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Meaning of Pulse Pressure Variation during ARDS
J.-L. Teboul and X. Monnet
J.-L. Vincent (ed.), Annual Update in Intensive Care and Emergency Medicine 2011
DOI 10.1007/978-3-642-18081-1, ˇ Springer Science+Business Media LLC 2011
Introduction
Fluid management is a crucial issue during acute respiratory distress syndrome
(ARDS). On the one hand, fluid administration is important to reverse adverse
hemodynamic effects of mechanical ventilation with positive end-expiratory
pressure (PEEP) or to restore adequate cardiovascular conditions in case of asso-
ciated sepsis. On the other hand, since ARDS is characterized by the development
of increased lung capillary permeability, fluid administration can result in lung
fluid overload and hence in worsening of hypoxemia and further alteration of
lung mechanics. Maintaining fluid balance is considered a major goal in the man-
agement of critically ill patients [1–3]. In comparison with a liberal strategy, a
conservative strategy of fluid management in patients with acute lung injury
(ALI) has been shown to shorten the duration of mechanical ventilation and
intensive care without increasing non-pulmonary organ failure [3]. Accurate
identification of patients who will not benefit from fluid administration in terms
of hemodynamics (‘preload unresponsive’ patients) will enable unnecessary fluid
loading to be avoided. In those identified as ‘preload responders’, the benefit/risk
ratio of fluid administration should be assessed carefully before infusing fluid
and must take into account not only indices of preload responsiveness but also
markers of the severity of circulatory failure versus respiratory failure.
Functional hemodynamic parameters such as arterial pressure variation have
gained wide popularity as predictors of the cardiovascular response to fluid
administration in mechanically ventilated patients [4]. In the present chapter, we
review the rationale, the practical use, and the limitations of measuring pulse
pressure variation (PPV) in patients with ARDS.
Why use PPV?
The Concept of Preload Responsiveness
The relationship between ventricular preload and stroke volume (Frank-Starling
relationship), is curvilinear: If the ventricle is operating on the steep part of the
curve, an increase in preload must induce an increase in stroke volume (preload
responsiveness). In contrast, if the ventricle is operating on the flat portion of the
curve, increasing preload will not induce any significant increase in stroke vol-
ume (preload unresponsiveness). Thus, the patient is considered as a ‘preload
responder’ only if both ventricles are operating on the steep part of the Frank-
Starling curve.
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The Cyclic Effects of Mechanical Ventilation on Hemodynamics
Biventricular preload responsiveness can be determined by analyzing the cyclic
consequences of mechanical ventilation on hemodynamics. Schematically,
mechanical insufflation decreases preload and increases afterload of the right
ventricle. The right ventricular preload reduction is due to the decrease in the
venous return pressure gradient related to the inspiratory increase in intratho-
racic pressure. The increase in right ventricular afterload is related to the inspira-
tory increase in transpulmonary pressure (alveolar minus intrathoracic pressure)
[5]. The reduction in right ventricular preload and the increase in right ventricu-
lar afterload both lead to a decrease in right ventricular stroke volume, which is
therefore minimal at the end of the inspiratory period [6]. The inspiratory
decrease in venous return is the main mechanism of the inspiratory reduction of
right ventricular stroke volume [7], which leads to a decrease in left ventricular
filling after a phase lag of 2–4 heart beats because of the long pulmonary blood
transit time. When conventional mechanical ventilation is applied, the decrease
in left ventricular filling thus occurs during expiration. Finally, the left ventricular
preload reduction may induce a decrease in left ventricular stroke volume, which
is thus minimal during the expiratory period [6].
Interestingly, the cyclic changes in right ventricular preload induced by
mechanical ventilation should result in greater cyclic changes in right ventricular
stroke volume when the right ventricle operates on the steep rather than on the
flat portion of the Frank-Starling curve [6]. The cyclic changes in right ventricu-
lar stroke volume – and hence in left ventricular preload – should also result in
greater cyclic changes in left ventricular stroke volume when the left ventricle
operates on the ascending and steep portion of the Frank-Starling curve [6].
Thus, the magnitude of the respiratory changes in left ventricular stroke volume
should be an indicator of biventricular preload responsiveness [6].
PPV and Preload Responsiveness
At the aortic level, the pulse pressure (systolic minus diastolic pressure) is
directly related to left ventricular stroke volume and inversely related to aortic
compliance. Assuming that aortic compliance does not change during the respira-
tory cycle, the magnitude of cyclic changes in pulse pressure induced by mechan-
ical ventilation (PPV) has been proposed to detect biventricular preload respon-
siveness in mechanically ventilated patients [8].
The PPV is calculated as the difference between the maximal (PPmax) and the
minimal (PPmin) value of arterial pulse pressure over a single respiratory cycle
(Fig. 1), divided by the mean of the two values, and expressed as a percentage:
PPV (%) = (PPmax – PPmin) / [(PPmax + PPmin) / 2] × 100.
PPV as a marker of fluid responsiveness
Numerous studies in various clinical settings have emphasized the usefulness of
PPV in determining fluid responsiveness in mechanically ventilated patients [8–31].
Threshold predictive PPV values ranging between 9 and 17 % have been reported,
although a cut-off value of 12 % has been more frequently reported [32, 33]. In the
majority of the studies, areas under the receiver operating characteristics (ROC)
curve greater than 0.90 have been reported, confirming the good predictive value of
PPV [33]. Interestingly, PPV was demonstrated to be more accurate than static
Meaning of Pulse Pressure Variation during ARDS 323
VIII
40
100
A
rt
e
ri
a
l
P
re
ss
u
re
m
m
H
g
PPmin
PPmax
PPmax – PPmin
(PPmax + PPmin) / 2
PPV (%) = X 100
Fig. 1. Arterial pressure tracing
in a mechanically ventilated
patient. Pulse pressure variation
(PPV) can be calculated as the
difference between the maximal
value of pulse pressure (PPmax)
and the minimal value of pulse
pressure (PPmin) divided by
their averaged value and
expressed as a percentage.
markers of preload in predicting fluid responsiveness [8, 10, 16–22, 33]. In addi-
tion, PPV can be used not only to predict fluid responsiveness but also to assess the
actual changes in cardiac output following volume expansion. Indeed, a good cor-
relation was found between the fluid-induced decrease in PPV and the increase in
cardiac output (or stroke volume) following fluid administration [8, 34, 35].
PPV as a marker of the hemodynamic effects of PEEP
PPV can also be used to predict and assess the hemodynamic effects of PEEP in
patients with ARDS. PEEP is frequently used with the aim of improving pulmo-
nary gas exchange; however it may also decrease cardiac output and thus offset the
expected benefits in terms of oxygen delivery. The adverse hemodynamic effects
of PEEP are not easily predictable in clinical practice. It has been hypothesized
that PPV could accurately predict the effects of PEEP on cardiac output [35].
Indeed, the PEEP-induced decrease in cardiac output and the decrease in right
ventricular output induced by mechanical insufflation share the same mecha-
nisms, i.e., the negative effects of the increased intrathoracic pressure on right
ventricular filling and of the increased transpulmonary pressure on right ventricu-
lar ejection. Thus, it was hypothesized that the PEEP-induced decrease in cardiac
output wouldcorrelate with the magnitude of the inspiratory decrease in right
ventricular stroke volume and of the expiratory decrease in left ventricular stroke
volume and hence with the magnitude of PPV [35]. In patients ventilated for ALI,
a very close relationship was reported between PPV prior to the application of
PEEP and the PEEP-induced decrease in cardiac output [35]. This finding strongly
suggested that PPV before applying PEEP could predict the hemodynamic effects
of PEEP [35]. Moreover, PEEP increased PPV such that the PEEP-induced decrease
in cardiac index also correlated with the PEEP-induced increase in PPV [35]. Thus,
the comparison of PPV prior to and after the application of PEEP may help to
assess the hemodynamic effects of PEEP. In a study in cardiac surgery patients, a
significant negative correlation was also found between PEEP-induced changes in
cardiac output and PPV before PEEP application [34].
324 J.-L. Teboul and X. Monnet
VIII
Practical Use of PPV in Patients with ARDS
The PPV is usually calculated from the arterial pressure waveform obtained with
an arterial fluid-filled catheter (either radial or femoral artery). The calculation of
PPV can be made either manually or automatically (Fig. 1). Manual determination
of PPV can be obtained after freezing the screen of the hemodynamic monitor.
Recent arterial pressure waveform-derived cardiac output monitors, such as
PiCCO™ and LidCO™, allow automatic calculation of PPV. The PPV value can be
displayed on the screen of the monitor and periodically updated.
As mentioned earlier, fluid management is a critical issue during ARDS since
fluid resuscitation, which is often required because of the coexistence of sepsis
and of PEEP application, can enhance pulmonary edema accumulation because of
the presence of increased lung permeability. In this context, where a conservative
fluid strategy is rather recommended [3], one may speculate that knowledge of
PPV could be particularly useful for limiting the amount of fluid administered to
the patient. Indeed, in the presence of low PPV (< 10 %), no beneficial hemody-
namic effect of fluid administration is expected to occur and the clinician may
judiciously choose to avoid volume resuscitation and might even adopt a fluid
depletion strategy in some cases until the appearance of a significant increase in
PPV [36]. In the presence of high PPV (above 12–15 %), the clinician has the
knowledge that a positive hemodynamic response to volume infusion would
occur if fluid were administered. The decision whether or not to infuse fluid will
then depend on the expected benefit/risk ratio and thus on the degree of severity
of other conditions such as circulatory failure, renal insufficiency or hypoxemia.
If available, quantitative markers of lung tolerance, such as extravascular lung
water (EVLW) measured using a PiCCOTM monitor or pulmonary artery occlu-
sion pressure (PAOP) using a pulmonary artery catheter can also be helpful in the
decision-making process.
PPV can also serve as a marker of the hemodynamic effects of PEEP in ARDS
patients. A high PPV before applying PEEP indicates that application of around
10 cmH2O of PEEP would significantly decrease the cardiac output [35]. More-
over, a significant increase in PPV after applying PEEP would confirm that the
cardiac output has actually decreased [35]. Thus, determination of PPV could
avoid the use of a sophisticated monitoring device with the only aim of assessing
the hemodynamic consequences of PEEP application. From a practical point of
view, it can be recommended that a trial at the initially desired level of PEEP is
conducted. If there is a large increase in PPV during the trial, the clinician may
then choose to infuse fluid or to reduce the level of PEEP, depending on other cri-
teria, such as the degree of PEEP-induced improvement in lung mechanics and
gas exchange and the severity of circulatory failure. In either case, the appropriate
interpretation of PPV requires perfect synchronization of the patient with the
ventilator (see below).
Limitations of the Use of PPV during ARDS
Although the usefulness of heart-lung interaction indices – such as PPV – to
detect preload responsiveness, is now well established, a number of limitations
must be remembered.
Meaning of Pulse Pressure Variation during ARDS 325
VIII
) Persistence of Spontaneous Breathing Activity
PPV cannot be used in patients with spontaneous breathing activity as has been
demonstrated in at least three studies in critically ill patients [18, 37, 38]. This
limitation is important since a large proportion of patients with ARDS may trig-
ger their ventilator.
) Cardiac Arrhythmias
In cases of cardiac arrhythmias, the pulse pressure may vary for obvious reasons
independent of mechanical ventilation, such that the PPV cannot be interpreted
reliably [18].
) Low Tidal Volume Ventilation
The influence of tidal volume is a matter of debate. Obviously, for a given volume
status, increasing tidal volume by increasing both transpulmonary pressure and
intrathoracic pressure must increase PPV and vice versa. This has been confirmed
in experimental as well as in clinical studies [39–42]. However, at the same time,
increasing tidal volume can also decrease cardiac output mainly through a
decrease in systemic venous return related to increased intrathoracic pressure. In
this regard, increasing tidal volume can make preload responsive a patient who
was not preload responsive [43]. Therefore, it is quite possible that PPV keeps its
significance as a preload responsiveness index in case of increase in tidal volume
[43]. Conversely, decreasing tidal volume should increase venous return and car-
diac output [44] and potentially make preload unresponsive a patient who was
previously preload responsive. Therefore, it is theoretically possible that PPV
keeps its significance as a preload responsiveness index in case of decrease in
tidal volume.
In almost all the studies examining the predictive value of PPV, patients were
ventilated with tidal volumes ranging from 8 to 10 ml/kg. In a limited series of
patients suffering from various critical illnesses, it has been reported that PPV
was less predictive of volume responsiveness when tidal volume was < 8 ml/kg
than when tidal volume was & 8 ml/kg [14]. In addition, the threshold predictive
value of PPV was lower in the case of tidal volume < 8 ml/kg (8 % vs. 12.8 %)
[14]. Similar results were reported in another series of critically ill patients [45].
It must be stressed however, that low tidal volumes (around 6 ml/kg) are not gen-
erally applied to subjects with normal lungs but rather applied to patients with
ARDS who exhibit high plateau pressure and reduced lung compliance. Conse-
quently, during low tidal volume ventilation in patients with ARDS, respiratory
changes in transpulmonary pressure should remain greater than normal and in
spite of reduced lung compliance, cyclic changes in intrathoracic pressure may
still be high enough for PPV to predict volume responsiveness [46]. Moreover, in
ARDS patients ventilated with low tidal volume ventilation, application of rela-
tively high levels of PEEP (between 10 and 15 cmH2O) is now recommended [47].
This will result in increases in both transpulmonary pressure and intrathoracic
pressure and hence in PPV [35]. Interestingly, in a study performed in patients
with severe ARDS (mean PaO2/FiO2 96, mean static compliance 26 ml/kg) venti-
lated with low tidal volume (mean value 6.4 ml/kg), and high PEEP (mean value
14 cmH2O), PPV was better than static markers of preload, such as cardiac filling
326 J.-L. Teboul and X. Monnet
VIII
pressures, to predict fluid responsiveness and a 12 % threshold value was found
[28]. Additional studies in severe ARDS patients are, however, necessary to inves-
tigate whether or not PPV could be used in cases of low tidal volume ventilation
and high PEEP application.
Attempts have been made to improve the interpretation of PPV in cases of low
tidal volume. For example,it was proposed that PPV be normalized to transalveo-
lar pressure (plateau pressure minus PEEP) [45]. Unfortunately, with low tidal
volume ventilation (< 8 ml/kg), the PPV/transalveolar pressure ratio did not per-
form better than PPV alone in predicting fluid responsiveness in a series of criti-
cally ill patients including only a few ARDS patients.
) High-frequency Ventilation
The hypothesis that PPV is a marker of preload responsiveness is based on the
assumption that the decrease in left ventricular filling secondary to the insuffla-
tion-induced decrease in right ventricular stroke volume occurs 2–4 heart beats
later owing to the long pulmonary transit time. This occurs during expiration
when conventional mechanical ventilation is used. In case of high frequency ven-
tilation, it may be possible for the two events (decrease in right ventricular output
and decrease in left ventricular filling) to occur at the same period of the respira-
tory cycle (i.e., insufflation). Therefore, only minimal changes in stroke volume
would occur during mechanical ventilation resulting in low PPV even in cases of
biventricular preload responsiveness. De Backer et al. [48] recently addressed this
issue in a series of 17 fluid responsive patients. PPV was measured at a low respi-
ratory rate (14–16 breaths/min) and at the highest respiratory rate (30 or 40
breaths/min) achievable without altering tidal volume or inspiratory/expiratory
ratio. Increase in heart rate resulted in a decrease in PPV from 21 % to 4 % and
in respiratory variation in aortic flow from 23 % to 6 % [48]. The authors consid-
ered that PPV could be interpreted reliably when the heart rate/respiratory rate is
higher than 3.6, a condition that is frequently encountered in ARDS patients, in
whom tachycardia is frequently present, especially when they are fluid responsive.
) Right Ventricular Dysfunction
Another potential limitation of PPV in ARDS is related to the fact that, in some
patients with marked right ventricular dysfunction (or with acute cor pulmo-
nale), a significant PPV could result from a marked increase in right ventricular
afterload during insufflation and thus could reflect preload responsiveness of the
left ventricle but not of the right ventricle [49]. In this hypothesis, a high PPV
could be observed in cases of fluid unresponsiveness (false positive cases). In a
study performed in a series of 35 critically ill patients including a majority of sur-
gical patients, the authors reported 34 % of false positive cases [50]. They attrib-
uted this finding to a predominant effect of transpulmonary pressure on the right
ventricular afterload in presence of right ventricular dysfunction. However, it is
hard to be totally convinced by such a hypothesis since the transpulmonary pres-
sure was not very high as attested by the quite low plateau pressure and the pres-
ence of right ventricular dysfunction was probably overestimated with the tools
used by the authors to detect it. It has to be stressed that few ARDS patients and
no patients suffering from chronic right ventricular disease were included in this
study. In other studies performed in septic and/or ARDS patients, a far lower
Meaning of Pulse Pressure Variation during ARDS 327
VIII
incidence of false positives was reported [8, 9, 14, 18, 21, 28] and the infusion of
fluid in patients with high PPV resulted in a decrease in PPV accompanying the
increase in cardiac output, even in cases of severe ARDS [35]. Interestingly, in
patients ventilated with tidal volumes & 8 ml/kg the PPV/transalveolar pressure
ratio was reported to perform better than PPV in predicting fluid responsiveness
by diminishing the number of false positive cases, presumably in relation to a
right ventricular ‘afterload effect’ [45].
Clearly, other markers of fluid responsiveness are thus required in cases of
spontaneous breathing activity, cardiac arrhythmias, high-frequency ventilation.
They may also be helpful in some dubious cases, for example, when a low PPV
is measured in case of low tidal volume, or when a high PPV is measured in
presence of severe right ventricular dysfunction. In all these conditions, a pas-
sive leg raising (PLR) test has been proposed [50] to assess preload responsive-
ness. In this short test, lifting the legs passively from the horizontal position
induces a gravitational transfer of blood from the lower limbs and from the
abdominal compartment toward the intrathoracic compartment, and thus may
act as a reversible ‘self volume challenge’ [51]. The real-time hemodynamic
response to PLR measured by ultrasonography or arterial pressure waveform-
derived cardiac output monitor has been demonstrated to accurately detect fluid
responsiveness in spontaneously breathing patients [18, 52–57]. Alternatively, an
end-expiratory occlusion test has been proposed in patients who are mechani-
cally ventilated but have conditions where PPV may potentially be unreliable
[57]. An increase in pulse contour cardiac output during a short end-expiratory
occlusion was reported to identify fluid responsive patients with a good accuracy
[56].
Finally, it must be stressed that preload responsiveness is a physiological phe-
nomenon related to a normal cardiac preload reserve, since both ventricles of
healthy subjects operate on the steep portion of the preload/stroke volume rela-
tionship. Therefore, detecting volume responsiveness cannot systematically lead
to the decision to infuse fluid. Such a decision must be based on the presence of
signs of cardiovascular compromise and must be balanced with the potential
risk of enhancing pulmonary edema development and/or worsening gas
exchange.
Conclusion
In mechanically ventilated patients, PPV has been demonstrated to be a more
accurate marker of preload responsiveness than static measures of preload.
Calculation of PPV can be helpful in the management of ARDS patients in
terms of fluid and PEEP titration. However, appropriate use of PPV requires
perfect synchronization of the patient with the ventilator and the presence of a
regular cardiac rhythm. Further studies are required to investigate whether
PPV and other heart-lung interaction indices can be appropriately used as pre-
dictors of preload responsiveness in severe ARDS patients ventilated with low
tidal volumes.
328 J.-L. Teboul and X. Monnet
VIII
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Meaning of Pulse Pressure Variation during ARDS 331
VIII
	Meaning of Pulse Pressure Variation during ARDS
	Introduction
	Why use PPV?
	The Concept of Preload Responsiveness
	The Cyclic Effects of Mechanical Ventilation on Hemodynamics
	PPV and Preload Responsiveness
	PPV as a marker of fluid responsiveness
	PPV as a marker of the hemodynamic effects of PEEP
	Practical Use of PPV in Patients with ARDS
	Limitations of the Use of PPV during ARDS
	Persistence of Spontaneous Breathing Activity
	Cardiac Arrhythmias
	Low Tidal Volume Ventilation
	High-frequency Ventilation
	Right Ventricular Dysfunction
	Conclusion
	References