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MCC 240303

REVIEW

CURRENT
OPINION Esophageal pressure monitoring: why, when
and how?
Takeshi Yoshida a,b and Laurent Brochard a,b

Purpose of review
Esophageal manometry has shown its usefulness to estimate transpulmonary pressure, that is lung stress,
and the intensity of spontaneous effort in patients with acute respiratory distress syndrome. However,
clinical uptake of esophageal manometry in ICU is still low. Thus, the purpose of review is to describe
technical tips to adequately measure esophageal pressure at the bedside, and then update the most
important clinical applications of esophageal manometry in ICU.

Recent findings
Each esophageal balloon has its own nonstressed volume and it should be calibrated properly to measure
pleural pressure accurately: transpulmonary pressure calculated on absolute esophageal pressure reflects
values in the lung regions adjacent to the esophageal balloon (i.e. dependent to middle lung). Inspiratory
transpulmonary pressure calculated from airway plateau pressure and the chest wall to respiratory system
elastance ratio reasonably reflects lung stress in the nondependent ‘baby’ lung, at highest risk of
hyperinflation. Also esophageal pressure can be used to detect and minimize patient self-inflicted lung
injury.

Summary
Esophageal manometry is not a complicated technique. There is a large potential to improve clinical
outcome in patients with acute respiratory distress syndrome, acting as an early detector of risk of lung
injury from mechanical ventilation and vigorous spontaneous effort.

Keywords
acute respiratory distress syndrome, esophageal pressure, spontaneous breathing, transpulmonary pressure

INTRODUCTION methods, early detection of the harm of spontane-

Esophageal manometry has shown to be useful for
more than 50 years of research. The clinical appli-
cations of esophageal manometry are potentially
various, for example to estimate pleural pressure
(Ppl) and hence transpulmonary pressure (PL), which
is the distending pressure of the lungs; to assess
patient’s effort when the respiratory muscles are
active; to monitor the patients-ventilator interac-
tions; to facilitate weaning process from mechanical
&&
ventilation [1 ]. However, the recent LUNG SAFE
international study revealed that esophageal
manometry was rarely employed in patients with
acute respiratory distress syndrome (ARDS) [2]. In
order words, there is a large potential for the uptake
of esophageal manometry in clinical practice.
Thus, we describe technical tips to be employed
to adequately measure esophageal pressure (Pes) at
the bedside, and then update the most important
clinical applications of esophageal manometry in
ICU, that is estimation of local PL with several
ous effort.
WHY DO CLINICIANS RARELY USE
ESOPHAGEAL MANOMETRY IN ICU?
Although esophageal manometry has been estab-
lished as an essential tool in research for a long time,
a large epidemiologic study covering 50 countries
reported that esophageal manometry was used in
less than 1% of patients with ARDS [2]; several
a
Keenan Research Centre, Li Ka Shing Knowledge Institute, St. Michael’s
Hospital and bInterdepartmental Division of Critical Care Medicine,
University of Toronto, Toronto, Ontario, Canada
Correspondence to Laurent Brochard, MD, Keenan Research Centre, Li
Ka Shing Knowledge Institute, St. Michael’s Hospital, 30 Bond St,
Toronto, ON, Canada M5B 1W8. Tel: +1 416 864 5686;
e-mail: BrochardL@smh.ca
Curr Opin Crit Care 2018, 24:000–000
DOI:10.1097/MCC.0000000000000494

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Cardiopulmonary monitoring
KEY POINTS
 The esophageal balloon should be inflated with
minimal nonstressed volume to measure esophageal
pressure accurately. This value in each commercially
available catheter is different.
 If calibrated properly, absolute esophageal pressure
reflects the value adjunct to the balloon, that is in the
middle-dependent lung regions. The elastance-derived
method (using tidal change in esophageal pressure)
reflects the value in the nondependent lung regions.
 The lung injury from spontaneous effort occurs in the
dependent lung regions, the same regions where strong
effort increases greater inspiratory stress and stretch.
The magnitude of negative ‘swing’ in esophageal
pressure, that is the intensity of spontaneous effort, is
linearly correlated with inspiratory stress and stretch in
the dependent lung regions. Thus monitoring of
esophageal pressure in patients with spontaneous effort
is highly recommended.
reasons may play a role: seemingly complicated
technical issues to measure Pes at bedside; uncertain
validity of Pes.
First, methodology to introduce Pes is seemingly
complicated. For instance, incorrect volumes of air
in the esophageal balloon are known to result in
overestimation or underestimation of the surround-
ing Ppl [3,4]. Second, in the supine position a gradient
of Ppl exists (higher in dorsal, lower in ventral) [5]; it
is not clearly known in which lung regions Pes
represents Ppl. Also it has been claimed that the
mass of the mediastinum could falsely elevate Pes
by direct compression [6]. In addition, two different
estimates of Ppl (and thus PL) – both derived from
esophageal manometry – are proposed. One esti-
mate of PL is based on measured absolute Pes [7], and
the other is based on the elastance ratio of chest wall
to respiratory system [8,9]. These two estimates of PL
have been shown to yield quite different results [10],
and this discrepancy also raised concerns about the
validity of esophageal manometry.
TECHNICAL TIPS: HOW TO START THE
MEASUREMENTS OF ESOPHAGEAL
PRESSURE
The technique of esophageal balloon was summa-
&&
rized in recent reviews [1 ,11].
Introducing the esophageal balloon
Several esophageal balloons are commercially avail-
able [3]. All types of esophageal balloon are introduced
transnasally (55 cm) or orally (40 cm) until the
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stomach and inflated with adequate volume. The
intragastric position of the esophageal balloon is con-
firmed by a positive pressure deflection during gentle
external manual compression of the abdomen. Then,
the balloon is withdrawn until appearing cardiac arti-
facts on the pressure tracings, indicating that the site
of pressure measurement (balloon) is in the lower third
of the esophagus. The presence of a nasogastric tube
does not seem to significantly affect Pes measurement
[12] and it is possible to use an esophageal catheter in
addition to a feeding tube already in place.
Inflating the esophageal balloon
It is important to emphasize that the nonstressed
volume varies depending on balloons and the sur-
rounding pressure [3,4]. Nonstressed volume is rec-
ognized as the adequate filling volume, not causing
underestimation of Pes due to low filling volume nor
overestimation of Pes due to the elastance of esopha-
gus. In addition, to minimize the effect of the ela-
stance of esophageal wall, the minimal nonstressed
volume should be used to measure Pes accurately.
This value in each commercially available catheter
was carefully evaluated in a previous study [3]. Thus,
we suggest checking what the minimal nonstress
volume is for each esophageal balloon before starting
to use it at bedside, referring to a previous elegant
study done by Mojoli et al. [3]. Alternatively, a simple
correction subtracting elastic pressure of the esopha-
gus imposed by filling balloon can be used [4].
Confirming the appropriate position
The position of esophageal balloon is validated with
an occlusion test, using a chest compression (passive
patient) or an inspiratory effort maneuver (spontane-
ously breathing patient) against an end-expiratory
&&
occlusion [1 ]. It is assumed that with no net change
in global PL (i.e. zero flow conditions) due to a closed
airway, changes in airway pressure (Paw) should mirror
the changes in local Ppl as measured by the esophageal
balloon [13]. Thus, the relationship between DPes and
DPaw should present a slope of 1.0  0.2 during an
occlusion test. When DPes/DPaw is out of range, that
is less than 0.8 or more than 1.2, during an occlusion
test, the position of esophageal balloon should be
modified since Pes does not reflect Ppl correctly.
CLINICAL APPLICATIONS OF
ESOPHAGEAL MANOMETRY IN ICU
Estimating (local) lung distending pressure
During a positive-pressure mechanical ventilation
(i.e. no active spontaneous effort), pressure applied
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MCC 240303
to the respiratory system by a ventilator is consumed
to inflate the lung and chest wall. Lung distending
pressure, that is transpulmonary pressure PL is cal-
culated as follows:
PL ¼ Paw  Ppl :
Two different methods have been proposed to
estimate Ppl and thus PL calculation from directly
measured Pes [7] or using airway plateau pressure
and the elastance ratio of chest wall to respiratory
system [8,9]. Both are derived from esophageal
manometry, and it is interesting to note that they
yield different estimates of PL [10]. The reason, as
explained below, is that there is not a single
Ppl value.
Absolute esophageal pressure
The first method is based on measured ‘absolute’
value of Pes [7]. This method has an assumption
that absolute Pes by itself can be used as a surrogate
of Ppl and then PL is directly calculated as follows:
PL ¼ Paw  Pes :
The static Ppl increases from nondependent to
dependent regions in supine position, creating a
vertical pressure gradient. This vertical gradient of
Ppl is known to reach approximately 10 cmH2O in
patients with ARDS, which is almost double than in
healthy adults [5]. Such a large pressure gradient can
explain inhomogeneous distribution of lung aera-
tion in ARDS, and it is uncertain in which lung
regions Pes reflects local Ppl. In accordance with a
previous study [14], a recent validation study (pigs
and human cadavers) of Pes using direct Ppl sensor
revealed that if properly calibrated (i.e. minimal
nonstressed volume), absolute ‘measured’ Pes accu-
rately reflects local Ppl in the mid to dependent lung
regions, adjacent to the esophageal balloon, inde-
pendently of the mediastinal structures (Fig. 1) [15 ].
& patients with ARDS [2,16], in part because oxygen-
Thus, the absolute Pes is a good surrogate for local Ppl
in the mid-dependent lung regions. Since atelectasis
usually predominates in the mid to dependent lung
regions in ARDS, setting positive end-expiratory
pressure (PEEP) using expiratory ‘measured’ Pes to
prevent dorsal (i.e. middle to dependent) atelectasis
makes sense. A clinical trial showed that a ventila-
tory strategy using Pes at end-expiration to maintain
a positive value of PL had physiological benefits in
patients with ARDS [7].
Elastance ratio of chest wall to respiratory
system
The second method is based on elastance ratio of chest
wall to respiratory system [8,9]. This method has two
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Esophageal pressure monitoring Yoshida and Brochard
assumptions: first, the ratio of chest wall elastance to
respiratory system elastance (ECW/ERS) determines
the fraction of airway driving pressure consumed to
inflate chest wall (and not harmful to the lungs);
second, Ppl is zero at functional residual capacity. At
functional residual capacity, lung is neither expand-
ing nor collapsing and thus PL must be zero: as Paw is
zero, Ppl must be zero for PL being zero. Thus, Ppl can
be calculated as Paw  (ECW/ERS) and then PL is cal-
culated as follows:
 
ECW
PL ¼ Paw  Paw  :
ERS
A recent study (pigs and human cadavers)
revealed that inspiratory PL calculated from ela-
stance ratio closely reflected the nondependent
&
actual (measured) values (Fig. 2) [15 ]. Bland–Alt-
man analysis revealed that PL calculated from ela-
stance ratio served a good surrogate for inspiratory
PL in the nondependent lung regions (i.e. mean
difference: 0.8 cmH2O). This happens because the
assumptions are true only in these regions, consid-
ering Ppl in nondependent lung (but not in other
lung regions) was the closest to zero at low PEEP
levels (close to functional residual capacity). Inspi-
ratory PL calculated from the elastance ratio reason-
ably reflects local PL in the nondependent ‘baby’
lung where is most vulnerable to ventilator-induced
lung injury. Thus inspiratory PL calculated from the
elastance ratio may represent a novel and testable
clinical target to reduce ventilator-induced lung
&
injury [15 ]. The distribution of Ppl and their meas-
urements are illustrated in Fig. 3.
Early detection of the harm of spontaneous
effort
Spontaneous breathing is often permitted in
ation is better [16] and diaphragm disuse is avoided
&
[17,18 ]. However, accumulating evidence indicates
that this may cause – or worsen – lung injury,
especially if ARDS is severe and/or spontaneous
effort is vigorous and dyssynchronous with the ven-
tilator [19–23]. Recent perspective termed this
effort-dependent lung injury as patient self-inflicted
lung injury (P-SILI) [24]. This may explain the find-
ings that high respiratory drive is independently
associated with failure of noninvasive ventilation
[25], and that such patients have a particularly poor
prognosis [26].
Here we described three main mechanisms of
lung injury from spontaneous effort: first, increased
local dependent lung stress; second, increased lung
perfusion; third, patient-ventilator asynchrony.
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Cardiopulmonary monitoring

(a) PEEP4 PEEP24

82mm
76mm

Expiratory Transpulmonary Pressure (cmH2O)

20

15mm 34mm
15
* +‡
* +‡
*+‡
* +‡
10 ‡ * +‡ ‡
*+ ‡
‡
*+ ‡
*+‡
*+ ‡ ‡
*+ *+ ‡ ‡
5 ‡ ‡
‡ ‡
‡ ‡
‡ ‡
‡ ‡
0 ‡
‡
Non-dependent sensor
Esophageal (absolute)
Dependent sensor
-5
4 6 8 10 12 14 16 18 20 22 24
PEEP (cmH2O)

PEEP12
(b)
105mm
Expiratory Transpulmonary Pressure (cmH2O)

15
57mm
10

-5

Non-dependent sensor
-10
Esophageal (absolute)
Dependent sensor
-15
5 10 15
PEEP (cmH2O)

FIGURE 1. The spatial relationship of expiratory transpulmonary pressures calculated from esophageal pressure in lung-injured
pigs and human cadavers. (a) In lung-injured pigs, expiratory transpulmonary pressure, calculated using Pes (i.e. positive end-
expiratory pressure  expiratory Pes), reflected the directly measured values in mid (at higher positive end-expiratory pressure
values) – dependent lung regions (at lower positive end-expiratory pressure values). Static computed tomography images in a
representative pig confirmed that the position of the esophagus was close to the dependent sensor at positive end-expiratory
pressure of 4 cmH2O, but was closer to mid-zone (i.e. more distant from the dependent sensor) at positive end-expiratory
pressure of 24 cmH2O. (b) In human cadavers, expiratory transpulmonary pressure, calculated using Pes, reflected the directly
measured values in mid-lung regions. A representative computed tomography was presented from acute respiratory distress
syndrome registry. The position of the esophagus was observed to be located mid-thorax in a patient with acute respiratory
distress syndrome. Taken together, these computed tomography images indicate that Pes reflected the local pleural pressure
that was adjacent to the esophageal balloon. ARDS, acute respiratory distress syndrome; CT, computed tomography; PEEP,
positive end-expiratory pressure; Pes, esophageal pressure. P < 0.05 compared with Pes; þP < 0.05 compared with dependent
sensor; zP < 0.05 compared with positive end-expiratory pressure 4. Reprinted with permission of the American Thoracic
Society. Copyright ß 2018 American Thoracic Society [15 ]. The American Journal of Respiratory and Critical Care Medicine &

is an official journal of the American Thoracic Society.

Increased local lung stress more negative local ‘swings’ in Ppl in the dependent
In normal ‘fluid like’ lung, the inspiratory deflection lung. The resulting higher local lung stress causes local
(swing) in Ppl resulting from diaphragmatic contrac- volutrauma [22] and huge tidal recruitment in the
tion is rapidly dissipated across the whole pleural dependent lung [23,28] by drawing gas either from
surface [27]. In contrast, in the injured ‘solid like’ lung, other lung regions, for example nondependent lung
the inspiratory Ppl swing is not dissipated, but is pre- (this is called pendelluft [22]) or from the ventilator.
dominantly localized to the dependent regions where Recent data confirmed that the bulk of effort-depen-
it is generated [22,23]. Thus, stronger effort results in dent lung injury occurred in the dependent lung, the

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Esophageal pressure monitoring Yoshida and Brochard

(a)

Inspiratory Transpulmonary Pressure (cmH2O)

25
Non-dependent sensor Elastance rao
*+‡
Esophageal Dependent sensor *+‡
20 +‡
*+‡

*+ ‡ +‡
‡
15 * +‡ +‡ ‡
*+ ‡ +‡
*+ +‡ ‡
+ *+ *+ *+
+ ‡
10 *+
+ ‡
+ *+ ‡
‡
‡ ‡

0
4 6 8 10 12 14 16 18 20 22 24
PEEP (cmH2O)

(b)
Inspiratory Transpulmonary Pressure (cmH2O)

30 Non-dependent sensor Esmated

Elastance from
rao dal changes in Pes
Esophageal (absolute) Dependent sensor
25
20
15
10
+

5
0
-5
-10
5 10 15
PEEP (cmH2O)

FIGURE 2. The spatial relationship of inspiratory transpulmonary pressures calculated from esophageal pressure vs. elastance
ratio in lung-injured pigs and human cadavers. In lung-injured pigs (a) and human cadavers (b), inspiratory transpulmonary
pressure, calculated using elastance ratio, closely matched the directly measured value in nondependent lung. However, note
that inspiratory transpulmonary pressure, calculated using Pes, reflected the directly measured values in mid and dependent
lung regions adjacent to the esophageal balloon. Pes, esophageal pressure. P < 0.05 compared with Pes; þP < 0.05
compared with dependent sensor; zP < 0.05 compared with positive end-expiratory pressure 4. Reprinted with permission of
the American Thoracic Society. Copyright ß 2018 American Thoracic Society [15 ]. The American Journal of Respiratory and &

Critical Care Medicine is an official journal of the American Thoracic Society.

same region where vigorous effort increased greater on the respiratory drive, could be used to control the
inspiratory stress and stretch [29]. intensity of the effort assessed by esophageal pressure
Of note, the intensity of spontaneous effort manometry [30,31].
(represented as negative ‘swing’ in Pes) is linearly
correlated to the magnitude of local dependent lung Increased lung perfusion
stress and stretch [22,23]. Spontaneous effort should Spontaneous effort generates a more negative Ppl
be maintained to be a modest level to prevent P-SILI which in turn increases transmural vascular pres-
and hence monitoring Pes in ARDS patients with sure, that is difference between intravascular pres-
&&
spontaneous effort is highly recommended [1 ]. sure and pressure outside the vessels. Transmural
Our recent review suggested to limit inspiratory PL vascular pressure is considered as the net pressure
less than 20–25 cmH2O and/or muscle pressure less distending the intrathoracic vessels. Hence vigorous
than 5–10 cmH2O in ARDS patients with spontane- spontaneous effort was recently shown to increase
&&
ous effort [1 ]. lung perfusion, propensity to edema and worsen
Significantly, recent reports showed that extracor- clinical outcome in children with acute asthma
&&
poreal removal of CO2, by decreasing the stimulation exacerbation [32 ]. Transmural vascular pressure

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Cardiopulmonary monitoring

Pleural pressures (Ppl) and their measurements

Non-Dependent regions
Sternum
Mediasnum

Pleural Pressure Gradient

Non-dependent Ppl
(esmated by elastance method)
Trachea
Esophagus

Middle Ppl
(esmated by esophageal pressure)
Dependent Ppl

Dependent regions
Lungs

FIGURE 3. The distribution of pleural pressures and their measurements. The Ppl increases from nondependent to dependent
regions in supine position, creating a vertical pressure gradient (indicated in the left side). This vertical gradient of Ppl is known
to reach approximately 10 cmH2O in patients with acute respiratory distress syndrome, explaining heterogeneous distribution
of lung aeration in acute respiratory distress syndrome, that is hyperinflation at nondependent and collapse in dependent lung
regions. Nondependent Ppl (and thus nondependent PL, the highest risk of hyperinflation) can be estimated with elastance
method. Middle to dependent Ppl (and thus middle to dependent PL where collapse is prevailed) can be estimated with
absolute ‘measured’ Pes.

can be calculated as intravascular pressure minus a huge potential to improve clinical outcome in
Pes. Thus, the use of Pes can potentially help to detect patients with ARDS as an early detector of the risk
the risk of pulmonary edema while patients preserve of lung injury from mechanical ventilation and
spontaneous effort. spontaneous effort.

Patient-ventilator asynchrony Acknowledgements

Asynchrony can potentially worsen lung injury. None.
‘Double triggering’ is the occurrence of two conse-
cutive inspirations following a single respiratory Financial support and sponsorship
effort [33], and is injurious because the delivered None.
tidal volume (VT) is now double. Double triggering is
more frequent in patients with higher respiratory Conflicts of interest
drive [34]. Reverse triggering can occur in heavily T.Y. declares no conflicts of interest. L.B.’s laboratory
sedated patients where the diaphragm is ‘triggered’ has received research grants or equipment from Covidien
by ventilator-driven inspiration [35]. This can (PAV), Maquet (NAVA), General Electric (recruitment;
increase PL and/or VT. The adverse impact of ultrasound), Philips (sleep), Air Liquide (Helium; CPR),
patients-ventilator asynchrony is increasingly rec- Fisher Paykel (high-flow).
ognized, and data from 50 ventilated patients sug-
gests an association between increased incidence of
asynchrony and higher mortality [36]. The conven- REFERENCES AND RECOMMENDED
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& of special interest
asynchrony. Thus, the careful monitoring of && of outstanding interest

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