Canadian Journal of Cardiology 33 (2017) 88e100

Review
Extracardiac Signs of Fluid Overload in the Critically Ill
Cardiac Patient: A Focused Evaluation Using Bedside
Ultrasound
William Beaubien-Souligny, MD, FRCPC,a Jos
ee Bouchard, MD, FRCPC,b
Georges Desjardins, MD, FRCPC,c Yoan Lamarche, MD, MSc, FRCSC,d
Mark Liszkowski, MD, FRCPC,e Pierre Robillard, MD,f and Andr
e Denault, MD, PhD, FRCPCc
a
Nephrology Department, Universit
e de Montr
e al, Montreal, Qu
e bec, Canada
b
Nephrology Department, Hôpital Sacr
e -Coeur de Montr
e al, Montreal, Qu
e bec, Canada
c
Department of Anesthesiology, Montreal Heart Institute, Universit
e de Montr
e al, Montreal, Qu
e bec, Canada
d
Department of Cardiac Surgery, Montreal Heart Institute, Universit
e de Montr
e al, Montreal, Qu
e bec, Canada
e
Department of Cardiology, Montreal Heart Institute, Universit
e de Montr
e al, Montreal, Qu
e bec, Canada
f
Department of Radiology, Montreal Heart Institute, Universit
e de Montr
e al, Montreal, Qu
e bec, Canada

ABSTRACT

RESUM

E
Fluid balance management is of great importance in the critically ill La gestion de l’e
quilibre hydroe

lectrolytique a une grande importance
cardiac patient. Although intravenous fluids are a cornerstone therapy chez le malade cardiaque en phase critique. Bien que l’administration
in the management of unstable patients, excessive administration de liquides par voie intraveineuse constitue la pierre angulaire de la
coupled with cardiac dysfunction leads to elevation in central venous prise en charge des patients instables, un apport liquidien excessif
pressure and end-organ venous congestion. Fluid overload is known to jumele
à la dysfonction cardiaque entraîne une augmentation de la
have a detrimental effect on organ function and is responsible for pression veineuse centrale et une congestion veineuse des organes.
significant morbidity in critically ill patients. Multisystem bedside point On sait qu’une surcharge liquidienne a un effet ne
faste sur la fonction
of care ultrasound imaging can be used to assess signs of fluid over- organique et qu’elle entraîne une morbidite
significative chez le pa-
load and venous congestion in critically ill patients. In this review we tient en phase critique. Il peut être utile d’utiliser, au chevet de pareil
describe the ultrasonographic extracardiac signs of fluid overload and patient, un appareil d’e
chographie afin de de
celer les signes d’une
how they can be used to complement clinical evaluation to individu- surcharge liquidienne et d’une congestion organique. Dans cet article,
alize patient management. nous de
crivons les signes e
chographiques extracardiaques de la sur-
charge liquidienne et la façon dont ils peuvent servir de comple
ment à

valuation clinique aux fins de personnalisation de la prise en charge
l’e
des patients.

Appropriate use of intravenous fluid therapy is a critical
component of patient management in the intensive care unit.
Fluid administration in the context of hypovolemia increases
cardiac output by the Frank-Starling mechanism and helps to
maintain systemic perfusion. When a significant inflammatory
reaction is initiated in the context of major surgery involving
cardiopulmonary bypass or during sepsis, the response to fluid
Received for publication June 6, 2016. Accepted August 8, 2016.
Corresponding author: Dr Andr
e Denault, Montreal Heart Institute,
5000 Belanger St, Montreal, Quebec H1T 1C8, Canada. Tel.: þ1-514-376-
3330; fax: þ1-514-376-1355.
E-mail: andre.denault@gmail.com
See page 97 for disclosure information.
administration is altered by increased vascular permeability
and impaired vasoconstriction (Fig. 1). In these settings, fluid
administration can lead to a significant positive fluid balance.
The progressive increase in central venous pressure (CVP) and
end-organ congestion in patients with heart failure can have a
prolonged detrimental effect on organ function.2
To assess fluid status, clinicians have relied on physical
examination. However, bedside ultrasound imaging has
significantly added to the clinical examination in the opti-
mization of fluid status. Although its use in assessing fluid
responsiveness has been described in multiple publications,3-5
a focused ultrasound assessment can also provide important
information on the effect of congestive heart failure on other
systems.

http://dx.doi.org/10.1016/j.cjca.2016.08.012
0828-282X/
2016 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.
Beaubien-Souligny et al. 89
Evaluation of Fluid Status Using Bedside Ultrasound

A Normal B Increased permeability

Extra Vascular Lung Water (EVLW)

Extra Vascular Lung Water (EVLW)

EVLW EVLW sepsis EV L W

Stroke Volume (SV)

Stroke Volume (SV)

2

2 SV SV

1 1

Preload Preload

C Normal D Increased permeability

Extra Vascular Lung Water (EVLW)

Extra Vascular Lung Water (EVLW)

EVLW EVLW sepsis EV L W
Stroke Volume (SV)

Stroke Volume (SV)

2

1 SV 1 SV

Preload Preload

Figure 1. Relationship between stroke volume (SV), preload, and extravascular lung water (EVLW). (A) Normal fluid-responsive patients: a fluid
challenge results in an increase in cardiac output with a small change in EVLW. (B) With increased permeability or sepsis, the increase in EVLW will
be more important. (C) Flat portion of the Starling relationship; no significant increase in cardiac output but elevation in EVLW in normal patients. (D)
However in patients with sepsis, the increase in EVLW will be even more significant for the same fluid challenge. Adapted from Marik et al.1 with
permission from Oxford University Press.

In this article we focus on the adverse effect of fluid Abdominal organs are also particularly vulnerable to an
overload on organ function and the multisystemic ultrasound increase in intra-abdominal pressure resulting from venous
features associated with organ congestion. Assessment of fluid hypertension. Fluid overload is an important risk factor for
responsiveness and the composition of fluid therapy are the development of intra-abdominal hypertension
beyond the scope of this review and can be found syndrome.13
elsewhere.6,7 The adverse effects of fluid overload on organ function are
now documented and might be responsible for significant
morbidity in critically ill patients.2 A summary of the effects on
Adverse Effects of Fluid Overload in Critically the different systems are presented in Table 1. In some patients,
Ill Patients organ congestion could represent a preventable and/or modi-
Vascular permeability is increased by the disruption of the fiable risk factor for organ failure in critically ill cardiac patients.
endothelial glycocalyx layer in sepsis8 and in ischemia- In this regard, an early detection of organ congestion is the first
reperfusion injury after surgery.9 The glycocalyx layer is a step to study this phenomenon and develop an appropriate
cell-bound structure composed of proteins and glycosamino- treatment strategy for this, often iatrogenic, complication.
glycans covering the surface of the capillary endothelium,
which creates a local oncotic gradient.10 The integrity of the
glycocalyx layer within the capillary lumen prevents hydro- The Bedside Diagnosis of Fluid Overload in
static fluid shifts from the intravascular space to the interstitial Critically Ill Patients
compartment in physiologic conditions.11 Hypervolemia also The early detection of fluid overload could offer the
increases the release of atrial natriuretic peptide, which has opportunity to induce a negative fluid balance using diuretics or
been shown to damage the endothelial glycocalyx.12 Rapid ultrafiltration combined with a restriction of fluid intake before
fluid loss from the vascular compartment leads to the accu- organ damage occurs. It must be noted that attempting to
mulation of fluid in the interstitial compartment resulting in induce a negative fluid balance in an unstable patient might lead
an increase in interstitial pressure, which could impair organ to marked deterioration of the cardiac output because the
perfusion, leading to injury. In the lungs, the effect of extravascular fluid might not be recruited easily. The identifi-
increased vascular permeability is shown by the increase in cation of the causal mechanisms of hemodynamic instability,
extravascular lung water (EVLW) as the capillary hydrostatic although beyond the scope of this article, is important and can
pressure increases with fluid administration (Fig. 1). be improved by the use of bedside ultrasound assessment.29
90
Table 1. Adverse effects of organ congestion
Involved system Clinical consequences
Gastrointestinal  Prolonged ileus
 Bacterial endotoxin translocation:
systemic inflammation
 Impaired hepatic function and
cholestasis
 Impaired drug absorption
Kidney  Acute kidney injury
Lungs  Pulmonary edema
 Decreased compliance
 Increased work of breathing
Central nervous system  Impairment in cognition
delirium
Heart  Conduction abnormalities
 Subendocardial ischemia
Soft tissues  Impaired wound healing
 Promote surgical site infections
ARDS, acute respiratory distress syndrome; CHF, chronic heart failure; CVP, central venous pressure; EVLW, extravascular lung water; LPS, lipopolysaccharide
(endotoxin).
Multiple mechanisms of shock, such as right ventricular failure
and postcardiopulmonary bypass vasoplegia, can coexist in a
single patient.30-32 Appropriate fluid administration guided by
clinical predictors of fluid responsiveness must be weighed
against the risk of inducing fluid overload.3,33-35 An appropriate
use of vasopressor therapy is of paramount importance and the
administration of fluids should be done to improve tissue
perfusion, and not for the sole purpose of decreasing vasopressor
requirements. A timely systemic decongestion strategy in the
postresuscitation period in selected patients who show features
of organ congestion could prevent complications associated
with fluid overload. Retrospective data in septic patients sup-
port this hypothesis.36 In the following section, we describe
ultrasonographic manifestations of organ congestion and how
they can complement other clinical signs of fluid overload.
Assessment of Central Vessels
Ultrasound measurements of the inferior vena cava (IVC)
have been used for the evaluation of fluid responsiveness
under the prerequisite that they are representative of right
ventricular preload. The IVC diameter and collapsibility are
now integrated in focused ultrasound assessment in trauma
patients37 and IVC collapse is the best predictor of hypo-
tension after induction of anaesthesia.38 Some measurements
might reflect abnormally high CVP (10-20 mm Hg), such as
an IVC diameter of > 20 mm, a collapse of IVC (collapsibility
index; CI) of < 50% with sudden inspiration39 or a variation
of < 20% of IVC diameter upon normal inspiration.40 Many
studies have evaluated the correlation between IVC diameter/
CI and CVP with variable results, showing a moderate cor-
relation and relatively fair accuracy to predict CVP.40-44
Although ultrasonographic measurements of the IVC do not
seem to be precise enough to estimate CVP values, they can
discriminate between normal/low CVP and high CVP
values.40,42 This distinction is useful because the presence of
Canadian Journal of Cardiology
Volume 33 2017
Evidence
 A restrictive fluid strategy leads to shorter hospital stay after intestinal
surgery14
 Higher measurements of serum LPS in decompensated CHF patients15
 Posthepatic portal hypertension and hyperbilirubinemia in CHF
patients16
 Diuretic resistance in CHF patients17
 Fluid overload is an independent risk factor for acute kidney injury in
critically ill adults18,19
 Elevated CVP is a predictive factor of renal impairment in CHF pa-
tients20 and in cardiac surgery patients21
 A restrictive fluid strategy has led to fewer ventilator days in patients
with ARDS22
 EVLW correlated with organ dysfunction and poor outcomes and with
increased risk of reintubation and respiratory failure23
and  Fluid overloaded patients could be at greater risk of delirium24
 CHF after surgery is a risk factor for postoperative delirium25
 In an animal model of intra-abdominal hypertension, intracranial
pressure correlated with CVP values26
 Myocardial edema might contribute to increased risk of atrial fibrilla-
tion and bundle branch block27
 A restrictive fluid regimen reduced postoperative wound healing com-
plications after colorectal surgery28
peripheral edema does not necessarily reflect increased CVP
and could be treated differently according to the cause. As
such, imaging of the IVC can be done as a first step. The
technique is shown in Figure 2. Longitudinal imaging of the
IVC can be done through the liver with a phased array
transducer (cardiac probe) or a curved array transducer
(abdominal probe) from the subxiphoid position down to the
posterior axillary line providing a large window for adequate
visualization. Using the liver as an acoustic window, the
success rate in visualizing the IVC is very high even for cli-
nicians with basic training.46 It should be noted there is some
limitation to the estimation of systemic venous pressure with
this technique because any supradiaphragmatic mechanical
obstruction can impair venous return.47 Consequently, tam-
ponade, pneumothorax, or direct obstruction of the IVC from
stenosis or thrombus should the sought. Measurements of the
IVC are modified by positive pressure ventilation and should
be interpreted with caution in mechanically ventilated pa-
tients.41 A high positive end expiratory pressure or lung hy-
perinflation can lead to a larger IVC size leading to potential
overestimation of cardiac preload.48
Jugular vein examination has been taught as a way to
evaluate fluid status with variable accuracy depending on the
skills of the observer.49 Direct visualization of the jugular
venous pulse can be difficult in patients who have more
subepithelial fat in the cervical region or with increased res-
piratory work with the use of sternocleidomastoid muscles.
Bedside ultrasound imaging can also be used to estimate CVP
noninvasively very quickly. The technique relies on the visu-
alization of the right jugular vein tapering point as presented
in Figure 3. Using a linear probe, the right jugular vein can be
located to obtain a longitudinal image. Minimal pressure must
be applied to the probe because the internal jugular vein is
easily collapsible. After identification of the taper point, CVP
can be estimated by measuring the height as for physical ex-
amination.50 This technique can predict CVP with moderate
Beaubien-Souligny et al. 91
Evaluation of Fluid Status Using Bedside Ultrasound

Figure 2. Examination of the inferior vena cava: (A) Axial T1-weighted magnetic resonance image of the liver showing different positions of the
ultrasound probe to obtain a longitudinal view of the inferior vena cava. The subxyphoid (1), anterior axillary line (2), and posterior axillary line (3) are
indicated. The subxyphoid (B), anterior axillary line (C), posterior axillary line, and (D) position is shown using the Vimedix simulator (Canadian
Aviation Electronic [CAE] Healthcare, Saint-Laurent, QC). Copyright ª 2016 from Basic Transesophageal and Critical Care Ultrasound by Denault
et al.45 Reproduced by permission of Taylor and Francis Group, LLC, a division of Informa plc.

accuracy in a few seconds at the bedside.51 It must be noted
that this technique has been reported to underestimate CVP
and should be interpreted with caution.52
Assessment of Abdominal Manifestations of
Fluid Overload
Excessive fluid administration and high CVP can have a
negative effect on abdominal organs. Intra-abdominal pres-
sures can be estimated by measuring intravesical pressures
through a Foley catheter.53 Importantly, early monitoring of
organ congestion could facilitate measures to avoid the
development of intra-abdominal hypertension.
Doppler ultrasound imaging of the liver offers the
possibility to assess flow in the portal and hepatic veins.
Hepatic venous flow can be used to evaluate right ven-
tricular diastolic function39 and stratify shock on the basis
of the aspect of the IVC and the hepatic venous flow
Doppler signal.54,55 Impairment of venous return from an
extracardiac cause can also alter hepatic blood flow pro-
ducing a reduction in phasicity and lower or absent
Doppler velocities.55 Hepatic vein flow can be obtained

Figure 3. Examination of the internal jugular vein (IJV). (A) Measurements of the vertical distance between the top of the IJV and the sternal angle.
Central venous pressure is estimated by adding 5 cm to the measured height at a 30 -45 angle.50 (B) Linear probe position to obtain a longitudinal
view of the IJV. (C) Visualization of the IJV taper point.
92 Canadian Journal of Cardiology
Volume 33 2017

Figure 4. Hepatic venous flow. Triphasic Doppler hepatic venous flow obtained from a subxyphoid abdominal ultrasound image with colour (A-C) and
pulsed-wave Doppler (D) has an atrial reversal (AR) in red, a systolic (S) phase in blue/green, which can be followed by a V wave, and a diastolic (D)
phase in dark blue. Images (E-H) show abnormal hepatic venous flow in the context of right ventricular dysfunction. Notice the change in the D to S
velocity ratio that is now < 1. Copyright ª 2016 from Basic Transesophageal and Critical Care Ultrasound by Denault et al.45 Reproduced by
permission of Taylor and Francis Group, LLC, a division of Informa plc.

using a phased array probe or a curved array probe in the
subxiphoid region as presented in Figure 4. Normal hepatic
flow is directed away from the liver and fluctuates during
the cardiac cycle as shown in Figure 4, A-D.56 Systolic flow
is usually of higher velocity than diastolic flow. In patients
with right heart failure, increased right atrial pressure and/
or tricuspid regurgitation during ventricular systole leads to
a reduction of the S wave and to a systolic to diastolic ratio
< 1 (Fig. 4, E-H).55,57,58 Although an abnormal hepatic
vein flow waveform can be found in stable chronic heart
failure patients and is not synonymous with fluid overload
and organ congestion, its presence in a critically ill patient
should prompt the clinician to consider the patient at
increased risk of organ congestion.

Figure 5. Portal venous flow (PoVF). (A) PoVF assessment from a posterior axillary line coronal view. (B) Using the same view, the inferior vena cava
(IVC), portal vein (PV), and hepatic vein (HV) can be seen. Note the increased echogenicity of the PV wall. (C) Normal PV pulsed-wave Doppler has a
monophasic signal indicating that blood is directed toward the transducer. Note the background pulsatile higher velocity of the hepatic artery, which
is in the same direction. (D) Abnormal pulsatile portal flow with a pulsatility fraction of > 50%.
Beaubien-Souligny et al. 93
Evaluation of Fluid Status Using Bedside Ultrasound

1.0 n = 117 1
Cumulative event-free probability S D

n = 51
0.8 2
2
0.6
n = 49

0.4 3 S D

0.2
Log Rank p < 0.001 3

0.0
0 100 200 300 365
Follow up days D

Figure 6. Kaplan-Meier curves at 1-year follow-up for the probability of freedom from death from cardiac causes and unplanned hospitalizations for
heart failure of 3 classifications of intrarenal venous flow which include the (1) continuous flow, (2) the biphasic discontinuous flow, and (3)
monophasic discontinuous flow. D, diastolic; S, systolic. Modified from Iida et al.65 with permission from Elsevier.

Flow in the portal vein can be assessed using a phased array
probe positioned in a right midaxillary coronal view as shown
in Figure 5. Venous flow through the portal vein is of low
velocity (20 cm/s) because this circulation is isolated from the
systemic circulation by the liver sinusoids and splanchnic
capillary bed. Therefore, portal venous flow does present
minimal variations through the cardiac cycle. A difference
between systolic and diastolic velocities (also named pulsatility
fraction; PF) of > 50% can be considered abnormal and is
called pulsatile flow. Pulsatile blood flow is a validated sign of
portal hypertension.59
PF ð%Þ ¼ 100 ð½VSystole  VDiastole =VSystole Þ
(V ¼ blood velocity in the portal vein)
Portal pulsatility has been studied as a sign of severity in
patients with congestive heart failure. The presence of an
abnormal portal pulsatility predicted increased CVP and worse
functional class in heart failure patients.60-62 Venous congestion
resulting from congestive heart failure begins with an elevation
of the CVP and dilatation of the IVC and its main tributaries
such as the hepatic veins. When the dilatation becomes severe,
the venous compliance of the IVC is decreased and pressure is
transduced through the hepatic sinusoids to the portal system.
This results in a decrease in velocities in the portal system or,
when severe, in a complete absence or reversal of portal flow.
Doppler evaluation of the portal flow could be used as a marker
of end-organ venous congestion. In decompensated heart fail-
ure, a portal pulsatility of > 50% was the best predictor of
increased serum bilirubin compared with other parameters such
as CVP.63 For the portal flow to be representative of central
venous congestion, other causes of portal hypertension such as
cirrhosis and portal thrombosis must be absent. A PF of > 50%

Figure 7. Pulmonary congestion. (A) Chest radiograph of an 86-year-old man and lung ultrasound images (B and C) show diffuse B-lines in zones 1
and 5. Copyright ª 2016 from Basic Transesophageal and Critical Care Ultrasound by Denault et al.45 Reproduced by permission of Taylor and
Francis Group, LLC, a division of Informa plc.
94 Canadian Journal of Cardiology
Volume 33 2017

Figure 8. Optic nerve sheath measurement. (A) The site for measuring the diameter of the optic nerve sheath is shown. A 3-mm perpendicular line
is drawn from the middle of the optic nerve, at which point the transverse measurement of the optic sheath is performed. Note that the mea-
surement includes the sheath and stops at the transition contrast between the optic nerve and surrounding tissue. (B) A 2-dimensional image
displays the ocular structures and optic nerve sheath. (C) Ultrasound of the eye orbit from an 85-year-old patient after aortic valve replacement with
significant postoperative fluid balance. The optic nerve diameter was 6.4 mm. (D) Optic nerve 2-dimensional image of papilledema (arrow) in a brain-
dead patient for organ donation. Copyright ª 2016 from Basic Transesophageal and Critical Care Ultrasound by Denault et al.45 Reproduced by
permission of Taylor and Francis Group, LLC, a division of Informa plc.

has also been reported in some individuals with low body mass
index and normal cardiac function.64 Consequently, this
finding should be supported by other signs of elevated CVP
such as IVC dilatation/noncollapsibility and an abnormal he-
patic vein flow waveform.
In decompensated heart failure patients, an elevated CVP is
the best predictor of renal failure compared with cardiac index,
systolic blood pressure, and pulmonary capillary wedge pres-
sure.20 The effect of elevated venous pressures on intrarenal
hemodynamics can be assessed using Doppler ultrasound ex-
amination. In physiological conditions, blood flow in the
interlobar veins is continuous during the cardiac cycle. With
high CVP, new evidence suggests that venous flow transforms
into a discontinuous biphasic pattern, and with further venous
hypertension, into a monophasic discontinuous pattern
(Fig. 6).65 Discontinuous flow in the interlobar renal veins can
be linked to the CVP waveform during the cardiac cycle. As CVP
increases and the IVC becomes noncompliant, flow in the
interlobar vein can be observed during the systolic and diastolic
filling of the right atria (during the X and Y descent on CVP
waveform). As right heart failure worsens, intrarenal venous flow
becomes monophasic reflecting the predominance of the Y
descent of the CVP waveform analogous to the variation in the
systolic/diastolic ratio in the hepatic vein waveform (decreased
filling of the right atria during systole).66 Iida et al. have shown
that the intrarenal venous flow pattern strongly correlated with
death from cardiovascular disease and unplanned hospitalization
for heart failure independent of renal resistance index, CVP, and
hemodynamic status including echocardiographic parameters.65
Assessment of Pulmonary Manifestations of
Fluid Overload
Detection of subclinical pulmonary edema or increased
EVLW could avoid pulmonary complications in critically ill
adults. Bedside physical examination, CVP measurements,
and chest x-ray do not predict increased EVLW measured
according to transpulmonary thermodilution, suggesting that
those techniques do not have sufficient sensitivity to detect
early fluid overload.67 Although normal lung parenchyma
Beaubien-Souligny et al. 95
Evaluation of Fluid Status Using Bedside Ultrasound

Figure 9. Transcranial Doppler colour-coded duplex sonography. The middle cerebral artery (MCA) is interrogated using a transthoracic probe
positioned over the right temporal region. (A) A 2-dimensional image of the circle of Willis with colour Doppler (Nyquist 43 cm/s) where flow
interrogation is obtained. (B) Sample volume positioning in the vessel allows precise determination of the MCA velocity spectral Doppler profile. (C)
Transcranial Doppler changes in the MCA mean flow with progressive increase in intracranial pressure (ICP) are shown compared with normal MCA
flow trace and normal ICP. DAP, diastolic arterial pressure; LACA, left anterior cerebral artery; LMCA, left MCA; LPCA, left posterior cerebral artery;
SAP, systolic arterial pressure. Copyright ª 2016 from Basic Transesophageal and Critical Care Ultrasound by Denault et al.45 Reproduced by
permission of Taylor and Francis Group, LLC, a division of Informa plc.

cannot be visualized with ultrasound imaging because of air,
which is impermeable to ultrasound, the image generated by
thickened interlobular septas produce an artifact called pul-
monary B-lines, also referred to as “comet tail artifacts”
(Fig. 7). The detection of pulmonary B-lines is possible with a
linear probe or a phased array probe placed over the para-
sternal, midclavicular, anterior axillary, and mid axillary lines
at the second, third, fourth, and fifth intercostal spaces.
Visualization of B-lines identifies the presence of alveolar-
interstitial syndrome, which can be explained by congestive
pulmonary edema secondary to heart failure or acute respi-
ratory distress syndrome. Edema can be semiquantitatively
assessed by recording the number of B-lines present in mul-
tiple lung fields.68 The presence of B-lines has been correlated
to capillary wedge pressure and invasively measured EVLW.69
B-lines have also been proven to be more reliable than chest
x-ray for the evaluation of EVLW in patients with acute res-
piratory distress syndrome.70 This information can be ob-
tained within a few minutes with a short learning curve.71
Lung ultrasound imaging has been used for the evaluation
of pulmonary congestion in a variety of different settings such
as the differential diagnosis of dyspnea in the emergency
department,72 the evaluation of chronic heart failure in an
outpatient setting,73 and fluid status in hemodialysis pa-
tients.74 In the intensive care setting, the predominance of
pleural B-lines can predict elevated EVLW measured ac-
cording to transpulmonary thermodilution.69 It is important
to note that interstitial lung disease such as idiopathic pul-
monary fibrosis can also produce B-lines on pulmonary ul-
trasound examination.75 To avoid this pitfall, pulmonary
ultrasound imaging must be interpreted in the light of other
historical, physical and 2-dimensional and Doppler findings
from the patient’s medical background.
Pleural effusions are usually present in patients with sig-
nificant fluid overload. A pleural effusion can be detected on a
posteroanterior chest x-ray at a volume of 200 mL.76 Bedside
pleural ultrasound examination can reliably detect pleural
effusion with better sensitivity than the chest x-ray and chest
auscultation.76 An anechoic pleural effusion is compatible
with a transudate that could be caused by congestive heart
96 Canadian Journal of Cardiology
Volume 33 2017

Table 2. Clinical and ultrasound signs of fluid overload and their associated characteristics
Sign Characteristic
Clinical signs of fluid overload
Fluid balance and weight  Advantages: objective and included in routine care
 Limitations: does not consider cardiac function, not necessarily representative of end-organ congestion, and
can lead to misinterpretation of fluid status
Peripheral edema  Advantages: part of routine examination
 Limitations: can be caused by hypoalbuminemia, venous insufficiency, and nonuse, not necessarily
representative of central organ congestion and can lead to misinterpretation of fluid status
CVP measurements  Advantages: usually available in critically ill patients
 Limitations: require a central venous access, important technical caveats, and measurements are modified by
pleural pressure in mechanically ventilated patients
Intra-abdominal pressure  Advantages: detection of intra-abdominal hypertension due to fluid overload is clinically important
monitoring  Limitations: intra-abdominal hypertension is not specific to fluid overload. A bladder catheter is required
Ultrasound signs of fluid overload
IVC collapsibility and diameter  Advantages: short learning curve and noninvasive
 Limitations: can be modified by other factors such as positive pressure ventilation and other conditions
impairing venous return to the right atria
 Cutoff for CVP > 10 mm Hg in spontaneously breathing patients85: CI < 40% (sensitivity: 73%;
specificity: 85%) or IVC diameter > 2.0 cm (sensitivity 73%; specificity 84%)
JVP estimation  Advantages: rapid and noninvasive
 Limitations: measurements are modified by pleural pressure in mechanically ventilated, estimated CVP
with ultrasound have been reported to underestimate CVP52
 PPV of 81.3% for CVP > 8 cm H2O, NPV of 96.4% for CVP  5 cm H2O86
Hepatic vein flow  Advantages: dynamic marker of central hemodynamics: a reduction in the systolic to diastolic ratio is
observed with right heart failure and/or tricuspid regurgitation58
 Limitations: not necessarily representative of end-organ venous congestion
Pulsatile portal flow  Advantages: marker of hepatic venous congestion63
 Limitations: not studied in critically ill patients
Pulmonary B-lines  Advantages: marker of pulmonary congestion: able to detect early increase in EVLW70
 Limitations: can be present in ARDS and pulmonary fibrosis
Discontinuous intrarenal venous  Advantages: marker of the effect of elevated venous pressure on renal hemodynamics65
flow  Limitations: not studied in critically ill patients
Optic nerve diameter  Hypothesis: potential marker of increased ICP caused by important cerebral congestion
 Diameter > 5.2-5.9 mm: sensibility: 90%; specificity: 85% for intracranial hypertension78
Transcranial Doppler  Hypothesis: assessment of cerebral hemodynamics, which could be altered by venous congestion
 PI > 1.26-1.34: sensitivity: 80%-89%; specificity 90%-97% for intracranial hypertension82
ARDS, acute respiratory distress syndrome; CI, collapsibility index; CVP, central venous pressure; EVLW, extravascular lung water; ICP, intracranial pressure;
IVC, inferior vena cava; JVP, jugular venous pressure; NPV, negative predictive value; PI, pulsatility index; PPV, positive predictive value.

failure. Bilateral anechoic pleura effusions in a patient with
normal serum albumin level is highly suggestive of fluid
overload.
Assessment of Neurological Manifestations of
Fluid Overload
Although the utility of ultrasound examination of the
nervous system in the setting of fluid overload is not yet clear,
we believe that it should be an area of active investigation
because cerebral congestion causing increased intracranial
pressure (ICP) could impair cerebral perfusion.
Bedside ultrasound imaging can be used to detect elevated
ICP using the measurement of the optic nerve sheath. The
technique is presented in Figure 8. The diameter threshold of
5.2-5.9 mm has been used to detect increased ICP. The
diagnostic accuracy for the detection of intracranial hyper-
tension has been assessed in multiple observational studies
showing good diagnostic accuracy compared with invasive
monitoring.77
Transcranial Doppler examination offers the possibility to
assess blood flow in the cerebral vessels when the probe is
positioned in the temporal region. This technique has been
used to monitor vasospasm in patients with subarachnoid
hemorrhage, for the diagnosis of cerebral circulatory arrest,
and for the monitoring of cerebral embolism during
surgery.79-81 In the context of an increase in ICP, transcranial
Doppler examination shows a reduction of flow velocity in
diastole as shown in Figure 9. Multiple studies have shown
good correlation between the pulsatility index and elevated
ICP.82-84 Although the relationship between CVP and cere-
bral blood flow has not been described systematically, our
local experience suggests that significant venous congestion
could impair diastolic blood flow in the cerebral arteries.
Transcranial Doppler imaging is a highly operator-dependent
technique and adequate imaging is impossible to achieve in up
to 10% of patients because of an inadequate temporal win-
dow. Anatomical variants of the circle of Willis can also alter
the interpretation of the examination. Finally, transcranial
Doppler waveforms are known to be modified by other factors
such as arterial pressure and steno-occlusive vessel disease.
Integrating Ultrasound Assessment Into
Practice
Clinical assessment of fluid status relies on the integration of
multiple parameters having their own advantages and caveats
(Table 2). As such, patient management should not be on the basis
of an individual finding in ultrasound assessment but enhancing
physical examination with the use of bedside ultrasound offers the
possibility for early detection of fluid overload and its effect on end
organs. An overview of the proposed multisystem organ
Beaubien-Souligny et al.
Evaluation of Fluid Status Using Bedside Ultrasound
Figure 10. Extracardiac ultrasound signs of fluid overload. (A) Internal jugular vein (IJV), (B) inferior vena cava (IVC), (C) hepatic venous flow, (D)
portal venous flow, (E) optic nerve diameter, (F) transcranial Doppler, (G) pulmonary B-lines, and (H) renal interlobar vein Doppler. AR, atrial reversal;
D, diastolic; HV, hepatic vein; RA, right atrium; S, systolic. Modified from Iida et al.65 with permission from Elsevier.
congestion evaluation using ultrasound is shown in Figure 10.
This assessment can be repeated to monitor the fluid status during
the course of the illness. The presence of multiple signs of organ
congestion might predict adverse outcomes and this hypothesis is
currently being studied (NCT02658006 and NCT02831907). It
should be noted that central nervous system evaluation for
congestion using transcranial Doppler and optic nerve measure-
ment is on the basis of local experience in selected cases and should
be further studied before being used at the bedside. To be
competent in the use of bedside ultrasound imaging, clinicians
should seek critical care ultrasound training based on current
recommendations from expert statements.87-89
Conclusions
The integration of the understanding of normal patho-
physiology of a clinical syndrome, clinical examination, and
ultrasonography as described in this report might help to
avoid the adverse effect of fluid overload in critically ill pa-
tients by initiating a timely and optimized fluid, vasopressor
and inotropic support, followed by early initiation of a
restrictive fluid balance when needed.
Funding Sources
Supported by the Richard I. Kaufman Endowment Fund
in Anesthesia and Critical Care and the Montreal Heart
Institute Foundation.
97
Disclosures
Dr Denault is on the Speakers Bureau for Covidien and
Canadian Aviation Electronic (CAE) Healthcare. The other
authors have no conflicts of interest to disclose.
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