Adult Respiratory Distress Syndrome (ARDS) is characterized by an inflammatory process affecting endothelial and epithelial lung tissue, with occurrence of hypoxemia, bilateral X-ray infiltrates, in absence of cardiogenic edema. The introduction of Computerized Tomography brought some improvements in understanding the ARDS lung, leading to a pulmonary model made up of three zones: 1) normally inflated, 2) recruitable and 3) consolidated. It has now been well established that mechanical ventilation of ARDS lung presents some iatrogenic effects that may affect mortality. Several mechanisms are considered responsible of ventilator-associated lung injury (VALI): high inspired oxygen fraction, high inspiratory plateau pressure and large tidal volume, and intratidal collapse and reinflation of alveolar units. In these years, different ventilatory strategies in the treatment of ARDS patients have been suggested to decrease and to prevent VALI. The most important one seems to be the application of an appropriate value of tidal volume and positive end-expiratory pressure (PEEP). Several randomized studies, which compared low versus high tidal volumes, have recently been finished. Despite some differences, it seems that a ventilatory management limiting inspiratory plateau pressure to 35 cmH2O or lower may be useful to reduce VALI and mortality, also in association with a PEEP level sufficient to decrease the end-expiratory collapse. Another useful ventilatory tool for improving gas exchange and decreasing VALI in ARDS patients is likely the prone positioning, even if further studies are necessary to understand how this maneuver may really affect mortality. Another therapeutic instrument for improving oxygenation in ARDS patients is the inhalation of NO. Unfortunately, this pharmacological agent does not seem to affect the outcome of these patients.

[Mechanical ventilation in acute respiratory distress syndrome. New Trends]

CAIRONI, Pietro;
2000-01-01

Abstract

Adult Respiratory Distress Syndrome (ARDS) is characterized by an inflammatory process affecting endothelial and epithelial lung tissue, with occurrence of hypoxemia, bilateral X-ray infiltrates, in absence of cardiogenic edema. The introduction of Computerized Tomography brought some improvements in understanding the ARDS lung, leading to a pulmonary model made up of three zones: 1) normally inflated, 2) recruitable and 3) consolidated. It has now been well established that mechanical ventilation of ARDS lung presents some iatrogenic effects that may affect mortality. Several mechanisms are considered responsible of ventilator-associated lung injury (VALI): high inspired oxygen fraction, high inspiratory plateau pressure and large tidal volume, and intratidal collapse and reinflation of alveolar units. In these years, different ventilatory strategies in the treatment of ARDS patients have been suggested to decrease and to prevent VALI. The most important one seems to be the application of an appropriate value of tidal volume and positive end-expiratory pressure (PEEP). Several randomized studies, which compared low versus high tidal volumes, have recently been finished. Despite some differences, it seems that a ventilatory management limiting inspiratory plateau pressure to 35 cmH2O or lower may be useful to reduce VALI and mortality, also in association with a PEEP level sufficient to decrease the end-expiratory collapse. Another useful ventilatory tool for improving gas exchange and decreasing VALI in ARDS patients is likely the prone positioning, even if further studies are necessary to understand how this maneuver may really affect mortality. Another therapeutic instrument for improving oxygenation in ARDS patients is the inhalation of NO. Unfortunately, this pharmacological agent does not seem to affect the outcome of these patients.
2000
66
12
875
882
Respiratory Function Tests; Respiratory Distress Syndrome; Adult; Lung Injury; Respiration; Artificial
P. Pelosi; M. Aspesi; D. Franchi; G. Colombo; C. Gamberoni; P. Caironi; N. Bottino
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2318/1613581
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