key: cord-0777107-epwocrte
authors: Mauri, Tommaso; Spinelli, Elena; Caccioppola, Alessio; Marongiu, Ines; Colombo, Sebastiano M.; Abbruzzese, Chiara; Lissoni, Alfredo; Tagliabue, Paola; Grasselli, Giacomo; Pesenti, Antonio
title: Interdependence between elevated intrabdominal, pleural and airway opening pressure in severe ARDS with ECMO
date: 2020-07-02
journal: Br J Anaesth
DOI: 10.1016/j.bja.2020.06.044
sha: ae5e749ef2015b32147dd82bbb262c4bbbfd7c1b
doc_id: 777107
cord_uid: epwocrte

nan

with relevant physiological and clinical consequences (1). AOP is the threshold level for start of alveolar inflation, and when it is higher than externally set positive end-expiratory pressure (PEEP), undetected AOP can lead to overestimation of driving pressure (2) and to underestimation of the potential for lung recruitment (3) . Several mechanisms contribute to the development of elevated AOP during ARDS, such as impaired surfactant (4, 5) . The recent Coronavirus Disease 19 (COVID-19) pandemic led to a dramatic surge in intubated ARDS patients admitted to intensive care (6) . The number of patients, the stress on healthcare workers and the need for careful isolation limited the ability to perform extensive clinical and physiological testing in these patients (7) . We present here unique physiological measures on the interdependence between AOP, pleural pressure (Ppl, estimated from oesophageal pressure) and intrabdominal pressure (IAP) obtained by 2 standard bedside monitoring, in a patient affected by COVID-19 ARDS fully supported by extracorporeal membrane oxygenation (ECMO). The institutional ethics board of Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, approved this study. The data used and/or analysed are available from the corresponding author on reasonable request. infection itself (8, 9) . The patient was ventilated on pressure-controlled mode and as Vt became minimal (0.7 ml kg -1 PBW, Supplementary Material Table S1 ). A switch to volume controlled mode with long inspiratory time (12 s), low RR (4 bpm), Vt >300 ml allowed us to perform a low-flow pressure-volume (P-V) curve between 5 and 45 cm H 2 O and to detect the AOP at the bedside (Figure 1, left) . We also manually collected the P-V Airway closure in ARDS might result from elevated pleural pressure with reduced lung size causing compression of distal airways (4) or depletion of surfactant with high surface tension causing airway collapse (5) . Moreover, pleural pressure can be increased by external (e.g., abdominal pressure) or intrinsic (e.g., increased lung weight) forces (8) .

Perfect correspondence between IAP, Ppl and AOP has not been reported previously and generates the hypothesis that the presence of extremely elevated IAP applied to a closed system (rigid abdominal and chest wall and collapsed non-ventilated lung) can become the only external force determining elevated pleural pressure and AOP. The persistence of elevated AOP even after the decrease of IAP may suggest that other mechanisms related to intrinsic compressive forces and surfactant dysfunction became predominant. Even though previous studies have not reported correspondence between AOP and pleural pressure (1), the almost complete lung collapse due to profound hypoventilation leading to a virtually closed intrathoracic system may explain the pressure equalization that we observed. From a clinical point of view, the measurement of AOP may be useful to personalize PEEP and/or to perform further diagnostic investigations targeted at intestinal function.

The physiological measures in this COVID-19 ARDS patient supported with ECMO suggest a new mechanism for elevated AOP: extremely elevated IAP is transmitted to the pleural space and, in presence of complete lung collapse becomes the threshold value for airway opening. 

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time waveforms from the ventilator. The cursor indicates the airway opening pressure (AOP) at 30 cm H 2 O. On the right, the P-V curve obtained by manual plotting of values obtained from the ventilator (see text for details). The dashed line shows the steep