Inspiratory preload obliteration may injure lungs via cyclical “on–off” vascular flow
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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  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 .
Increased perfusion and...
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.
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