REVIEW

CURRENT
OPINION Focused ultrasonography for septic
shock resuscitation
Sara Nikravan a, Pingping Song a, Nibras Bughrara b,
and José L. Dı´az-Gómez c

Purpose of review
Severe sepsis with septic shock is the most common cause of death among critically ill patients. Mortality
has decreased substantially over the last decade but recent data has shown that opportunities remain for
the improvement of early and targeted therapy. This review discusses published data regarding the role of
focused ultrasonography in septic shock resuscitation.
Recent findings
Downloaded from http://journals.lww.com/co-criticalcare by BhDMf5ePHKbH4TTImqenVFDg6RAyiLhSBM/EWM9lEYSl4uZyXm20HJL3IuiX2AslHkcmjt61vlc= on 05/02/2020

Early categorization of the cardiovascular phenotypes with echocardiography can be crucial for timely
diagnosis and targeted therapy of patients with septic shock. In the last few years, markers of volume status
and volume responsiveness have been investigated, serving as valuable tools for targeting volume therapy
in the care of both spontaneously breathing and mechanically ventilated patients. In tandem, investigators
have highlighted findings of extravascular volume with ultrasonographic evaluation to compliment de-
escalation of resuscitation efforts when appropriate. Furthermore, special attention has been given to
resuscitation efforts of patients in septic shock with right ventricular failure.
Summary
Severe sepsis with septic shock is an insidious disease process that continues to take lives. In more recent
years, data have emerged suggesting the utility of bedside ultrasonography for early cardiovascular
categorization, goal directed resuscitation, and appropriate cardiovascular support based on its changing
phenotypes.
Keywords
cardiovascular phenotypes, point of care ultrasound, septic shock, volume responsiveness

INTRODUCTION characterized by inappropriate systemic vasodila-

Shock is a life-threatening form of acute circulatory
failure associated with cellular dysfunction from a
dysoxia that occurs from an imbalance in the supply
of oxygen in the setting of increased requirements
and consumption [1,2]. The most common shock
mechanisms are decreased venous return secondary
to volume loss, impaired cardiac function from
either a loss in contractility or new onset major
arrhythmia, presence of an obstructive process, or
loss of systemic vascular resistance [3]. While cate-
gorization is helpful for overall conceptualization of
the causes of shock, these features often overlap and,
worse yet, tend to morph into the other overtime.
Septic shock, in particular, presents classification
challenges, blurring these boundaries secondary to
the nature of the disease process: a maladaptive
inflammatory reaction to an infectious insult that
can cause organ dysfunction (severe sepsis) and
volume refractory shock (septic shock). The cardio-
vascular response to septic shock is very complex,
tion, varying grades of myocardial depression, and
hypovolemia causing tissue hypoperfusion and hyp-
oxia [4]. Although the Surviving Sepsis Campaign
guidelines have improved the rates of patient sur-
vival, there is some suggestion that early
a
Department of Anesthesiology and Pain Medicine, University of Wash-
ington Medical Center, Seattle, Washington, bCritical Care Echocardi-
ography Training Program, Anesthesia Critical Care Division, Albany
Medical College, Albany, New York and cDivision of Cardiovascular
Anesthesia and Critical Care Medicine/Critical Medicine Services, Texas
Heart Institute, Baylor St Luke’s Medical Center, Baylor College of
Medicine, Houston, Texas, USA
Correspondence to Sara Nikravan, Associate Professor of Cardiotho-
racic Anesthesiology & Critical Care Medicine; Director of Point of Care
Ultrasound; Associate Director, Residency Program, Department of
Anesthesiology and Pain Medicine, University of Washington Medical
Center, 1959 N.E. Pacific Street, Seattle, WA 98195, USA.
Tel: +1 214 282 9774; e-mail: nikravan@uw.edu
Curr Opin Crit Care 2020, 26:296–302
DOI:10.1097/MCC.0000000000000730

www.co-criticalcare.com Volume 26  Number 3  June 2020

Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.

 Focused ultrasonography for septic shock resuscitation Nikravan et al.
KEY POINTS
 Ultrasonography can be used to categorize phenotypes
of shock so as to target appropriate therapy.
 A variety of ultrasonographic parameters can help
predict fluid responsiveness in septic patients.
 Evaluating patients for fluid tolerance by assessing for
extravascular volume or congestion has been used to
supplement a targeted approach to volume resuscitation
in shock.
 Serial ultrasonography with both qualitative and
quantitative assessments can play a role in assessing
volume responsiveness in patients with right
ventricular failure.
echocardiography-driven monitoring leads to a dif-
ferent approach to initial resuscitation strategies in
sepsis. Moreover, lack of agreement between fluid/
inotropic therapy derived from echocardiography
and Surviving Sepsis Campaign guidelines in
patients presenting with septic shock has been
reported [5]. The goal of this review aims at
highlighting how bedside ultrasonography can be
used to potentially categorize the phenotypes of
shock while underscoring the utility of tailoring
therapy based on a timely, targeted approach.
ECHOCARDIOGRAPHY AS A
‘BIOMARKER’: AN ECHOCARDIOGRAPHIC-
DRIVEN APPROACH FOR
CHARACTERIZATION OF
CARDIOVASCULAR PHENOTYPES
Early characterization of cardiovascular phenoypes is
essential in the initial assessment of septic shock. The
utilization of patient clusters and phenotypes can
facilitate a more tailored hemodynamic manage-
ment regimen. Although the pathophysiology of
septic shock is complex and multifactorial, previous
echocardiography-driven management was limited
to specific measures such as administration of intra-
venous fluids or inotropes versus vasopressors. Sig-
nificantly, critical care echocardiography (CCE) can
better facilitate the recognition of combined mecha-
nisms of shock, particularly when paired with clinical
&&
hemodynamic variables. Geri et al. [6 ] recently pro-
posed five different clusters utilizing a large database
of septic shock patients who received transesopha-
geal CCE monitoring. The authors, highly trained
CCE intensivists, characterized the following clus-
ters: first, patients who are ‘well resuscitated’
(16.9%); second, patients with left ventricular (LV)
systolic dysfunction (17.7%); third, patients with
hyperkinetic profile (23.3%); fourth, patients with
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Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.
right ventricular (RV) failure (22.5%); and fifth,
patients who present with sustained hypovolemia
(19.4%). Overall, these clusters represent the macro-
circulatory derangements of shock and should be
used in conjunction with other clinical parameters.
For instance, a patient in shock with LV dysfunction
(Cluster 2) on higher doses of vasopressors with
increasing lactate levels may benefit from an accept-
able albeit lower target mean arterial pressure (MAP)
goal to assist with decreasing the afterload of the LV.
The contrast between Clusters 3 and 5 patients
deserves attention given the mounting evidence to
support the importance of response targeted volume
resuscitation [7] so as to determine the necessity for
further fluid administration. Significantly, Cluster 3
was associated with higher pulse pressure variability
(PPV), limiting the reliability of this hemodynamic
modality for fluid responsiveness. Instead, they found
better reliability differentiating Cluster 3 from Cluster
5 patients by using a dynamic echocardiographic
marker such as superior vena cava (SVC) variability.
Furthermore, Cluster 4 patients exhibited lower oxy-
genation indices suggesting that RV failure was indeed
associated with acute lung injury related to septic
shock or mechanical ventilatory support. Lastly, the
finding of Cluster 5 patients requiring further fluid
resuscitation suggest that individualization of fluid
therapy in septic shock is necessary. Indeed, detrimen-
tal effects from both higher vasopressors and more
aggressive fluid resuscitation in the early phase of
septic shock remain to be fully determined.
Bughrara et al. has recently proposed the utiliza-
tion of a single subxiphoid view [Echocardiographic
Assessment Using Subxiphoid-only (EASy)] exam for
qualitative assessment and echocardiographic phe-
notyping instead of a full Focused Transthoracic
Echocardiography (FoTE) exam to characterize undif-
ferentiated shock. In their study, the EASy exam was
obtained in 88% of the patients, and its image quality
was categorized as good or adequate in 75% of the
cases. Surprisingly, the EASy findings of ventricular
function, volume status, and pericardial effusion
were consistent in 89% of patients with interpretable
EASy images when compared with the formal FoTE
&&
exam [8 ]. These authors are proposing three pri-
mary clusters with seven distinct phenotypes in sep-
tic shock patients who require perioperative care.
Cluster 1 includes phenotypes representing patients
with normal or increased ventricular systolic func-
tion; Cluster 2 includes phenotypes associated with
LV systolic dysfunction with or without RV dysfunc-
tion; Cluster 3 represent the phenotype of acute, or
acute on chronic isolated RV dysfunction. Uncom-
mon phenotypes such as gross valvular regurgitation
or cardiac tamponade in the setting of septic shock
were classified apart from the main three clusters for
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Cardiopulmonary monitoring

FIGURE 1. Initial and subsequent echocardiographic assessment using subxiphoid-only phenotypes for septic shock patients.
echocardiographic assessment using subxiphoid-only-acute lung syndrome (ALS) phenotypes are based on the subcostal 4 chamber
view (top row), subcostal inferior vena cava view (middle row), and lung evaluation in the upper lung fields (bottom row).
Phenotypes 1–3 are grouped within Cluster 1, phenotypes 4 and 5 are part of Cluster 2, and phenotypes 6 and 7 are part of
Cluster 3. In general, cardiac evaluation assesses myocardial performance, inferior vena cava evaluation provides information
regarding fluid responsiveness and the lung exam differentiates fluid tolerance (A-profile) from fluid intolerance (B-profile). Phenotype
1 is more characteristic of hypovolemic shock as is evident by the small diastolic ventricular chamber size, collapsed inferior vena
cava with respiratory variation, and A-profile on the lung exam. Phenotype 2 is consistent with distributive shock in an adequately
fluid resuscitated patient with good cardiac filling, normal inferior vena cava size, and A-profile on lung evaluation. Phenotype 3
describes a patient with left ventricular hypertrophy, commonly dilated left atrium, and a small and collapsible inferior vena cava
with an A-profile on lung exam. Phenotypes 4 and 5 highlight isolated left ventricular and biventricular dysfunction, respectively,
which are usually affiliated with a plethoric inferior vena cava and B-profile on lung exam when no longer fluid responsive.
Phenotype 6 could be found in an acute respiratory distress syndrome (ARDS) patient with right ventricular dysfunction as is evident
by the enlarged right ventricular, plethoric inferior vena cava, and B-profile on lung exam reflecting nonhydrostatic edema.
Phenotype 7 takes in consideration patients with underlying pulmonary hypertension and right ventricular hypertrophy who develop
acute on chronic right ventricular failure. These patients will have an enlarged and hypertrophic right ventricular, plethoric inferior
vena cava, and variable lung profile (B-profile shown here). Bi A, Bi atrial; Bi V, Bi ventricular; HTN, hypertension; LA, left atrium; LVH,
left ventricular hypertrophy; RA, right atrium; RVH, right ventricular hypertrophy. (Courtesy of N. Bughrara, MD, Albany, NY, USA).

practicality purposes of the EASy exam. All clusters
and phenotypes are depicted in Fig. 1. Moreover, an
EASy exam-driven therapeutic management algo-
rithm has also been proposed (Fig. 2). In contrast
to Geri’s study, Bughrara et al. [9] emphasize the
utilization of the EASy exam as a transthoracic rather
than a transesophageal tool for a relatively rapid
initial assessment of shock.
VOLUME STATUS AND FLUID
RESPONSIVENESS: THE HOLY GRAIL
In septic shock, due to increased vascular permeabil-
ity, fluid administration can lead to a significant
positive fluid balance. However, the adverse effects
of fluid overload have been well documented and
might be responsible for significant morbidity in
patients with shock, including increased risk of
delirium, cardiac arrhythmias, pulmonary edema,
prolonged ileus, hepatic congestion, acute kidney
injury, and impaired wound healing [10–12]. Thus,
it is crucial to find a balanced state where patients
have adequate intravascular volume without over-
resuscitation.
A variety of parameters obtained via transtho-
racic echocardiography (TTE) have been evaluated
to predict fluid responsiveness in septic patients.
TTE offers timely assessment of fluid challenges,

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 Focused ultrasonography for septic shock resuscitation Nikravan et al.

FIGURE 2. Echocardiographic assessment using subxiphoid-only phenotype driven therapeutic management algorithms. Based
on the different clusters and phenotypes, a management algorithm can be adopted. For patients in Cluster 1, preload
optimization with volume resuscitation first can be initiated with subsequent addition of vasopressors if adequate volume
expansion (as is evident by normalization of inferior vena cava size, loss of respiratory variability, and presence of B-profile
on lung exam) does not result in resolution of shock. If left atrium dilation and left ventricular hypertrophy exist, gentle volume
expansion with frequent reassessment of fluid responsiveness and tolerance are needed as these patients typically have
diastolic dysfunction and have a narrow therapeutic window for fluid resuscitation. Cluster 2 patients can be fluid responsive if
they show signs of inferior vena cava respiratory variability and A-lung profile but their management should be judicious with
small fluid challenges (reversible or not) coupled with assessments of stroke volume variability or responsiveness. Vasoactive
medications with ionotropic properties should be considered if the shock state exists in the setting dilated inferior vena cava
without respiratory variation and presence of B-profile on the lung exam. Cluster 3 patients are at high risk for spurious
decompensation. The initial goal is to convert right ventricular failure with hypotension to right ventricular failure without
hypotension [mean arterial pressure (MAP) > 65] by using vasopressors that do not increase pulmonary vascular resistance
(PVR) (such as vasopressin) to maintain right ventricular myocardial perfusion while supporting right ventricular contractility
with ionotropic agents. The second goal is to improve right ventricular loading conditions and pursuing diuresis particularly if
signs of volume overload exist such as intraventricular septal bowing in diastole. D, HVF diastolic wave; HVF, hepatic vein
flow; IVC, inferior vena cava; IVF, intravenous fluid; IVS, interventricular septum; LA, left atrium; LV, left ventricle; LVH, left
ventricular hypertrophy; NE, norepinephrine; PPV, pulse pressure variation; RA, right atrium; S, HVF systolic wave. (Courtesy
of N. Bughrara, MD, Albany, NY, USA).

with significant advantages over static parameters
such as central venous pressure (CVP), pulmonary
artery occlusion pressure or cardiac output (CO).
Dynamic parameters obtained by echocardiography
include maximal aortic blood flow velocity and
velocity time integral (VTI) in the LV outflow tract
(LVOT), SVC collapsibility index, inferior vena cava
(IVC) collapsibility index and changes in stroke
volume (SV) with volume expansion.
Vignon et al. [13] evaluated the diagnostic accu-
racy of dynamic parameters using echocardiography
in predicting fluid responsiveness in mechanically
ventilated patients with all causes of shock in the
ICU. Fluid loading was conducted using the passive
leg raise maneuver. They concluded that DVmax LVOT
had the best sensitivity and SVC collapsibility index
had the best specificity in predicting fluid responsive-
ness. SVC collapsibility index had a greater diagnostic
accuracy than IVC collapsibility index, but its mea-
surement requires transesophageal echocardiography.
In patients not requiring mechanical ventilation,
numerous studies have evaluated the correlation

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Cardiopulmonary monitoring
Table 1. Dynamic parameters for predicting fluid responsiveness with echocardiography in mechanically ventilated patients
Dynamic parameter
Respiratory variation of SVC
Respiratory variation of IVC
Respiratory variation of maximal Doppler velocity in LVOT
These are commonly used dynamic parameters using echocardiography in predicting fluid responsiveness in mechanically ventilated patients with all causes of
shock in the ICU. diamMAX, maximum diameter; diamMIN, minimum diameter; Exp, diameter of the vessel in question during expiration; Ins, diameter of the vessel
in question during inspiration; IVC, inferior vena cava; LVOT VMAX, left ventricular outflow tract maximal velocity; LVOT VMIN, LVOT minimal velocity, SVC,
superior vena cava. (Adapted from [13]).
between IVC diameter or collapsibility index and
CVP. In general, there is a moderate correlation at
best and relatively fair accuracy to predict CVP by
measuring IVC diameter and collapsibility index.
More specifically, an IVC collapsibility index lower
than 50% and a large IVC diameter (>2.5 cm) has
been correlated with higher CVPs (>10 mmHg) and a
lower likelihood for hemodynamic respond to vol-
&
ume expansion [14,15 ,16]. Of note, previous inves-
tigations have attempted to detect fluid
responsiveness using mini volume challenges. Muller
et al. [17] evaluated the change of subaortic VTI after
an infusion of 100-ml colloid over 1 min and con-
cluded that the change of VTI accurately predicts
fluid responsiveness. Wu et al. [18] demonstrated that
with even smaller volume infusion (50-ml crystalloid
solution given over 10 s), the change of CO and aortic
VTI measured by TTE can reliably predict fluid
responsiveness among critically ill patients (Table 1).
To completely avoid undesirable fluid loading,
alternative maneuvers have been evaluated to predict
fluid responsiveness in ventilated patients with
shock. These include a transient increase in tidal
volume, lung recruitment maneuver, and end-expi-
ratory occlusion test (EEO). Myatra et al. [19] demon-
strated that when tidal volume is increased from 6 to
8 ml/kg predicted body weight (tidal volume chal-
lenge), the absolute change in pulse pressure varia-
tion (PPV > 3.5%) and SV variation (SVV > 2.5%)
reliably predicts fluid responsiveness, whereas PPV
and SVV at tidal volume of 6 ml/kg do not. Biais et al.
evaluated the magnitude of SV decrease during lung
recruitment in neurosurgical patients. Their results
suggest that a decrease in SV of at least 30% during
lung recruitment detects preload responsiveness.
There was a strong correlation between the change
of SV during lung recruitment and the change of SV
during volume expansion [20]. Despite the novelty of
the alternative maneuvers that avoided exogenous
fluid administration, those studies relied on invasive
hemodynamic data (PPV, SVV). Georges et al. vali-
dated the use of EEO to predict fluid responsiveness
using dynamic TTE parameters. They measured the
maximal aortic blood flow velocity (Vmax) and VTI at
300 www.co-criticalcare.com
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Formula
(Exp SVC diamMAX  Ins SVC diamMIN)/Exp SVC diamMAX
(Exp IVC diamMAX – Ins IVC diamMIN)/Exp IVC diamMAX
(LVOT VMAX – LVOT VMIN)/LVOT VMAX
the LVOT. End-expiratory occlusion (EEO) was car-
ried out by producing an end-expiratory pause for
12 s on the ventilator. They demonstrated that a 9%
increase in the aortic VTI predicted fluid responsive-
&
ness with satisfactory sensitivity and specificity [21 ].
In another study, Jozwiak et al. [22] included 30 ICU
patients and found that a 5% increase in VTI at the
end of a 15-s EEO predicted fluid responsiveness with
good sensitivity and specificity.
A TARGETED APPROACH TO VOLUME
RESUSCITATION: LOOKING FOR SIGNS OF
EXTRAVASCULAR FLUID OR VENOUS
CONGESTION WITH ULTRASONOGRAPHY
The proven benefit of early volume expansion in
severe sepsis with septic shock juxtaposed with the
risk for organ injury with over resuscitation has
created a practical dilemma for the care provider.
Understanding when to de-escalate volume expan-
sion, especially early on can be challenging. In
addition to using indices of fluid responsiveness,
another approach focuses on identifying signs of
extravascular volume with ultrasound.
Under lung ultrasonography, the presence of
pulmonary B-lines has been shown to detect early
increase in extravascular lung water and correlates
well with pulmonary edema on chest radiograph. In
acute decompensated heart failure, lung ultrasonog-
raphy was found to be more sensitive than chest
radiography for the detection of cardiogenic pulmo-
nary edema and had comparable specificity [23].
Another modality that can be employed to
understand the risk of volume overload is Doppler
interrogation of hepatic venous flow. A reduction in
the systolic to diastolic flow velocity ratio is
observed with right heart failure and/or tricuspid
regurgitation. It does not represent hepatic venous
congestion. Although an abnormal hepatic vein
flow waveform can be found in stable chronic heart
failure patients and is not synonymous with fluid
overload, its presence in a critically ill patient should
prompt the clinician to consider the patient at
increased risk of RV dysfunction and organ
Volume 26  Number 3  June 2020
 Focused ultrasonography for septic shock resuscitation Nikravan et al.
congestion, prompting consideration of a more
restrictive fluid strategy.
Portal venous flow pulsatility has been evaluated
as a marker of hepatic congestion and RV failure.
Venous flow through the portal vein is of low velocity
(10–30 cm/s) and presents minimal variations
throughout the cardiac cycle. When congestive heart
failure develops, CVP is elevated and the IVC starts to
dilate. When the dilatation exceeds the compliance
of the IVC, pressure is transduced through the
hepatic sinusoids to the portal system. This results
in high venous retrograde flow, leading to a signifi-
cant difference between systolic and diastolic veloci-
ties in the portal vein. Using pulse-wave Doppler,
portal vein pulsatility fraction (PPF, the difference
between systolic and diastolic portal vein velocities)
can be obtained using a phased array transducer
positioned in a right posterior-axillary coronal view
in the 9th to 11th intercostal spaces. The portal vein is
confirmed using pulsed-wave Doppler to differenti-
ate portal venous flow (monophasic to biphasic) from
that seen in the hepatic artery (sharp systolic
upstroke) and the hepatic veins (triphasic). PPF of
more than 50% is considered abnormal and it is called
pulsatile flow. High PPF has been validated as a strong
predictor of elevated CVP, worse functional class in
heart failure and hepatic congestion (elevated serum
bilirubin) [24,25]. In the acute setting, PPF more than
50% correlates with RV systolic and diastolic dysfunc-
tion during cardiac surgery. High PPF was also asso-
ciated with hemodynamic indicators of venous
congestion (high CVP and pulmonary arterial pres-
sure) and those of low systemic perfusion (mean
arterial pressure, cardiac index, mean perfusion pres-
&
sure) [26 ]. When ruling out other causes of portal
hypertension such as cirrhosis and portal thrombosis,
high PPF is suggestive of cardiogenic portal hyper-
tension secondary to pulmonary hypertension, RV
failure, and/or tricuspid regurgitation. Additional
fluid expansion should be carried out with extreme
caution. Of note, pulsatile portal venous flow has also
been reported in healthy individuals with low BMI
(<20) and therefore should be interpreted carefully in
thin patients.
FLUID RESPONSIVENESS AND RIGHT
VENTRICULAR FAILURE
RV dysfunction is common in patients presenting in
septic shock, with a reported incidence of 30–60%,
with or without concomitant LV dysfunction
[27,28]. In these patients, isolated RV dysfunction
has been shown to be an independent predictor of
worse 1-year survival [29].
Proper management of volume status is essential
for the failing RV, as both hypovolemia and
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hypervolemia may result in reduced CO and further
stress. Optimal right-sided filling pressures may vary
considerably between individual patients based on
RV contractility and afterload. When RV failure
occurs in the setting of contractile dysfunction but
the afterload is normal (as can be seen in acute RV
infarction), a higher preload is needed to maintain
CO. The RV end-diastolic pressure or the CVP is
usually kept moderately elevated at 8–12 mmHg.
However, when RV failure occurs in the setting of
increased RV afterload, excessive volume loading
can result in left displacement of the intraventricular
septum, impairing LV diastolic filling, and further
decreasing CO. This is a phenomenon known as
ventricular interdependence. RV preload reduction
with is key to reducing RV dilatation and free
wall tension, thereby minimizing RV ischemia and
optimizing contractility. Serial TTE examinations of
dynamic assessments of RV function and loading
condition that may be useful in determining an
adequate response to changes in treatment modali-
ties, including, fluid or at time more importantly
inotropic, rather than vasopressor, support in RV
&&
dysfunction [30 ]. Qualitative evaluation by visual
assessment of RV wall motion and thickening can
distinguish normal ventricular function from mild,
moderate or severely depressed function. Quantitative
measures include tricuspid annular plane systolic
excursion, tricuspid annular systolic velocity (S0 )
and RV fractional area change. RV strain analysis
and RV index of myocardial performance (Tei index)
are especially valuable due to their independence of
loading conditions and Doppler angle alignment. Of
note, invasive monitoring such as CVP and pulmo-
nary artery pressure (including central and mixed
venous oxygen saturation) can provide valuable
information on the RV preload and afterload, com-
plimenting TTE assessments in the setting of RVF.
CONCLUSION
With over 260 000 sepsis-related deaths per year
[31], improved care of these patients remains of
high priority. Ultrasonography has emerged as a
modality for guidance in resuscitation, particularly
in the face of ongoing discussions regarding goals
for fluid therapy versus vasopressor/inotropic sup-
port. Certainly, studies such as the CLOVERS trial of
fluid treatment strategies in early sepsis and others
seeking to understand best practices will help to
enlighten the critical care community. In the mean-
time, evidence to support targeting therapy while
avoiding the negative effects of inappropriate vol-
ume expansion and/or vasopressor/inotropic use
suggests real utility in ultrasonographic evaluation
of these patients.
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Cardiopulmonary monitoring
Acknowledgements
None.
Financial support and sponsorship
None.
Conflicts of interest
S.N. has received honorarium from Philips Inc. and
Caption Health. J.L.D.-G. has received honorarium from
Philips Inc. and Caption Health. The remaining authors
have no conflicts of interest.
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mini-fluid challenge study. Anesthesiology 2011; 115:541–547.
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echocardiography can predict fluid responsiveness. Crit Care 2014;
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19. Myatra SN, Monnet X, Teboul J-L. Use of ‘tidal volume challenge’ to improve
the reliability of pulse pressure variation. Crit Care 2017; 21:60.
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recruitment maneuver predict fluid responsiveness in mechanically ventilated
patients in the operating room. Anesthes 2017; 126:260–267.
21. Georges D, de Courson H, Lanchon R, et al. End-expiratory occlusion
& maneuver to predict fluid responsiveness in the intensive care unit: an
echocardiographic study. Crit Care 2018; 22:32.
A recent publication investigating the utility of a ventilator maneuver as a reversible
modality for assessing fluid responsiveness and how this affects echocardio-
graphic findings.
22. Jozwiak M, Depret F, Teboul J-L, et al. Predicting fluid responsiveness in
critically ill patients by using combined end-expiratory and end-inspiratory
occlusions with echocardiography. Crit Care Med 2017; 45:e1131–e1138.
23. Maw AM, Hassanin A, Ho PM, et al. Diagnostic accuracy of point-of-care
lung ultrasonography and chest radiography in adults with symptoms
suggestive of acute decompensated heart failure. JAMA Netw Open
2019; 2:e190703.
24. Shih C-Y, Yang S-S, Hu J-T, et al. Portal vein pulsatility index is a more
important indicator than congestion index in the clinical evaluation of right
heart function. World J Gastroenterol 2006; 12:768–771.
25. Hu J-T, Yang S-S, Lai Y-C, et al. Percentage of peak-to-peak pulsatility of
portal blood flow can predict right-sided congestive heart failure. World J
Gastroenterol 2003; 9:1828–1831.
26. Eljaiek R, Cavayas YA, Rodrigue E, et al. High postoperative portal venous
& flow pulsatility indicates right ventricular dysfunction and predicts complica-
tions in cardiac surgery patients. Br J Anaesth 2019; 122:206–214.
An original publication on the utility of ultrasonographic portal vein assessments as
a predictor of right ventricular dysfunction and right-sided congestion.
27. Pulido JN, Afessa B, Masaki M, et al. Clinical spectrum, frequency, and
significance of myocardial dysfunction in severe sepsis and septic shock.
Mayo Clin Proc 2012; 87:620–628.
28. Landesberg G, Jaffe AS, Gilon D, et al. Troponin elevation in severe sepsis
and septic shock: the role of left ventricular diastolic dysfunction and right
ventricular dilatation. Crit Care Med 2014; 42:790.
29. Vallabhajosyula S, Kumar M, Pandompatam G, et al. Prognostic impact of
isolated right ventricular dysfunction in sepsis and septic shock: an 8-year
historical cohort study. Ann Intensive Care 2017; 7:94.
30. Vieillard-Baron A, Naeije R, Haddad F, et al. Diagnostic workup, etiologies and
&& management of acute right ventricle failure: a state-of-the-art paper. Intensive
Care Med 2018; 44:774–790.
A thorough and well formulated review of acute right heart failure to include causes
of right heart failure, diagnostic tools, as well as management techniques and
challenges.
31. Rhee C, Dantes R, Epstein L, et al. Incidence and trends of sepsis in US
hospitals using clinical vs claims data. JAMA 2017; 318:1241–1249.
Volume 26  Number 3  June 2020