# Transpulmonary pressure in SARS-CoV-2-associated acute respiratory distress syndrome: a single-center observational study

Séverin Ramin, Jonathan Charbit, Geoffrey Dagod, Mehdi Girard, Samir Jaber, Xavier Capdevila

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Séverin Ramin, Jonathan Charbit, Geoffrey Dagod, Mehdi Girard, Samir Jaber, et al. Transpulmonary pressure in SARS-CoV-2-associated acute respiratory distress syndrome: a single-center observational study. Critical Care, 2020, 24 (1), pp.408. 10.1186/s13054-020-03129-5. hal-02897053

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# Transpulmonary pressure in SARS-CoV-2-associated acute respiratory distress syndrome: a single-center observational study

Severin Ramin<sup>1,2* ID</sup>, Jonathan Charbit<sup>1,2</sup>, Geoffrey Dagod<sup>1,2</sup>, Mehdi Girard<sup>1,2</sup>, Samir Jaber<sup>3,4</sup> and Xavier Capdevila<sup>1,2</sup>

Dear Editor,

Gattinoni et al. [1] have recently described that the ARDS related to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was not a “typical” ARDS. Patients indeed presented a significant hypoxemia, which was surprisingly associated with a high compliance of the respiratory system. The cornerstone of current treatment is the use of “lung protective” ventilation strategy with especially maintaining sufficiently high positive end-expiratory pressures (PEEP). However, high levels of PEEP may lead to lung overdistension associated with an increase of alveolar dead space and an alteration of gas exchanges. The airway pressures commonly monitored on respirators do not reliably reflect the impact of pressures on the lung parenchyma. In contrast, transpulmonary pressures allow to highlight directly lung overdistension risk and lung properties. In order to better know this new kind of ARDS, transpulmonary pressures’ assessment seems to be essential [2].

We wish to report the preliminary findings of a
prospective monocentric physiological work, which is
approved by the institutional ethics review board of the
Montpellier University Hospital, France (IRB ID:
202000432). All consecutive ARDS adult patients with
confirmed Covid-19 admitted in our critical care unit are
included if they received invasive mechanical. Manage-
ment of patients followed international recommendations.

PEEP was set according to the low PEEP arm of the PEEP/F₁O₂ table used in previous trials. Esophageal pressures were recorded with Cooper Surgical® device.

Sixteen patients were assessed (body mass index 29 [range 26–31] kg/m<fnref n="2" />, age 70 years [range 61–72 years]). The median worst value of PaO₂/FiO₂ ratio was 144 mmHg [range 138–149 mmHg]. Baseline of patient characteristics may be observed in the Table 1. Six patients received at least one session of prone positioning. One of them also benefited from VV-ECMO. We observed that median transpulmonary end-expiratory pressure was positive during mechanical ventilation (2 cm H₂O at D1 [range –1–3 cm H₂O]) and median transpulmonary elastance (E_L) remained low at day 1 (19 cm H₂O/L [range 8–20 cm H₂O/L]) and during the first week. All our findings are shown in Fig. 1.

Many reports have highlighted specificities of SARS-
CoV-2, particularly that the elastance of respiratory
system (ERS) was slightly altered. Driving pressures of
the respiratory system are therefore quite low in these
patients. Unsurprisingly, our study showed that the EL
was not elevated in the first days of mechanical ventila-
tion. The main finding of the present work is that end-
expiratory transpulmonary pressure remained positive in
most patients with the use of moderate PEEP (8–13
cm H2O). To summarize, our analysis is in agreement
with the descriptions of Gattinoni et al. [3]. Most of
these patients present indeed low ERS, low ventilation to
perfusion ratio (VA/Q), and low lung recruitability due
to the low amount of non-aerated tissue (L profile). Hy-
poxemia and intrapulmonary shunt might thus be better
explained by dysregulation of pulmonary perfusion and
by alteration of hypoxic vasoconstriction. This would

<footnote>* Correspondence: severin.ramin@gmail.com</footnote>

<footnote n="1">¹Anesthesiology and Intensive Care, Anesthesia and Critical Care Department
A, Lapeyronie Teaching Hospital, Montpellier Cedex 5, France</footnote>

<footnote n="2">²Département d'Anesthésie Réanimation Lapeyronie, Hôpital Lapeyronie, 371 Avenue du Doyen G. Giraud, 34090 Montpellier, France</footnote>

<footnote>Full list of author information is available at the end of the article</footnote>
<table><caption>**Table 1** Baseline characteristics of the patients and respiratory mechanics (n = 16)</caption><thead><tr><th colspan="2">Characteristics</th></tr></thead><tbody><tr><td>Male, n (%)</td><td>11 (69)</td></tr><tr><td>Age (years)</td><td>70 (61-72)</td></tr><tr><td>Body mass index (kg/m<sup>2</sup>)</td><td>29 (26-31)</td></tr><tr><td>Organ failure at baseline (SOFA), n (%)</td><td></td></tr><tr><td>Hemodynamic</td><td>12 (75)</td></tr><tr><td>Renal</td><td>4 (25)</td></tr><tr><td>Hepatic</td><td>2 (13)</td></tr><tr><td>Hematological</td><td>1 (6)</td></tr><tr><td>Arterial blood gas</td><td></td></tr><tr><td>PaO2/FiO2 ratio</td><td>170 (150-208)</td></tr><tr><td>pH</td><td>7.43 (7.38-7.47)</td></tr><tr><td>PaO2 (mmHg)</td><td>71 (62-89)</td></tr><tr><td>PaCO2 (mmHg)</td><td>40 (37-45)</td></tr><tr><td>Lactates (mmol/l)</td><td>1.2 (1-1.4)</td></tr><tr><td>Radiologic characteristics, n (%)</td><td></td></tr><tr><td>Bilateral pneumonia</td><td>4 (25)</td></tr><tr><td>Multiple mottling and ground-glass opacity</td><td>12 (75)</td></tr><tr><td>Time between admission and intubation (day)</td><td>2 (2-3)</td></tr><tr><td colspan="2">Respiratory mechanics at day 1</td></tr><tr><td>Tidal volume (ml/kg PBW)</td><td>7 (6.6-7.3)</td></tr><tr><td>Respiratory rate (beats/min)</td><td>22 (20-24)</td></tr><tr><td>PEEPtot,rs (cm H<sub>2</sub>O)</td><td>10 (10-13)</td></tr><tr><td>PEEPtot,es (cm H<sub>2</sub>O)</td><td>8 (8-12)</td></tr><tr><td>PEEPtot,L (cm H<sub>2</sub>O)</td><td>2 (-1-3)</td></tr><tr><td>Pplat,rs (cm H<sub>2</sub>O)</td><td>19 (18-22)</td></tr><tr><td>Pplat,es (cm H<sub>2</sub>O)</td><td>13 (11-16)</td></tr><tr><td>Pplat,L (cm H<sub>2</sub>O)</td><td>6 (6-11)</td></tr><tr><td>DP,rs (cm H<sub>2</sub>O)</td><td>9 (6-12)</td></tr><tr><td>DP,cw (cm H<sub>2</sub>O)</td><td>5 (3-5)</td></tr><tr><td>DP,L (cm H<sub>2</sub>O)</td><td>4 (2-9)</td></tr><tr><td>Est,rs (cm H<sub>2</sub>O/L)</td><td>23 (18-30)</td></tr><tr><td>Est,cw (cm H<sub>2</sub>O/L)</td><td>4 (4-10)</td></tr><tr><td>Est,L (cm H<sub>2</sub>O/L)</td><td>19 (8-20)</td></tr></tbody></table>

Results are expressed as median (IQR) or as number of patients (percentage) as appropriate

PBW, predicted body weight; SOFA, sepsis-related organ failure; PEEPtot,rs, static end-expiratory pressure of the respiratory system; PEEPtot,es, static end-expiratory esophageal pressure; PEEPtot,L, static end-expiratory

transpulmonary pressure; Pplat,rs, static end-inspiratory pressure of the respiratory system; Pplat,es, static end-inspiratory esophageal pressure; Pplat,L, static end-inspiratory transpulmonary pressure; DP,rs, DP,cw, DP,L, driving pressure of respiratory system, chest wall, and lung, respectively; Est,rs, Est,cw, Est,L, static elastance of respiratory system, chest wall, and lung, respectively
<figure><img src="image_3.png" /></figure>

<figure><img src="image_4.png" /></figure>

<figure><img src="image_5.png" /><figcaption>**Fig. 1** (See legend on next page.)</figcaption></figure>
(See figure on previous page.)

**Fig. 1** Respiratory physiological measures during mechanical ventilation. Boxes represent median and interquartile range. The number of patients with available respiratory physiological data decreases over successive study days due to deaths and discontinuation of invasive mechanical ventilation. Transpulmonary pressure (PL) equals respiratory system pressure minus esophageal pressure. Respiratory system driving pressure equals plateau pressure minus positive end expiratory pressure (PEEP). Transpulmonary driving pressure equals end-inspiratory PL minus end-expiratory PL

justify the use of moderate levels of PEEP to limit alveolar dead space and optimize the CO₂ removal. Gattinoni et al. [4] also described that 20–30% of patients presented a delayed aggravation with more usual pulmonary parameters: high E<sub>RS</sub>, high right-to-left shunt, high lung recruitability (H profile). Constitution of atelectasis or bacterial overinfection is associated with H profile. This is observable in our series since a part of patients experienced an increase of E<sub>RS</sub> as E<sub>L</sub> (Fig. 1c). For the latter, elevated PEEP seems to be more legitimate [5]. To conclude, identification of respiratory phenotype seems therefore essential in ventilated SARS-CoV-2 patients to determine optimal mechanical ventilation strategy. Our observations support the concept of using low PEEP in a large part of SARS-CoV-2 patients.

**Acknowledgements**

No acknowledgements.

**Authors' contributions**

SR, JC, and XC conceived of the study. SR, JC, and SJ analyzed the data. SR, JC, SJ, and XC drafted the manuscript. All authors interpreted the data, revised the manuscript, and approved the final version.

**Funding**

No finding received.

**Availability of data and materials**

Not applicable.

**Ethics approval and consent to participate**

Institutional ethics review board of the Montpellier University Hospital, France (IRB ID: 202000432).

**Consent for publication**

Obtained.

**Competing interests**

No competing interests.

**Author details**

¹Anesthesiology and Intensive Care, Anesthesia and Critical Care Department A, Lapeyronie Teaching Hospital, Montpellier Cedex 5, France. ²Département d'Anesthésie Réanimation Lapeyronie, Hôpital Lapeyronie, 371 Avenue du Doyen G. Giraud, 34090 Montpellier, France. ³Anesthesiology and Intensive Care, Anesthesia and Critical Care Department B, Saint Eloi Teaching Hospital, PhyMedExp, University of Montpellier, INSERM U1046, CNRS, UMR 9214, 80 Avenue Augustin Fliche, 34295 Montpellier Cedex 5, France. ⁴Département d'Anesthésie Réanimation Saint-Eloi, Hôpital Saint-Eloi, 80 Avenue Augustin Fliche, 34090 Montpellier, France.

Received: 27 May 2020 Accepted: 1 July 2020

Published online: 09 July 2020

**References**

1. Gattinoni L, Coppola S, Cressoni M, Busana M, Chiumello D. Covid-19 does not lead to a "typical" acute respiratory distress syndrome. Am J Respir Crit Care Med. 2020;201(10):1299-300.

2. Gattinoni L, Giosa L, Bonifazi M, Pasticci I, Busana M, Macri M, et al. Targeting transpulmonary pressure to prevent ventilator-induced lung injury. Expert Rev Respir Med. 2019;13(8):737-46.

3. Gattinoni L, Chiumello D, Caironi P, Busana M, Romitti F, Brazzi L, et al. COVID-19 pneumonia: different respiratory treatments for different phenotypes? Intensive Care Med. 2020;46(6):1099-102.

4. Gattinoni L, Chiumello D, Rossi S. COVID-19 pneumonia: ARDS or not? Crit Care Lond Engl. 2020;24(1):154.

5. Marini JJ, Gattinoni L. Management of COVID-19 respiratory distress. JAMA. 2020;323(22):2329-30.

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