Feature

Passive Leg-Raising
and Prediction of Fluid
Responsiveness:
Systematic Review
Joya D. Pickett, RN, PhD, ARNP-CNS, CCNS, ACNS-BC, CCRN
Elizabeth Bridges, RN, PhD, CCNS
Patricia A. Kritek, MD, EdM
JoAnne D. Whitney, RN, PhD

Fluid boluses are often administered with the aim of improving tissue hypoperfusion in shock. However,
only approximately 50% of patients respond to fluid administration with a clinically significant increase
in stroke volume. Fluid overload can exacerbate pulmonary edema, precipitate respiratory failure, and
prolong mechanical ventilation. Therefore, it is important to predict which hemodynamically unstable
patients will increase their stroke volume in response to fluid administration, thereby avoiding deleterious
effects. Passive leg-raising (lowering the head and upper torso from a 45° angle to lying supine [flat] while
simultaneously raising the legs to a 45° angle) is a transient, reversible autotransfusion that simulates a
fluid bolus and is performed to predict a response to fluid administration. The article reviews the accuracy,
physiological effects, and factors affecting the response to passive-leg raising to predict fluid responsive-
ness in critically ill patients. (Critical Care Nurse. 2017;37[2]:32-48)

luid resuscitation with a goal of hemodynamic optimization is important in the clinical

F management of patients in shock.1 However, only approximately 50% of patients respond to

fluid administration with a clinically significant (≥ 10% to 15%) increase in stroke volume (SV).2,3
The administration of fluids to patients whose SV does not improve in response to fluid administration

CE 1.0 hour, CERP A

This article has been designated for CE contact hour(s). The evaluation demonstrates your knowledge of the following objectives:
1. Outline the importance and physiology of fluid responsiveness
2. Identify the passive leg-raising–induced hemodynamic parameters and the cutoff values used as accurate predictors of fluid responsiveness
3. State 2 factors that affect the response to the passive leg-raising maneuver
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may cause fluid overload, which can exacerbate pulmo-
nary edema, precipitate respiratory failure, and prolong
mechanical ventilation (MV).3-5 Alternatively, under-
treated hypovolemia may lead to inappropriate use of
vasopressors and may increase organ hypoperfusion and
ischemia.3 In patients with septic shock, a more positive
fluid balance at 12 hours (positive fluid balance of ≥ 4.2 L)
and on day 4 (positive fluid balance of ≥ 11 L) from ini-
tial treatment was associated with increased mortality.5
To avoid the deleterious effects associated with fluid
overload and undertreated hypovolemia, it is import-
ant to predict which patients in shock with signs of
hypoperfusion will increase their SV in response to
fluid administration.3,6
Recently, the response to the passive leg-raising
(PLR) maneuver has been an accurate predictor of fluid
responsiveness in critically ill patients in several stud-
ies.7-12 Additionally, revisions to the Surviving Sepsis
Campaign Bundle,13 a national, evidence-based protocol,
include the use of PLR to assess a patient’s volume sta-
tus. PLR causes a transient reversible autotransfusion
that temporarily increases preload, thus mimicking a
fluid bolus. If the patient responds to PLR with a clini-
cally significant increase in SV or its surrogates (eg,
aortic blood flow [ABF]), the patient would most likely
respond to a fluid bolus.
This article synthesizes the evidence on PLR as a
predictor of fluid responsiveness in critically ill patients.
Topics include accuracy of prediction, physiological
Authors
Joya D. Pickett completed her doctoral degree at the University
of Washington, School of Nursing, and practices as a critical care
clinical nurse specialist at Swedish Medical Center in Seattle,
Washington.
Elizabeth Bridges is an associate professor at the University of
Washington School of Nursing and the clinical nurse researcher at
the University of Washington Medical Center, Seattle, Washington.
Patricia (Trish) A. Kritek is the medical director of Critical Care
at the University of Washington Medical Center.
JoAnne D. Whitney is a professor of nursing at the University of
Washington, School of Nursing, and a nurse scientist at Harborview
Medical Center, Seattle, Washington.
Corresponding author: Joya D. Pickett, RN, PhD, ARNP-CNS, CCNS, ACNS-BC, CCRN,
System, Critical Care Clinical Nurse Specialist, Swedish Medical Center, 747
Broadway, Seattle, WA 98122 (e-mail: joyap@u.washington.edu).
To purchase electronic or print reprints, contact the American Association of Critical-
Care Nurses, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 899-1712 or
(949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, reprints@aacn.org.
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effects of PLR, factors affecting the response to PLR,
safety, and implications for practice and future research.
Literature Review Search Strategies
A literature search was conducted using the follow-
ing databases: PubMed (MEDLINE), CINAHL Plus,
COCHRANE library, EMBASE, and Clinical Trials.gov.
The following search terms were used: passive leg raising
(n = 142 articles), fluid responsiveness and passive leg rais-
ing and fluid responsiveness (n = 48 articles), and passive
leg raising and device (n = 13 articles). Studies evaluated
included (1) prospective design, (2) use of a device to
assess the changes in SV or cardiac output (CO) induced
by PLR, (3) use of a predefined cutoff point to stratify
patients as “responders” versus “nonresponders” in
response to a fluid bolus, and (4) studies measuring the
response to PLR at baseline and after performing PLR to
predict an increase in SV or CO. Fifteen studies published
between 2002 and 2015 were reviewed.
Fluid Responsiveness and the
Frank-Starling Law of the Heart:
Responder Versus Nonresponder
The purpose of administering a fluid bolus to a
patient in shock is to increase the SV. Therefore, resus-
citation of patients in shock requires an assessment
of the probability that the patient will respond (ie,
increase SV) to a fluid bolus (fluid responsiveness).3,14
Fluid responsiveness is generally defined as an increase
in SV or CO of 10% to 15% in response to a 500-mL
crystalloid fluid bolus.8,9,15
The Frank-Starling law of the heart explains the rela-
tionship among preload (amount of myocardial fiber
stretch at end diastole), cardiac function, and SV. When
both the right and the left ventricles are operating on
the ascending portion of the Frank-Starling curve, an
increase in
preload To prevent deleterious effects associated
will induce with fluid overload, it is important to
a similar, predict which patients will increase their
but not SV in response to fluid administration.
necessarily
proportional, increase in SV (Figure 1). The relationship
between preload and SV is not linear; rather, it is curvi-
linear (as the preload increases the SV does not necessar-
ily go up in the same proportion). Thus, an increase in
preload will induce a significant increase in SV only if
CriticalCareNurse Vol 37, No. 2, APRIL 2017 33

b'
b
Fluid nonresponsive
a'
Stroke volume
Fluid responsive
a thus mimicking a fluid bolus. PLR recruits a portion of
Ventricular preload
Figure 1 Frank-Starling curve shows relationship between
ventricular preload and stroke volume. When the ventricle
is operating on the ascending part of the curve, an increase
in preload (eg, fluid bolus, passive leg-raising maneuver)
induces an increase in stroke volume (a-a'). When the ven-
tricle is operating on the flat part of the curve, an increase in
preload does not induce an increase in stroke volume (b-b').
b h ventricles
both l are operating on the h ascending
d portion
of the curve. In contrast, if one or both ventricles operate
on the flat portion of the curve (eg, in patients with heart
failure), a similar increase in preload will not induce a
significant increase in SV. Therefore, a patient most likely
will be a responder (ie, SV will increase significantly
in response to a fluid bolus) to volume expansion
only if both ventricles are operating on the ascending
Figure 2 Passive leg-raising is performed by raising the patient’s legs to a 45º angle while simultaneously lowering the patient’s
head and upper torso from a semirecumbent (head of bed elevated 45º) to a supine (flat) position. This maneuver tests for fluid
responsiveness.
Adapted with permission from Marik et al.3
34 CriticalCareNurse Vol 37, No. 2, APRIL 2017
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portion of the ventricular curve. If one or both ventricles
operate on the flat portion of the ventricular curve, then
the patient will most likely be a nonresponder (ie, SV will
not increase significantly in response to a fluid bolus).
The Passive Leg-Raising Maneuver
Lifting the legs is a rescue maneuver that has been
used for years in providing immediate first aid to patients
with circulatory shock. PLR is a transient, reversible
autotransfusion that temporarily increases preload,
the unstressed venous volume of blood from the legs
and splanchnic compartment and shunts it toward the
central circulation, causing a transient increase in sys-
temic venous return and increasing cardiac preload.16-18
As noted, if both ventricles are operating on the ascend-
ing portion of the Frank-Starling curve, the PLR-induced
increase in preload will cause a clinically significant
increase in SV. Studies conducted in various hemody-
namic conditions have demonstrated a PLR-induced
increase in central venous pressure8,9,18 and pulmonary
artery occlusion pressure,19,20 providing evidence that
the volume of blood transferred to the heart in response
to PLR is sufficient to increase the right and left ventric-
ular preload.
PLR can be performed using 2 slightly different
methods. The semirecumbent method involves lowering
the head and upper torso from a 45° angle to lying
supine (flat) while simultaneously raising the legs to a
45° angle18 (Figure 2). In the supine method, the legs
Transfer of blood
from legs and abdominal
compartments
passive leg raising
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are lifted passively from the horizontal position to a
30° to 45° elevation while the head of the bed is flat. A
study comparing the 2 PLR methods showed that the
45° semirecumbent position induced additional venous
blood recruitment from the splanchnic reservoir.18 The
PLR-induced increase in central venous pressure was
greater during semirecumbent PLR (33%; range, 22%-
50%; P < .05) compared with supine PLR (20%; range,
15%-29%; P < .05), suggesting a difference in the change
in preload depending on the position. Additionally,
semirecumbent PLR increased the cardiac index (CI,
calculated as cardiac output in liters per minute
divided by body surface area in square meters) by 22%
(range, 17%-28%), compared with a 10% increase in CI
in response to supine PLR (range, 7%-14%; P < .05).
Researchers measuring the response to supine PLR19,21
estimated that this method recruits approximately 300
mL of unstressed blood, whereas semirecumbent PLR22
recruits approximately 450 to 500 mL of unstressed
blood. Therefore, the semirecumbent PLR method is
recommended.18
The peak effects of PLR occur within 30 to 90 sec-
onds; therefore, response to PLR needs to be assessed
within this period.12,20,23 The varied peak response time
is affected by the device used to measure the response
to PLR. For example, the peak effect of PLR was noted
within 30 seconds when the ABF was measured using
an esophageal Doppler ultrasound device,16 compared
with 90 seconds or less when measured by transthoracic
echocardiography (TTE).12,24 The effects of PLR are rap-
idly reversed when the legs are returned to a horizontal
position16,19,20,24,25; therefore, PLR constitutes a transient,
reversible “self-volume” challenge.16,20,25
The hemodynamic effects of PLR persist over several
respiratory and cardiac cycles. Thus, in addition to
patients receiving MV, PLR can be used to predict fluid
responsiveness in spontaneously breathing patients and
patients with cardiac arrhythmias.7,16
Clinical Studies Evaluating PLR
Studies have been conducted to assess the accuracy
of PLR-induced changes in SV or a surrogate for predict-
ing fluid responsiveness. Measurement of the response
to PLR as a predictor of fluid responsiveness has been
studied in patients receiving total MV, MV with assist,
spontaneously breathing patients, patients with car-
diac arrhythmias, and patients receiving vasoactive
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medications. Table 1 summarizes the characteristics of
the PLR studies that evaluated the accuracy of PLR in
critically ill patients. Table 2 describes key statistical
terms used in the review of the literature.
To evaluate the effect of PLR, hemodynamic measure-
ments were obtained with the patient in the semirecum-
bent position (head-of-bed elevation, 45°) and then within
30 to 90 seconds after PLR was completed. Most studies
measured the response to PLR using a change in SV. How-
ever, other studies measured the stroke volume index
(SVI, calculated as SV divided by body surface area in
square meters), CO, CI, and ABF. Surrogate indicators
of the change in SV such as changes in systolic blood
pressure or pulse pressure (PP) have also been used.
Six studies,12,19,22,24-26 including 254 critically ill
patients, examined the PLR-induced changes in SV
and SVI. Five studies9-11,26,27 evaluated 299 critically ill
patients for the PLR-induced change in CO and CI.
Two studies16,21 evaluated 93 critically ill patients for
the PLR-induced change in ABF. Five studies9,16,19,22,27
evaluated the change in PP in 280 critically ill patients,
and the
PLR recruits about 300 to 500 mL of
change in
unstressed blood from the legs and
systolic
splanchnic compartment and shunts it
blood pres-
toward the central circulation, mimicking
sure was
a fluid bolus.
evaluated
in 1 study8 that included 112 patients. Inclusion criteria
focused on the health care provider ordering a fluid
bolus on the basis of their clinical assessment of inade-
quate tissue perfusion (eg, hypotension, oliguria,
altered mental status). Primary exclusion criteria were
related to contraindications for a fluid challenge (eg,
pulmonary edema). Other exclusion criteria included
hemorrhage, head trauma,10 leg amputation, intra-
abdominal balloon pump support, limb and pelvic
fractures,7 and increased abdominal pressure.12 Exclu-
sion criteria specific to the hemodynamic measurement
method (eg, patients with suspected esophageal mal-
formations when an esophageal Doppler ultrasound
device was used21) were also considered. In 2 studies,8,10
the use of a lower-extremity compression device was
considered an exclusion criterion, whereas in another
study,25 the compression device was removed before
initiation of the study.
In all the studies, patients were categorized as respond-
ers or nonresponders, on the basis of predetermined
CriticalCareNurse Vol 37, No. 2, APRIL 2017 35
 Table 1 Characteristics of passive leg-raising studies in critically ill patients
No. in Cardiac Initial HOB° Bolus, Type and
Studyª/patients’ characteristics population rhythm BLeg° mL/min No. of vaso meds
Stroke volume/stroke volume index
Preau et al,22 2010 34 Sinus Semi 500/30 – 6
Sepsis 30-45
Pancreatitis
Spontaneous breathing
Biais et al,12 2009 34 – Semi 500 0
General surgical (4 exclusions)
Mechanical ventilation/assist
Spontaneous breathing
Thiel et al,25 2009 89 Sinus Semi 500 – 59
Sepsis (102 challenges) Arrhy 45
General medical
Mechanical ventilation/assist
Lamia et al,24 2007 24 Sinus Semi 500/15 NE 11
Respiratory Arrhy 45 Dobut 1
Sepsis
Mechanical ventilation/assist
Spontaneous breathing
Maizel et al,26 2007 34 Sinus Supine 500/15 0
Medical cardiac 30 15
General medical
Spontaneous breathing
Boulain et al,19 2002 39 – Supine 300 NE 5
Sepsis Legs 45 > 20 Dopa 35
Cardiovascular Dobut 15
Mechanical ventilation/assist Epi 5
Cardiac output/cardiac index
Monnet et al,10 2012 54 Sinus Semi 500 NE 23
ARDS/ – 20
Nonsepsis
Mechanical ventilation
Benomar et al,11 2010 75 – – 500 NE 3
Cardiac surgery Epi 6
Mechanical ventilation Dobut 18
Lakhal et al,9 2010 102 Sinus Supine 500 –
Sepsis Legs 45 < 15
Cardiac
Respiratory
Mechanical ventilation
Monnet et al,27 2009 34 Sinus Semi 500 NE 23
Sepsis Arrhy 45 10
ARDS
Mechanical ventilation/assist
Maizel et al,26 2007 34 Sinus Supine 500/15 0
Medical cardiac 30 15
General medical
Spontaneous breathing
Aortic blood flow
Lafanechere et al,21 2006 22 Sinus Supine 500 NE 10
Sepsis Legs 45 Epi 11
General medical
Mechanical ventilation
Monnet et al,16 2006 71 Sinus Semi 500 NE 29
Sepsis Arrhy 45 10 Dopa 5
General medical Dobut 2
Mechanical ventilation/assist
Mechanical ventilation

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 R/NR, Fluid response, PLR response,
No. (%) %/device %/device Sens, % Spec, % AUC (95% CI) PPV/NPV, %

14 (41)/20 (59) SV ≥ 15 SV ≥ 10 86 90 0.94 (0.86-1.00) 86/92

TTE TTE

20 (67)/10 (33) SV ≥ 15 SV ≥ 13, TTE 100 80 0.96 (0.90-1.00) 91/100

TTE SV ≥ 16, pulse contour 85 90 0.92 (0.82-1.00) 95/80

47 (46)/55 (54) SV > 15 SV ≥ 15 81 93 0.89 (0.81-0.97) 91/85

TTDU TTDU

13 (54)/11 (46) SVI ≥ 15 SVI ≥ 12.5 77 100 – 100/79

TTE TTE

17 (50)/17 (50) CO ≥ 12 SV ≥ 12 69 89 0.90 (0.74-0.97) 85/76

TTE TTE

– BSV BSV – – – –
PAC PAC

30 (56)/24 (44) CI ≥ 15 CI ≥ 10 Crs ≤ 30, 94 Crs ≤ 30, 100 0.94 (0.84-1.00) 100/93
TPTD TPTD Crs > 30, 93 Crs > 30, 91 0.91 (0.80-1.00) 93/93

64 (85)/11 (15) CO ≥ 9 CO > 9 68 95 0.84 99/41

Bioreactance Bioreactance

43 (42)/59 (58) CO ≥ 10 CO ≥ 7b 93c 97c 0.98 (0.89-1.00)b –

TPTD/PAC TPTD/PAC

23 (68)/11 (32) CI ≥ 15 CI ≥ 10 91 100 0.94 (0.80-0.99) 100/84

TPTD TPTD

17 (50)/17 (50) CO ≥ 12 CO ≥ 12 63 89 0.89 (0.73-0.97) 83/73

TTE TTE

10 (45)/12 (55) ABF ≥ 15 ABF > 8 90 83 – 82/91

EDoppler EDoppler

37 (52)/34 (48) ABF ≥ 15 ABF ≥ 10 97 94 0.96 (0.92-0.99) 95/97

EDoppler EDoppler

Continued

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 Table 1 Continued
No. in Cardiac Initial HOB° Bolus, Type and
Studyª/patients’ characteristics population rhythm BLeg° mL/min No. of vaso meds
Pulse pressure
Preau et al,22 2010 34 Sinus Semi 500 – 6
Sepsis 30-45 30
Pancreatitis
Spontaneous breathing
Lakhal et al,9 2010 102 Sinus Supine 500 –
Sepsis Legs 45 < 15
Cardiac
Respiratory
Mechanical ventilation
Monnet et al,27 2009 34 Sinus Semi 500 NE 23
Sepsis Arrhy 45 10
ARDS
Mechanical ventilation/assist
Monnet et al,16 2006 71 Sinus Semi 500 NE 29
Sepsis Arrhy 45 10 Dopa 5
General medical Dobut 2
Mechanical ventilation/assist
Mechanical ventilation
Boulain et al,19 2002 39 – Supine 300 NE 5
Sepsis Legs 45 > 20 Dopa 35
Cardiovascular Dobut 15
Mechanical ventilation Epi 5
Systolic blood pressure, noninvasive
Lakhal et al,8 2012 112 Sinus Supine 500 NE 97
Sepsis Arrhy Legs 45 30 Epi 44
Cardiac Dobut 53
General medical
Mechanical ventilation
Meta-analysis
Cavallaro et al,7 2010 353 Arrhy Semi 300-500 –
9 studies Supine
Abbreviations: –, not reported; A-line, arterial pressure catheter; ABF, aortic blood flow; ARDS, acute respiratory distress syndrome; Arrhy, arrhythmia; AUC, area under the
curve; CI, cardiac index; CO, cardiac output; Crs, compliance of respiratory system (cm H2O/mL); CVP, central venous pressure; Dobut, dobutamine; Dopa, dopamine;
EDoppler, esophageal Doppler ultrasound; Epi, epinephrine; HOB, head of bed; Mechanical ventilation/assist, mechanical ventilation with spontaneous breathing; NE, norepi-
nephrine; NPV, negative predictive value; NR, nonresponder; Oscillo NIBP, oscillometric noninvasive blood pressure; PAC, pulmonary artery catheter; PLR, passive leg-raising;
PP, pulse pressure; PPV, positive predictive value; R, responder; SBP, systolic blood pressure, noninvasive; SE, standard error; Semi, semirecumbent; Sens, sensitivity; Spec,
specificity; Supine, head of bed flat; Surg, surgery; SV, stroke volume; SVI, stroke volume index; TPTD, transpulmonary thermodilution; TTDU, transthoracic Doppler ultra-
sound; TTE, transthoracic echocardiography; vaso meds, vasoactive medications.
a
Studies are organized by the hemodynamic parameter(s) used to measure the PLR-induced response.
b
Concomitant increase in CVP ≥ 2 mm Hg.
c
Values calculated from data in source article.

cutoff points used to define the changes in the SV or a
surrogate (eg, ABF) in response to a fluid bolus. The
amount of fluid administered in the bolus varied between
studies; however, in general, 500 mL was delivered. In 1
study,21 it was noted that if the bolus volume was not
sufficient, the patient may have been classified as nonre-
sponsive simply because the patient did not receive
enough volume to affect preload.
Studies Using Changes in SV and SVI to
Measure the Response to PLR
SV (ie, the amount of blood ejected from the left
ventricle with each heartbeat) is often the hemodynamic
parameter used to measure the response to PLR. In a
study25 of 89 critically ill patients receiving MV with
various amounts of ventilator-assisted breathing and/or
arrhythmias, a PLR-induced increase in SV of 15% or

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 R/NR, Fluid response, PLR response,
No. (%) %/device %/device Sens, % Spec, % AUC (95% CI) PPV/NPV, %

14 (41)/20 (59) SV ≥ 15 PP ≥ 9 79 85 0.86 (0.60-1.00) 79/88

TTE A-line

43 (42)/59 (58) CO ≥ 10 PP ≥ 8b 87c 91c 0.91 (0.79-0.97)b –

TPTD/PAC A-line

23 (68)/11 (32) CI ≥ 15 PP ≥ 11 48 91 0.68 (0.50-0.83) 92/52

TPTD A-line

37 (52)/34 (48) ABF ≥ 15 PP ≥ 12 60 85 0.75 (0.63-0.87) 81/73

EDoppler A-line

– BSV B PP – – – –
PAC A-line

44 (39)/68 (61) CO > 10 SBP ≥ 9b 94 83 0.94 (0.85-0.98) 78/97

TPTD Oscillo NIBP

– CO/surrogate CO ≥ 8-15 89 91 0.95 (0.92-0.97) –

≥ 12-15 PP ≥ 9-12 60 86 0.76 (0.67-0.86)

more, measured using transthoracic Doppler ultra-
sound, predicted the response to a subsequent fluid
bolus, with a sensitivity of 81% and a specificity of
93%.The lower sensitivity was attributed to the inclu-
sion of patients who had conditions that might lessen
the effect of PLR (eg, abdominal ascites, lower extrem-
ity contracture and amputations, deep venous thrombo-
sis in the leg). In another study19 of 15 patients with
sepsis or who had undergone cardiac surgery, the
PLR-induced increase in SV correlated with the fluid
bolus–induced increase in SV (r = 0.89; P < .001), as
measured with a pulmonary artery catheter.
In a study12 of 34 patients receiving MV with various
amounts of assisted ventilation and/or with arrhythmias,
changes in SV induced by PLR and by a fluid bolus were
measured using TTE and a minimally invasive radial

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 Table 2 Key statistical terms
Term Explanation
Test validity The extent a test measures what it is supposed to measure, also known as the accuracy
of a test. The accuracy of a test depends on how well a test separates the individuals
being tested into those with and without the condition. Measures of a test’s accuracy
include sensitivity, specificity, area under the receiver operating characteristic curve, posi-
tive predictive value, and negative predictive value.
Test thresholds or cut-point values Established for tests to identify the true-positive test results from the true-negative test results.
For example, when using changes in stroke volume to identify fluid responders from fluid
nonresponders, a cutoff point of ≥ 15% increase as compared with baseline has been
studied and is accurate for distinguishing fluid responders from fluid nonresponders.
Sensitivity The ability of a test to identify the proportion of people who have a condition, also known
as the true positives. Sensitivity of passive leg-raising (PLR) indicates the proportion of
fluid responders who are correctly identified by a given cutoff point (eg, an increase in
stroke volume of ≥ 15%).
Specificity The ability of a test to identify the proportion of people who do not have a condition, also
known as the true negatives. Specificity of PLR indicates the proportion of fluid nonre-
sponders who are correctly identified by a given cutoff point (eg, a change in stroke vol-
ume of < 15%).
Area under the curve (AUC) Measures how well a test discriminates between those with a condition (true positives) and
those without a condition (false positives) for different cutoff points. The true-positive rate
(sensitivity) is plotted against the false-positive rate (1 - specificity). Each plot on the curve
measures a sensitivity/specificity pair corresponding to a particular cutoff point. The test
classifies or “tests” the 2 conditions in the pair. With an AUC of 1.0 (1.0 representing a per-
fect score and 0.5 representing the worst score), an AUC of 0.5 to 0.7 represents an inac-
curate test. For example, an AUC of 0.60 indicates the test is unable to identify the patients
who are fluid responders from those who are nonresponders for a given cutoff point.
Example: In a study by Lakhal and colleagues,8 a PLR-induced increase in systolic blood
pressure (SBP) of ≥ 9% (in patients who also had a ≥ 2 mm Hg increase in central venous
pressure) identified fluid responsiveness with a sensitivity of 94% and a specificity of
83%. This means that an SBP cutoff of ≥ 9% accurately predicted fluid responsiveness
94% of the time (few false negatives) and accurately predicted fluid nonresponsiveness 83%
of the time (moderate false positives). The AUC was 0.94, indicating that the test could
discriminate between those who were responders (true positives) and nonresponders
(false positives).
Positive predictive value (PPV) Answers the question, what is the chance a person with a positive test result truly has the
condition? PPV is the proportion of people with positive test results who actually have the
condition. If the number is close to 100, it suggests that the new test is doing as well as
the “gold standard” test.
Negative predictive value (NPV) Answers the question what is the chance a person with a negative test truly does not have
the condition? NPV is the proportion of people with negative test results who actually do
not have the condition. If the number is close to 100, it suggests that the new test is
doing as well as the “gold standard” test.
Example: In a study by Lafanechere and colleagues,21 a PLR-induced increase in aortic
blood flow > 8 L/min, measured by esophageal Doppler ultrasound, predicted fluid respon-
siveness with a PPV of 82% and an NPV of 91%. This means if the patient had a positive
test result (a PLR-induced increase indicating that the patient is a fluid responder), the
patient was actually responsive to a fluid bolus 82% of the time. If the test was negative (a
fluid nonresponder), the patient failed to respond to a fluid bolus 91% of the time.

artery device. In the same patients, a PLR-induced
increase in SV of 13% or more, measured using TTE,
was predictive of a response to a fluid bolus (sensitivity,
100%; specificity, 80%), whereas a PLR-induced increase
in SV of 16% or greater, measured by the radial artery
device, had a sensitivity of 85% and a specificity of 90%.
In another study24 of 24 patients with sepsis who were
receiving ventilatory support, an SVI greater than 12.5%,
measured using TTE, had a sensitivity of 77% and a spec-
ificity of 100% in predicting fluid responsiveness. These
studies demonstrate that the specification of the optimal
threshold may vary depending on how SV was measured.

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 SV has also been used to measure the response to
PLR in nonintubated, spontaneously breathing patients.
In a study22 of 34 spontaneously breathing patients with
severe sepsis or acute pancreatitis, a PLR-induced increase
in SV of at least 10%, measured using TTE, was predic-
tive of fluid responsiveness (sensitivity, 86%; specificity,
90%). In another study26 that used TTE in 34 sponta-
neously breathing patients,the PLR-induced increase in
SV of 12% or more predicted a response to a fluid bolus
with a sensitivity of 69% and specificity of 89%. Overall,
these studies suggest that the PLR-induced change in SV
is an accurate predictor of fluid responsiveness in the
critically ill patient.
Studies Using Changes in CO and CI to
Measure the Response to PLR
In a study10 of 54 patients receiving ventilatory
support who were in circulatory shock and respiratory
distress, and who were not initiating ventilator breaths
(27 patients had acute respiratory distress syndrome
vs 27 with nonacute respiratory distress), the change in
CI was measured using transpulmonary thermodilu-
tion. If compliance of the respiratory system was 30 cm
H2O/mL or less (n = 28), the best cutoff was a CI of less
than 10% (mean area under the curve [AUC], 0.94 [SD,
0.05]; P < .001); if compliance of the respiratory system
was greater than 30 cm H2O/mL, at the same cutoff,
mean AUC was 0.91 (SD, 0.06; P < .001). These data sug-
gest that PLR is reliable in patients with various degrees
of (ie, low and normal) respiratory system compliance.
In a 2-center study11 of 75 consecutive, critically ill
patients after cardiac surgery, noninvasive hemody-
namic monitoring with bioreactance technology was
used to measure the CO in response to PLR. A PLR-
induced increase in CO of more than 9% had a sensitiv-
ity of 68% and a specificity of 95%. These studies suggest
that PLR-induced changes in CO or CI are accurate pre-
dictors of fluid responsiveness.
Studies Using Changes in ABF to Measure
the Response to PLR
In a study21 of 22 critically ill patients receiving
MV who were in acute circulatory shock, supine PLR–
induced increase in ABF of greater than 8% predicted
fluid responsiveness (sensitivity, 90%; specificity, 83%).
Monnet et al16 determined fluid responsiveness in 71
patients who were in shock and receiving MV, 31 of
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whom were spontaneously breathing and/or had arrhyth-
mias. A PLR-induced increase in ABF of 10% or more
predicted fluid responsiveness (sensitivity, 97%; specific-
ity, 94%). These studies suggest the PLR-induced increase
in ABF is an accurate predictor of fluid responsiveness.
Studies Using Changes in PP to Measure the
Response to PLR
In studies measuring the response to PLR, the
change in PP has been used as a surrogate for the change
in SV. The change in PP indirectly reflects the change in
SV; however, a limitation of the PP is that it may be
affected by arterial compliance and arterial resistance. In
a study19 of 15 patients with sepsis or who had undergone
cardiac surgery, the PLR-induced change in radial artery
PP was significantly correlated with the PLR-induced
change in SV (r = 0.77; P < .001) and with fluid bolus–
induced change in SV (r = 0.84; P < .001). In the same
study, in a second group of 24 critically ill patients, the
PLR-induced changes in radial artery PP were also sig-
nificantly related to the fluid bolus–induced change in
SV (r = 0.73; P < .001).
In the study by Monnet et al16 cited earlier, a PLR-
induced increase in radial artery PP of 12% or greater
predicted a response to a subsequent fluid bolus (sensi-
tivity, 60%;
Some studies suggest that PLR-induced
specificity,
changes in cardiac output and cardiac
85%). The
index are accurate predictors of fluid
researchers
responsiveness.
noted that
although PLR-induced changes in PP had lower sensi-
tivity than PLR-induced changes in ABF, PLR-induced
changes in PP provided a fair prediction of fluid respon-
siveness, even in patients with inspiratory efforts and
arrhythmias who were receiving ventilatory support.
In 34 spontaneously breathing patients with severe sep-
sis or pancreatitis, a 9% or greater PLR-induced increase
in radial artery PP predicted a response to a fluid bolus
(sensitivity, 79%; specificity, 85%).22 A meta-analysis7
using pooled data from 4 studies found that a PLR-
induced increase in radial artery PP predicted a response
to a fluid bolus with sensitivity of 60% (95% CI, 47%-
71%) and specificity of 86% (95% CI, 75%-94%). The
threshold for a PLR-induced increase in radial artery PP
varied between 9% and 12%.
In a study9 of 102 patients with septic and cardiogenic
shock and acute respiratory failure, a PLR-induced 8%
CriticalCareNurse Vol 37, No. 2, APRIL 2017 41
 increase in PP, with a concurrent increase in central
venous pressure (n = 48) of 2 mm Hg or greater (suggest-
ing that PLR increased cardiac preload), had higher pre-
dictive values than seen in patients who did not have
an increase (AUC, 0.91 [95% CI, 0.79-0.97] vs 0.66 [95%
CI, 0.51-0.78)]; P < .05). Researchers in some studies sug-
gest that PLR-induced changes in PP are fairly accurate
predictors, whereas others did not report similar findings.
The PLR-induced change in radial artery PP is a weaker
but significant predictor of fluid responsiveness.7,23
PLR and Prediction of Fluid Responsiveness:
Meta-Analysis
A systematic review and meta-analysis7 published
in 2010 evaluated 9 studies, including 353 critically ill
patients, on the ability of PLR-induced changes in CO
or similar physiological variables (eg, SV, CI, ABF) to
predict fluid responsiveness. The PLR-induced changes
in these physiological variables discriminated between
fluid responders and nonresponders, when compared
with fluid bolus–induced increases in CO. The cutoff
threshold for the increase in CO or its surrogates in
response to a fluid bolus, for determination of respond-
ers, was between 8% and 15%. The pooled sensitivity and
specificity were 89.4% (95% CI, 84.1%-93.4%) and 91.4%
(95% CI, 85.9%-95.2%), respectively. The pooled AUC
was 0.95 (95% CI, 0.92-0.97). No significant differences
were noted between patients receiving total MV and
those with
Because the hemodynamic effects of inspiratory
PLR are rapid and transient, the use of efforts or
a real-time, fast-response device is between
essential to the measurement of the patients in
response to PLR. sinus rhythm
and those
with an arrhythmia. This meta-analysis suggests that
measurement of the response to PLR using SV, CO, CI,
or ABF is accurate for predicting fluid responsiveness in
various patient populations (eg, total MV, MV with
assist ventilation, and spontaneously breathing).
Findings from the meta-analysis were independent
of the device used to measure the response to PLR (eg,
transpulmonary thermodilution, radial artery device,
esophageal Doppler ultrasound, or echocardiography).
One limitation of the meta-analysis is the pooling of
data from studies that used different hemodynamic
parameters to measure the response to PLR; however,
42 CriticalCareNurse Vol 37, No. 2, APRIL 2017
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Table 3 Methods to measure response to passive
leg-raising (stroke volume/cardiac output or surrogate)a
Type of method Methods
Invasive Transesophageal Doppler imaging
Arterial-catheter pressure monitoring
Arterial pulse-contour–pressure waveform
analysis using an indicator dilution
Arterial pulse-contour–pressure wave-
form analysis using transpulmonary
thermodilution
Arterial pulse-contour–pressure wave-
form analysis using demographic data
and physical characteristics
Noninvasive Bioreactance
Echocardiography
Transthoracic Doppler ultrasound
a
Based on analysis of the literature.
subgroup analysis did not show statistical differences.
Another limitation is that the studies did not classify
patients by their ejection fraction. Future research needs
to consider evaluating patients with normal versus
impaired cardiac function.
How to Assess the Effects of PLR
Multiple hemodynamic parameters have been used
to assess the effects of PLR to predict fluid responsive-
ness, including the change in SV/SVI, CO/CI, ABF, PP,
systolic blood pressure, and left ventricular stroke
area. Because the hemodynamic effects of PLR are rapid
and transient, the response to PLR should be assessed
within 30 to 90 seconds after the onset of the test.20,23
Therefore, the use of a real-time, fast-response device is
essential to the measurement of the response to PLR.12,28
Table 3 summarizes the devices used to measure the
response to PLR, based on analysis of the review of
the literature.
Various hemodynamic monitoring devices can be
used to measure the response to PLR, and the time
frame used to measure the response depends on the spe-
cific device. Transesophageal Doppler,16,21 TTE,12,22,24,26
and transthoracic Doppler ultrasound25 all have been
used to measure the response to PLR and can do it rap-
idly. Transthoracic Doppler CO uses transaortic or
transpulmonary Doppler ultrasound flow to calculate
the SV and is noninvasive. A limitation of these methods
is that they require significant training and skill, and
they may not be readily available at the bedside.
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 Other researchers used transpulmonary thermodi-
lution,10 pulse-contour analysis,12,29 and arterial pressure
monitoring.9,16,27,19,22 However, these methods limit the
use of PLR to a small proportion of critically ill patients
who have invasive monitoring. A clinical factor to con-
sider when using an arterial catheter to measure PLR-
induced changes is the need to reference the system again
because of changes in the backrest position. Bioreac-
tance is a noninvasive method of CO determination that
also has been used to measure the response to PLR.11,23,30
Plethysmographic waveform analysis has also been stud-
ied to detect changes in preload in response to PLR.31
However, it had weak predictive value of fluid respon-
siveness (sensitivity, 82%; specificity, 57%; mean AUC,
0.7 [SD, 0.1]).
Recently, oscillometric noninvasive blood pressure
monitoring was used to measure the PLR response in
patients receiving total MV with cardiac arrhythmias.8
A PLR-induced increase in systolic blood pressure of
9% or greater, concurrent with an increase in the central
venous pressure of 2 mm Hg or more (suggesting that the
PLR increased cardiac preload) was predictive of fluid
responsiveness (AUC, 0.94; 95% CI, 0.85-0.98). However,
research on the use of noninvasive blood pressure moni-
toring to measure the response to PLR is so limited that
it cannot currently be recommended.
Limitations of PLR
Patient safety is a key consideration in applying
evidence to practice. PLR is a safe and simple maneuver.
Several researchers have noted that the effects of PLR
in the critically ill are reversed when the legs are returned
to the horizontal position16,19,20,24,25 and it does not result
in acute fluid overload in patients who are not respon-
sive to preload.16 In the studies presented on PLR, there
were no reports of patients leaving the study because
of the maneuver.
A study of PLR was conducted in anesthetized patients
undergoing coronary artery bypass surgery.32 Six patients
had depressed right ventricular (RV) function (RV ejection
fraction < 40%) compared with 10 patients with preserved
RV function. The patients with preserved RV function
had a PLR-induced increase in the RV end-diastolic vol-
ume index (mean [SD], from 105 [17] to 133 [29] mL/m2;
P < .05), and the RV end-systolic volume index (from
61 [13] to 77 [24] mL/m2; P < .05). In contrast, in the
patients with depressed RV function, PLR caused a
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decrease in the RV end-diastolic volume index (from 171
[50] to 142 [32] mL/m2; P < .05) and the RV end-systolic
volume index (from 124 [45] to 91 [22] mL/m2; not
significantly different). One implication of this finding
is to use caution when performing PLR in cardiac sur-
gery patients with depressed RV function (ie, ejection
fraction < 40%). Further research is necessary in other
patient populations to confirm the effect of the PLR-
induced changes in patients with depressed RV function.
Changes in arterial compliance, in comparison with
normal vascular tone, may cause the change in PP to
inaccurately reflect the change in SV. If the arterial com-
pliance decreases (eg, vasoconstriction due to pain or
vasopressor medications), the PP may increase. Con-
versely, if the arterial compliance increases (eg, vaso-
dilatation due to sepsis), the PP may be decreased.
Contraindications to the use of the PLR include patients
with traumatic brain injury, because the PLR may
increase intracranial pressure. Other limitations include
patients
Contraindications to the use of the PLR
with frac-
include patients with traumatic brain
tures of the
injury, because the PLR may increase
lower
intracranial pressure.
extremities
and leg amputations, because these conditions may
cause a difference in the volume of unstressed blood
recruited by the maneuver.23
Implications for Practice
There are inconsistencies in clinical practice on the
use of hemodynamic monitoring to determine fluid
administration in critically ill patients. According to a
recent study33 of critically ill patients with shock, only
23.6% of all fluid boluses (635 of 2694) administered had
concurrent hemodynamic assessment (eg, central venous
pressure, predictive index of fluid responsiveness, echo-
cardiography, or CO measurement) during the first 4 days
in the intensive care unit. Traditionally, static hemody-
namic indicators, such as central venous pressure and
pulmonary artery occlusion pressure, have been used to
guide fluid administration. However, these indicators are
not predictive of the response to a fluid bolus.34-37
Dynamic or functional hemodynamic parameters, such
as arterial pulse pressure variation and SV variation,
can be used to predict the response to a fluid bolus.3,15
These dynamic indices reflect ventilator-induced cyclic
changes in cardiac preload.38 Therefore, these indices
CriticalCareNurse Vol 37, No. 2, APRIL 2017 43
 can be used only in patients receiving total MV with
adequate tidal volumes (eg, tidal volume of > 8 mL/kg)39
and cannot be used in spontaneously breathing patients.
PLR, which causes a transient, reversible autotransfusion
that increases preload and simulates a fluid bolus, is an
accurate test to determine if a patient will increase SV or
CO in response to a fluid bolus.
In accordance with the American Association of
Critical-Care Nurses levels of evidence,40 the studies
reviewed are primarily of level of evidence B; that is,
the recommendations are based on experimental studies
designed to test the effects of an intervention on selected
outcomes. Overall, the evidence supports the use of PLR
in predicting the response to a subsequent fluid bolus
in various populations of patients (eg, total MV, MV
with assist, spontaneously breathing, and patients with
arrhythmias). In general, a PLR-induced increase in SV
or CO of 10% to 15% or greater is an accurate predictor
of fluid responsiveness, and an increase in invasive radial
artery PP of 9% to 12% or greater is a weaker but signifi-
cant predictor of the response to a fluid bolus. Further
research is needed regarding noninvasive blood pressure
monitoring measurements.
The decision to administer fluids must be made on
an individual patient basis.15,41 One factor to consider is
whether the patient has indications of altered perfusion.
Fluid resuscitation is indicated only in patients with
evidence of inadequate tissue perfusion (eg, mean arte-
rial pressure, ≤ 65 mm Hg; systolic blood pressure, < 90
mm Hg; decrease of 40 mm Hg from baseline; increased
lactate level).29,42 Administering fluid boluses to increase
the CO in patients with adequate organ perfusion is not
recommended and may be harmful.3 If there are indica-
tions of
Vasoconstrictor medications, such as altered per-
norepinephrine, may alter the response fusion that
to PLR. Maintain a constant rate of may be
administration of vasoactive medications affected by a
while performing PLR. fluid bolus,
preload
responsiveness (a positive PLR test) and the patient’s
risk of fluid overload should be assessed. If the results
of PLR on the patient indicate that the patient is not
fluid responsive and/or at risk for fluid overload, alter-
native measures such as vasoactive medications or inotro-
pic agents to improve perfusion must be considered. If
the patient has a positive PLR examination and is not
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Table 4 Passive leg-raising (PLR) scenario
Mr AT was admitted to the intensive care unit from the
general care area. After receiving 30 mL/kg of crystal-
loid intravenous fluid, the patient remained hypoten-
sive (ie, mean arterial pressure ≤65 mm Hg, systolic
blood pressure <90 mm Hg) and his skin was mottled,
indicating poor capillary refill. PLR was performed,
and a pulse-contour analysis of change in stroke vol-
ume was used to evaluate the response to PLR. Ninety
seconds after PLR was performed, the patient’s stroke
volume had increased only 6%. In this case, the
patient would be considered a fluid nonresponder
(ie, the patient would not be expected to increase his
stroke volume in response to a fluid bolus), and con-
sideration of other therapies (eg, vasopressor, inotro-
pic therapy) would be appropriate. The continued
administration of fluids may place the patient at an
increased risk of fluid overload.
at risk for fluid overload, fluid boluses may be adminis-
tered. Table 4 presents a scenario that depicts how PLR
can be applied in practice.
PLR is a simple maneuver. The most effective way to
perform PLR is to lower the head and upper torso from a
45º angle to lying supine (flat) while simultaneously rais-
ing the legs to a 45° angle (Figure 2). Generalization of
the evidence using different modifications of PLR (eg,
recumbent vs semirecumbent methods) is not recom-
mended, because the differences in body position may
transfer a different volume of blood to the central circu-
lation, potentially altering differences in preload and,
therefore, the response to PLR.
Several factors may affect the response to PLR. Pain
induced during PLR, due to sympathetic stimulation,
may alter the response to PLR and result in inaccurate
interpretation of the PLR-induced changes.8,29,41 Several
researchers12,16,19,23,26,41 noted that PLR did not produce
alterations in heart rate (eg, tachycardia) in patients
who were awake, suggesting the absence of catechol-
amine stimulation. Therefore, an increase in heart rate
may suggest autonomic stimulation, which may be an
indicator of an altered test result. Assessment of the
patient’s pain and a plan for effective management of
pain needs to be considered before performing PLR.
Vasoactive medications may also alter the response to
PLR.11,16,19,24,43 Therefore, when considering an optimal
time to perform PLR, nurses need to identify a stable
period when they are not titrating vasoactive medica-
tions immediately before or during PLR. Do not change
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 Table 5 Factors potentially affecting the response to passive leg-raising (PLR)
Factor Mechanism Evidence Conclusion
Cardiac arrhythmias Irregular heart rhythms 7
Meta-analysis of critically ill patients The accuracy of PLR is not
can cause alterations demonstrated that PLR similarly predicted affected by cardiac
(eg, decrease in stroke the response to fluid bolus in patients with arrhythmias.
volume). sinus rhythm (area under curve, 0.96; 95%
CI, 0.92-0.99), vs those with arrhythmias
(area under the curve, 0.96; 95% CI,
0.89-1.03).
Norepinephrine Catecholamines, owing Multiple studies11,16,19,24,43 maintained a con- Maintain a constant infusion
to their vasoconstrictor stant rate of infusion while PLR was per- rate while performing PLR.
effects, may alter the formed. In a study44 of the effects of
response to PLR. norepinephrine on cardiac preload, after an
increase in the dose of norepinephrine, a
second PLR test, compared with the base-
line PLR, was able to predict fluid respon-
siveness with a sensitivity of 95% (95% CI,
76%-99%) and a specificity of 100% (95%
CI, 30%-100%).
Intra-abdominal Intra-abdominal hyper- In a study45 of 41 patients with a baseline An intra-abdominal pressure
hypertension tension causes a pulse pressure variation > 12% (ie, fluid ≥ 16 mm Hg may affect
decrease in cardiac responders), and if the intra-abdominal the accuracy of PLR for
output (CO) by decreas- pressure cutoff value was < 16 mm Hg, predicting fluid
ing venous return. fluid responsiveness was predicted with responsiveness.
sensitivity of 100% (95% CI, 78%-100%)
and specificity of 87.5% (95% CI,
62%-98%).
Pregnancy Pregnancy may affect the In a study46 of 47 pregnant women (gesta- PLR did not increase CO in
accuracy of PLR. tional weeks, mean [SD], 39 [0.6]) to deter- healthy women during the
mine if supine, left and/or right lateral third trimester of
decubitus PLRs increase CO. Mean (SD) pregnancy.
baseline CO was 7.8% (1.2%) vs 7.7%
(1.0%) for supine PLR (P < .40), vs 7.8%
(1.0%) for left lateral decubitus PLR (P < .90,
compared with baseline), vs 7.6% (1.0%) for
right lateral decubitus PLR (P < .01, com-
pared with baseline). After right lateral decu-
bitus PLR, CO decreased significantly.

vasoactive drug dosage when performing the PLR test.
Table 5 summarizes the potential factors affecting the
response to PLR.
A limitation of this literature review is that other tech-
niques of performing PLR (eg, variations of the Trende-
lenburg position) are not discussed. Table 6 is a summary
of considerations for future research.
Conclusion
Studies suggest that PLR-induced changes in SV and
its surrogates are reliable predictors of fluid responsive-
ness regardless of type of ventilation and cardiac
rhythm. The PLR-induced change in invasive radial
artery PP is a weaker but significant predictor of fluid
responsiveness.7 &&1
Financial Disclosures
None reported.
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in Patients With Urinary Catheter–Associated Bacteriuria” by Conway
et al in the American Journal of Critical Care, January 2017;26:43-52.
Available at www.ajcconline.org.
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 Table 6
Review of the literature
Lack of studies using non-
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Lower-extremity compres-
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Considerations for future research on passive leg-raising (PLR)
Future research
Noninvasive blood pressure measurement
is often used as an initial assessment of
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response to PLR that can be used during
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 CCN Fast Facts CriticalCareNurse
The journal for high acuity, progressive, and critical care nursing

Passive Leg-Raising and Prediction of

Fluid Responsiveness

luid boluses are often administered with the 45º angle while simultaneously lowering the head

F aim of improving tissue hypoperfusion in shock.

However, only approximately 50% of patients
respond to fluid administration with a clinically signifi-
of bed from a 45° semirecumbent position to a
supine position.
• Vasoactive medications may alter the response to
cant increase in stroke volume (SV). Fluid overload can
the PLR. When performing the PLR, maintain a
exacerbate pulmonary edema, precipitate respiratory
constant vasoactive drip rate. Identify a stable
failure, and prolong mechanical ventilation. Therefore,
period when vasoactive drip titration (either
it is important to predict which hemodynamically unsta-
increase or decrease) is not occurring immediately
ble patients will increase their SV in response to fluid
before or during the PLR. &&1
administration, thereby avoiding deleterious effects.
Passive leg-raising (PLR), that is, lowering the head
and upper torso from a 45° angle to lying supine (flat) b'
while simultaneously raising the legs to a 45° angle, is b
a transient, reversible autotransfusion that simulates a Fluid nonresponsive
fluid bolus and is performed to predict a response to
fluid administration. a'
Stroke volume

• The Frank-Starling law of the heart explains the

relationship among preload, cardiac function,
and SV (see Figure). When both the right and
Fluid responsive
left ventricles are operating on the ascending
portion of the Frank-Starling curve, an increase
a
in preload (ie, PLR, fluid bolus) will induce a
similar, but not necessarily proportional,
increase in stroke volume.
• Overall, the evidence supports the use of PLR in Ventricular preload
predicting the response to a subsequent fluid
Figure Frank-Starling curve shows relationship between
bolus in various populations of patients (eg, total ventricular preload and stroke volume. When the ventricle is
mechanical ventilation, mechanical ventilation operating on the ascending part of the curve, an increase in
with assist, spontaneously breathing, and patients preload (eg, fluid bolus, passive leg-raising maneuver)
induces an increase in stroke volume (a-a'). When the
with arrhythmias). ventricle is operating on the flat part of the curve, an
increase in preload does not induce an increase in stroke
• PLR is a simple maneuver. The most effective way volume (b-b').
to perform PLR is to elevate the lower limbs to a

Picket JD, Bridges E, Kritek PA, Whitney JD. Passive Leg-Raising and Prediction of Fluid Responsiveness: Systematic Review. Critical Care Nurse. 2017;37(2):32-48.

48 CriticalCareNurse Vol 37, No. 2, APRIL 2017 www.ccnonline.org

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Passive Leg-Raising and Prediction of Fluid Responsiveness: Systematic Review
Joya D. Pickett, Elizabeth Bridges, Patricia A. Kritek and JoAnne D. Whitney
Crit Care Nurse 2017;37 32-47 10.4037/ccn2017205
©2017 American Association of Critical-Care Nurses
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