08 Assessment of volume status and fluid responsiveness in the emergency department

Übersichten
Med Klin Intensivmed Notfmed 2017 · 112:326–333
DOI 10.1007/s00063-015-0124-x
Received: 25 August 2015
Revised: 13 October 2015
Accepted: 29 October 2015
Published online: 16 December 2015
© Springer-Verlag Berlin Heidelberg 2015
Redaktion
M. Buerke, Siegen
C. Maurer 1 · J.Y. Wagner 2 · R.M. Schmid 1 · B. Saugel 2
1
II. Medizinische Klinik und Poliklinik, Klinikum rechts der Isar der
Technischen Universität München, München, Germany
2
Department of Anesthesiology, Center of Anesthesiology and Intensive Care Medicine,
University Medical Center Hamburg-Eppendorf, Hamburg, Germany
Assessment of volume status
and fluid responsiveness in
the emergency department:
a systematic approach
Introduction
Fluid therapy is a crucial therapeutic intervention
in the treatment of acutely ill
patients admitted to the emergency department
(ED). In ED patients with conditions
such as sepsis, acute kidney injury,
pancreatitis or trauma, early fluid resuscitation
constitutes one of the most potent
and important therapeutic interventions
and a delay in its implementation may
contribute to an increase in mortality [1–
3]. However, after the initial resuscitation
period, continued aggressive hydration
may cause interstitial edema which is associated
with a worse outcome. Therefore,
fluid therapy needs to be performed based
on the patient’s volume status and fluid responsiveness.
Although we can apply advanced
invasive hemodynamic monitoring
in intensive care medicine, clinical,
laboratory, and static hemodynamic parameters
remain the key instruments in
an ED setting to guide therapy during the
early period of critical disease. In this review
we want to outline established and
promising means for the assessment of a
patient’s volume status and fluid responsiveness
in the ED.
In a clinical context, the term “dehydration”
is often used synonymously for
the following two conditions: (a) hypertonicity,
that is, intracellular water deficits
resulting from hypertonicity and a disturbance
in water metabolism and (b) deficit
in extracellular fluid volume, that is, a
net loss of total body sodium and a reduction
in intravascular volume [4]. Basically,
although both dehydrated and volume
depleted patients may present with similar
symptoms and signs in physical examination,
the underlying pathophysiology of
dehydration and volume depletion is different
and may require different treatment
strategies [4].
Physical examination
Physical examination remains the foundation
of every patient encounter and may
contribute valuable information to volume
status assessment. Initially, identifying
patients with circulatory shock remains
the most important task during triage
in the ED [5]. Besides arterial hypotension,
evaluating the three “windows
of the body” [6] may yield clues to ongoing
tissue hypoperfusion: (a) the presence
of mottled and clammy skin, (b) oliguria
(< 0.5 mL urine output per kg body
weight per hour), and (c) an altered mental
state (e.g., confusion). In the absence
of the findings above, physical examination
should proceed with the assessment
of a combination of clinical indicators [7,
8]. Signs and symptoms that might indicate
hypovolemia are dry membranes of
mouth and nose, dry tongue, longitudinal
furrows on tongue, decreased skin turgor,
dry axilla, sunken eyes, reduced production
of saliva, confusion, and weakness.
Orthostatic (postural) changes in heart
rate and blood pressure are often interpreted
as indicators of intravascular volume
status in the emergency setting [9].
However, even the detection of moderate
to large amounts of blood loss based on
physical examination has been demonstrated
to be a challenge [10].
The accuracy of clinical signs and
symptoms of hypervolemia has mostly
been studied in patients with congestive
heart failure [11, 12]. Symptoms that point
towards a diagnosis of hypervolemia due
to heart failure with moderate specificity
Abbreviations
BUN
CO
CTR
CVP
CXR
Ea dyn
EABV
ED
FE UN
IVC
PAOP
PLR
blood urea nitrogen
cardiac output
cardiothoracic ratio
central venous pressure
chest x-ray
dynamic arterial elastance
effective arterial blood volume
emergency department
fractional excretion of urea
inferior vena cava
pulmonary artery occlusion pressure
passive leg raising
ROC-AUC area under the receiver operating
characteristic curve
VPW
vascular pedicle width
326 | Medizinische Klinik - Intensivmedizin und Notfallmedizin 4 · 2017

include paroxysmal nocturnal dyspnea
and orthopnea whereas dyspnea on exertion
is the most sensitive anamnestic hint.
During physical examination, jugular venous
distention and abdominojugular reflux
may secure the diagnosis of heart
failure (however, these signs have very
low sensitivity). Among the more sensitive
findings, lower extremity edema and
rales on lung auscultation may provide evidence
for hypervolemia and heart failure.
In cardiac patients, the synopsis of
clinical findings can be used to assign the
patient to a Killip class that was initially
proposed for risk stratification in patients
with myocardial infarction [13].
Taken together, we consider the clinical
examination as an immediately available
and cost-effective means to evaluate
a patient’s volume status early after his arrival
in the ED, which can help to guide
the initial resuscitation therapy. However,
clinical studies revealed significant limitations
of clinical signs and symptoms in
the assessment of a patient’s volume status
[8, 10, 14, 15].
Laboratory parameters
Blood urea nitrogen/
creatinine ratio
Volume depletion induces a neurohumeral
response which enhances the reabsorption
of sodium and water in the proximal
tubule. Since urea reabsorption occurs
passively in this very part of the nephron,
volume depletion also causes an increase
in urea reabsorption. The blood urea nitrogen
(BUN)/serum creatinine ratio is
approximately 10:1 in normal subjects but
may be substantially elevated in hypovolemic
states [16]. In a state called “prerenal
azotemia,” true volume depletion or
decreased effective arterial blood volume
(EABV) go along with BUN/creatinine ratios
of 20:1 and higher. Decreased EABV
volume may occur in edematous disorders
such as cardiac failure, liver cirrhosis,
and more rarely nephrotic syndrome
[17]. Although there are quite a few confounding
conditions such as intake of steroid
medication or upper gastrointestinal
bleeding, the BUN/creatinine ratio remains
an easily obtainable tool for volume
status assessment. We would like to point
out that mere creatinine levels are poor indicators
of kidney function in the elderly,
and the use of formulas to estimate glomerular
filtration rate is strongly suggested
in this patient group [18].
Urinary sodium and fractional
excretion of urea
Urinalysis is often performed in the ED
during the evaluation of common symptoms
such as fever or abdominal discomfort.
A “spot urine” sample may also aid in
evaluating volume status. The aforementioned
neurohumeral response to volume
depletion or decreased EABV induces the
kidneys to retain sodium and subsequently
water in order to (re-)expand the extracellular
fluid compartment. Chung and
colleagues were able to demonstrate that
in contrast to clinical assessment by two
experienced nephrologists the spot urinary
sodium concentration was highly
sensitive to distinguish between hypovolemic
and euvolemic patients with hyponatremia
[15]. In their study, a spot urinary
sodium concentration of less than
30 mmol/L was 100 % specific and 80 %
sensitive to detect patients with hyponatremia
who had elevated plasma renin and
norepinephrine concentrations, responded
to infusion of isotonic saline, and were
thus deemed to be hypovolemic.
However, when hypovolemia occurs
due to an overzealous use of loop and thiazide
diuretics, low urinary sodium concentrations
lose their sensitivity to detect
volume depletion. As sodium and water
are reabsorbed in the proximal tubulus,
the fractional excretion of urea (FE UN )
remains unaffected. In patients with renal
hypoperfusion, a FE UN of ≤ 35 % was
found to be indicative of kidney injury
due to hypovolemia or decreased EABV
even after administration of diuretic therapy
(sensitivity and specificity of 90 and
96 %, respectively [19]). However, these
results were challenged by another study
in which the diagnostic accuracy of FE UN
was explored prospectively. Pépin et al.
demonstrated that FE UN performed rather
poorly, irrespective of whether diuretics
had been administered or not [20].
In summary, a urinary spot sodium of
less than 30 mmol/L is very specific and
moderately sensitive to detect hypovolemia.
After diuretic therapy, a FE UN of
≤ 35 % may still be able to support the diagnosis
of hypovolemia, although reports
on its diagnostic accuracy are contradictive.
Blood lactate
Screening for hypotension alone might
miss patients at risk for circulatory failure
[21]. Elevated serum lactate levels indicate
ongoing tissue hypoxia and are associated
with a worse prognosis in acutely
ill patients [22], independent of age,
blood pressure, or other comorbidities
[23]. Therefore, we advocate a liberal use
of sequential [24] lactate measurements
in the ED while being aware of potential
confounders such as biguanide or antiretroviral
medications and liver disease.
Bedside ultrasound
Bedside ultrasound may provide valuable
information on circulatory function that
cannot be obtained by clinical assessment.
It may detect the presence of pericardial
and pleural effusions or ascites, which
may give important diagnostic clues both
for patients suspected to have decreased
EABV and patients with fluid loss to the
abdominal or thoracic compartment (e.g.,
pancreatitis). Furthermore, the diameter
of the inferior vena cava (IVC) can be used
to estimate right cardiac function and central
venous pressure (CVP). According to
current guidelines, a low right atrial pressure
(0–5 mmHg) can be inferred from
an IVC diameter of ≤ 2.1 cm that collapses
> 50 % with a sniff. On the contrary,
an IVC diameter > 2.1 cm without a collapse
of 50 % with a sniff suggests a high
right atrial pressure (10–20 mmHg). Values
found in between are considered indeterminate
and an intermediate pressure is
then assumed [25].
The IVC diameter is not affected by
the neurohumeral stress response but will
adapt to changes in CVP such as volume
depletion or fluid resuscitation [26, 27].
In particular, the expiratory IVC (IVCe)
diameter correlated well with complete
blood volume, as determined by I131-labeled
albumin dilution, in patients with
iatrogenic volume depletion, that is hemodialysis
[28]. Although ultrasonographic
Medizinische Klinik - Intensivmedizin und Notfallmedizin 4 · 2017 |
327

Abstract · Zusammenfassung
evaluation is known to be dependent on
sonographer experience, M-Mode IVC
diameter measurements as perfomed by
ED residents after a short course of training
had a high degree of interrater reliability
[29].
IVCe was consistently and significantly
lower in hypovolemic trauma patients
with confirmed or suspected blood loss
[30–32]. Weekes and colleagues showed
that in hypovolemic ED patients, the IVCe
diameter and caval index increased and
decreased, respectively, after a mean fluid
bolus of 2580 mL [27].
In summary, IVCe diameter and caval
index provide a noninvasive, quickly obtainable,
and reproducible tool to assess
intravascular volume status before and after
fluid resucitation that seems well suited
for the ED.
However, ultrasonographic examination
of the IVC diameter has several limitations:
in patients with right ventricular
failure the IVC diameter will be elevated
even in the presence of hypovolemia and
shock.
Despite its ability to estimate CVP and
intravascular volume status, IVC diameter
and collapsibility index will not provide
information on a patient’s fluid responsiveness.
Corl and colleagues showed that
neither the initial nor the dynamic (i.e., after
a passive leg raise maneuver) caval index
could predict fluid responsiveness in
an ED patient cohort [33].
Echocardiography plays a crucial role
in the initial evaluation of ED patients for
the differentiation of different etiologies
of hemodynamic instability or shock [34,
35]. Besides the differential diagnosis of
cardiac and noncardiac causes of shock,
echocardiography allows the estimation of
left and right ventricular dysfunction and
valvular dysfunction [34]. In addition to
static parameters, it provides noninvasive
means to examine dynamic parameters of
volume responsiveness (for details please
see below) [36]. Stroke volume and cardiac
output (CO) can be estimated by measuring
the velocity–time integral of the
aortic outflow and the aortic valve area in
the apical five-chamber and parasternal
long-axis view, respectively.
Med Klin Intensivmed Notfmed 2017 · 112:326–333
© Springer-Verlag Berlin Heidelberg 2015
Chest x-ray
Results obtained from a chest x-ray (CXR)
will add additional information on the
presence or absence of hypervolemia.
However, classic radiographic signs of
volume overload such as pleural effusions
or peribronchial cuffings correlate poorly
with the invasive determination of volume
status or extravascular lung water [14,
37, 38]. Unlike those classic signs of increased
pulmonary hydration, the vascular
pedicle width (VPW)—that is, the distance
between a perpendicular line from
the point where the left subclavian artery
exits the aortic arch and the crossing of
the superior vena cava and the left main
DOI 10.1007/s00063-015-0124-x
C. Maurer · J.Y. Wagner · R.M. Schmid · B. Saugel
Assessment of volume status and fluid responsiveness in
the emergency department: a systematic approach
Abstract
When treating acutely ill patients in the
emergency department (ED), the successful
management of a variety of medical conditions,
such as sepsis, acute kidney injury, and
pancreatitis, is highly dependent on the correct
assessment and optimization of a patient’s
intravascular volume status. Therefore,
it is crucial that the ED physician knows
and uses available means to assess intravascular
volume status to adequately guide fluid
therapy. This review focuses on techniques
for volume status assessment that are available
in the ED including basic clinical and laboratory
findings, apparatus-based tests such
as sonography and chest x-ray, and functional
tests to evaluate fluid responsiveness. Furthermore,
we provide an outlook on promising
innovative, noninvasive technologies that
might be used for advanced hemodynamic
monitoring in the ED.
Keywords
Shock · Sepsis · Volume therapy ·
Fluid deficiency · Passive leg raising ·
Fluid challenge · Advanced hemodynamic
monitoring · Noninvasive cardiac output
Die Bestimmung des Volumenstatus und der Volumenreagibilität
in der Notaufnahme – ein systematischer Ansatz
Zusammenfassung
Bei der Behandlung akut kranker Patienten
in der Notaufnahme hängt die erfolgreiche
Behandlung einer Reihe von Erkrankungen
(z. B. Sepsis, akutes Nierenversagen,
Pankreatitis) in hohem Maße von der
korrekten Einschätzung und Optimierung
des intravaskulären Volumenstatus des
Patienten ab. Daher ist es entscheidend für
eine adäquate Steuerung der Volumentherapie,
dass der Notfallmediziner die verschiedenen
Methoden zur Abschätzung des
intravaskulären Volumenstatus kennt und zur
Anwendung bringt. Dieser Übersichtsartikel
behandelt Methoden zur Abschätzung des
Volumenstatus, die in der Notaufnahme verfügbar
sind, wie grundlegende klinische und
laborchemische Untersuchungen, Ultraschallund
Röntgendiagnostik und funktionelle
Tests zur Beurteilung der Volumenreagibilität.
Desweiteren wird ein Ausblick gegeben
auf vielversprechende, innovative, nicht-invasive
Technologien, die für ein erweitertes
hämodynamisches Monitoring in der Notaufnahme
verwendet werden könnten.
Schlüsselwörter
Schock · Sepsis · Volumentherapie ·
Volumenmangel · Passive leg raising ·
Fluid challenge · Erweitertes
hämodynamisches Monitoring ·
Nicht-invasives Herzzeitvolumen
bronchus—and the cardiothoracic ratio
(CTR) seem to provide a more robust estimation
of cardiac preload [39]. Ely and
colleagues divided mechanically ventilated
intensive care unit patients into groups
of high and low/normal volume status after
measuring pulmonary artery occlusion
pressure (PAOP) [40]. By integrating
the objective parameters VPW and CTR
into the analysis of a portable supine CXR,
radiologists were able to increase the likelihood
ratio of the CXR to correctly determine
volume status. The optimal cutoff
for the distinction between high and
normal/low volume status in this investigation
was 70 mm for VPW and 0.55 for
CTR. Limitations of this cost-effective and
328 | Medizinische Klinik - Intensivmedizin und Notfallmedizin 4 · 2017

quickly obtainable technique include the
inability of the CXR to detect hypovolemia
[14], an accuracy of at best 70 % (leaving
a substantial 30 % of patients misclassified),
and missing data on the significance
of VPW and CTR in a spontaneously
breathing ED patient cohort. Despite
these limitations, we agree with Ely
et al. to “use the information already available
on the patient’s CXR to its maximum
potential” [37].
Central venous pressure
The implantation of a central line and the
measurement of CVP are among the invasive
procedures that can be performed
in the ED.
However, there are considerable differences
in the clinical practice of central venous
catheterization in the ED among different
countries [41, 42]. Whereas in specific
patient groups placement of a central
venous catheter seems to be routine clinical
ED practice in the USA and Australia
(e.g., treatment of the control group in
the ProCESS and ARISE studies [43, 44]),
central venous catheterization is rarely
performed in European ED settings.
In this context, it is questionable
whether ED patients benefit from the
placement of a central venous line with
regard to their hemodynamic management
as there is abundant evidence that
CVP is a poor predictor of cardiac preload
and fluid responsiveness [45–47]. Marik
and Cavallazzi performed a meta-analysis
including 43 studies that reported the
correlation coefficient or area under the
receiver operating characteristic curve
(ROC-AUC) between CVP and changes
in stroke volume index or cardiac index
following an intervention-related change
in cardiac preload [47]. The authors demonstrated
that the CVP is able to predict
fluid responsiveness with a ROC-AUC of
only 56 %. Therefore, CVP as a static measure
of cardiac preload should not be used
to guide fluid therapy and assess fluid responsiveness
[48].
Functional tests for
the assessment of fluid
responsiveness in the ED
The aforementioned tests may quickly
aid to determine a patient’s intravascular
volume status after his arrival in the
ED. However, they provide no information
on whether this patient will benefit
from fluid therapy or not. To come to
the crucial decision of whether to administer
fluid therapy or not, two functional
tests—the passive leg-raising test (PLR)
and the fluid challenge test—are available
and have been studied primarily in intensive
care unit patients. However, in the ED
setting, the clinical applicability of these
tests might be limited due to restraints
in hemodynamic monitoring modalities.
However, despite the limited availability
of advanced hemodynamic monitoring,
the ED physician might perform a PLR or
fluid challenge test using surrogate endpoints
available in the ED setting.
Passive leg-raising test
Lifting the legs of the patient passively
from the horizontal position recruits
venous blood volume and transfers it to
the intrathoracic compartment [49–51].
By using the PLR maneuver, a prediction
whether a patient will be fluid responsive
or not is possible without the need to
give a fluid bolus [49, 51]. PLR is applicable
even in arrhythmic and spontaneously
breathing patients [51]. As an endpoint
to define fluid responsiveness different
hemodynamic parameters have been
proposed. Although it has been shown
that changes in radial pulse pressure induced
by PLR can be used for the prediction
of fluid responsiveness in nonintubated
patients [52], for an optimal utilization
of this functional test, the immediate
hemodynamic effects of PLR on blood
flow (i.e., CO or stroke volume) should
be assessed 30–90 s after the onset of the
test [51, 53, 54] because the predictive value
of PLR-induced changes in CO is higher
compared with changes in arterial pulse
pressure [55]. Because usually invasive real-time
measurement of blood flow (e.g.,
using pulse contour analysis) is not possible
in the ED, in this setting, alternative
methods for the estimation of CO/stroke
volume or surrogate parameters might be
considered.
According to recent guidelines [56],
PLR maneuver-induced blood pressure
changes can be used as a surrogate marker
for the initial assessment of fluid responsiveness.
In this context, Lakhal et al.
demonstrated that PLR-induced changes
in systolic arterial pressure measured with
a brachial cuff are able to identify fluid responsive
patients [57]. Lamia and coworkers
described the assessment of PLR-induced
changes of stroke volume by echocardiography
in critically ill patients with
spontaneous breathing activity [58]. In
addition, it was suggested that changes
in the pulse oximetry plethysmographic
waveform amplitude might be used during
PLR in spontaneously breathing patients
[59].
Fluid challenge
In order to assess fluid responsiveness, a
fluid challenge test following a structured
protocol can be performed [60, 61]. During
a fluid challenge test a certain amount
of fluid is given intravenously over a predefined
period of time, and the induced
changes in hemodynamic parameters
are observed [62]. The best way to monitor
hemodynamic effects of a fluid challenge
is to continuously observe CO [60].
A fluid challenge-induced increase in
blood flow (i.e., stroke volume or CO) of
10–15 % indicates that the patient is in the
volume-dependent upward slope of the
Frank–Starling curve and thus fluid responsive
[60, 63]. Because the fluid challenge
maneuver directly assesses the actual
hemodynamic response to fluid loading,
it can be considered the standard criterion
method for the evaluation of fluid
responsiveness. Since only about 50 % of
critically ill patients are fluid responsive,
careful hemodynamic monitoring during
a fluid challenge is of utmost importance
to promptly identify “non-responders”
and avoid unnecessary fluid loading.
The fact that assessment of CO is not routinely
possible in the ED limits the clinical
applicability of the fluid challenge test
in this setting. Blood pressure can only be
considered as a surrogate marker for fluid
responsiveness. However, for the assessment
of fluid responsiveness based on a
Medizinische Klinik - Intensivmedizin und Notfallmedizin 4 · 2017 |
329

Übersichten
Patient admitted to ED
Initial assessment
1) focussed history + physical examination
2) basic monitoring: blood pressure, heart rate, SaO2
3) i.v. access + blood withdrawal
Evidence for shock
+
Detailed physical examination
–
Signs of hypovolemia
+
Biochemistry/laboratory tests
–
Indicative for
a) hypovolemia
b) microcirculatory failure
+
–
IVC ultrasound
Intravascular
hypovolemia
+
–
Chest X-ray
+
Indicative for
pulmonary fluid
overload
–
Assess fluid responsiveness
1. Passive leg raising test
2. Fluid challenge test
Consider negative
fluid balance
Preserve fluid
status
Fluid responsivenss
–
+
1. Consider advanced hemodynamic monitoring
2. Further diagnostic workup
Fluid
administration
Fig. 1 8 Algorithm for evaluating volume status and fluid responsiveness in the emergency department
330 | Medizinische Klinik - Intensivmedizin und Notfallmedizin 4 · 2017

fluid challenge, the use of the mean arterial
pressure as the clinical endpoint and
the CVP as the “safety limit” has been proposed
[61] and is feasible in the ED setting.
Although it has been shown that B-
type natriuretic peptide is not able to accurately
predict fluid responsiveness in
patients with acute circulatory failure
[64], it might be to identify patients with
systolic cardiac dysfunction and a high
risk for fluid overload prior to a fluid challenge
test.
Innovative continuous
noninvasive concepts for
advanced hemodynamic
monitoring: the future in the ED?
The commonly used hemodynamic measures
in the ED are heart rate and intermittently
obtained noninvasive blood
pressure measurements using oscillometry.
In recent years, however, large studies
revealed severe limitations of the oscillometric
method, for example, in obese
and arrhythmic patients [65, 66]. Moreover,
clinically relevant discrepancies between
invasive arterial catheter-derived
and oscillometrically obtained blood pressure
were demonstrated in critically ill patients
[67].
Invasive advanced hemodynamic
monitoring technologies can still usually
not be applied in an ED setting. In the
future, however, innovative technologies
allowing for a continuous and completely
noninvasive estimation of blood pressure,
CO, and other hemodynamic variables
(e.g., pulse pressure variation, stroke
volume variation) might allow advanced
hemodynamic monitoring even in ED patients.
Among the multiple applications,
the option to monitor changes in CO in
real time during functional tests (PLR,
fluid challenge) via noninvasive continuous
CO measurements appears particularly
intriguing. Since CO and stroke volume
are the hemodynamic variables that
are most reliable in the prediction of fluid
responsiveness [63], their continuous recording
would help to identify those patients
who are not fluid responsive, and
thus might be harmed by further fluid administration
[60]. Together with a potentially
reduced probability of missing rapid
changes in vital parameters [68, 69], continuous
noninvasive monitoring of arterial
pressure and blood flow in the ED may
therefore markedly improve both patient
safety and optimization of volume status
and blood flow.
A variety of noninvasive technologies
have been proposed during the past years
that might contribute to assessing a patient’s
volume status, fluid responsiveness,
and guiding fluid therapy in the ED in the
future. The vascular unloading technique,
for example, has already been proven to be
feasible in continuous noninvasive blood
pressure measurements in the ED setting
[68, 69]. This method uses an inflatable
finger cuff applying pressure to the finger
and contains an infrared transmission plethysmograph
to measure the finger artery
diameter (i.e., blood volume) [70]. The arterial
blood pressure waveform can then
be indirectly deduced from the pressure
that is needed to keep the volume in the
finger artery constant throughout the cardiac
cycle. Another noninvasive technology
that allows continuous blood pressure
monitoring and the estimation of CO is
radial artery applanation tonometry [71–
74]. Additional techniques that allow for
the estimation of CO include thoracic
electrical bioimpedance, thoracic bioreactance,
and pulse wave transit time [75].
As mentioned above, the use of these
noninvasive technologies for continuous
hemodynamic monitoring during the
functional tests for fluid responsiveness
might pose a powerful approach. In this
context, it is important that Cecconi et
al. determined dynamic arterial elastance
(Ea dyn ) by using arterial pulse pressure
analysis obtained by the aforementioned
vascular unloading technology in spontaneously
breathing patients [76]. Ea dyn was
defined as the ratio between pulse pressure
variation and stroke volume variation
during one respiratory cycle. Importantly,
patients who had an increase in
MAP of ≥ 10 % after a fluid challenge possessed
a significantly higher preinfusion-
Ea dyn value than nonresponders. As a result,
a preinfusion-Ea dyn > 1.06 identified
fluid responders with both sensitivity and
specificity of 88.2 %. While awaiting further
validation, these findings underscore
the potential of noninvasive arterial pulse
pressure analysis for the assessment of fluid
responsiveness that appears particularly
well suited for the ED.
At this point, however, these innovative
technologies for continuous advanced
hemodynamic monitoring still need to be
further evaluated in the ED setting with
regard to their clinical applicability and
their measurement performance [77, 78].
Conclusions
The correct assessment of the patient’s
volume status and fluid responsiveness
constitutes a fundamental and yet challenging
task for the effective management
of a wide variety of medical conditions
that physicians encounter in the
ED. In this review, we provide a detailed
guide through a variety of methods applicable
in the ED environment for the
assessment of a patient’s intravascular
volume status and fluid responsiveness.
Based upon history, physical examination,
laboratory tests, and ultrasound we
propose an algorithm to estimate the intravascular
volume status (. Fig. 1). In
addition, we describe the functional tests
to assess fluid responsiveness and their
limitations in an ED setting. In the future,
innovative noninvasive means of continuous
hemodynamic monitoring may allow
advanced hemodynamic monitoring
in the ED.
Authors’ contributions. C. Maurer was
responsible for the conception and drafting
of the review. J.Y. Wagner has made
substantial contributions to the conception,
was involved in drafting, and revised
the manuscript for important intellectual
content. R.M. Schmid revised the manuscript
for important intellectual content.
B. Saugel was responsible for the conception
and drafting of the review. All authors
read and approved the final manuscript.
Corresponding address
B. Saugel MD
Department of Anesthesiology, Center of
Anesthesiology and Intensive Care Medicine,
University Medical Center Hamburg-Eppendorf
Martinistrasse 52, 20246 Hamburg
bernd.saugel@gmx.de
Medizinische Klinik - Intensivmedizin und Notfallmedizin 4 · 2017 |
331

Übersichten
Compliance with
ethics guidelines
Conflict of interest. B. Saugel collaborates with
Pulsion Medical Systems SE (Feldkirchen, Germany)
as a member of the Medical Advisory Board. Saugel
received honoraria for giving lectures and refunds
of travel expenses from Pulsion Medical Systems SE
(Feldkirchen, Germany).
Saugel received institutional research grants, unrestricted
research grants, and refunds of travel expenses
from Tensys Medical Inc. (San Diego, CA, USA). BS
received honoraria for giving lectures and refunds of
travel expenses from CNSystems Medizintechnik AG
(Graz, Austria).
J.Y. Wagner received institutional research grants, unrestricted
research grants, and refunds of travel expenses
from Tensys Medical Inc. (San Diego, CA, USA). J.Y.
Wagner received refunds of travel expenses from CN-
Systems Medizintechnik AG (Graz, Austria).
For C. Maurer and R.M. Schmid there is no conflict of
interest to disclose.
This article does not contain studies on human or animal
subjects.
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