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

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 Focused ultrasonography for septic shock resuscitation Nikravan et al.

right ventricular (RV) failure (22.5%); and fifth,

KEY POINTS patients who present with sustained hypovolemia
 Ultrasonography can be used to categorize phenotypes (19.4%). Overall, these clusters represent the macro-
of shock so as to target appropriate therapy. circulatory derangements of shock and should be
used in conjunction with other clinical parameters.
 A variety of ultrasonographic parameters can help For instance, a patient in shock with LV dysfunction
predict fluid responsiveness in septic patients.
(Cluster 2) on higher doses of vasopressors with
 Evaluating patients for fluid tolerance by assessing for increasing lactate levels may benefit from an accept-
extravascular volume or congestion has been used to able albeit lower target mean arterial pressure (MAP)
supplement a targeted approach to volume resuscitation goal to assist with decreasing the afterload of the LV.
in shock. The contrast between Clusters 3 and 5 patients
 Serial ultrasonography with both qualitative and deserves attention given the mounting evidence to
quantitative assessments can play a role in assessing support the importance of response targeted volume
volume responsiveness in patients with right resuscitation [7] so as to determine the necessity for
ventricular failure. further fluid administration. Significantly, Cluster 3
was associated with higher pulse pressure variability
(PPV), limiting the reliability of this hemodynamic
echocardiography-driven monitoring leads to a dif- modality for fluid responsiveness. Instead, they found
ferent approach to initial resuscitation strategies in better reliability differentiating Cluster 3 from Cluster
sepsis. Moreover, lack of agreement between fluid/ 5 patients by using a dynamic echocardiographic
inotropic therapy derived from echocardiography marker such as superior vena cava (SVC) variability.
and Surviving Sepsis Campaign guidelines in Furthermore, Cluster 4 patients exhibited lower oxy-
patients presenting with septic shock has been genation indices suggesting that RV failure was indeed
reported [5]. The goal of this review aims at associated with acute lung injury related to septic
highlighting how bedside ultrasonography can be shock or mechanical ventilatory support. Lastly, the
used to potentially categorize the phenotypes of finding of Cluster 5 patients requiring further fluid
shock while underscoring the utility of tailoring resuscitation suggest that individualization of fluid
therapy based on a timely, targeted approach. therapy in septic shock is necessary. Indeed, detrimen-
tal effects from both higher vasopressors and more
aggressive fluid resuscitation in the early phase of
ECHOCARDIOGRAPHY AS A septic shock remain to be fully determined.
‘BIOMARKER’: AN ECHOCARDIOGRAPHIC- Bughrara et al. has recently proposed the utiliza-
DRIVEN APPROACH FOR tion of a single subxiphoid view [Echocardiographic
CHARACTERIZATION OF Assessment Using Subxiphoid-only (EASy)] exam for
CARDIOVASCULAR PHENOTYPES qualitative assessment and echocardiographic phe-
Early characterization of cardiovascular phenoypes is notyping instead of a full Focused Transthoracic
essential in the initial assessment of septic shock. The Echocardiography (FoTE) exam to characterize undif-
utilization of patient clusters and phenotypes can ferentiated shock. In their study, the EASy exam was
facilitate a more tailored hemodynamic manage- obtained in 88% of the patients, and its image quality
ment regimen. Although the pathophysiology of was categorized as good or adequate in 75% of the
septic shock is complex and multifactorial, previous cases. Surprisingly, the EASy findings of ventricular
echocardiography-driven management was limited function, volume status, and pericardial effusion
to specific measures such as administration of intra- were consistent in 89% of patients with interpretable
venous fluids or inotropes versus vasopressors. Sig- EASy images when compared with the formal FoTE
nificantly, critical care echocardiography (CCE) can
&&
exam [8 ]. These authors are proposing three pri-
better facilitate the recognition of combined mecha- mary clusters with seven distinct phenotypes in sep-
nisms of shock, particularly when paired with clinical tic shock patients who require perioperative care.
&&
hemodynamic variables. Geri et al. [6 ] recently pro- Cluster 1 includes phenotypes representing patients
posed five different clusters utilizing a large database with normal or increased ventricular systolic func-
of septic shock patients who received transesopha- tion; Cluster 2 includes phenotypes associated with
geal CCE monitoring. The authors, highly trained LV systolic dysfunction with or without RV dysfunc-
CCE intensivists, characterized the following clus- tion; Cluster 3 represent the phenotype of acute, or
ters: first, patients who are ‘well resuscitated’ acute on chronic isolated RV dysfunction. Uncom-
(16.9%); second, patients with left ventricular (LV) mon phenotypes such as gross valvular regurgitation
systolic dysfunction (17.7%); third, patients with or cardiac tamponade in the setting of septic shock
hyperkinetic profile (23.3%); fourth, patients with 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 positive fluid balance. However, the adverse effects
and phenotypes are depicted in Fig. 1. Moreover, an of fluid overload have been well documented and
EASy exam-driven therapeutic management algo- might be responsible for significant morbidity in
rithm has also been proposed (Fig. 2). In contrast patients with shock, including increased risk of
to Geri’s study, Bughrara et al. [9] emphasize the delirium, cardiac arrhythmias, pulmonary edema,
utilization of the EASy exam as a transthoracic rather prolonged ileus, hepatic congestion, acute kidney
than a transesophageal tool for a relatively rapid injury, and impaired wound healing [10–12]. Thus,
initial assessment of shock. it is crucial to find a balanced state where patients
have adequate intravascular volume without over-
resuscitation.
VOLUME STATUS AND FLUID A variety of parameters obtained via transtho-
RESPONSIVENESS: THE HOLY GRAIL racic echocardiography (TTE) have been evaluated
In septic shock, due to increased vascular permeabil- to predict fluid responsiveness in septic patients.
ity, fluid administration can lead to a significant 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 in predicting fluid responsiveness in mechanically
such as central venous pressure (CVP), pulmonary ventilated patients with all causes of shock in the
artery occlusion pressure or cardiac output (CO). ICU. Fluid loading was conducted using the passive
Dynamic parameters obtained by echocardiography leg raise maneuver. They concluded that DVmax LVOT
include maximal aortic blood flow velocity and had the best sensitivity and SVC collapsibility index
velocity time integral (VTI) in the LV outflow tract had the best specificity in predicting fluid responsive-
(LVOT), SVC collapsibility index, inferior vena cava ness. SVC collapsibility index had a greater diagnostic
(IVC) collapsibility index and changes in stroke accuracy than IVC collapsibility index, but its mea-
volume (SV) with volume expansion. surement requires transesophageal echocardiography.
Vignon et al. [13] evaluated the diagnostic accu- In patients not requiring mechanical ventilation,
racy of dynamic parameters using echocardiography 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 Formula

Respiratory variation of SVC (Exp SVC diamMAX  Ins SVC diamMIN)/Exp SVC diamMAX
Respiratory variation of IVC (Exp IVC diamMAX – Ins IVC diamMIN)/Exp IVC diamMAX
Respiratory variation of maximal Doppler velocity in LVOT (LVOT VMAX – LVOT VMIN)/LVOT VMAX

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 the LVOT. End-expiratory occlusion (EEO) was car-
CVP. In general, there is a moderate correlation at ried out by producing an end-expiratory pause for
best and relatively fair accuracy to predict CVP by 12 s on the ventilator. They demonstrated that a 9%
measuring IVC diameter and collapsibility index. increase in the aortic VTI predicted fluid responsive-
&
More specifically, an IVC collapsibility index lower ness with satisfactory sensitivity and specificity [21 ].
than 50% and a large IVC diameter (>2.5 cm) has In another study, Jozwiak et al. [22] included 30 ICU
been correlated with higher CVPs (>10 mmHg) and a patients and found that a 5% increase in VTI at the
lower likelihood for hemodynamic respond to vol- end of a 15-s EEO predicted fluid responsiveness with
&
ume expansion [14,15 ,16]. Of note, previous inves- good sensitivity and specificity.
tigations have attempted to detect fluid
responsiveness using mini volume challenges. Muller
et al. [17] evaluated the change of subaortic VTI after A TARGETED APPROACH TO VOLUME
an infusion of 100-ml colloid over 1 min and con- RESUSCITATION: LOOKING FOR SIGNS OF
cluded that the change of VTI accurately predicts EXTRAVASCULAR FLUID OR VENOUS
fluid responsiveness. Wu et al. [18] demonstrated that CONGESTION WITH ULTRASONOGRAPHY
with even smaller volume infusion (50-ml crystalloid The proven benefit of early volume expansion in
solution given over 10 s), the change of CO and aortic severe sepsis with septic shock juxtaposed with the
VTI measured by TTE can reliably predict fluid risk for organ injury with over resuscitation has
responsiveness among critically ill patients (Table 1). created a practical dilemma for the care provider.
To completely avoid undesirable fluid loading, Understanding when to de-escalate volume expan-
alternative maneuvers have been evaluated to predict sion, especially early on can be challenging. In
fluid responsiveness in ventilated patients with addition to using indices of fluid responsiveness,
shock. These include a transient increase in tidal another approach focuses on identifying signs of
volume, lung recruitment maneuver, and end-expi- extravascular volume with ultrasound.
ratory occlusion test (EEO). Myatra et al. [19] demon- Under lung ultrasonography, the presence of
strated that when tidal volume is increased from 6 to pulmonary B-lines has been shown to detect early
8 ml/kg predicted body weight (tidal volume chal- increase in extravascular lung water and correlates
lenge), the absolute change in pulse pressure varia- well with pulmonary edema on chest radiograph. In
tion (PPV > 3.5%) and SV variation (SVV > 2.5%) acute decompensated heart failure, lung ultrasonog-
reliably predicts fluid responsiveness, whereas PPV raphy was found to be more sensitive than chest
and SVV at tidal volume of 6 ml/kg do not. Biais et al. radiography for the detection of cardiogenic pulmo-
evaluated the magnitude of SV decrease during lung nary edema and had comparable specificity [23].
recruitment in neurosurgical patients. Their results Another modality that can be employed to
suggest that a decrease in SV of at least 30% during understand the risk of volume overload is Doppler
lung recruitment detects preload responsiveness. interrogation of hepatic venous flow. A reduction in
There was a strong correlation between the change the systolic to diastolic flow velocity ratio is
of SV during lung recruitment and the change of SV observed with right heart failure and/or tricuspid
during volume expansion [20]. Despite the novelty of regurgitation. It does not represent hepatic venous
the alternative maneuvers that avoided exogenous congestion. Although an abnormal hepatic vein
fluid administration, those studies relied on invasive flow waveform can be found in stable chronic heart
hemodynamic data (PPV, SVV). Georges et al. vali- failure patients and is not synonymous with fluid
dated the use of EEO to predict fluid responsiveness overload, its presence in a critically ill patient should
using dynamic TTE parameters. They measured the prompt the clinician to consider the patient at
maximal aortic blood flow velocity (Vmax) and VTI at increased risk of RV dysfunction and organ

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 Focused ultrasonography for septic shock resuscitation Nikravan et al.

congestion, prompting consideration of a more hypervolemia may result in reduced CO and further
restrictive fluid strategy. stress. Optimal right-sided filling pressures may vary
Portal venous flow pulsatility has been evaluated considerably between individual patients based on
as a marker of hepatic congestion and RV failure. RV contractility and afterload. When RV failure
Venous flow through the portal vein is of low velocity occurs in the setting of contractile dysfunction but
(10–30 cm/s) and presents minimal variations the afterload is normal (as can be seen in acute RV
throughout the cardiac cycle. When congestive heart infarction), a higher preload is needed to maintain
failure develops, CVP is elevated and the IVC starts to CO. The RV end-diastolic pressure or the CVP is
dilate. When the dilatation exceeds the compliance usually kept moderately elevated at 8–12 mmHg.
of the IVC, pressure is transduced through the However, when RV failure occurs in the setting of
hepatic sinusoids to the portal system. This results increased RV afterload, excessive volume loading
in high venous retrograde flow, leading to a signifi- can result in left displacement of the intraventricular
cant difference between systolic and diastolic veloci- septum, impairing LV diastolic filling, and further
ties in the portal vein. Using pulse-wave Doppler, decreasing CO. This is a phenomenon known as
portal vein pulsatility fraction (PPF, the difference ventricular interdependence. RV preload reduction
between systolic and diastolic portal vein velocities) with is key to reducing RV dilatation and free
can be obtained using a phased array transducer wall tension, thereby minimizing RV ischemia and
positioned in a right posterior-axillary coronal view optimizing contractility. Serial TTE examinations of
in the 9th to 11th intercostal spaces. The portal vein is dynamic assessments of RV function and loading
confirmed using pulsed-wave Doppler to differenti- condition that may be useful in determining an
ate portal venous flow (monophasic to biphasic) from adequate response to changes in treatment modali-
that seen in the hepatic artery (sharp systolic ties, including, fluid or at time more importantly
upstroke) and the hepatic veins (triphasic). PPF of inotropic, rather than vasopressor, support in RV
&&
more than 50% is considered abnormal and it is called dysfunction [30 ]. Qualitative evaluation by visual
pulsatile flow. High PPF has been validated as a strong assessment of RV wall motion and thickening can
predictor of elevated CVP, worse functional class in distinguish normal ventricular function from mild,
heart failure and hepatic congestion (elevated serum moderate or severely depressed function. Quantitative
bilirubin) [24,25]. In the acute setting, PPF more than measures include tricuspid annular plane systolic
50% correlates with RV systolic and diastolic dysfunc- excursion, tricuspid annular systolic velocity (S0 )
tion during cardiac surgery. High PPF was also asso- and RV fractional area change. RV strain analysis
ciated with hemodynamic indicators of venous and RV index of myocardial performance (Tei index)
congestion (high CVP and pulmonary arterial pres- are especially valuable due to their independence of
sure) and those of low systemic perfusion (mean loading conditions and Doppler angle alignment. Of
arterial pressure, cardiac index, mean perfusion pres- note, invasive monitoring such as CVP and pulmo-
&
sure) [26 ]. When ruling out other causes of portal nary artery pressure (including central and mixed
hypertension such as cirrhosis and portal thrombosis, venous oxygen saturation) can provide valuable
high PPF is suggestive of cardiogenic portal hyper- information on the RV preload and afterload, com-
tension secondary to pulmonary hypertension, RV plimenting TTE assessments in the setting of RVF.
failure, and/or tricuspid regurgitation. Additional
fluid expansion should be carried out with extreme
caution. Of note, pulsatile portal venous flow has also CONCLUSION
been reported in healthy individuals with low BMI With over 260 000 sepsis-related deaths per year
(<20) and therefore should be interpreted carefully in [31], improved care of these patients remains of
thin patients. high priority. Ultrasonography has emerged as a
modality for guidance in resuscitation, particularly
in the face of ongoing discussions regarding goals
FLUID RESPONSIVENESS AND RIGHT for fluid therapy versus vasopressor/inotropic sup-
VENTRICULAR FAILURE port. Certainly, studies such as the CLOVERS trial of
RV dysfunction is common in patients presenting in fluid treatment strategies in early sepsis and others
septic shock, with a reported incidence of 30–60%, seeking to understand best practices will help to
with or without concomitant LV dysfunction enlighten the critical care community. In the mean-
[27,28]. In these patients, isolated RV dysfunction time, evidence to support targeting therapy while
has been shown to be an independent predictor of avoiding the negative effects of inappropriate vol-
worse 1-year survival [29]. ume expansion and/or vasopressor/inotropic use
Proper management of volume status is essential suggests real utility in ultrasonographic evaluation
for the failing RV, as both hypovolemia and of these patients.

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Cardiopulmonary monitoring

13. Vignon P, Repessé X, Bégot E, et al. Comparison of echocardiographic

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