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Critical Care Research Letters
Paradoxical Effect of Chest
Wall Compression on
Respiratory System
A Multicenter Case Series of Patients
With ARDS, With Multimodal
Different modalities were used to detect the effect of chest wall
compression on changes in: (1) partitioned respiratory mechanics
Case 1
During patient positioning of a 63-year-old woman
(BMI, 28 kg/m2) with severe ARDS on veno-venous
extracorporeal membrane oxygenation (San Gerardo
Hospital) from semi-recumbent to horizontal, we
observed a “paradoxical” (at least toward common
expectations) decrease of the driving pressure of the
respiratory system (DP,rs) leading to a higher Cpl,rs.
Three positions were formally tested: (1) supine (0 ); (2)
Trendelenburg (–30 ); and (3) reverse Trendelenburg
(30 ).
Increased abdominal compression on the lungs in the
Trendelenburg position decreased plateau pressure and
led to higher Cpl,rs, with a decreased stress index (Fig 1,
panel 1). The EIT analysis suggested decreased lung
overdistension in the nondependent areas in the
Trendelenburg position and greater overdistension in
the reverse Trendelenburg position (Fig 1, panel 2).
Changes in respiratory mechanics observed during
postural changes are described in the Video 1, part 1.
Case 2
Chest compression with a 5-kg weight is sometimes used
in patients with ARDS to assess respiratory mechanics
despite lack of evidence on its benefit.4
To the Editor:
The lungs of patients with ARDS are characterized by
marked heterogeneity, resulting in the coexistence of
collapsed and hyperinflated tissue.1 Gravitational forces
and chest wall geometry help govern the balance
between these components.2
In this research letter, we present four cases in which chest
wall compression caused an apparently “paradoxical”
increase in the compliance of the respiratory system
(Cpl,rs), likely explained by reduction of overdistension.
using static respiratory maneuvers and an esophageal balloon; (2)
distribution of the tidal ventilation and end-expiratory lung volume
(EELV) by electrical impedance tomography (EIT)3; and (3) lung
aeration by lung CT analysis.
We report the effect of a 5-kg bag applied on the chest of
a 69-year-old man (BMI, 22.5 kg/m2) admitted to the
Neuro-ICU (Niguarda Hospital) with legionellosis
causing severe ARDS. We hypothesized that a
continuous external weight on the chest might change
the mechanical properties of the respiratory system,
reducing overdistension of the nondependent lung areas
and, in contrast, recruiting the dependent lung areas. We
explored this mechanism by EIT.5
We tested three steps, each lasting 10 min: step A,
baseline; step B, 5-kg bag continuous compression; and
step C, no compression. Compared with baseline, chest
weight application led to a sudden improvement of
Cpl,rs by reduced DP,rs and reduced end-expiratory
lung impedance (EELI), a surrogate of EELV (Fig 2,
panel 1). The EELI reduction was localized mainly in the
ventral regions (Fig 2, panel 2, solid lines). At the same
time, we observed a change in regional tidal volume
(TV) distribution from dorsal to ventral lungs,
suggesting an increased regional Cpl,rs in nondependent
areas (Fig 2, panel 2, dashed lines).
In the nondependent lung, we observed an apparently
paradoxical behavior: an increased Cpl,rs with a
reduction of EELV, which we might interpret as a
reduction of regional hyperinflation. In the dependent
lung, we observed a decrease in both EELI and regional
Paw = 22.8 cmH2O
Paw = 26.7 cmH2O
Paw = 24.8 cmH2O
Stress index < 1
Stress index = 1
Stress index > 1
CW [%]
CL [%]
Tidal Volume =
Tidal Volume =
Tidal Volume =
Driving Pressure = 12.8
Driving Pressure = 16.7
Driving Pressure = 14.8
Figure 1 – Case 1. Body positional changes. We positioned the patient as follows: (1) Trendelenburg position (–30 ), left side; (2) supine (0 ), center;
and (3) reverse Trendelenburg position (30 ), right side. The ventilator was set as follows: volume-controlled mode with a tidal volume of 180 mL,
respiratory rate of 10 breaths/min, FIO2 of 0.65, PEEP of 10 cm H2O, and a Pplat of 25 cm H2O. In the supine position, Pplat was 24.8 cm H2O,
leading to a driving pressure of 14.8 cm H2O. The tidal volume was 178 mL, leading to a compliance of the respiratory system (Cpl,rs) of 12 mL/cm
H2O. In the Trendelenburg position, driving pressure decreased to 12.8 cm H2O, leading to a Cpl,rs of 14.1 mL/cm H2O. Finally, in a reverse
Trendelenburg position, driving pressure increased to 16.7 cm H2O (Cpl,rs ¼ 10.7 mL/cm H2O). Interestingly, the stress index of the airway pressure
changed from < 1 to 1 to > 1, moving from the Trendelenburg to 0 to the reverse Trendelenburg position, respectively (panel 1). At electrical
impedance tomography evaluation, we observed, compared with the reference (supine positioning [0 ]), a significant improvement of Cpl,rs (CW) in
the Trendelenburg position (–30 ), accounting for 21% of decrease of overdistension, with a minimal decrease of Cpl,rs (CL), which suggested 6% of
lung de-recruitment. In contrast, in the reverse Trendelenburg position (30 ), we reported a low CW with 7% of lung recruitment, in the presence of
a significant CL, which suggested 12% of lung overdistension (panel 2). The change in the mechanical properties of the respiratory system from
horizontal to the Trendelenburg position may be suggested by a right-shifting of the pressure-volume curve of the chest wall and, consequently, of the
entire respiratory system. Although the global end-expiratory lung volume decreases (from a to a0 , center to the left side), tidal ventilation occurs in a
steeper (ie, more compliant) part of the pressure-volume curve, leading to a decreased driving pressure, for the same tidal volume. The opposite
happens in the reverse Trendelenburg position, right side (panel 3). CL ¼ compliance “loss”; CW ¼ compliance “win”; Paw ¼ airway pressure;
PEEP ¼ positive end-expiratory pressure; Pplat ¼ plateau pressure.
TV, suggesting a loss of Cpl,rs likely caused by a certain
degree of de-recruitment. Time seems to be a meaningful
factor, as the global EELI trend during Step B shows a
progressive reduction over time (Fig 2, panel 1).
In summary, this case suggests that external chest
compression might improve the Cpl,rs by reducing
EELV. Although this seems to lead to reduced alveolar
overdistension in the nondependent areas, it might also
favor dorsal de-recruitment.
Case 3
A 64-year-old man (21.5 kg/m2), with a medical history
of Hodgkin’s lymphoma and bilateral pneumonia caused
by Pneumocystis jirovecii, was admitted to the general
1336 Research Letters
ICU (Ospedale Maggiore Policlinico) for ARDS. To
reduce tidal overdistension, 3 cm H2O of positive endexpiratory pressure (PEEP) and 6 mL/kg predicted body
weight TV were used. However, ventilation was not
protective (DP,rs ¼ 25 cm H2O). A weight was therefore
placed on the patient’s chest, with an immediate
improvement in respiratory mechanics (Fig 2). A chest
CT scan was acquired at end-inspiration and endexpiration, both with and without the weight on the
chest, to optimize ventilator settings. Figure 2 (panel 3)
shows a representative slice with color-mapped
qualitative density analysis.6 Application of the weight
reduced EELV, with an end-expiratory reduction and
increase of hyperinflated and poorly aerated lung tissue,
160#4 CHEST OCTOBER 2021
Without Weight
Lung density
Delta Regional TV (mL)
Delta End-Expiratory Lung Impedance
With Weight
Nondependent Delta impedance
Dependent Delta impedance
Nondependent Delta TV
Dependent Delta TV
Figure 2 – Chest compression. Case 2. Lung mechanics and electrical impedance tomography behavior during baseline (step A), chest compression (step
B), and following removal of the chest weight (step C). Ventilatory settings were as follows: volume-controlled mode, tidal volume of 400 mL, respiratory
rate of 25 breaths/min, and positive end-expiratory pressure of 8 cm H2O with an FIO2 of 0.50. The chest compression led to a global end-expiratory
lung impedance (EELI) decrease (step B, panel 1) compared with baseline (step A, panel 1); once the compression is discontinued, the EELI increased
without returning to baseline values (step C, panel 1). We observed two effects on the regional ventilation: in the dependent lung (dorsal), the chest
compression decreased both EELI and regional ventilation (step B, panel 2, solid and dashed black lines); in the nondependent lung (ventral), the
compression led to a decrease in EELI (to a greater extent compared with dorsal) and an increase in tidal volume (step B, panel 2, solid and dashed red
lines). We also analyzed these regional effects at the beginning and at the end of step B (step B, panel 1, dashed yellow lines, and panel 2); no difference
was observed in the dependent lung, whereas a further reduction in EELI was observed in the nondependent lung region. These effects in regional
ventilation and EELI disappeared once the chest weight was removed, without a return to baseline values (step C, panel 2). Compliance of the respiratory system was increased during chest compression (from 30 to 36 mL/cm H2O), and driving pressure of the respiratory system was reduced from
13 to 11 cm H2O. These effects immediately reverted following removal of the chest weight. We observed a reduction of the following parameters from
baseline to step B: blood oxygen saturation, 98% to 96%; PaO2, 81 to 70 mm Hg; end tidal CO2, 41 to 38 mm Hg; PaCO2, 56 to 50 mm Hg; and alveolar
dead space, 26% to 24%. After removal of the chest weight, blood oxygen saturation and end tidal CO2 were 96% and 40 mm Hg, respectively. Case 3.
Color-mapped CT scan. Representative CT slices of the lung obtained without (left) and with (right) application of a chest weight. Images were acquired
during an end-expiratory (boxes A and B) or end-inspiratory (boxes C and D) hold. The images are visualized by using a color map; color maps
represent different ranges of HU, which are reported on the right side of the graphic. Of note, images acquired with a lung weight have lower quality
because they were acquired using a low-dose radiation protocol. This, however, does not significantly affect the quantitative results. Following are the
respiratory mechanics and lung CT data at baseline and following the application of a chest weight during an end-expiratory hold with a positive endexpiratory pressure of 3 cm H2O: plateau pressure, 28 to 23 cm H2O; driving pressure of the respiratory system, 25 to 20 cm H2O; compliance of the
respiratory system, 15 to 19 mL/cm H2O; compliance of the lung, 19 to 24 mL/cm H2O; compliance of the chest wall, 80 to 93 mL/cm H2O; endexpiratory lung volume, 614 to 469 mL; mean CT number, –270 to –220 HU; lung weight, 1,661 to 1,659 g; hyperinflated lung tissue, 0 to 0%; normally
aerated lung tissue, 13% to 10%; poorly aerated lung tissue, 27% to 29%; and nonaerated lung tissue, 60% to 61%. HU ¼ Hounsfield units; TV ¼ tidal
Case 4
A 62-year-old man (BMI, 28 kg/m2) with severe
COVID-19 ARDS was in the ICU (Milan Fair)7 on
volume-controlled ventilation with the following
settings: TV, 400 mL; respiratory rate, 35 beats/min;
PEEP, 8 cm H2O; FIO2, 0.9; and peak inspiratory
pressure (PIP), 42 cm H2O. The patient experienced
decreased PIP when the head of the bed was lowered
to 0 for nursing. To test whether this observation
was related to an increased transmission of the
abdominal pressure to the chest wall, we performed a
transient abdominal compression in semi-recumbent
position (~15 s). A sudden decrease of PIP to 26 cm
H2O was observed. After releasing the abdominal
compression, PIP immediately increased to 38 cm
H2O. Blood oxygen saturation and hemodynamics
were unaffected by the transient change in PIP (Video
1, part 2).
To further investigate this mechanism, we performed a
formal test applying a 5-kg saline bag to the abdomen
for 10 min while recording airway and esophageal
pressures during end-inspiratory and end-expiratory
holds. The following was noted after application of the
abdominal weight: DP,rs decreased (28 to 17 cm
H2O); driving pressure of the chest wall increased (1
to 3 cm H2O); and driving pressure of the lung
decreased by 13 cm H2O. Consequently, compliance of
the lung doubled (15 to 29 mL/cm H2O), whereas
compliance of the chest wall worsened (400 to
133 mL/cm H2O).
During this test, PaO2/FIO2 and PaCO2 remained
unchanged. This finding suggests that the improvement
of the lung mechanical properties is unlikely determined
by lung recruitment, and more likely the consequence of
a decreased lung resting volume preventing endinspiratory overdistention.
The presented cases show that, in some patients with
ARDS, compression on the chest wall decreases the
amount of hyperinflation, improving respiratory
mechanics without causing alveolar recruitment. Our
explanation resides in a right shift of the chest wall
pressure-volume loop, which decreases lung volume,
causing ventilation to occur in a more compliant region
of the lung pressure-volume loop (Fig 1, panel 3). The
measurement of partitioned respiratory mechanics
suggests that an extrinsic weight does not worsen the
compliance of the chest wall in a clinically relevant way.
However, it reduces chest wall and lung volume,
similarly to what is observed in obese patients.8 This
might be an additional explanation for the protective
effects determined by prone position9 and for the obesity
paradox.10 Chest wall compression does not seem to
favor alveolar recruitment, which is also unlikely given
the decreased airway pressure during weight placement.
Our work suggests that an increase of respiratory system
compliance during chest or abdominal compression
should be regarded as a sign of tidal overinflation and
should be taken into account to optimize mechanical
ventilation. It remains unknown if improvement of lung
mechanics due to patient positioning or chest wall
compression has an impact on gas exchange and,
ultimately, on patient outcome.
Emanuele Rezoagli, MD, PhD
Luca Bastia, MD
Alice Grassi, MD
Arturo Chieregato, MD
Thomas Langer, MD
Giacomo Grasselli, MD
Pietro Caironi, MD
Andrea Pradella, MD
Alessandro Santini, MD
1338 Research Letters
Alessandro Protti, MD
Roberto Fumagalli, MD
Giuseppe Foti, MD
Giacomo Bellani, MD, PhD
AFFILIATIONS: From the Department of Medicine and Surgery (E.
Rezoagli, A. Grassi, T. Langer, R. Fumagalli, G. Foti, and G. Bellani),
University of Milan-Bicocca, Monza, Italy; ASST Monza (E. Rezoagli,
G. Foti, and G. Bellani), San Gerardo Hospital, Monza, Italy;
Neurointensive Care Unit (L. Bastia and A. Chieregato), ASST
Grande Ospedale Metropolitano Niguarda, Milan, Italy; Department
of Anesthesiology and Pain Medicine (A. Grassi), University of
Toronto, Toronto, ON, Canada; Department of Anaesthesia and
Intensive Care Medicine (T. Langer and R. Fumagalli), Niguarda Ca’
Granda, Milan, Italy; Department of Anesthesia, Critical Care and
Emergency (G. Grasselli) and Surgery and Liver Transplant Center
(G. Grasselli), Fondazione IRCCS Ca’ Granda-Ospedale Maggiore
Policlinico, Milan, Italy; Department of Anesthesia and Critical Care
(P. Caironi), Azienda Ospedaliero-Universitara S. Luigi Gonzaga,
Orbassano, Italy; Department of Oncology (P. Caironi), University of
Turin, Turin, Italy; IRCCS Humanitas Research Hospital (A.
Pradella, A. Santini, and A. Protti), Rozzano-Milan, Italy; and the
Department of Biomedical Sciences (A. Protti), Humanitas
University, Pieve Emanuele-Milan, Italy.
Drs Rezoagli and Bastia contributed equally to the manuscript.
FUNDING/SUPPORT: The authors have reported to CHEST that no
funding was received for this study.
reported to CHEST the following: G. B. and G. F. received fees from
Draeger Medical for lectures also on EIT. None declared (E. R., L. B.,
A. G., A. C., T. L., G. G., P. C., A. P., A. S., A. P., R. F.).
CORRESPONDENCE TO: Giacomo Bellani, MD, PhD; email: giacomo.
bellani1@unimib.it, emanuele.rezoagli@unimib.it
Copyright Ó 2021 American College of Chest Physicians. Published
by Elsevier Inc. All rights reserved.
DOI: https://doi.org/10.1016/j.chest.2021.05.057
Other contributions: The authors are highly grateful to Laurent
Brochard, MD, for helpful discussions and his constructive feedback in
regard to this work. The authors are indebted to Dario Manzolini, MD,
and Manuela Marotta, MD, Department of Medicine and Surgery of
the University of Milano-Bicocca, Monza, Italy, for their valuable
support with the making of the Video about case 1; to Serena Brusatori,
MD, Department of Pathophysiology and Transplantation of the
University of Milan, for her valuable support with qualitative colormapped analysis of Figure 2, panel 3; and to Manuela Chiodi, MD,
Department of Pathophysiology and Transplantation of the University
of Milan, for her valuable support with quantitative CT analysis of
Figure 2, panel 3.
Additional information: The Video can be found in the Supplemental
Materials section of the online article.
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