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Positive End-expiratory Pressure and Mechanical Power

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Positive End-expiratory Pressure and Mechanical Power. / Collino, Francesca; Rapetti, Francesca; Vasques, Francesco; Maiolo, Giorgia; Tonetti, Tommaso; Romitti, Federica; Niewenhuys, Julia; Behnemann, Tim; Camporota, Luigi; Hahn, Günter; Reupke, Verena; Holke, Karin; Herrmann, Peter; Duscio, Eleonora; Cipulli, Francesco; Moerer, Onnen; Marini, John J.; Quintel, Michael; Gattinoni, Luciano.

In: Anesthesiology, Vol. 130, No. 1, 01.01.2019, p. 119-130.

Research output: Contribution to journalArticle

Harvard

Collino, F, Rapetti, F, Vasques, F, Maiolo, G, Tonetti, T, Romitti, F, Niewenhuys, J, Behnemann, T, Camporota, L, Hahn, G, Reupke, V, Holke, K, Herrmann, P, Duscio, E, Cipulli, F, Moerer, O, Marini, JJ, Quintel, M & Gattinoni, L 2019, 'Positive End-expiratory Pressure and Mechanical Power', Anesthesiology, vol. 130, no. 1, pp. 119-130. https://doi.org/10.1097/ALN.0000000000002458

APA

Collino, F., Rapetti, F., Vasques, F., Maiolo, G., Tonetti, T., Romitti, F., Niewenhuys, J., Behnemann, T., Camporota, L., Hahn, G., Reupke, V., Holke, K., Herrmann, P., Duscio, E., Cipulli, F., Moerer, O., Marini, J. J., Quintel, M., & Gattinoni, L. (2019). Positive End-expiratory Pressure and Mechanical Power. Anesthesiology, 130(1), 119-130. https://doi.org/10.1097/ALN.0000000000002458

Vancouver

Collino F, Rapetti F, Vasques F, Maiolo G, Tonetti T, Romitti F et al. Positive End-expiratory Pressure and Mechanical Power. Anesthesiology. 2019 Jan 1;130(1):119-130. https://doi.org/10.1097/ALN.0000000000002458

Author

Collino, Francesca ; Rapetti, Francesca ; Vasques, Francesco ; Maiolo, Giorgia ; Tonetti, Tommaso ; Romitti, Federica ; Niewenhuys, Julia ; Behnemann, Tim ; Camporota, Luigi ; Hahn, Günter ; Reupke, Verena ; Holke, Karin ; Herrmann, Peter ; Duscio, Eleonora ; Cipulli, Francesco ; Moerer, Onnen ; Marini, John J. ; Quintel, Michael ; Gattinoni, Luciano. / Positive End-expiratory Pressure and Mechanical Power. In: Anesthesiology. 2019 ; Vol. 130, No. 1. pp. 119-130.

Bibtex Download

@article{1b3f42ede69c4d6a8a04b597f09a9a7c,
title = "Positive End-expiratory Pressure and Mechanical Power",
abstract = "WHAT WE ALREADY KNOW ABOUT THIS TOPIC: WHAT THIS ARTICLE TELLS US THAT IS NEW: BACKGROUND:: Positive end-expiratory pressure is usually considered protective against ventilation-induced lung injury by reducing atelectrauma and improving lung homogeneity. However, positive end-expiratory pressure, together with tidal volume, gas flow, and respiratory rate, contributes to the mechanical power required to ventilate the lung. This study aimed at investigating the effects of increasing mechanical power by selectively modifying its positive end-expiratory pressure component. METHODS: Thirty-six healthy piglets (23.3 ± 2.3 kg) were ventilated prone for 50 h at 30 breaths/min and with a tidal volume equal to functional residual capacity. Positive end-expiratory pressure levels (0, 4, 7, 11, 14, and 18 cm H2O) were applied to six groups of six animals. Respiratory, gas exchange, and hemodynamic variables were recorded every 6 h. Lung weight and wet-to-dry ratio were measured, and histologic samples were collected. RESULTS: Lung mechanical power was similar at 0 (8.8 ± 3.8 J/min), 4 (8.9 ± 4.4 J/min), and 7 (9.6 ± 4.3 J/min) cm H2O positive end-expiratory pressure, and it linearly increased thereafter from 15.5 ± 3.6 J/min (positive end-expiratory pressure, 11 cm H2O) to 18.7 ± 6 J/min (positive end-expiratory pressure, 14 cm H2O) and 22 ± 6.1 J/min (positive end-expiratory pressure, 18 cm H2O). Lung elastances, vascular congestion, atelectasis, inflammation, and septal rupture decreased from zero end-expiratory pressure to 4 to 7 cm H2O (P < 0.0001) and increased progressively at higher positive end-expiratory pressure. At these higher positive end-expiratory pressure levels, striking hemodynamic impairment and death manifested (mortality 0% at positive end-expiratory pressure 0 to 11 cm H2O, 33% at 14 cm H2O, and 50% at 18 cm H2O positive end-expiratory pressure). From zero end-expiratory pressure to 18 cm H2O, mean pulmonary arterial pressure (from 19.7 ± 5.3 to 32.2 ± 9.2 mmHg), fluid administration (from 537 ± 403 to 2043 ± 930 ml), and noradrenaline infusion (0.04 ± 0.09 to 0.34 ± 0.31 μg · kg · min) progressively increased (P < 0.0001). Lung weight and lung wet-to-dry ratios were not significantly different across the groups. The lung mechanical power level that best discriminated between more versus less severe damage was 13 ± 1 J/min. CONCLUSIONS: Less than 7 cm H2O positive end-expiratory pressure reduced atelectrauma encountered at zero end-expiratory pressure. Above a defined power threshold, sustained positive end-expiratory pressure contributed to potentially lethal lung damage and hemodynamic impairment.",
author = "Francesca Collino and Francesca Rapetti and Francesco Vasques and Giorgia Maiolo and Tommaso Tonetti and Federica Romitti and Julia Niewenhuys and Tim Behnemann and Luigi Camporota and G{\"u}nter Hahn and Verena Reupke and Karin Holke and Peter Herrmann and Eleonora Duscio and Francesco Cipulli and Onnen Moerer and Marini, {John J.} and Michael Quintel and Luciano Gattinoni",
year = "2019",
month = jan,
day = "1",
doi = "10.1097/ALN.0000000000002458",
language = "English",
volume = "130",
pages = "119--130",
journal = "Anesthesiology",
issn = "0003-3022",
publisher = "Lippincott Williams and Wilkins",
number = "1",

}

RIS (suitable for import to EndNote) Download

TY - JOUR

T1 - Positive End-expiratory Pressure and Mechanical Power

AU - Collino, Francesca

AU - Rapetti, Francesca

AU - Vasques, Francesco

AU - Maiolo, Giorgia

AU - Tonetti, Tommaso

AU - Romitti, Federica

AU - Niewenhuys, Julia

AU - Behnemann, Tim

AU - Camporota, Luigi

AU - Hahn, Günter

AU - Reupke, Verena

AU - Holke, Karin

AU - Herrmann, Peter

AU - Duscio, Eleonora

AU - Cipulli, Francesco

AU - Moerer, Onnen

AU - Marini, John J.

AU - Quintel, Michael

AU - Gattinoni, Luciano

PY - 2019/1/1

Y1 - 2019/1/1

N2 - WHAT WE ALREADY KNOW ABOUT THIS TOPIC: WHAT THIS ARTICLE TELLS US THAT IS NEW: BACKGROUND:: Positive end-expiratory pressure is usually considered protective against ventilation-induced lung injury by reducing atelectrauma and improving lung homogeneity. However, positive end-expiratory pressure, together with tidal volume, gas flow, and respiratory rate, contributes to the mechanical power required to ventilate the lung. This study aimed at investigating the effects of increasing mechanical power by selectively modifying its positive end-expiratory pressure component. METHODS: Thirty-six healthy piglets (23.3 ± 2.3 kg) were ventilated prone for 50 h at 30 breaths/min and with a tidal volume equal to functional residual capacity. Positive end-expiratory pressure levels (0, 4, 7, 11, 14, and 18 cm H2O) were applied to six groups of six animals. Respiratory, gas exchange, and hemodynamic variables were recorded every 6 h. Lung weight and wet-to-dry ratio were measured, and histologic samples were collected. RESULTS: Lung mechanical power was similar at 0 (8.8 ± 3.8 J/min), 4 (8.9 ± 4.4 J/min), and 7 (9.6 ± 4.3 J/min) cm H2O positive end-expiratory pressure, and it linearly increased thereafter from 15.5 ± 3.6 J/min (positive end-expiratory pressure, 11 cm H2O) to 18.7 ± 6 J/min (positive end-expiratory pressure, 14 cm H2O) and 22 ± 6.1 J/min (positive end-expiratory pressure, 18 cm H2O). Lung elastances, vascular congestion, atelectasis, inflammation, and septal rupture decreased from zero end-expiratory pressure to 4 to 7 cm H2O (P < 0.0001) and increased progressively at higher positive end-expiratory pressure. At these higher positive end-expiratory pressure levels, striking hemodynamic impairment and death manifested (mortality 0% at positive end-expiratory pressure 0 to 11 cm H2O, 33% at 14 cm H2O, and 50% at 18 cm H2O positive end-expiratory pressure). From zero end-expiratory pressure to 18 cm H2O, mean pulmonary arterial pressure (from 19.7 ± 5.3 to 32.2 ± 9.2 mmHg), fluid administration (from 537 ± 403 to 2043 ± 930 ml), and noradrenaline infusion (0.04 ± 0.09 to 0.34 ± 0.31 μg · kg · min) progressively increased (P < 0.0001). Lung weight and lung wet-to-dry ratios were not significantly different across the groups. The lung mechanical power level that best discriminated between more versus less severe damage was 13 ± 1 J/min. CONCLUSIONS: Less than 7 cm H2O positive end-expiratory pressure reduced atelectrauma encountered at zero end-expiratory pressure. Above a defined power threshold, sustained positive end-expiratory pressure contributed to potentially lethal lung damage and hemodynamic impairment.

AB - WHAT WE ALREADY KNOW ABOUT THIS TOPIC: WHAT THIS ARTICLE TELLS US THAT IS NEW: BACKGROUND:: Positive end-expiratory pressure is usually considered protective against ventilation-induced lung injury by reducing atelectrauma and improving lung homogeneity. However, positive end-expiratory pressure, together with tidal volume, gas flow, and respiratory rate, contributes to the mechanical power required to ventilate the lung. This study aimed at investigating the effects of increasing mechanical power by selectively modifying its positive end-expiratory pressure component. METHODS: Thirty-six healthy piglets (23.3 ± 2.3 kg) were ventilated prone for 50 h at 30 breaths/min and with a tidal volume equal to functional residual capacity. Positive end-expiratory pressure levels (0, 4, 7, 11, 14, and 18 cm H2O) were applied to six groups of six animals. Respiratory, gas exchange, and hemodynamic variables were recorded every 6 h. Lung weight and wet-to-dry ratio were measured, and histologic samples were collected. RESULTS: Lung mechanical power was similar at 0 (8.8 ± 3.8 J/min), 4 (8.9 ± 4.4 J/min), and 7 (9.6 ± 4.3 J/min) cm H2O positive end-expiratory pressure, and it linearly increased thereafter from 15.5 ± 3.6 J/min (positive end-expiratory pressure, 11 cm H2O) to 18.7 ± 6 J/min (positive end-expiratory pressure, 14 cm H2O) and 22 ± 6.1 J/min (positive end-expiratory pressure, 18 cm H2O). Lung elastances, vascular congestion, atelectasis, inflammation, and septal rupture decreased from zero end-expiratory pressure to 4 to 7 cm H2O (P < 0.0001) and increased progressively at higher positive end-expiratory pressure. At these higher positive end-expiratory pressure levels, striking hemodynamic impairment and death manifested (mortality 0% at positive end-expiratory pressure 0 to 11 cm H2O, 33% at 14 cm H2O, and 50% at 18 cm H2O positive end-expiratory pressure). From zero end-expiratory pressure to 18 cm H2O, mean pulmonary arterial pressure (from 19.7 ± 5.3 to 32.2 ± 9.2 mmHg), fluid administration (from 537 ± 403 to 2043 ± 930 ml), and noradrenaline infusion (0.04 ± 0.09 to 0.34 ± 0.31 μg · kg · min) progressively increased (P < 0.0001). Lung weight and lung wet-to-dry ratios were not significantly different across the groups. The lung mechanical power level that best discriminated between more versus less severe damage was 13 ± 1 J/min. CONCLUSIONS: Less than 7 cm H2O positive end-expiratory pressure reduced atelectrauma encountered at zero end-expiratory pressure. Above a defined power threshold, sustained positive end-expiratory pressure contributed to potentially lethal lung damage and hemodynamic impairment.

UR - http://www.scopus.com/inward/record.url?scp=85059253266&partnerID=8YFLogxK

U2 - 10.1097/ALN.0000000000002458

DO - 10.1097/ALN.0000000000002458

M3 - Article

C2 - 30277932

AN - SCOPUS:85059253266

VL - 130

SP - 119

EP - 130

JO - Anesthesiology

JF - Anesthesiology

SN - 0003-3022

IS - 1

ER -

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