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Intensive Care Medicine

, Volume 44, Issue 9, pp 1521–1523 | Cite as

Inspiratory preload obliteration may injure lungs via cyclical “on–off” vascular flow

  • B. H. Katira
  • W. M. Kuebler
  • B. P. KavanaghEmail author
What's New in Intensive Care

Introduction

Mechanical ventilation is the mainstay of supportive treatment for acute respiratory distress syndrome (ARDS) and high tidal volumes worsen outcome [1, 2]. The current paper considers how the pulmonary vasculature might participate in the development of ventilator-associated lung injury, and how recent research insights might ultimately be exploited in practice.

Vascular contributions to VILI

The status of the pulmonary vasculature can directly impact the development of ventilator-induced lung injury (VILI) via several mechanisms. Elevated pulmonary artery pressure, flow, or pulse frequency [3] can each potentiate VILI. Also, increased hydrostatic pressure in the microvasculature augments edema formation, and if permeability is also increased, the impact is synergistic. In addition, higher flow and hydrostatic pressure potentiate injury, as dopamine, administered to increase flow and pressure, caused injury despite “protective” ventilation [4].

Increased perfusion and...

Notes

Acknowledegements

Supported by the Canadian Institutes of Health Research, and the Dr. Geoffrey Barker Chair in Critical Care Research (BPK).

Compliance with ethical standards

Conflicts of interest

None of the authors have a financial conflict of interest with the subject matter of this manuscript.

Supplementary material

134_2017_5024_MOESM1_ESM.ppsx (39 kb)
Animation of heart–lung interaction during high V T ventilation. During inspiration, expanding lung obliterates the right ventricle and the pulmonary blood flow is absent. During expiration, with lung deflation the right ventricle overfills and pulmonary blood flow is high (PPSX 40 kb)

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Copyright information

© Springer-Verlag GmbH Germany, part of Springer Nature and ESICM 2017

Authors and Affiliations

  • B. H. Katira
    • 1
    • 3
  • W. M. Kuebler
    • 4
  • B. P. Kavanagh
    • 1
    • 2
    • 3
    Email author
  1. 1.Department of Critical Care MedicineHospital for Sick Children, University of TorontoTorontoCanada
  2. 2.Department of AnesthesiaHospital for Sick Children, University of TorontoTorontoCanada
  3. 3.Research Institute, Hospital for Sick ChildrenUniversity of TorontoTorontoCanada
  4. 4.Institute of Physiology, Charité, UniversitätsmedizineBerlinGermany

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