the probe; calculated by the time elapsed between signal pulse and the
received echo
Direction - the crystals precisely differentiate the direction of the returning echoes
The sound wave is calculated to be traveling through human tissue at body temperature
(approx. 1540 m/sec) and the system measures the round-trip time and intensity of the
returning “echo”

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 The returning intensity determines (is proportional to) the grayscale assignment of the pixel
(dot) of information on the screen
The surface area of a transducer in contact with the patient is referred to as the “footprint” of
the probe (small probes=small footprint; e.g. cardiac probe)
In general, organized molecules=better image
>iver ŚĞůĚƐhůƚƌĂƐŽƵŶĚ/ŵĂŐŝŶŐ
¾ Also, it is referred to as an “acoustic window”
¾ In other words, the liver helps to improve visualization of other structures
¾ We use the liver to see the IVC, the cardiac subxiphoid view, the gallbladder, etc.
Fluid densities are ideal for imaging
Air is bad disrupts propagation of sound waves.
Fat is also bad because it also does not transmit waves well.
B-mode Ultrasound:
x The gray-scale ultrasound you see on the screen
x Strong echoes represented by white dots
x Absence of echoes represented by black dots
x Everything else is somewhere in-between
x Hyperechoic=bright (white) objects
x Anechoic=dark (black) objects
x Everything else is somewhere in-between=Isoechoic (same echogenicity), hypoechoic
(less echoic), etc.

 '(6&5,%(7+(,'($/8/75$6281'%($0
The beam produced by the transducer has a typical theoretical description involving a Near Field
where the beam is at its narrowest, and a Far Field where the beam starts to diverge from the
midline. The angle of divergence is related to the wavelength and the diameter of the beam by the
equation

8. WHAT IS THE ACTUAL ULTRASOUND BEAM ?

The actual beam shape is somewhat different from the textbook description, with “off-axis
energy” (side lobes and grating lobes) propagating at angles to the direction of main beam.
Reflected echoes from these beams will be received by the transducer, and interpreted as
though they originated from within the main beam field. This also forms the basis for side lobe
artifacts.

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 9. DESCRIBE BRIEFLY ABOUT TRANSDUCERS?

TABLE 1.3
Comparison of the three types of transducers
Linear array Curvilinear array Phased array
Frequency range (Hz) 4–12 2–4 1–4
Footprint (cm2) Large (~5 × 1) Large (~6 × 1.5) Small (~2.5 × 1.5)
Axial resolution Very good Good to average Good to average
Penetration Poor Good Good
Coverage Small Large Large
Uses • Vascular ultrasound Abdominal ultrasound • Echocardiography
• Ultrasound-guided • Lung ultrasound
vascular access • Pleural ultrasound
Comparisons of the three types of transducers

10.WHAT DETERMINES THE QUALITY OF IMAGE ?

Impedance & Attenuation
Impedance:
x The resistance to the propagation of sound, resulting in reflection of sound waves
(echoes)
x The amount of reflection is proportional to the difference in the acoustic impedance
between the two media
x Low impedance: liquid
x Moderate impedance: liver
x High impedance: bone, stones
x The higher the impedance, the greater the reflected signal; this produces a brighter
image on the monitor

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 x If no reflection occurs, the monitor shows BLACK (echo-free)
x In summary: Reflections occur at points where there are changes in the conducting
medium’s acoustic impedance
Attenuation:

As ultrasound traverses tissue, it loses energy with a resultant reduction in amplitude and
intensity. This process is known as attenuation. The rate of attenuation is dependent on the
medium, for example, the attenuation rate in bone is thousands of times greater than in water.

Reflection= the amount of reflection is proportional to the difference in the acoustic impedance
between the two media; bones, stones reflect the most

A. B. C. D.
Refraction=redirection of part of the sound wave as it obliquely crosses a boundary of mediums
possessing different propagation speeds; especially next to a fluid-filled structure
Scatter=sound waves reflected away from the transducer (due to gas, skin density, scanning angle, etc.);
when the ultrasound beam encounters an interface that is smaller than the sound beam or irregular in
shape
Absorption=energy is contained within the tissue (acoustic energy is converted to thermal energy), and
dissipates as heat within the tissue

11.HOW DO I MANAGE ATTENUATION ?

Returning echoes, by nature, are weaker than ultrasound pulses

Need to amplify the signal=GAIN
The GAIN control amplifies the returning echoes from ALL parts of the screen
However, echoes from deeper structures are progressively weaker (attenuated)
Distant structures appear artifactually less echogenic
Need a way to adjust gain for deeper echoes: Time Gain Compensation

12.BASICS OF IMAGE SPATIAL RESOLUTION

The ability of the sound waves to discriminate between two different objects and to generate a
separate image for each

Axial resolution=parallel to the ultrasound beam (resolving shallower and deeper object)
The size of the wavelength (shorter, more resolution) is the major determinant of axial resolution;
so higher frequency means better axial resolution, but more attenuation and decreased tissue
penetration

Lateral resolution=perpendicular to the ultrasound beam (resolving objects next to one another)

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 The width of the ultrasound beam (array of crystals, distance between individual crystal rays) is the
major determinant of lateral resolution, though frequency also plays a role
The “focus” allows for enhanced resolution at particular depths of the scanning area, improving the
lateral resolution

13.WHAT IS THE ANGLE OF INCIDENCE / INSONATION?

The angle between the incident ultrasound beam and an imaginary line that is perpendicular to
the boundary of the object of interest; important for defining the boundaries of a vessel for a
vascular study

14.WHAT IS REAL TIME ULTRASONOGRAPHY?

The term real-time simply refers to the ability of the machine to display a rapid sequence of B-
scan images such that any motion is visualized as it actually occurs. Typically between 15 and 60
image frames per second can be shown in modern equipment. It is worth noting that as the
number of frames shown per second (the framing rate) is increased, the smoother is the
appearance of any motion. To produce the effect of continuous movement, >16 frames/sec
need to be displayed.

15. ARTFACTS
There are many types of artifacts associated with the technology of medical ultrasound, and
they are not all a disadvantage. Here is a brief description of important ones:
a. ACOUSTIC SHADOWING: Sound waves cannot penetrate VERY DENSE structures- BONE,
CALCIFICATION. The image will be “black” or have a “shadow posterior-beneath- the DENSE
structure.(Fig A)

A. B. C. D.

b. Distal Enhancement: Just posterior to a FLUID filled structure- (like cyst) is a brighter
enhancement in the image (Fig B). This is caused by the sound waves traveling through the
liquid-then interfacing with the tissue beneath it.

c. Mirror Images: Sound can bounce off a strong, smooth reflector such as the diaphragm.
The surface acts as mirror and reflects the pulse to another tissue interface. The ultrasound
system believes the second interface is beyond the first surface, and this is where it appears
on the scan. In Figure C, the arrow shows the real object, which appears as if reflected in a
mirror.
d. Reverberation: Reverberation artifacts appear as multiple equally spaced lines along a ray
line. Reverberation is caused by the sound bouncing back and forth between tissue
boundaries and then returning to the receiver. (Fig D)

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16.HOW dK OPTIMIZE IMAGE?
Frequency: ↑ Frequency = ↑ Resolution = ↓ Penetration
Gain: controls the brightness of the displayed image ( Insufficient gain can result in missed
structures of low reflectivity, such as thrombus. Excessive gain can result in false echoes or
oversaturation)
Depth: Adjust the depth so that the target structure lies in center of the image.

A. Too Close B. Too Far  C. ŽƌƌĞĐƚŝƐƚĂŶĐĞ

17. Transducer orientation
A. Transverse

B. Longitudinal

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CHAPTER 2
Lung Ultrasound - Basics
From Auscultation & X Ray -------- to Ultrasonation

1. PROBE SELECTION:

a. Linear high frequency probe – 5-10 Hz: (higher resolution, lesser penetrance)
: For superficial structures (lung sliding, comet artifact)

b. Curvilinear low frequency probe- 3-5 Hz: (lesser resolution, deeper penetrance)
: For deeper structures (consolidation, effusion)

2. PROBE ORIENTATION

LONGITUDINAL TRANSVERSE

3. CHEST AREAS: TOPOGRAPHY

ANTERIOR POSTERIOR

PAL 6 5

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 4. KNOW THE 4 BASICS IN NORMAL LUNG USG:
The pleural line
The bat sign
The A-line
Lung sliding

a) Pleural Line
Starting with the long axis view, the anterior chest wall can be seen: the echogenic layer of
subcutaneous fat superficially, followed by the hypoechoic layers of intercostal muscles and their thin
echogenic fascia planes. The superior rib is sited on the left of the image, producing intense posterior
acoustic shadowing. About 0.5cm below and between the two ribs, a thick echogenic line will be seen.
This is the pleural line, which represents the two layers of the pleura, the outer parietal and the inner
visceral layer

In Fig A, a linear probe is used, in the midclavicular line at approximately 3rd intercostal space. At the
posterior edge of the rib, a hyperechoic (bright) pleural line is seen (Static Image), which is the interface
between the visceral and parietal pleura. In a moving image(Dynamic Image) of a normal lung, shimmering
or “sliding” would be seen at the pleural line.

b) Bat Sign
The wings are formed by: superior rib to the left, inferior rib to the right , with intense posterior
acoustic shadow. The body of the bat: pleural line between the two ribs and about 0.5cm below
them. The bat sign is a basic step. It allows to easily locating the lung surface in almost every
circumstances

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c) A line
Horizontal, regularly spaced hyperechogenic lines representing reverberations of the pleural line.
These are motionless and are artifacts of repetition. In two-thirds of normal lungs, this is the only
artifact pattern that can be seen.

d) Lung Sliding & Sea Shore Sign

The pleural line, on real time USG (Dynamic Scan), moves with respiration horizontally and is actually
the visceral layer moving along with the lung, while the chest wall and parietal pleura are still or
move in an opposite direction to the lung, so this is called the lung sliding in real time imaging. Its
amplitude is greater at the base than at the apex where it may be imperceptible. The static image of
same is best seen in an M mode, which can be documented as an image - as the superficial pareital
layers are motionless and have a horizontal pattern of lines while the area deep to the pleural line
appears "granular" as the motion of the pleural line is reflected all over this area. This is also known
as the "seashore sign". In simple words - the motion of the lung (sea) as it relates to the chest wall
(shore).

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 5. UNDERSTANDING MORE LINES

a. B lines
Alveolar interstitial syndrome is an ultrasonographic finding in several conditions. In an acute event, it
may represent pulmonary edema, but it may be seen in other conditions such as ARDS, interstitial
diseases or as a focal finding in infectious or ischemic processes.
Seven required points to define B line are:
- Comet tail artefact emerging from pleural line or consolidations
- Well-defined & laser-ray like
- Spreading to the edge of the screen without fading
- Sliding with the pleural line
- Erasing normal horizontal A lines
- Hyperechoic as pleural line

Essential point for defining AIS: Three or more B lines in a single view between 2 ribs are called B
+ lines or lung rockets.

In the emergency care setting, the presence of B lines on pleural ultrasonography predicts fluid overload,
adding to diagnostic accuracy to the physical examination.

Multiple B-lines 7 mm apart are caused by thickened interlobular septa characterizing interstitial edema,
represented by B-7 lines (Fig a). In contrast, B-lines 3 mm or less apart are caused by ground-glass areas
characterizing alveolar edema, represented as B-3 lines (Fig b)

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 Fig A Fig B

b. Artefactual E lines: (Differs from B line)

Generated by Subcutaneous Emphysema
Vertical, laser like, reach screen edge (similar to B lines)
Arise from chest wall and not the pleural line (different from B line)

c. Artefactual Z Lines:(differentiate from B Lines)

-Short, broad, ill defined vertical lines
-Arising from pleural line- but not reaching edge of screen- taper off after 2- 4 cm
-Less echogenic than pleural line
-Do not erase A lines
-May be seen in normal persons and in pneumothorax

6. DIAGNOSING LUNG CONDITIONS:

a. Pneumothorax (3 SIGNS)
In the supine patient, a pneumothorax tends to collect in the anterior and non dependent
area. The signs are best elicited with a high frequency probe. A probe > 5 MHz is preferred.
High frequency linear (such as a vascular) probes will give a clearer & better picture.

i. Absence of lung sliding/ Stratoshpere Sign: This is the first sign of pneumothorax. If lung sliding
is present, pneumothorax can be ruled out. However, loculated posterior, mediastinal and apical
pneumothoracies can be missed. For a complete examination, the probe must be placed along the
anterior, lateral and posterior intercostals spaces and observation must include a whole respiratory
cycle at each point.
Documentation can be done on M Mode by eliciting stratosphere sign. In the absence of lung
sliding the pattern observed is called the stratosphere sign, also called the bar code sign. The
granular or sandy beach pattern (normally seen in sea shore sign) below the pleural line is replaced
by horizontal lines.

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 Abolished lung sliding though is essential to diagnose pneumothorax but is alone non-
confirmatory, as lung sliding may be absent in severe ARDS, tube block, lung fibrosis, phrenic palsy,
apnea, esophageal intubation etc. Therefore we must confirm by other signs.
ii. The A-line sign (i.e., no B-line seen)
B-lines, also called comet tail artifacts, are vertical artifacts that arise from the visceral
pleura. Since B-lines originate from visceral pleura, their presence rules out pneumothorax.
The A lines are reverberation artifacts of the pleural line. A lines without B lines and no lung
sliding, on real time US, are highly suggestive of pneumothorax & is called A+-profile in the
BLUE-protocol
B-lines with absent lung sliding may be seen in lower lobe consolidations. Absent B-lines
with lung sliding present may be seen in emphysema or hyperinflated lung states.

iii. Lung Point is pathogonomic

Partially collapsed lung is in contact with the chest wall at some point, where the visceral and
parietal pleura are in contact, and slide against each other with respiration. A thorough
examination may reveal this point where the pleura slide in with inspiration as the lung expands,
but during expiration as the lung contracts, lung sliding disappears. This sign is 100% specific for
pneumothorax, but has low sensitivity. Low sensitivity could be due to multiple reasons operator
skills, completely collapsed lung with no chest wall contact, incomplete examination, or the rib
and sternum could be obscuring visualization. This sign can be recorded on M mode.

Fig Lung Point : Alternating seashore sign (indicating lung sliding - vertical arrow), with
stratosphere sign (indicating absent lung sliding - horizontal arrow)

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 b. Lung Consolidation: (Shred Sign, Hepatization of lung, Dynamic Air Bronchogram)

Lung consolidations are fluid disorders and, therefore, are easily diagnosed by ultrasound. Lung
consolidations touch the wall in most of cases. In the critically ill, consolidations are nontranslobar or
translobar & the sign of nontranslobar consolidation (most cases) is the shred sign: the border
between consolidated and aerated lung is irregular, drawing the fractal line, fully opposed to the
lung line. The sign of translobar consolidation is the tissue-like sign: it looks like liver, meaning it has
an echogenicity similar to that of the liver, hence the term, sonographic hepatization of the lung. Air
bronchograms when visualized, appear as punctiform or linear hyperechoic artifacts within the
consolidated lung. When the centrifugal inspiratory movement of the air bronchogram is > 1mm, it is
called a dynamic air bronchogram. The presence of dynamic air bronchogram indicates patent
bronchi, with air bubbling within the bronchi with inspiration, and has a 94% specificity and a 97%
positive predictive value for diagnosing pneumonia, and distinguishing it from resorptive atelectasis

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TISSUE LIKE SIGN (HEPATISATION) AIR BRONCHOGRAM

SHRED-LINE INSTEAD OF LUNG LINE

c. Atelectasis vs Consolidation:
-Static vs dynamic air bronchogram
-Penetration of gas into bronchial tree of consolidation during inspiration produces
inspiratory re- inforcement of air-bronchogram: this is absent in atelectasis

d. Pleural Effusion
-Hypoechoic and homogeneous structure with no gas inside
-Present during expiration and inspiration
-Present above diaphragm
-Should be sought in longitudinal view, in dependant lung regions

Few Precautions:
- It must be located above the diaphragm (to avoid confusion with intraperitoneal fluid)
- Identification of the lung behind the pleura is necessary before introducing a needle - it may
be consolidated or aerated. In massive effusions, the lung will seem to swim in the effusion
with frank undulations

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 Quad Sign: The deep boundary of the collection is regular, roughly parallel to the pleural line, and is called
the lung line (visceral pleura) . Image between pleural line, rib shadow and lung line is quad sign.

Sinusoidal Sign: Inspiratory movement of lung line towards pleural line

Effusions can have one of the following sonographic patterns:

(1) Anechoic: echo-free (black) space between the visceral and parietal pleura
(2) Complex non septated: echogenic material is present in a non homogenous pattern without
septations (Fig A)
(3) Complex septated: floating fibrin strands or septae in a lattice like pattern are present (Fig B),
like in malignant effusion, complicated empyma
(4) Homogenously echogenic: very cellular echogenic material is strewn homogenously in the
effusion, as in an empyema or hemorrhagic effusions

Fig A Fig B Fig C

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 7. DIAPHRAGM
Diaphragmatic motion is well evaluated with M-mode. The transducer is located either in
the low intercostal spaces, between midclavicular and midaxillary lines, for separate
examination of each hemidiaphragm or at the subxyphoid space for comparative
evaluation. During inspiration diaphragm descents, moving toward the ultrasound probe
and appears as an upward slope on M- mode. In contrast, during expiration the diaphragm
moves away from the probe and this is a downward slope on M-mode. In diaphragmatic
paralysis M-mode shows absent movement during quiet respiration and paradoxical
movement-away from the transducer- when the patient sniffs

USG lung is useful in the evaluation of many pediatric chest queries.

Apart from differential diagnosis, it contributes to avoid additional radiation exposure

(Multiple x-rays/CT) when frequent follow-up is required (pleural effusions, complicated
pneumonias, pneumothorax).

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CHAPTER 3
Summarzing Lung USG
Pleural Fluid
Characterized by:

1. An echo free space surrounded by

typical anatomic boundaries:
diaphragm, chest wall, and lung
2. Dynamic changes: e.g. lung flapping,
diaphragmatic movement, plankton
sign

Alveolar Consolidation (dynamic evaluation)

Characterized by:

Tissue density of lung often in a

segmental or lobar pattern. The lung
looks like the liver or spleen (sonographic
hepatization of lung). Within the tissue
density lung are often seen echogenic
foci that represent air bronchograms.
Caution! Alveolar consolidation pattern is
descriptive i.e. it has many causes such
as pneumonia, atelectasis, infiltrative
lung diseases etc.

Alveolar-interstitial disease
Characterized by

B-lines defined as:

1. One or more ray like echo dense lines

that are vertical on the screen
2. They are mobile in synchrony with
respirations
3. They reach the bottom of the screen
4. They originate at the pleural line
5. They efface A-lines (see below)

B-lines (AKA as lung rockets or comet

tails) are strongly correlated with ground
glass abnormality of chest CT and Kerley B lines. They are powerful evidence of
alveolar interstitial disease. Caution! B-lines are descriptive i.e. they have many
causes such as cardiogenic pulmonary edema, ILD, PCP, etc. Also, normal
individuals may have a few at the lateral lower chest wall.

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Normal aeration pattern

Characterized by:

A-lines and sliding lung defined as

1. One or more horizontal lines that are in

multiplicative distance from the pleural line.
These represent reverberation artifact of
normal lung.
2. Sliding lung sign is normally observed at
the pleural interface. It is a subtle
shimmering movement that derives
from the movement of the visceral
pleura against the parietal pleura. Its
presence excludes pneumothorax.

Normal aeration pattern observed at multiple points on the thorax (the exam may
be done rapidly) is strongly associated with normal lung CT scan results.

R/O Pneumothorax (dynamic evaluation)

Characterized by:

1. A-lines
2. absence of sliding lung
3. Lung point

This makes sense, as air gives A-lines whether

in normally aerated lung or in a pneumothorax
space. Lung sliding is lost because the visceral
pleura is no longer against the parietal pleura
in pneumothorax. Caution! There are other
causes for loss of lung sliding other than
pneumothorax. Absence of lung sliding may
“suggest” that a pneumothorax is in the
provisional diagnosis, and is not a confirmation
of the condition.

Documentation
Clips are often used in documenting sliding
lung or various conditions which are best
documented in a dynamic format. M-Mode
however, may be employed to demonstrate
sliding lung in a static image with what is Chest Wall
known as the sea-shore sign which documents
the motion of the chest lung (sea) as it relates
to the chest wall (shore). Lung

21
CHAPTER 4
Echocardiography - Basics
Understandings ECHO image – know the 3 P’s: Patient, Probe and Picture

Knowing the anatomy and orientation of the standard 2D images of the heart is the starting point of
learning basic echocardiography.

TRANSDUCER

Echocardiography is done using a low-frequency, phased array probe, typically with a frequency of 2.5 -
3.5 MHZ .

Fig 1. ECHO transducer with mentioned parts

EXAM PRESET in USG MACHINES

When available, a "cardiac" exam preset should be selected when looking at the heart.

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SCREEN MARKER

By convention, the screen marker is set at the upper right hand corner of the screen (note it is different
from other critical care organ scanning where the orientation marker is usually set to the top left of the
screen. Also note that most machines automatically switch orientation when switching exam preset (but
still it’s better to cross check to reduce operator "mistakes")

PROBE HOLD

The probe should be held like a pencil to allow you to easily perform subtle adjustments of angle and
rotation, and also to reduce operator induced image instability, you can place (SHOULD PLACE) the
thenar eminence on the patient.

PROBE MANIPULATION

Five types of movement are used ECHO to obtain the optimal image:

Sliding: Slide the transducer on the body to find the optimal window or to move to a different area of
the body in any direction. For example, this fig shows sliding from the location of the parasternal view to
the the apical view.

Rocking: Rocking the transducer toward the indicator or away from the indicator allows centering of the
area of interest or extending the field of view in one direction or the other, ie, cephalic/caudal or
right/left.

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 Tilting: Tilting the transducer from side to side allows other planes in the same axis to come into view .
This is also called cross-plane1 motion. (“Cross-plane” refers to a motion that is perpendicular to the
visualized plane.)

Rotation: Rotation depends on the viewing window. For example, in these parasternal views: Rotating
the transducer approximately from 11 to 2 o’clock switches correctly from long to short axis.

Compression: Compression is usually used to make adequate contact between the transducer face and
scanning surface of the patient, thus improving image quality. For example, the figure shows
compression being used for the subcostal view. The sonographer must always keep in mind the
patient’s comfort level while compressing.

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SCANNING TECHNIQUE AND PATIENT POSITION
Since a portion of the heart is often located beneath the sternum, the patient's body should be
preferably positioned in a left lateral decubitus for parasternal and apical 4-chamber views. For the
subcostal views, the patient should be preferably placed in the supine position with the knees flexed

Axis
Short axis: cuts heart anterior to posterior
Long axis: cuts Heart through Apex to Base

BASIC CARDIAC VIEWS

There are five basic trans-thoracic views that we usually rely on for goal-directed echocardiographic
exams in the. Each view has strengths and weaknesses dependant on the clinical question and structure
of interest. Learning to compile a complete picture of function requires compiling the information from
each view obtained. Another practical problem is the frequent inability to obtain all views - for patients
on the ventilator, but the sub-costal view is also called the "bail-out" view by many as it is most often
easily obtainable.

BASIC TRANS-THORACIC CARDIC VIEWS

Parasternal Long Axis

Apical 4 Chamber
Apical 5 Chamber
Subcostal/ Sun Xiphoid
IVC view

25
 Subcostal 4-chamber view

Place patient in supine position. Place transducer just below xiphoid/ sternum, with the probe relatively
flat on the abdominal wall and the PROBE FACE pointing to the left shoulder with the PROBE MARKER
pointing to the patients left. Hold transducer on top surface only to allow for probe to be placed flat on
the patient. Unlike other cardiac views, this view is dependent on the left lobe of the liver as an acoustic
window in the near field.

Fig: Sub Coastal View

Apical 4-chamber view

Place the transducer at the anatomical apex of the heart, with the PROBE FACE pointing towards the
right shoulder and the PROBE MARKER pointing toward the left shoulder. Multiple adjustments are often
needed to obtain the ideal view (i.e. one where the RV and LV are side-by-side and the MV and TV are
seen in the same plane. Also note that rotating the probe can make the RV look bigger or smaller -
make sure that you are not over- or under-rotated. For optimal imaging try to get an image of a "bullet"
shaped heart (not rounded like a soccer ball, this indicates an off-axis view (i.e. not at the true point or
apex).

26
Fig: Apical 4 chamber view

Parasternal long-axis (The only view where you point towards patient’s right shoulder – for beginners)

The transducer should be placed in the left third or fourth ICS, just adjacent to the sternum. The probe
marker should point toward the patient's right shoulder creating a "slice" of the heart through the long
axis of the left ventricle. Optimal image of the heart is one that bisects the mitral and aortic valves in the
same plane and has the heart horizontally across screen (not always possible). Note that the apex of the
LV is not normally seen, only up to the mid ventricle unless the probe is tilted.

Fig: Parasternal Long Axis View

Apical 5 chamber view

To get the apical 5 chamber view, you need to have a good apical 4 chamber view. The objective will be
to visualize the 5th chamber: the aorta. Since the aorta is the most anterior, you will need to tilt your
probe upwards (=angle up): the tricuspid valve and RA will go out of the imaging plane, the aorta will
appear in the middle of the screen.

27
 Fig: Apical 5 chamber View

RECOMMENDED VIEWS FOR CLINICAL QUESTIONS:

Pericardial Effusion – subcoastal or PSLA
LV function – PSLA or A4C or SC
Regional wall motion - A4C and PSLA
Cardiac Output - Apical 5 chamber
Fluid Responsiveness - IVC view or A5C looking for respiratory variation of aortic outflow (advanced)
Severe Hypovolemia - IVC view looking for a "virtual or flat IVC"
RV size - A4C.

28
CHAPTER 5
Focussed Assessment with Sonography in
Trauma (FAST)
GOAL:
1. Detection of intraperitoneal free fluid
2. Detection of pericardial fluid
3. Extended-FAST(E-FAST): Detection of hemo/pneumothorax

HISTORY:
The acronym “FAST”— was originally “Focused Abdominal Sonography for Trauma”— was first
mentioned in the literature in 1996. As the role of ultrasonography in trauma increased, some thought
that this definition did not appropriately describe all uses of trauma ultrasonography. Thereby, in 1997,
the FAST Consensus Conference Committee concluded : FAST should stand for “Focused Assessment
with Sonography for Trauma.” The term FAST is synonymous with trauma ultrasonography and is
clearly accepted as an integral part of the bedside assessment of patients with blunt or penetrating
trauma, where though detection of bowel injury/ parenchymal injuries - although possible with
ultrasonography- is not goal of current FAST examination

ERGONOMICS & PROBE:

PROBE: Curvilinear

POSITION: Head low for upper quadrants

Reverse head low for pelvis

FAST works because fluid preferentially pools in these predictable locations:

29
 STANDARD FAST VIEWS:
1. The Right Upper Quadrant View (also known as the Perihepatic, Morison Pouch, or Right Flank
View)

2. The Left Upper Quadrant View (also known as the Perisplenic or Left Flank View)

3. The Pelvic View (also known as the Retrovesical, Retrouterine, or Pouch of Douglas View)

4. The Pericardial View (also known as the Subcostal or Subxiphoid View)

Positive FAST exam:

Detection of intraperitoneal fluid on any of 3 abdominal windows or
Detection of pericardial fluid on the cardiac window

Negative FAST exam:

Absence of intraperitoneal fluid on all 3abdominal windows and pericardial fluid on the cardiac window

Indeterminate FAST exam:

In which any of the windows is inadequately visualized and there is no fluid detected on the views that
are visualized

Extended FAST- includes Lung fields

Includes evaluation for hemothorax & pneumothorax
x Expand UQ views to visualize diaphragm: Lack of mirror artifact indicates fluid/hemothorax
x Scan anterior chest: Lack of lung slide with presence of lung point indicates pneumothorax

30
 1. Right upper quadrant ( peri-hepatic) view:

The operator should stand or sit to the right of the patient and, ideally, scan with the dominant
hand. The ultrasound machine should be at eye level or have the screen tilted to minimize
reflection.

INTERCOSTAL TECHNIQUE
SUBCOSTAL TECHNIQUE
Commonly used
Probe in right infracostal margin lateral to
Probe in midaxillary line between 8-11 rib midclavicular line

Probe indicator towards pt posterior axilla Deep breath pushes subcostal structures into view
(pt co-operation needed)
Rotate counterclockwise to reduce rib
shadowing Colonic gas in hepatic flexure-limits visualisation

NEGATIVE RUQ SCAN POSITIVE RUQ SCAN

Free
floating tip
Liver
of liver

Diaphragm
Kidney

31
 2. LEFT UPPER QUADRANT (PERISPLENIC WINDOW)

Intercostal approach-between ribs 9 and 10 or

10 and 11 in posterior axillary line – indicator to
pt’s head

NEGATIVE LUQ SCAN POSITIVE LUQ SCAN

32
 3. CARDIAC VIEW

SUBCOSTAL VIEW (subxiphoid view)

In supine position provides information regarding

pericardial fluid gross chamber enlargement, and gross
wall motion abnormalities.
Probe in the epigastrium directed toward the patient’s left
shoulder probe indicator directed toward the patient’s
right side.
Difficult to obtain if the patient is having significant
abdominal pain & in obese patient

33
 PARASTERNAL VIEW

When adequate subcostal view not possible

Probe placed to the left of the sternum at 2-4th
intercostal space

Long Axis

Probe indicator to patient’s

right shoulder

PARASTERNAL VIEW

RV

LV

LA

Pericardial fluid

ABNORMAL SCANS SHOWING PERICARDIAL FLUID

34
 4. PELVIC (SUPRAPUBIC )WINDOW

LONGITUDINAL TRANSVERSE

Probe in the midline just above pubic bone Probe in the midline just above pubic
Probe indicator pointed towards pt’s head bone: directed inferiorly to the pelvic
region
Probe indicator pointed to pt’s right

LONGITUDINAL TRANSVERSE

35
 EXTENDED FAST:
Includes lung views to r/o hemothorax/pneumothorax

HEMOTHORAX:

-Probe placed laterally on lower thorax just above diaphragm

-Lack of mirror artifact
-Blood appears as an anechoic stripe in the thorax

PNEUMOTHORAX:

-Anterior chest scan

- Absence of B lines
-lack of lung sliding
-presence of lung point
-Stratosphere sign on M mode
Advantages of FAST:

– Can be performed in 5 minutes at the bedside

– Non-invasive
– Repeat exams
– Sensitivity and specificity for free fluid equal to DPL and CT
Disadvantages of FAST:
– Operator dependent
– May not identify specific injury
– Poor for hollow viscus or retroperitoneal injury
– Obesity, subcutaneous air may interfere with exam
Blunt Injury Abdomen Algorithm:

36
CHAPTER 6
Ultrasonographic Assessment of Inferior Vena
Cava (IVC): A tool to guide fluid resuscitation
in patients with shock

Introduction

Traditionally, it has been believed that central venous pressure (CVP) is a key
physiologic estimate of preload, which helps to define the intravascular fluid
volume status and guide fluid management. It is a particularly important parameter
in critically-ill patients who may require fluid resuscitation. A European survey of
intensivists/anesthesiologists reported that more than 90% used CVP to guide fluid
management(1). Another Canadian survey reported that 90% of intensivists used
CVP to monitor fluid resuscitation in patients with septic shock(2). However, CVP
measurement requires invasive central venous catheter placement which is time-
consuming and may be associated with a number of complications associated with
percutaneous insertion method e.g. arterial puncture, hemothorax, pneumothorax,
venous air embolism,or even damage to a major vein of the arm The size and shape
of the inferior vena cava (IVC) is correlated to the CVP and circulating blood
volume, and the IVC is a highly compliant vessel with no valve whose size varies
easily with changes of intravascular pressure. As a result, normal respiratory cycle
causes changes in intra-thoracic pressure which in turn influence venous return
from the IVC and also affect the variation of IVC diameter. IVC diameter
measurements can assist in ongoing resuscitation by providing a means to measure
CVP non-invasively. Clinician-performed bedside ultrasonographic evaluation of
the IVC is a tool that could potentially provide an instant and noninvasive measure
of volume status(3) which in turn could be rapidly deployed for initial assessment
to guide subsequent therapy(4,5).

37
 Method of IVC Assessment

The examination of the IVC is particularly easy and can be done by someone with
limited experience in echocardiography.Echocardiography of the IVC can be done
by a transthoracic, subcostal approach. To measure the IVC diameter and its
respiratory variations, the IVC should first be identified in a transverse plane
(Figure 1a and 1b), with the cardiac probe in a sub-xiphoid position perpendicular
to the skin.

Figure 1: Identification of the inferior vena cava (IVC) in transverse view. The probe is positioned
at the sub-xiphoid level, perpendicular to the skin. This view is useful to localize the IVC.
Ao = aorta.

The probe is moved progressively to the right to visualize the IVC in the center of
the field. The probe is then rotated by 90˚ to obtain a longitudinal plane. It is
important to identify the hepatic veins and entrance of the IVC into the right atrium
(Figure 2a and 2b).

38
 Figure 2a and 2b: Identification of inferior vena cava (IVC) in longitudinal view. From the previous
view (Figure 1), the probe is rotated by 90˚. The time-mode sampling cursor is positioned
perpendicular to the IVC, 1 cm caudal to the junction of the hepatic veins.

After obtaining a 2-D image of the IVC entering the right atrium and verifying that
the IVC visualization is not lost during movements of respiration, place a M-mode
line through the IVC 1 cm caudal from its junction with the hepatic vein, and
obtain a M-mode tracing (figure 3). This placement ensures that we do not measure
the intra-thoracic IVC during any part of the respiratory cycle.

Figure 3: Time-mode visualization of inferior vena cava respiratory variations (IVC).

Time-mode acquisition of the IVC at a speed of 25 mm/s. The beam is positioned 1 cm caudal
to the hepatic vein–IVC junction. Three respiratory cycles are visualized.

39
 Freeze the M-mode image and using calipers, measure the maximum (A) and
minimum (B) diameter of the IVC tracing as shown in figure 3. Three
measurements should be averaged. These measurements are valid only when there
are no active contractions of abdominal wall muscles or raised intra-abdominal
pressure (6).

Clinical implications of IVC indexes

Normal respiratory cycle causes changes in intra-thoracic pressure which in turn

influence venous return from the IVC and also affect the variation of IVC
diameter. Consequently, the IVC collapses with inspiration as the blood is pumped
out of the IVC due to the negative pressure created by chest expansion. In healthy
subjects breathing spontaneously, cyclic changes in thoracic pressure may result in
collapse of the IVC diameter of approximately 50%.Therefore, IVC diameter
measurements canassist in ongoing resuscitation by providing a means to measure
CVP non-invasively.

In a patient requiring ventilatory support, the inspiratory phase induces an increase

in pleural pressure, which is transmitted to the right atrium, thus reducing venous
return. The result is an inversion of the cyclic changes in IVC diameter, leading to
increases in the inspiratory phase and decreases in the expiratory phase. The
respiratory variations in IVC diameter in a mechanically ventilated patient are
therefore only observed when right atrial pressure is normal, that is low. In a
patient presenting with signs of circulatory insufficiency, this finding may indicate
hypovolemia. Measurement of IVC diameter in a patient receiving mechanical
ventilation does not accurately predict right atrial pressure. Absence of respiratory
variations in IVC diameter in a mechanically ventilated patient presenting with
signs of circulatory insufficiency suggests that volume expansion will be
ineffective in 90% of cases.

40
Various IVC indexes for measurement of volume status

1. Maximum IVC diameter

In spontaneously breathing adults, an IVC diameter less than 20 mm was

associated with a CVP less than 10 mm Hg (7). On the other hand, an IVC
diameter greater than 20 mm Hg with no respiratory variation is associated with an
elevated CVP. Sometimes the IVC is completely collapsed and may be difficult to
visualize (virtual IVC). Such a situation in a mechanically ventilated or
spontaneously breathing patient always indicates severe hypovolemia in the
absence of raised intra-abdominal pressure. Unfortunately, as with invasive
measurements of CVP, maximal or minimal IVC diameters fail to predict fluid
responsiveness (6). No pediatric specific IVC diameters for fluid responsiveness
are available.

2. IVC Collapsibility Index

It is expressed as the difference between the value of the maximum diameter and
the minimum diameter, divided by the maximum of the two values. It should be
noted that the denominator here is the maximum diameter. This index is used only
for spontaneously breathing non ventilated patients. In a spontaneously breathing,
healthy subject, cyclic variations in pleural pressure, which are transmitted to the
right atrium, produce cyclic variations in venous return, which is increased by
inspiration, leading to an inspiratory reduction of about 50% in IVC diameter.This
is an index of volume status (hypovolemia, hypervolemia) and right atrial pressure,
but has never been studied as an indicator of volume responsiveness.

3. IVC Variability Index

This variation is quantified by measuring the difference between the maximum and
minimum diameters on the M-mode tracing and dividing it by the mean of the two.
It should be noted that the denominator here is the mean diameter. This index is
used in mechanically ventilated patients.In mechanically ventilated patients, a 12%
or more variation identified patients likely to respond to vascular filling, in terms

41
 of increased cardiac output, from those who would not respond, with a positive
predictive value of 93% and a negative predictive value of 92%. It must be
remembered that the measurements should be taken during mandatory ventilator
breaths and the tidal volume should be at least 8 ml/kgwith the patient in sinus
rhythm.

4. IVC Distensibility Index

It is quantified by measuring the difference between the maximum and minimum

diameters on the M-mode tracing and dividing it by the minimum of the two. It
should be noted that the denominator here is the minimum diameter. It is also used
in mechanically ventilated patients. The cutoff for this index is 18%. IVC
variability index and IVC distensibility index are not reliable in spontaneously
breathing patients.

References
1. Kastrup M, Markewitz A, Spies C, Carl M, Erb J, Grosse J, et al. Current practice of
hemodynamic monitoring and vasopressor and inotropic therapy in post-operative cardiac
surgery patients in Germany: results from a postal survey. ActaAnaesthesiolScand 2007; 51:
347-58.
2. McIntyre LA, Hebert PC, Fergusson D, Cook DJ, Aziz A. A survey of Canadian intensivists’
resuscitation practices in early septic shock. Crit Care 2007; 11: R74
3. Natori H, Tamaki S, Kira S. Ultrasonographic evaluation of ventilatory effect on inferior
vena caval configuration. Am Rev Respir Dis 1979; 120: 421-7.
4. Carr BG, Dean AJ, Everett WW, Ku BS, Mark DG, Okusanya O, et al. Intensivist bedside
ultrasound (INBU) for volume assessment in the intensive care unit: a pilot study. J Trauma
2007; 63: 495-500.
5. Manasia AR, Nagaraj HM, Kodali RB, Croft LB, Oropello JM, Kohli-Seth R, et al.
Feasibility and potential clinical utility of goal-directed transthoracic echocardiography
performed by noncardiologist intensivists using a small handcarried device (SonoHeart) in
critically ill patients. J CardiothoracVascAnesth 2005; 19: 155-9.
6. Bendjelid K, Viale JP, Duperret S, Colling J, Piriou V, Merlani P,Jacques D. Impact of intra-
abdominal pressure on retrohepatic vena cava shape and flow in mechanically ventilated
pigs. PhysiolMeas2012;33:615–627.
7. Prekker ME, Scott NL, Hart D, Sprenkle MD, Leatherman JW. Point-ofcare ultrasound to
estimate central venous pressure: a comparison of three techniques. Crit Care Med
2013;41:833–841.

42
CHAPTER 7
Cranial Ultrasound
INTRODUCTION
Cranial Sonography is an accurate and adequate method to identify cranial
morphology and detect intracranial pathology in infants. Cranial ultrasound is less
expensive, spares the patient from radiation, does not require sedation, and its
portability allows for bedside evaluation in gravely ill infants who cannot be
transported to radiology for imaging.

TECHNIQUE
The cranial ultrasound examination is performed with a linear-array transducer
probe (5-10MHz).
Commonly, the anterior fontanel is used. But other sites may be used.

43
 Anterior fontanel is scanned in both saggital and coronal planes.

Conventionally, six coronal plane images are taken through the anterior fontanel,
beginning in the frontal lobes anterior to the frontal horns and progressing
posteriorly to the occipital lobes.

First coronal image acquired at the level of the frontal lobes allows the observer
to examine the frontal lobes, orbital cones, and the hyperechoic falx cerebri
located within the interhemispheric fissure.

44
Second coronal image is taken through the frontal horns of the lateral ventricles,
which allows multiple structures to be imaged at once. The frontal horns and
cavum septum pellucidumappear anechoic, CSF-filled spaces. The corpus
callosum is a linear, hypoechoic structure crossing the hemispheres that is
contained within echogenic superior and inferior borders. Finally, the globus
pallidus, putamen, caudate nucleus, and thalamus of each side can also be
visualized.

Third image is obtained at the level of the foramen of Monro. The third ventricle
can be visualized as an anechoic structure beneath the septum pellucidum.
Brainstem structures such as the pons and medulla can also be seen.

45
 Moving posteriorly, the fourth image is taken at the level of the cerebral
peduncles and shows hyperechoic choroid plexus along the floor of the lateral
ventricles and the roof of the third ventricle. The tentorium cerebelli and fourth
ventricle are also seen.

The quadrigeminal plate cistern serves as a marker for the fifth image, which
enables to see both temporal horns of the lateral ventricles as well as cerebellar

46
structures including the hemispheres and vermis. Below the vermis, the cisterna
magna is visible.

The final image is obtained through the cerebral convexities and displays the
interhemispheric fissure and occipital lobes

47
 Next, the transducer is turned 90 degrees on the anterior fontanel, and five more
images are acquired in the sagittal and parasagittal planes.
The first midline sagittal image displays a number of important structures. TheC-
shaped corpus callosum appears as a hypoechoic structure bound by echogenic
superior and inferior borders. The cingulate gyrus is seen above the corpus
callosum, while the septum cavum pellucidum is seen below. The third and fourth
ventricles along with the cisterna magna appear anechoic. The white matter
containing pons and cerebellar vermis are also seen.

Parasagittal view passes through each lateral ventricle showing the anterior and
posterior horns, with the caudothalamic notch (germinal matrix area).

48
The tangential parasagittal view shows the hemisphere lateral to the ventricle for
deep white matter.

49
 USES OF CRANIAL ULTRASOUND
Cranial ultrasound is commonly used in infants to evaluate for congenital
abnormalities, hydrocephalus, intracranial bleeds and periventricular
leukomalacia (PVL).

A. Dandy Walker malformation

50
B. Intraventricular hemorrhage with hydrocephalus

C. Periventricular calcification in congenital CMV

51
 D. Cysttic Periven
ntricular Leukomala
L acia

OP
PTIC NERV
VE SHEA
ATH DIAM
METER

DUCTION
INTROD

Measurrement of o optic nerve sheath

s diam
meter is a simple, non invasive,
i beedside tool to
t diagnose
e
intracraanial hyperttension in IC
CU setting.

nial pressure is a neeurologic emergency. The mostt reliable method

Elevated intracran m forr
measurrement of ICCP involves direct inseertion of a catheter
c into the craniaal cavity. Bu
ut this is an
n
invasivee and comp
plicated proccedure.

Measurrement of OONSD provid

des a simple
e and effecttive alternaative. Dilatation of the optic nervee
sheath has been sh
hown to be a much earrlier manifeestation of ICP rise thann papilledem
ma

ANATOMY

52
The optic nerve sheath is an anatomical extension of the duramater and the subarachnoid
space around the optic nerve is continuous with the intracranial subarachnoid space. When CSF
pressure is increased, this pressure is transmitted to the CSF space in the Optic Nerve Sheath
and causes it to distend. This distension can be detected as a change in the diameter of the
sheath and can be measured on imaging techniques like MRI, CT and ultrasound.

TECHNIQUE

High frequency (> 7.5 MHz) linear probes are used for measuring ONSD.

The probe is placed over the closed eyelid with the patient in supine position. Eyes are covered
with a transparent dressing before applying ultrasound gel. The beam is directed posteriorly
towards the optic disc and nerve. A good view of the nerve often necessitates moving the
probe slightly to the temporal side and angulating the beam a little nasally.

The normal sonographic veiw of the optic nerve from center to peripheral: hypoechogenic
nerve fibers closely surrounded by the echogenic pia mater; the subarachnoid space appears
anechogenic or hypoechogenic and is surrounded by hyperechogenic dura mater and
periorbital fat.The ONSD as the distance inside the dura mater.

The ONSD is measured 3 mm posterior to the globe. Two measurements are made for each
optic nerve: one in the sagittal plane and the other in the transverse plane, by rotating the
probe clockwise. The mean of value obtained for both eyes is taken as the ONSD.

53
 INTERPRETATION

There are no standard charts for ONSD. There are many studies which have found different cut
offs of ONSD for raised ICP. In general, ONSD more than 5 mm, in the setting of raised ICP,
should be viewed with caution.

54
CHAPTER 8
Cases
€ Case 1 –

3 month old
d male presented with Co
ough x 5 dayss , Respiratory distress x 4 days ,

Examination
n revealed – Heart rate 160 min , RR 505 /Min , mild respiratorry distress with bilateral
conducted sounds
s , no hepatomegal
h ly . Chest Xraay not showiing cardiomeegaly or pulmonary
oedema (Figgure a).

RPA

Figu
ure a – X ray of
o case number 1 – 3 mo onth old with
h suspected bronchiolitiss.
Normal lung fields,
f no sign
ns of pulmon
nary edema except right interlobar
pulmmonary enlarggement (RPAA)

At admission
n patient deccongestive measures
m d as there weere no signs of
was not started
congestive cardiac faailure . Ultrasonography lung was peerformed and d surprisinglyy showed siggnificant ‘B’
lines (figgure b) . Baseed on USG findings decongestive measures were started therreafter patie ent also
showed improvement over next 48 hours. Leearning point from this case is that ultrasound is not only
sensitivee but also abble to detect interstitial flluid before alveolar
a oedeema developps (patient deevelops
frank resspiratory sym mptoms seco ondary to hyypoxemia).

55
 B lines

Figure b – USG Lung case number 1 – 3 month old with normal X ray USG
showing significant B lines

56
 Case number 2- 2 month old case of VSD – On post operative day 6 patient was requiring
high ventilator settings. Chest X ray showing bilateral infiltrates. Two differential diagnosis were kept
ventilator associated pneumonia and pulmonary oedema . Patient also had thrombocytopenia and fever
which was favoring sepsis . Ultrasonographic finding helped in differentiating the two . Left lung showed
B lines and right lung showed shred sign (represents air bronchogram) suggestive of consolidation. Not
only antibiotics were changed but decongestive measures were also increased . After 48 hours chest X
ray was repeated which showed improvement in oedema ie left side but as expected (infection is going
to take time) infiltrate persisted on right side . (shown in figure c)

Figure c – Case 2 – Left X ray – Bilateral infiltrates , Right X ray – showing left
clearance , right infiltration in upper zone persisting

Learning point – USG lung can differentiate between consolidation and

pulmonary oedema

57
 Case 3 –1 year male presented in emergency room with mild respiratory distress
for past 3 days with signs suggestive of viral infection . This child was operated for
gastric pull up two months back with ICU stay of 30 days . Chest X ray showed left
paracardiac linear border suggestive of pneumothorax . Since clinically patient
was not fitting into diagnosis of pneumothorax therefore ultrasound was done .
Finding on USG were suggestive of normal lung (Figure d - A lines , seashore sign
on M mode )

Figure d-Case 3-USG finding-A Lines (LEFT SIDE), M mode (Rt side) showing seashore sign

58
 Case 4 - 14 year old male child previously diagnosed as a case of asthma
developed respiratory distress for one day . Chest X ray was suggestive of left
hydrpneumothorax (Figure e) . Ultrasound lung revealed normal A lines and
seashore appearance . In view of disparity between chart X-ray & Ultrasound
finding findings CT scan chest was performed . Left Diaphragmatic hernia
diagnosis was made and was operated .

Figure e – Case 4 – Hydropneumothorax

59
 Case 5
› 11 year old female fell 4 days back from by cycle and developed
swelling over right leg. After 24 hours developed high grade fever
and respiratory distress. At the time of admission she had ARDS and
shock was intubated ,ventilated and given fluid boluses followed by
vasoactive drugs(dopamine 10 mic /kg /min, epinephrine. one and
half after resuscitation she was on high ventilator settings (100% fio2,
Spo2 88%) suggestive of refractory hypoxemia and poor perfusion
markers (143 pulse rate, 94/43 BP, 55mm mean, High lactate , low
Scvo2 ). Question at this time was how to improve perfusion and
oxygen saturation . She had non recruitable lungs and optimum PEEP
was 8 . She did not tolerated HFO and since hemodynamically
unstable therefore could not prone the child. At this moment there
were two school of thoughts .
› Give fluid boluses – as no cardiomegaly on chest X ray (figure f ), no
crepitations in chest or hepatomegaly
› No fluid boluses – X ray chest cannot be taken as dyanamic marker
and patient had frothing through endotracheal tube which may
indicate pulmonary oedema and there was no pulse pressure
variation as seen in figure below . USG was used to further delineate
fluid responders and non responders (mentioned below).

60
Functional Echocardiographic markers(fluid non responsiveness)
1) IVC variability less than 12% (Figure g)
2) Velocity time integral variation with respiration . In above case it is less than 15%
indicative of fluid non responsiveness (figure h)
3) There was no increase in VTI by doing PLR (figure i)

Figure g – Case 5 – M Mode – No IVC variation in Inferior vena cava ( variability < 12% )

61
 Figure h-Case 5 –Calculation of velocity time integral and relation with respiration. In abov
case it is less than 15% indicative of fluid non responsiveness
After doing all above tests it was concluded that mentioned case ( number 5 ) should not be given fluid.
Then systemic vascular resistance was calculated by calculating cardiac output ( VTI X HR X CROSS
SECTIONAL AREA OF AORTA ) and then substituting values of CVP(central venous pressure ) and MAP
(Mean Arterial pressure ) in following formulae .

SVR (Systemic vascular resistance )=

MAP – CVP
--------------------------x 80 = 800-1200dynes-sec/cm5
Cardiac Output

SystemicVascularResistanceIndex (SVRI = 80x(MAP-RAP)/CI = 1970-2390dynes-

sec/cm5/m2)

62
In this child SVR was low therefore norepinphrine was started (Figure I). Child
showed improvement over next 30 minutes

Figure J – Case 5 – SVR was found to be less than 600 (800-1200dynes-sec/cm–5) therefore nor
epinephrine was started. After 30 minutes there was decrease in heart rate and improvement in
mean arterial pressure (Right)

63
 Case 6

21 month old female presented with history of fever of 21 days duration, lethargy, altered
sensorium and seizures of 3 day duration. On examination, child had tachycardia, hypotension,
delayed CRT, cool peripheries, bulging AF, GCS of 4/ 15, brisk DTJ's and extensor plantars. She was
intubated and started on mechanical ventilation. Fluid boluses and inotropes were started in view
of hemodynamic instability. CT scan was planned on suspicion of meningitis, however it could not be
carried out because of hemodynamic instability. Optic nerve sheath diameter was measured on the
bedside using portable USG machine which showed an increased diameter bilaterally (6 mm).

Anti raised ICP measures were started, and neurosurgery reference was taken. CT scan done after
hemodynamic stabilization showed communicating hydrocephalus with basal ganglia infarcts. EVD
was placed urgently, and CSF fluid analysis was positive for tuberculosis, for which appropriate
therapy has been instituted. VP shunt was placed at a later date for further decompression.

64
 CHAPTER 9
Predicting and measuring fluid
responsiveness with echocardiography

Introduction
Echocardiography is an essential tool for guiding
resuscitation in critically ill patients. Resuscitation often
requires the infusion of intravenous fluid in an effort to
reverse organ dysfunction. The harms of inappropriate
use of fluid are becoming increasingly apparent (1, 2).
Although the purpose of fluid resuscitation is often to
increase cardiac output, blood flow is not routinely used
to guide resuscitation. Sufficient mean arterial pressure
(MAP) is rightly targeted but is proportional to flow only
for a given systemic vascular resistance (SVR), which is a
dynamic component of circulatory state.
Measurement of flow requires more equipment, time
and expertise than standard parameters such as blood
pressure, and the value that achieves adequate perfusion
for an individual patient is not predictable. Mixed venous
oxygen saturations and lactate are useful but only reveal
a large mismatch between supply and demand, missing
subtler shock states.
The question of whether the patient improves with
fluid, additional vasopressors or inotropes can be difficult
to answer. Echocardiography is an evidence-based
approach and ideally suited to address this problem.
This article first outlines the physiological basis of fluid
resuscitation. Then there is a description of the concept
of fluid responsiveness (FR) and how this can be assessed
with echocardiography. In addition, the limitations and
pitfalls are discussed.
Background to fluid responsiveness
The ultimate goal of resuscitation with fluids, vasopressors
and inotropes is to ensure adequate oxygen delivery (DO2)
to prevent or treat organ dysfunction. There are some
fundamental principles that must be appreciated:
DO 2 = CaO 2 ´ CO
CO = SV ´ HR
MAP = CO ´ SVR
where DO2 refers to oxygen delivery, CaO2 refers to oxygen
content of arterial blood, CO refers to cardiac output,
SV refers to stroke volume, HR refers to heart rate, MAP

65
refers to mean arterial pressure and SVR refers to systemic
vascular resistance.
SV is the amount of blood ejected from the heart with
each beat and is dependent on preload (end-diastolic wall
tension), contractility and afterload (end-systolic wall
tension). When myocytes are stretched, they contract
more forcefully and so SV increases as venous return (VR)
increases (Frank–Starling law). This is the foundation
for the concept of fluid responsiveness. However, when
stretched beyond a certain level, they are unable to contract
more forcefully and so SV does not increase further (fluid
‘unresponsiveness’). This is depicted in Fig. 1.
Increased pressure in the left atrium and pulmonary
vasculature may then result in excessive capillary
engorgement, resulting in pulmonary oedema. In
clinical practice, a fluid responder is generally defined
as someone who increases their stroke volume by >15%
after a 500 mL fluid challenge. Around 50% of fluid
challenges administered in critically ill patients do not
result in an increase in SV, exposing these patients to
potential harm (3, 4).
Preload, or VR, is determined by the pressure gradient
between capacitance veins and the right atrium (RA). The
pressure in the veins is termed ‘mean circulatory filling
pressure’ (MCFP) or ‘mean systemic pressure’ (MSP) (5):
system. This contains 20% of the total blood volume, is
30 times more compliant than the arterial circulation
and is heavily innervated with α-adrenoceptors. It
serves as a reservoir of blood made up of capacitance
vessels easily able to change in volume to maintain VR
to the heart (6).
A visual analogy is shown in Fig. 2. MSP is increased
by fluid administration and by vasoconstriction. This
partly explains the improvement in cardiac output
sometimes seen with vasopressor administration. If
both ventricles are preload dependent, that is they lie
on the steep part of the Starling curve, stroke volume
increases appreciably.
Static parameters
Preload is defined as end-diastolic wall tension which,
while related to, is not the same as LV pressure or
volume. Consequently, an individual’s Starling curve is

( MSP -RAP )
VR =
SVR

where VR refers to venous return, MSP refers to mean

systemic pressure, RAP refers to right atrial pressure and
SVR refers to systemic vascular resistance.
MSP is regulated to a great extent by the effect of
sympathetic nervous system on the splanchnic venous

Figure 1
The Frank–Starling curve. Lower on the curve a given change in preload
results in a large change in stroke volume. On the higher, flatter portion,
the same preload change has minimal effect on stroke volume.
Figure 2
Stressed volume and venous return. (A) The fluid below the outlet is
unstressed venous volume and does not contribute to flow out of the
tank. The additional fluid in the tank is stressed volume, which drives
venous return. Lowering RAP or increasing MSP in isolation would
increase VR. (B) The proportion of the circulation that is stressed volume
can be increased by giving fluid (attenuated somewhat by reflex
venodilatation) or reducing the size of the tank (giving a vasopressor to
convert unstressed to stressed volume).

66
governed by their myocardial contractility. This means
that, although they say something about preload,
static markers such as CVP, pulmonary capillary wedge
pressure and ventricular volumes do not reliably
predict FR. This has been borne out in over 100 studies
since 1970s (7).
Dynamic parameters
Dynamic parameters are information gained from provoking
the circulation by inducing changes in the loading conditions
of the heart. In reality, this provocation is either in the form
of heart–lung interactions or a change in posture.
Heart–lung interactions
Ventilation induces cyclical changes in intrathoracic
pressure (ITP), which in turn cause alterations in SV
(Fig.  3). These changes are composed of two elements
termed delta-Up and delta-Down (8).
dDown In positive pressure inspiration:
t
Increased ITP reduces venous return. If hypovolaemia is
present, this is exaggerated by collapse of the SVC.
t
Increased transpulmonary pressure (TPP) compresses
pulmonary vessels and increases RV afterload. At higher
levels, small increases in pressure can result in large
increases in PVR, explaining the sensitivity of the RV to
high ventilation pressures.
Both these phenomena reduce RV output. This causes
reduced LV output a few heartbeats later.
Decrease in venous return plays the biggest role in
normovolaemia and hypovolaemia. Increased afterload
dominates if there is significantly reduced lung compliance
(with normovolaemia), pulmonary hypertension
or significant right heart failure (9). Although both
mechanisms lead to the same result, the appropriate
treatment is very different. Fluid may be indicated if there
is reduced venous return, whereas it could be detrimental
with increased TTP.
Figure 3
The physiology of respiratory-induced flow and
pressure changes during positive pressure
ventilation without additional respiratory effort.
The inspiratory rise in intrathoracic pressure is
transmitted, at least in part, to the pericardium
and causes increased transmural pressure across
the RV wall, plethora within the IVC and
compression of the SVC. The RV stroke volume
immediately falls. Concurrently, the pulmonary
vasculature is compressed, forcing blood into the
LV causing an initial increase in LV stroke volume.
After the pulmonary transition time, the LV
receives less blood and its stroke volume falls.
This effect is exaggerated in states of low
circulating volume and attenuated in the
overloaded system or when either ventricle is
failing. PP pulse pressure, IVC D inferior vena cava
diameter, SVC D superior vena cava diameter.
67
dUp Increased TPP reduces LV afterload and compresses
pulmonary capillaries in inspiration, forcing blood into
the left heart, and increasing stroke volume. Therefore,
dUp is unrelated to fluid responsiveness (10).
Biventricular failure has an exaggerated dDown and
dUp causing false positives for FR.
It can be appreciated from the explanations above
that the cyclical changes in intrathoracic pressure from
mechanical ventilation induce cyclical changes in preload
and SV if the ventricles are on the steep ascending part of
the Starling curve, i.e. if they are fluid responsive.
Postural change
Changes in posture such as from a head up to head down
position also alter the heart’s loading conditions by
transferring blood between the leg veins and the central
circulation. A manoeuvre termed passive leg raising (PLR)
and the interpretation of the physiological response to
this are now well studied. The PLR test and its assessment
with echocardiography are discussed later.
Predicting fluid responsiveness
There is now a large body of evidence to show that various
dynamic parameters (both invasive and non-invasive) have
a high sensitivity and specificity for predicting FR. These
include pulse pressure variation, systolic pressure variation,
stroke volume variation, systolic velocity variation, end-
expiratory occlusion and leg raise-induced changes (11).
The variation in pulse pressure, measured by analysis of
the arterial waveform, has been shown to be a valid method
when a threshold of around 12% is used. The variation in
stroke volume as determined by cardiac output monitoring,
usually also done by arterial waveform analysis, appears
equally valid when a similar cut-off value is employed.
End-expiratory occlusion involves holding the patient
at end-expiration for approximately 15 s and examining
the change in cardiac output that results. A rise in stroke
volume strongly suggests fluid responsiveness.
Ultrasound devices using Doppler to study the
descending aortic flow use the same principles as those
used in echocardiography. The most common of these is
the oesophageal Doppler device. This is ‘semi-invasive’
and usually requires the patient to be asleep. Positioning
of the probe to achieve an accurate signal can sometimes
be difficult.
These methods are clearly useful but are limited by the
requirement of an arterial cannula and a precise arterial
68
trace. Movement artefact, kinking of the catheter and
over- or under-damping of the waveform affect accuracy.
Echocardiography provides much more information
on the causes of shock than just FR and is increasingly
considered the first-line monitoring tool of choice in
haemodynamically compromised patients. Both static
and dynamic parameters may be assessed to build a
picture of the circulatory state.
Before the fluid challenge; using
echocardiography to predict fluid
responsiveness
Echocardiography avoids the need for invasive lines and
probes. Although it suffers from its own set of limitations,
it is non-invasive and also provides a wealth of qualitative
information in addition to the quantitative assessment
for accurate circulating volume assessment. It can be used
to assess the effect of a fluid challenge.
The most prevalent ways of using echocardiography
for assessing volume status are discussed here.
Left ventricle
LV size Although static parameters have a poor ability
to predict FR, there are some suggestive features that are
seen with overt hypovolaemia. The size of the LV is
predictive of FR only when it is very small. A
hyperdynamic LV with an end-diastolic area in the
PSAX view of less than 10 cm2 or papillary apposition
(kissing ventricles) is strongly indicative of
hypovolaemia (10, 12). Remember this appearance is
Figure 4
PW Doppler of MV inflow demonstrating high LV filling pressure.
also found in LV hypertrophy, highly inotropic and
vasodilated states, so care should be taken when
interpreting these findings. It is usually obvious from
clinical signs where there is profound hypovolaemia.
Changes in LV size as assessed by TOE reflect
changes in preload (13). However, increasing preload
does not necessarily increase SV, and LV size is a
poor predictor of fluid responsiveness. Variation in
LV stroke area with respiration has been shown to
predict fluid responsiveness (change >16%). This is
impractical without appropriate software in the echo
machine as it uses automated border detection on a
beat-to-beat basis (14).
An additional important LV feature to check for
is dynamic outflow tract obstruction. In patients with
known hypertrophic obstructive cardiomyopathy,
hypovolaemia accentuates the obstruction and can
be fatal. Significant narrowing of the outflow tract
during systole can be induced by under filling of the
LV in patients, particularly when in a hyperdynamic
state such as sepsis, or during inotrope infusions in the
presence or absence of proximal septal thickening (15).
Careful assessment of the outflow tract is, therefore,
obligatory and should include searching for systolic
high outflow tract velocity and anterior movement of
the anterior mitral valve leaflet.
LVEDP A restrictive pattern in MV flow should
prompt caution with fluid administration as it reflects
elevated LV diastolic pressure (Fig.  4). It should
be remembered, however, that if LV compliance is
reduced, the LVED pressure–volume relationship is
shifted up and left so:
Figure 5
PLAX view optimized for measuring the LVOT diameter.
t
The LV can be under-filled despite high filling pressures.
t
The optimum filling range is narrow: it is under or
overfilled easily.
Therefore, a hypovolaemic LV with diastolic
dysfunction may have elevated filling pressures, may
respond well to fluid, but will easily be overloaded with
pulmonary oedema resulting.
An additional reason for caution in using LV inflow
pattern is the occurrence of mild diastolic impairment in
hypovolaemia (9).
LV outflow variation
Stroke volume variation Stroke volume variation
is a good indicator of fluid responsiveness (4).
Measurement of stroke volume is relatively simple with
echocardiography:
t
Flow through a tube is velocity × cross-sectional area if
flow is constant.
t
Blood flow is pulsatile rather than constant, so we need
to calculate volume per contraction.
t
Measuring the velocity time integral VTI (measurement
of all the velocities of RBCs for each contraction at a
certain point) can be done by tracing the spectral
Doppler envelope.
t
This is measured in centimetres and represents how far
the column of blood is ejected (stroke distance).
volume = area × length
therefore:
volume = area × velocity × time
Figure 6
Tracing the PWD waveform to get the VTI value.
69
 So the area under the PW Doppler trace (VTI) is the SVmax - SVmin
stroke distance (SD): mean
flow volume (SV) = SD (or VTI) ´ CSA or in full

CSA = pr 2
( SVmax - SVmin )
variation = 100 ´
(( SVmax + SVmin )´0.5)
or

CSA = 0.785 ´ ( diameter )2

Pitfalls of using LV outflow variation SVV, SPV,
PPV, peak velocity and VTI variation are only valid with
Thus, SV can be calculated by measuring VTI and certain preconditions:
diameter at the same point. This is best performed by
measuring the diameter of the LVOT in the parasternal 1. The patient must be in sinus rhythm otherwise stroke
long axis (PLAX) view, remembering an error is squared. volume may vary because of the arrhythmia.
Optimize the view by minimizing the sector width and
depth (Fig. 5).
After switching to an apical five-chamber view (A5C),
the PW Doppler sample box should be placed at the same
point at which the LVOT was measured in the PLAX view.
The VTI can then be traced (Fig. 6).
Decreasing the sweep speed allows aortic flows to be
seen over more than one respiratory cycle. Tracing the
largest and smallest VTI over a respiratory cycle allows the
percentage change to be calculated.
Stroke volume variation of more than 12% accurately
predicts fluid responsiveness with values over 14% having
a very high positive predictive value and less than 10% a
high negative predictive value (4). Variation of 12–14%
represents a grey area and should encourage a search for
other markers.

Aortic peak velocity and VTI variation The

LVOT can be assumed not to change in size over the
respiratory and cardiac cycle and so changes in aortic
blood flow reflect changes in stroke volume. This can be
demonstrated with CW or PW Doppler with the sweep
speed set to ensure that several respiratory cycles are
represented. Evidence to date has used PW Doppler to
show changes in Vmax or VTI, so we recommend using
PW Doppler. The sample box should be placed at the
level of the aortic valve or within 1 cm of it, in the
LVOT, just as it would be when measuring SV. Peak
velocity variation of 12% in both adults and children
predicts fluid responsiveness (12) and VTI variation is
also predictive (Fig. 7).
It is essential to remember that these percentage Figure 7
(A) PWD in the LV outflow tract. VTI measurement of the smallest and
variations in SV, VTI or peak velocity are calculated using largest envelope within the respiratory cycle. (B) Measuring Vmax variation
the following equation: with appropriate sweep speed.

70
2. For the more established methods, there must be no
spontaneous respiratory effort, which would alter
preload and SV and make variations a reflection of
work of breathing rather than FR.
3. Tidal volumes should be around 8 mL/kg. Lower,
although now desirable, tidal volumes cause small
amplitude changes in intravascular pressure and have
been shown to cause false negatives (consequently, it
may be necessary to increase tidal volumes during the
study) (16).
4. Intra-abdominal pressure should be normal as
although respiratory variations are still predictive,
the cut-off value has to be raised by an amount as yet
undefined (17).
5. The thorax should be intact - an open chest invalidates
any conclusions based on flow variation (18).
This variation is abolished when RAP is high.
The absence of respiratory variation strongly suggests
that the patient is not fluid responsive (23). In contrast,
and similarly to LV outflow, large variations in IVC
size with IPPV accurately predict FR. A diameter
‘variability’ cut-off value of more than 12% identifies
responders (24):
( Dmax - Dmin )
DVIVC = 100 ´
Dmean
DVIVC refers to IVC diameter variability, Dmax refers to
maximum diameter, Dmin refers to minimum diameter and
Dmean refers to mean diameter over the respiratory cycle.

These limitations have brought into question the

usefulness of these tests when applied to a general
body of critically ill patients (19). However, when the
preconditions are met, these tests have a very high
positive predictive value for identifying fluid responders.

The great veins

The size and variation in size over the respiratory cycle of

both the IVC and SVC give information about volume status.

IVC size IVC size, measured just distal to the hepat-

ic vein, in spontaneously breathing patients correlates
with RAP (20). Ventilated patients demonstrate a low
correlation between IVC size and RAP; however, an RAP
of less than 10 mm of Mercury can be assumed if the
IVC is less than 12 mm (21). In spontaneously breathing
patients, the best cut-off value for an RAP above or below
10 mm of Mercury is 2 cm (22). As already discussed, this
is of little clinical value. However, a small (<10 mm) IVC
suggests that fluid is tolerated (23). Invasively ventilated
patients often have a dilated IVC because of increased
intrathoracic pressure rather than as a reflection of their
intravascular volume status.

IVC diameter variation Cyclical changes in intratho-

racic pressure induce changes in RAP, which alters venous
return. In controlled ventilation, the IVC expands in in-
spiration and reduces in expiration (Fig. 8A). This can be
assessed in M-mode but is often best done in 2D as the ves-
sel does not always lie perpendicular to the beam (Fig. 8B).
Figure 8
IVC measurement just distal to the hepatic vein. M-mode (A) can be used
if the vessel is perpendicular to the ultrasound incidence; however, 2D
measurements (B) are often more reliable.

71
 A variation threshold of 18% is used if the following
formula for the ‘IVC distensibility index’ is used. IVC
variability is as follows (23):
( Dmax - Dmin )
DIIVC =
Dmin
DIIVC refers to IVC distensibility index.
IVC diameter variation has also been studied in
spontaneously breathing patients without respiratory
support; however, the evidence to support its use is weak
and cannot be advocated at this time (25).
SVC variation The SVC is difficult to see with TTE but
can be easily visualized with TOE in the longitudinal 90- to
100-degree view. Diameter changes are opposite of the IVC in
IPPV. The SVC partially collapses in mechanical inspira-
tion, as the increase in pleural pressure is greater than
the increase in RAP with a positive pressure breath.
The collapsibility index of the SVC has been shown to
be predictive of FR with a variation in SVC size of 36%,
being an appropriate cut-off value using the equation
100 × (Dmax – Dmin/Dmin) (26).
Pitfalls of great vein variations With
respiration, the IVC can move out of the plane of the
US beam, falsely mimicking changes in diameter.
The IVC wall must be clearly visualized throughout
the respiratory cycle and the bright edges kept in
view. Work of breathing with any spontaneous
ventilation has a significant impact on IVC size over the
respiratory cycle and, similar to LVOT flow variations,
spontaneous breathing and TVs of less than 8 mm/kg
may invalidate conclusions on FR. Arrhythmia seems to
be less confounding for IVC interpretation than for LV
outflow variation.
Right ventricle
RV size A dilated right ventricle is commonly seen in
critically ill patients due to acute cor pulmonale
compounded by fluid administration. Acute cor
pulmonale can be caused by high ventilation pressures,
which are sometimes necessary to ventilate stiff lungs, so
the mode of ventilation and pressures delivered should be
noted. The RV can easily dilate to accommodate increased
72
volume loading but tolerates acute pressure loading
poorly. Patients with RV dilatation from pulmonary
embolism have been shown to increase their SV with a
fluid challenge; however, a dilated RV should prompt
caution in fluid administration (27). As both ventricles
occupy a relatively fixed space constrained by the
pericardium, the RV dilates at the expense of LV size
(Fig. 9). An increase in RV size with no increase in SV is a
definite stopping point for fluid administration.
Paradoxical septal wall motion demonstrating very high
RV pressure may be a contraindication to IV fluid.
Importantly, RV failure results in false positives for
fluid responsiveness. The increased afterload induced by
a positive pressure breath exaggerates dDown producing
significant SV or VTI variation.
Passive leg raising
Passive leg raising is a simple method of predicting fluid
responsiveness (28). It is performed by tilting a patient
from a 45-degree semi-recumbent head up position
to a 45-degree leg up position, which transfers up to
300 mL of blood into the central circulation. Tipping
the whole bed and not lifting the legs avoids compression
of the femoral veins. Stroke volume or simply VTI across
either outflow tract is measured before and 1 min after
the PLR. An increment of 10% suggests FR.
The fluid shift settles within a few minutes, so
runs none of the risks of excess administration. It also
overcomes some of the limitations of the dynamic
Figure 9
RV dilatation and septal flattening is evident in this PSAX view. LV filling
is being impaired.
parameters above, as it can be used in spontaneous
ventilation and arrhythmias.
Pain on tilting, lower limb amputation or severe
peripheral vascular disease, and raised intracranial
pressure are contraindications to PLR.
After a fluid challenge
As seen above, dynamic parameters in particular are
extremely useful for predicting fluid responsiveness. The
gold standard, however, must be whether SV actually
increases with a fluid challenge. A fluid challenge is
generally defined as rapid administration of 250–500 mm
of intravenous fluid (29).
Assessment of the response in flow to a fluid
challenge is easy with echocardiography. It is really
only necessary to measure LVOT VTI rather than adding
in an LVOT measurement to get SV. Measurement
of VTI should occur immediately before and after a
fluid challenge. Measurements should ideally be end-
expiratory or averaged over several consecutive beats.
Recently, it has been shown that a mini-fluid
challenge of only 100 mL accurately predicts FR using
variations in aortic VTI with TTE (30). It should be
noted that significant improvements in SV may not be
reflected by changes in blood pressure; however, blood
flow and calculated oxygen delivery are improved.
The length of time that cardiac output remains
increased after a successful fluid bolus is poorly studied.
In health, redistribution of most of a crystalloid bolus
occurs within 45 min, slightly longer for colloids. In
disease states, this duration is very variable and may be
as brief as 20 min (31). As such, the need for frequent
reassessment of circulating volume is important.
Figure 10
A typical ROC curve for the power of echocardiography to predict fluid
responsiveness. The ‘optimum’ threshold is neither the most sensitive nor
specific.
A further consideration is the dilutional effects of
fluid administration. Although cardiac output may be
increased, haemoglobin has been necessarily diluted.
The balance of these effects determines whether overall
oxygen delivery has been augmented. Equally frequent
checks on haemoglobin or haematocrit are, therefore,
often advised.
Fluid tolerance
When there is doubt about whether a fluid challenge
is appropriate, it can be reassuring to elicit signs with
echocardiography that suggest that fluid administration
will at least not lead to pulmonary oedema or right heart
failure. In both spontaneously breathing and ventilated
patients, a small IVC that varies in size with respiration,
non-dilated right heart chambers, a non-displaced inter-
ventricular septum, absence of right and left ventricular
systolic failure and absence of markers of raised LVEDP all
suggest that fluid administration will not cause acute harm.
Fluid administration should stop when VTI no longer
significantly increases with a fluid bolus. False negatives
can be excluded by demonstrating that preload has
increased by measuring an increase in LV E velocity, LV
E:A ratio or RV size.
Clinical judgement
The tests that predict fluid responsiveness do not always
give a dichotomic answer. Where a study’s ROC curve
analysis yields a best cut-off of 12% between responders
Figure 11
The ‘grey zone’ approach to flow variation assessment means that when
the result is around the threshold value, further corroborating evidence
should be sort from other modalities (e.g. IVC evaluation).
73
and non-responders, it must be recognized that this is a
balance between sensitivity and specificity (Fig.  10). If
the tests produce a result around the threshold, then this
should trigger a search for other markers of FR (Fig. 11).
FR means SV increases with fluid in the immediate
term. However, a patient being fluid responsive does not
necessarily mean that fluid is beneficial. Administration of
a fluid challenge to a healthy normovolaemic individual
very likely results in increased SV. This does not mean
they needed fluid or that it was of benefit to them. It
is vital for the physician to be aware of the dangers of
74
unnecessary fluid loading and take the whole clinical
picture into account.
Conclusion
Echocardiography is an ideal imaging modality for rapid
assessment of the circulation in the shocked patient. It
usually elucidates the cause, whether cardiac ischaemia,
cardiomyopathy, acute valve disease, tamponade,
significant pulmonary embolism, aortic root pathology or
Figure 12
An algorithm to guide fluid resuscitation using
echocardiography.
distributive shock. This article has focused on the fluid
optimization phase of resuscitation.
Intravenous fluid boluses can benefit the circulation
but also cause harm. The presence of signs that fluid
delivery improves cardiac output does not mean that a
greater cardiac output is necessary.
Echocardiography is an invaluable tool for assessing
both whether a patient will be fluid responsive and what
effects the fluid administration has on the heart. There are
limitations to its use and interpretation; no single test is
immune to false positives and negatives. For example, it
has been shown that between 2 and 30% of patients may
have tidal volumes outside the range for which outflow
tract flow variations are technically valid. However,
acknowledging such weaknesses, taking into account the
pre-test probability and gathering as many markers as
possible, leads to good clinical decision making.
The methods outlined in this article are summed up
in an algorithm to assess for fluid responsiveness (Fig. 12).
The principles of the use of echocardiography for
volume assessment used in the critically ill are as follows:
1. Small hyperdynamic ventricles with a small IVC
suggest significant hypovolaemia.
2. In a shocked patient without signs of overt
hypovolaemia, dynamic indices of FR should be sought.
3. Echocardiography can give additional information
regarding the validity of other clinical and monitoring
markers.
4. Echocardiography informs about the dangers
of delivering a fluid bolus in terms of adding to
extravascular fluid or worsening LV filling.
5. When interpreting echocardiography findings,
the limitations of that particular technique in that
particular patient must be taken into account.
Further research
Although there are numerous signals in the literature
that higher overall fluid balance correlates with poorer
outcome, the prospective evidence is lacking. Indeed, it
is not known whether it is actually better to maintain the
patient in a state of fluid responsiveness rather than so
often try to maximize stroke volume.
Further research in the use of echocardiography for
optimizing circulating volume might explore the in-depth
use of diastolic assessment of both LV and RV, the use of
strain imaging and the changes induced by small rapid
fluid boluses.
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Lehot J-J 2006 Prediction of fluid responsiveness using respiratory
variations in left ventricular stroke area by transoesophageal
echocardiographic automated border detection in mechanically
ventilated patients. Critical Care 10 R171. (doi:10.1186/cc5123)
15 Chauvet J-L, El-Dash S, Delastre O, Bouffandeau B, Jusserand D,
Michot J-B, Bauer F, Maizel J & Slama M 2015 Early dynamic left
intraventricular obstruction is associated with hypovolemia and high
mortality in septic shock patients. Critical Care 19 262. (doi:10.1186/
s13054-015-0980-z)
16 Muller L, Louart G, Bousquet P-J, Candela D, Zoric L,
Coussaye J-E, Jaber S & Lefrant J-Y 2009 The influence of the
airway driving pressure on pulsed pressure variation as a predictor
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18 de Waal EEC, Rex S, Kruitwagen CLJJ, Kalkman CJ & Buhre WF 2009
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CHAPTER 10
Echocardiography Atlas

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 Subcostal view projection 1

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CHAPTER 11
Echocardiographic Calculations

Calculation of stroke volume with echo:

Fig. 1 : Volume of cylinder principle for stroke volume

Fig. 2: A5C calculation of VTi

Area of cylinder =stroke volume = š r2 h

R = aortic valve radius

H = Vti

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Fig 3: Echo Doppler image for VTi

Fig 4: Echo Image VTI

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 Fig 5: Aortic Valve diameter for Cross sectional area calculation

1. Assessment of Cardiac Contractility by Echo:

Simple methods include

– Visual assessment – “Eyeballing”; reasonably accurate……Two views – A4C
and Psax
– M mode – ejection fraction and fractional shortening
• Principle: Difference in systolic and diastolic LV dimensions

LVEDD – LVESD
FS = -------------------- X 100
LVEDD
Normal value is 30 -45%

EDV - ESV
EF = ----------------- X 100
EDV
Normal – 50 – 75%

M-Mode Quantification calculation:

• Use Parasternal Short-Axis (recommended by Mayo) or Long-Axis (recommeneded

by American Society of Echocardiography) views to measure LVEDD and LVESD
• May take several measurements at different levels and calculate average
• Assumes no significant regional wall motion abnormalities present….

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 The ventricular functions should always be interpreted keeping in mind loading factors and
degree of inotropic support. When assessing ventricular function, each ventricle should be
considered in isolation and also in conjunction with the other ventricle.

Left ventricular size and functions:

The left ventricular diameter is measured in parasternal long axis, at the tip of the mitral
leaflets, at the interface of the blood- internal wall

Diastolic diameter: Measured at end diastole, on the frame after mitral closure. Normally
corresponds to the largest cardiac dimension

Systolic diameter: Measured at end systole, on the frame preceding mitral opening.
Corresponds to the smallest cardiac dimension

LV systolic function indices include

1. Ejection fraction and fractional shortening:- M Mode LV dimensional method,

Simpson’s method and Visual Gestalt i.e. eyeballing the LV in real time
2. dP/dT of the mitral regurgitant jet
3. Doppler measurement of stroke volume and cardiac output

Linear Measurements by M Mode

Made in PLAX

Beyond the tip of mitral leaflets

Easy to learn and perform

Some theoretical drawbacks: perfect sphere??, regional wall motion abnormalities

Still the most popular and simple way to measure LV functions

Left ventricle fractional shortening:

LVEDD – LVESD
FS = -------------------- X 100
LVEDD
Normal value is 30 -45%

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Left ventricle ejection fraction:

Ejection fraction is calculated from derived volumes

Volumes are computed based on the “cubed” or “Teichholtz” equations

EDV - ESV
EF = ----------------- X 100
EDV
Normal – 50 – 75%

“Eye Ball” estimation of left ventricular systolic function:

Reasonably accurate

A semi quantitative scaling proposed is:

Normal LV function (30% change in radius)

Mild – moderately decreased LV function (10 – 30% decrease in radius)

Severely impaired LV function (< 10% change in radius)

For better accuracy, checked in two different views (A4C and PSAX)

Pitfalls in LV diameter measurement:

Be careful to exclude chordate and papillary muscles

Measure perpendicular to long axis of ventricle

PLAX view should be parallel to LV axis (septum and posterior wall should be parallel)

Doppler assessment of Cardiac Output:

The stroke volume and cardiac output can be measured by echo.

This is calculated using Doppler measurements at the LVOT

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 Principle: Stroke volume is volume of cylinder ʌ r2 h (or cross sectional area ʌ r2 x Stroke
distance (VTi)

Velocity = distance/time >>> so distance (H) is velocity x time (Velocity of blood at LVOT
during cardiac contraction)

1st step : Measure LVOT diameter in PLAX at hinge of aortic leaflets (in cm)

2nd step: on A5C, place PW Doppler gate in LVOT as close to aortic valve as possible and
acquire PW trace

3rd step: Calculate VTi from PW trace (cm)

Stroke volume is then ʌ x (aortic valve radius)2 x VTi (in ml)

Cardiac output is SV x HR/ 1000 (in l/min)

This is indexed to BSA to get cardiac index >>>>(CO/BSA)

Other uses of VTi to Intensivist:

Vti variation with respiration of > 12% (some studies more than 15%) predicts fluid
responsivenesss (Sensitivity of 100% and specificity of 89%)

Vmax variations similar and easier to do

LVOT VTi variation with PLR > 12.5% (some studies more than 10%) also predicts fluid
responsiveness (sensitivity of 77% and specificity of 100%)

Systemic Vascular Resistance using echo:

SVR = (Mean Arterial Pressure – CVP)

Cardiac output

This gives value in Hybrid reference units(HRU) or Wood units

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SVR = 80 x (Mean Arterial Pressure – CVP)

Cardiac output

This gives value in dyn·s·cmí5 (this is standard unit)

Normal values are: (indexed to BSA)

Reference Range

Measurement
mmHg·min/l or
dyn·s/cm5 MPa·s/m3
HRU/Wood units

Systemic vascular resistance 700–1600[2] 70–160[3] 9–20[3]

Pulmonary vascular resistance 20–130[2] 2–13[3] 0.25–1.6[3]

Calculation of SVR can be objective and real time tool used for titration of inotropes in shock
patient.

Assessment of LV diastolic dysfunction:

Ideally measured as elevated EDP during cardiac cath

LV diastolic dysfunction is common in the ICU

Assessing diastolic dysfunction in useful in optimising volume status and hemodynamics in

critically ill patients

Echo indices used to assess diastolic dysfunction include:

1. Mitral inflow patterns: E/A, deceleration time, isovolemic relaxation time (IVRT)
2. Pulmonary venous inflow patterns: S/D ratio
3. Myocardial performance index (MPI) or Tei index

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 E/A ratio:

Flow from LA to LV occurs in 3 phases:

initial rush of blood when MV opens causes a peak velocity in early diastole – E
wave

Period of low or no flow (diastasis)

Second rush of blood during atrial contraction – A wave

PW (Doppler) gate is placed between tips of open mitral leaflets in A4C (see below )

Size of E and A waves seen

Normal E/A is between 1 and 2

A wave greater than E wave indicates diastolic dysfunction (an A-wave twice as large as the E-
wave indicates impaired LV relaxation – see figure below )

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Spectral tissue Doppler (TDI) - Mitral annular velocities examination

Slow wall velocities can be assessed with Tissue Doppler Imaging (TDI). The sample volume, when
placed at the medial mitral annulus, shows slower velocities as when placed at the lateral annulus.
The E/E' relationship will be different according to each case, making more difficult the
interpretation of results

Placement of sample volume (medial mitral annulus )

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Pulmonary artery (PA) pressure estimation-

Assessment of PA-pressure is an important part of a correctly and comprehensive conducted

echocardiographic examination. Assessment of pulmonary artery systolic pressure (PASP) can be
carried out by measuring maximal tricuspid regurgitation velocity, and applying the modified
Bernoulli equation to convert this value into pressure values. Estimated right atrial pressure (RAP)
must be added to this obtained value. Mean (PAMP) and diastolic PA-pressures (PADP) can be
estimated by assessment of the pulmonary regurgitation

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