This Article Has Been Retracted

SHOCK, Vol. 30, Supplement 1, pp. 18Y22, 2008

ARTERIAL PULSE PRESSURE VARIATION PREDICTING FLUID

RESPONSIVENESS IN CRITICALLY ILL PATIENTS

Jose Otavio C. Auler Jr, Filomena R.B.G. Galas, Marcia R. Sundin,

and Ludhmila A. Hajjar
Department of Anesthesia and Surgical Intensive Care, Incor, Heart Institute, Hospital das Clı́nicas,
Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil

Received 17 Dec 2007; first review completed 18 Feb 2008; accepted in final form 11 Mar 2008

ABSTRACT—In critically ill patients, it is important to predict which patients will have their systemic blood flow increased in
response to volume expansion to avoid undesired hypovolemia and fluid overloading. Static parameters such as the
central venous pressure, the pulmonary arterial occlusion pressure, and the left ventricular end-diastolic dimension cannot
accurately discriminate between responders and nonresponders to a fluid challenge. In this regard, respiratory-induced
changes in arterial pulse pressure have been demonstrated to accurately predict preload responsiveness in mechanically
ventilated patients. Some experimental and clinical studies confirm the usefulness of arterial pulse pressure as a useful
tool to guide fluid therapy in critically ill patients.
KEYWORDS—Dynamic, parameters, stroke volume variation, fluid responsiveness

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INTRODUCTION The key questions to the whole issue of volume responsive-

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ness are (1) On which portion of Frank-Starling curve is the
Recent guidelines for the hemodynamic management of

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patient in the time of fluid challenge? (2) Which are the best

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critically ill patients have emphasized the importance of
tools to predict fluid responsiveness?

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adequate volume resuscitation in predicting favorable out-
Considering the Frank-Starling relationship, the response to
comes (1Y3). However, only 40% to 72% of the intensive care

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volume infusion is more likely to occur when the ventricular
unit patients with hemodynamic instability are able to respond

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preload is low than when it is high. Thus, markers of

CT
to fluid loading by a significant increase in stroke volume or
ventricular preload have been proposed to predict volume
cardiac output (1, 4). This finding emphasizes the need for
responsiveness.

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predictive factors of fluid responsiveness to select patients

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who might benefit from volume expansion and to avoid

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ineffective or even deleterious volume expansion (1). This STATIC MARKERS OF CARDIAC PRELOAD AND

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variety of responses to a volume challenge is explained by the VOLUME RESPONSIVENESS

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shape of the Frank-Starling curve that relates stroke volume
and cardiac preload (Fig. 1). The shape of the Frank-Starling
curve, which relates stroke volume and cardiac preload
(Fig. 1), explains this variety of responses to a volume chal-
lenge. The curve is divided into two parts. On the initial and
steep limb, the stroke volume is highly dependent on preload;
if the heart is working on this part of the curve, increasing
preload by fluid administration will probably result in a
significant increase in stroke volume and cardiac output (3).
On the other hand, if the heart is working on the terminal and
flat portion of the curve, it cannot use any preload reserve, and
fluid administration will not significantly increase stroke
volume (3).
Recent studies in surgical patients have demonstrated that
liberal fluid administration results in worse outcomes, includ-
ing longer stay in the intensive care unit, prolonged time of
mechanical ventilation, and higher rates of infection (5Y7). It
is then essential to predict who are the patients that will
benefit from volume challenge and who will not.
Address reprint requests to Jose Otavio C. Auler Jr., Department of Anesthesia
and Surgical Intensive Care, Incor, Heart Institute, Hospital das Clı́nicas, Faculdade
de Medicina da Universidade de São Paulo, São Paulo, Brazil. E-mail: auler@
incor.usp.br.
DOI: 10.1097/SHK.0b013e3181818708
Copyright Ó 2008 by the Shock Society
18
Numerous studies have demonstrated that none of the
cardiac preload measures enables an accurate prediction of
fluid responsiveness. The central venous pressure, the pulmo-
nary arterial occlusion pressure, the left ventricular end-
diastolic dimension, the early/late diastolic wave ratio, and the
duration of the left ventricular ejection time cannot accurately
discriminate between responders and nonresponders to fluid
therapy (1, 3, 8, 9). Data from recent studies show that filling
pressures are poor indicators of cardiac preload because they
are highly dependent on ventricular compliance, which is
frequently altered in critically ill patients. Even in healthy
volunteers, pulmonary arterial occlusion pressure and central
venous pressure have been reported as poor markers of
preload responsiveness (10). Moreover, there is a physiolog-
ical reason explaining that even the most accurate marker of
ventricular preload will never be a reliable predictor of
volume responsiveness. Indeed, the slope of the Frank-
Starling curve (ventricular preload versus stroke volume)
depends on systolic function. In this respect, in the middle
range of preload, a given value of preload can be associated
with either some preload reserve and, thus, volume respon-
siveness for a normal heart (steep part of the curve) or with
the absence of preload reserve in the case of a failing heart
(flat part of the curve). This explanation probably accounts for
the superiority of dynamic indices attempting to approach the

Copyright @ 2008 by the Shock Society. Unauthorized reproduction of this article is prohibited.
 This Article Has Been Retracted
SHOCK OCTOBER 2008
FIG. 1. The Frank-Starling relationship. The ventricular function is an
important determinant of the relationship between stroke volume and
preload.
slope of the Frank-Starling curve over static markers of
preload (1, 9). In this regard, the magnitude of respiratory
changes as a surrogate of stroke volume has been emphasized
as a reliable index of volume responsiveness.
DYNAMIC PARAMETERS OF VOLUME
RESPONSIVENESSVTHE CONCEPT OF ARTERIAL
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PRESSURE PULSE VARIATION AND USEFULNESS
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IN CRITICALLY ILL PATIENTS
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The concept of respiratory variation of hemodynamic
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signals is based on the assumption that the cyclic changes in
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right ventricular preload induced by mechanical ventilation
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should result in greater cyclic changes in right ventricular
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stroke volume when the right ventricle operates on the steep,
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rather than on the flat, portion of the Frank-Starling curve (3,
4, 11). The cyclic changes in right ventricular stroke volume
and, thus, in left ventricular preload should result in greater
cyclic changes in left ventricular stroke volume when the left
ventricle operates in the ascending portion of the Frank-
Starling curve. Therefore, large variation in arterial pressure
induced by mechanical ventilation occurs in case of biven-
tricular preload preservation. Meanwhile, no change in left
ventricular stroke volume should occur when one of the two
ventricles is preload independent. Thus, in patients who are
preload responsive, positive pressure ventilation will induce
cyclical changes in left ventricular stroke volume. Because the
principle of the method is the tidal volume-induced change in
intrathoracic pressure, the greater the increase in tidal volume
for the same lung compliance, the greater the transient de-
crease in venous return, and, subsequently, the decrease in left
ventricular output becomes even more significant (12). The
degree of changes in either arterial pulse pressure ($PP) or
systolic blood pressure in response to a series of increasing
tidal breaths quantifies the degree of preload responsiveness.
On the other hand, when fixed tidal volume is delivered
during positive pressure ventilation, the degree of variations
in systolic pressure, pulse pressure, left ventricular stroke
volume, and aortic flow accurately reflects preload respon-
siveness (3, 4, 8). In summary, the left ventricular stroke
Copyright @ 2008 by the Shock Society. Unauthorized reproduction of this article is prohibited.
$PP PREDICTING FLUID RESPONSIVENESS 19
volume increases during inspiration because left ventricular
preload increases, whereas left ventricular afterload decreases.
In contrast, the right ventricular stroke volume decreases
during inspiration because right ventricular preload decreases,
whereas right ventricular afterload increases.
The $PP (the difference between the systolic and the
preceding diastolic pressure) is directly proportional to stroke
volume and inversely related to arterial compliance (13).
Therefore, for a given arterial compliance, the amplitude of
pulse pressure is directly related to left ventricular stroke
volume. Thus, the respiratory variation in left ventricular
stroke volume has been shown to be the main determinant of
the respiratory variation in pulse pressure (13). The systolic
pressure is less related to stroke volume than the pulse
pressure because it depends not only on stroke volume and
arterial compliance but also directly on diastolic pressure. The
systolic pressure may vary over a single mechanical breath,
whereas the pulse pressure and the left ventricular stroke
volume do not change significantly (13).
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In hypovolemic patients, the respiratory variations in stroke
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volume and arterial pressure are of greater magnitude because
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the venous system is more collapsible. The inspiratory in-
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crease in right atrial pressure may be greater in hypovolemic
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conditions because of the higher transmission of pleural
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pressure inside the right atrium when it is underfilled and,
thus, more compliant. In addition, in hypovolemic patients,
West zone I (pulmonary arterial pressure G alveolar pressure)
or II (pulmonary venous pressure G alveolar pressure)
conditions are more likely encountered, and, thus, the effect
of inspiration on right ventricular afterload is also more
marked in this context. Finally, the right and left ventricles are
more sensitive to changes in preload when they operate on the
steep (left) portion of the Frank-Starling curve than on the flat
(right) portion of it. The lower the ventricular preload is, the
more likely the ventricles are operating on the steep portion of
the curve (13). Because the four previously described
mechanisms are responsible for a decrease in right ventricular
output during inspiration, such phenomenon has been clearly
shown by many experimental and clinical studies. (1, 3, 4, 9,
10, 13) Thus, in hypovolemic conditions, the magnitude of the
variation in $PP is large, and the main component of this
variation is the expiratory decrease in left ventricular output
that is after the inspiratory decrease in right ventricular output.
In contrast, hypervolemia counteracts these four mechanisms
and increases the amount of blood boosted from the pul-
monary capillary bed toward the left side of the heart during
each lung inflation. Therefore, in hypervolemic conditions,
the magnitude of the respiratory variation in arterial pressure
is low, and the main component of this variation becomes the
inspiratory increase in left ventricular output (13).
The arterial pressure curve is usually displayed on bedside
monitors, and the noninvasive observation of the curve can be
considered an adequate method to assess the respiratory
variation in arterial pressure produced by mechanical ven-
tilation (9, 12, 13).
The first method that has been proposed to analyze and
quantify the respiratory variation in blood pressure produced
by mechanical ventilation is the calculation of the difference
 This Article Has Been Retracted

20 SHOCK VOL. 30, SUPPLEMENT 1 AULER ET AL.

thus, the quantification of its variation during a short period of

a few seconds. The Doppler recording of aortic blood flow has
been used to quantify the respiratory variation in aortic peak
velocity or in velocity time integral at the level of the aortic
annulus or in the descending aorta. The pulse oximeter
plethysmographic waveforms have been compared with the
arterial pressure variation, but despite significant relations
between the two phenomena, discrepancies have been reported,
supporting the notion that pulse oximetry cannot be recom-
mended to accurately assess the respiratory variation in arterial
pressure in mechanically ventilated patients (15Y20).

$PP VARIATIONVEVIDENCE FROM

FIG. 2. Description of respiratory changes in arterial pressure during
mechanical ventilation. Pa indicates arterial pressure; Paw, airway
pressure; SPV, systolic pressure variation.
between the maximum and the minimum systolic pressure
CLINICAL STUDIES
Numerous studies have consistently demonstrated that the
magnitude of respiratory variation of surrogates of stroke vol-
ume allows fluid responsiveness to be predicted with accura-
cy. The respiratory variations of $PP have been extensively

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over a single respiratory cycle, the systolic pressure variation

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(SPV). To discriminate between what is happening during
TABLE 1. Studies that have investigated the arterial PPV for

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inspiration and during expiration, the SPV is divided into two predicting volume responsiveness and the respective

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components ([DELTA]up and [DELTA]down) (8, 13). These threshold value for diagnosis (modified from Curr

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two components are calculated using a reference systolic Opin Crit Care 13:549Y553, 2007)

A
pressure, which is the systolic pressure measured during a PPV
short apnea or end-expiratory pause of 5 to 30 s. The

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Year of threshold

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[DELTA]up can be calculated as the difference between the Reference publication Clinical setting value, %

CT
maximal value of systolic pressure over a single respiratory Michard and Teboul (1) 2000 Medical ICU patients 13
cycle and the reference systolic pressure, reflecting the Vieillard-Baron et al. (21) 2004 Medical ICU patients 12

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inspiratory increase in systolic pressure. That may result from

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Kramer et al. (22) 2004 Coronary artery 11
an increase in left ventricular stroke volume (i.e. increase in

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bypass grafting
pulse pressure), an increase in extramural aortic pressure (i.e.

RE
Preisman et al. (23) 2005 Coronary artery 9
increase in diastolic pressure), or both. The [DELTA]down is bypass grafting
calculated as the difference between the reference systolic
Hofer et al. (24) 2005 Coronary artery 13
pressure and the minimal value of systolic pressure over a bypass grafting
single respiratory cycle, reflecting the expiratory decrease in
Feissel et al. (25) 2005 Mix of surgical and 17
left ventricular stroke volume related to the inspiratory medical ICU
decrease in right ventricular stroke volume (13). patients
To track changes in left ventricular stroke volume more De Backer et al. (19) 2005 Mix of surgical and 12
accurately, the respiratory variation in $PP (DELTAPP) medical ICU
should be measured by calculating the difference between patients
the maximum and minimum pulse pressures (PPmax and Cannesson et al. (15) 2006 Coronary artery 12
PPmin, respectively) over a single mechanical breath. Then, bypass grafting
it can be normalized by the mean of the two values and ex- Solus-Biguenet et al. (26) 2006 Hepatic resection 14
pressed as a percentage: [DELTA]PP (%) = 100  (PPmax j Lafanéchère et al. (27) 2006 Medical ICU patients 12
PPmin) / [(PPmax + PPmin) / 2], as shown in Figure 2. Recently,
Monnet et al. (28) 2006 Medical ICU patients 12
it has also been proposed to quantify the expiratory decrease
Charron et al. (18) 2006 Surgical ICU patients 10
in $PP using the pulse pressure measured during an end-
expiratory pause as the reference pulse pressure. In a recent Natalini et al. (29) 2006 Mix of surgical and 15
medical ICU
study, we proposed an automatic method to detect online
patients
arterial pressure variation as an effective guide to monitor
Feissel et al. (17) 2007 Medical ICU patients 12
fluid therapy after cardiac surgery (14).
Other techniques have been proposed to assess the Cannesson et al. (30) 2007 Coronary artery 11
bypass grafting
respiratory variation in left ventricular stroke volume. The
pulse contour analysis, based on the computation of the area Lopes et al. (31) 2007 Surgical ICU patients 10
under the systolic portion of the arterial pressure curve Auler et al. (14) 2008 Cardiac surgery 12
according to a modified Wesseling algorithm, allows a beat- patients
to-beat measurement of left ventricular stroke volume and, ICU indicates intensive care unit; PPV, pulse pressure variation.

Copyright @ 2008 by the Shock Society. Unauthorized reproduction of this article is prohibited.
 This Article Has Been Retracted
SHOCK OCTOBER 2008
investigated, and the threshold value of pulse pressure that
enables volume responsiveness to be predicted is fairly com-
parable between studies (Table 1) performed in various
clinical settings (1, 14, 15, 17Y19, 21Y31).
In a review of 12 studies comparing predictive factors of
fluid responsiveness, dynamic parameters discriminated more
accurately between responders and nonresponders (1). In
sedated patients receiving mechanical ventilation, $PP was
significantly greater in responders than in nonresponders, and
a $PP threshold value of 13% allowed discrimination between
responders and nonresponders with a positive predictive value
of 94% and a negative predictive value of 96%, respectively
(1). The higher the $PP at the baseline, the greater the
increase in cardiac output after fluid infusion.
In a critical examination of the evidence, comparing dy-
namic measurements of fluid responsiveness, the analysis of
the arterial blood pressure curve may remain the simplest and
most accurate way to predict response to a fluid challenge.
Few studies have compared the value of dynamic different
parameters in the same population and with the same meth-
odology. However, two studies (14, 32), using receiver
operator curve analysis, demonstrated a slight but significant
superiority of $PP over SPV in identifying responders and
nonresponders to a volume load.
D
LIMITATIONS OF PRESSURE PULSE VARIATION
E
CT
The usefulness of heart-lung interaction to detect volume
responsiveness is indisputable and based in both experimental
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and clinical studies (33, 34). However, some limitations must be
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commented. First, as in clinical practice, the arterial pressure
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tracing is obtained from fluid-filled catheters. Several factors (air
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bubbles, kinks, clot formation, compliant tubing, excessive
R
tubing length) may affect the dynamic response of the monitor-
ing system. Second, and more importantly, the beat-to-beat
variations in hemodynamic signals may be due to factors other
than preload reserve in cases of spontaneous breathing activity or
cardiac arrhythmias (3). Then, the method is only adequate for
patients with sinus rhythm and mechanically ventilated. Third,
different tidal volume or positive end-expiratory pressure can
influence the method accuracy (11). As a result, investigators
have studied alternative predictors of fluid responsiveness in
cases when respiratory variation of hemodynamic signals can-
not be appropriately interpreted. In this scenario, passive leg
raising test and the amplitude of pulse oximetry plethysmog-
raphy signal can be performed (28, 35).
CONCLUSIONS AND PERSPECTIVES
Recently published data have showed that in critically ill
patients, goal-directed therapy may improve outcomes, treat-
ing adequately hypovolemia and avoiding fluid overloading
(2, 36, 37). In assessing critically patients with hemodynamic
instability, we should establish objective goals to preserve
tissue perfusion. In this context, variables that would predict
fluid responsiveness are of paramount importance. In recent
years, acquiring more physiological knowledge, the literature
have pointed out through experimental and clinical studies
Copyright @ 2008 by the Shock Society. Unauthorized reproduction of this article is prohibited.
$PP PREDICTING FLUID RESPONSIVENESS 21
that static parameters do not assess fluid responsiveness
adequately. The heart and lung interaction allow us to predict,
dynamically, the individual response to fluid therapy. The
respiratory variation in arterial pressure induced by mechan-
ical ventilation has been evaluated in several studies as a good
predictor of fluid responsiveness. The analysis of the arterial
blood pressure curve may remain the simplest and most
accurate way to guide fluid therapy. It remains to be
determined whether a goal-directed therapy based on the
assessment of the respiratory variation of arterial pressure
may improve the outcome of patients.
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