Newly Published
Critical Care Medicine  |   October 2018
Positive End-expiratory Pressure and Mechanical Power
Author Notes
  • From the Departments of Anesthesiology, Emergency and Intensive Care Medicine (F. Collino, F. Rapetti, F.V., G.M., T.T., F. Romitti, J.N., T.B., G.H., P.H., E.D., F. Cipulli, O.M., M.Q., L.G.), Experimental Animal Medicine (V.R.), and Pathology (K.H.), University of Göttingen, Göttingen, Germany; Department of Adult Critical Care, Guy’s and St Thomas’ National Health Service Foundation Trust, King’s Health Partners, and Division of Asthma, Allergy and Lung Biology, King’s College London, London, United Kingdom (L.C.); and Department of Pulmonary and Critical Care Medicine, Regions Hospital and University of Minnesota, Minneapolis/St. Paul, Minnesota (J.J.M.).
  • F. Collino and F. Rapetti contributed equally to this article.
    F. Collino and F. Rapetti contributed equally to this article.×
  • Supplemental Digital Content is available for this article. Direct URL citations appear in the printed text and are available in both the HTML and PDF versions of this article. Links to the digital files are provided in the HTML text of this article on the Journal’s Web site (www.anesthesiology.org).
    Supplemental Digital Content is available for this article. Direct URL citations appear in the printed text and are available in both the HTML and PDF versions of this article. Links to the digital files are provided in the HTML text of this article on the Journal’s Web site (www.anesthesiology.org).×
  • Submitted for publication April 3, 2018. Accepted for publication August 30, 2018.
    Submitted for publication April 3, 2018. Accepted for publication August 30, 2018.×
  • Acknowledgments: This work was made possible by the generous donation of Charlotte Munz, Göttingen, to the Department of Anesthesiology of Göttingen.
    Acknowledgments: This work was made possible by the generous donation of Charlotte Munz, Göttingen, to the Department of Anesthesiology of Göttingen.×
  • Research Support: Support was provided solely from institutional and/or departmental sources.
    Research Support: Support was provided solely from institutional and/or departmental sources.×
  • Competing Interests: The authors declare no competing interests.
    Competing Interests: The authors declare no competing interests.×
  • Correspondence: Address correspondence to Dr. Gattinoni: University of Göttingen, Robert-Koch-Straße 40, 37075 Göttingen, Germany. gattinoniluciano@gmail.com. Information on purchasing reprints may be found at www.anesthesiology.org or on the masthead page at the beginning of this issue. ANESTHESIOLOGY’s articles are made freely accessible to all readers, for personal use only, 6 months from the cover date of the issue.
Article Information
Critical Care Medicine / Critical Care / Respiratory System
Critical Care Medicine   |   October 2018
Positive End-expiratory Pressure and Mechanical Power
Anesthesiology Newly Published on October 1, 2018. doi:10.1097/ALN.0000000000002458
Anesthesiology Newly Published on October 1, 2018. doi:10.1097/ALN.0000000000002458
Abstract

Editor’s Perspective:

What We Already Know about This Topic:

  • Positive end-expiratory pressure protects against ventilation-induced lung injury by improving homogeneity of ventilation, but positive end-expiratory pressure contributes to the mechanical power required to ventilate the lung

What This Article Tells Us That Is New:

  • This in vivo study (36 pigs mechanically ventilated in the prone position) suggests that low levels of positive end-expiratory pressure reduce injury associated with atelectasis, and above a threshold level of power, positive end-expiratory pressure causes lung injury and adverse hemodynamics

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−1 · min−1) 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.