Current opinion in critical care
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The clinical relevance of experimental ventilator-induced lung injury has recently received a resounding illustration by the Acute Respiratory Distress Syndrome Network trial that showed a 22% reduction of mortality in patients with acute respiratory disease syndrome when lung mechanical stress was lessened by tidal volume reduction during mechanical ventilation. This clinical confirmation of the concept of ventilator-induced lung injury has also undisputedly substantiated the experimental observation that excessive tidal volume and/or end-inspiratory lung volume is the main determinant of ventilator-induced lung injury. More recently, attention has focused on the roles and implication in the pathogenesis of ventilator-induced lung injury of inflammatory cells and mediators that may be activated and released either in the alveolar space or in the systemic circulation because of the rupture of the alveolar-capillary barrier and on the cellular response to mechanical stress.
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Curr Opin Crit Care · Feb 2002
ReviewReduced tidal volumes and lung protective ventilatory strategies: where do we go from here?
Three major determinants of lung injury associated with mechanical ventilation have been clearly identified: high pressure/high volume, the shear forces caused by intratidal collapse and decollapse leading to barotrauma/volotrauma/biotrauma. The lung protective strategy aims to reduce the impact of all three determinants. A groundbreaking study showed that reduced tidal volume is less dangerous than high tidal volume, but the researchers did not apply "full" lung protective strategy and did not take into account the shear forces. "Full" protective lung strategy was tested in only one study and in a limited number of patients. Several physiologic studies strongly suggest the advantages of the lung protective strategy.
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Curr Opin Crit Care · Feb 2002
ReviewPulmonary versus extrapulmonary acute respiratory distress syndrome: different diseases or just a useful concept?
The acute respiratory distress syndrome may complicate both pulmonary and extrapulmonary conditions. There is a growing belief that the predisposition to, and clinical course of, the syndrome may be influenced by the extent to which the lung is directly involved in the precipitating pathologic changes. Several studies have highlighted differences in morphology and respiratory physiology between the two subgroups in the early stages of acute respiratory distress syndrome. ⋯ There are, however, inconsistencies between various studies addressing these issues, which may relate in part to differences in etiologic case mix. There are also practical difficulties in assigning certain cases to one of these two groups. Finally, there are as yet no outcome data to support any modification of clinical management on the basis of this distinction.
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Increased knowledge of the pathophysiologic mechanisms of impaired gas exchange during acute respiratory failure during recent years has stimulated many studies that evaluate different treatments to improve oxygenation and outcome. Changes in body position (mainly prone positioning) can significantly improve gas exchange in patients with acute respiratory distress syndrome and acute lung failure, with few complications related to the maneuver; however, no survival advantage has yet been detected. A correlation between aerated lung tissue and oxygenation also confirms the importance of recruitment maneuvers in improving gas exchange. ⋯ New data support the hypothesis that maintenance of even small amount of spontaneous breathing during mechanical ventilation (with airway pressure release ventilation or biphasic positive airway pressure) can improve gas exchange, whereas other unconventional ventilatory modes have not yet proved advantageous. Some mechanisms responsible for the high percentage of nonresponse to inhaled nitric oxide have recently been proposed, and combinations of inhaled nitric oxide with other therapies have been tested. Increased knowledge in this area may, in the future, make inhaled nitric oxide more attractive in the treatment of adult respiratory failure as well as in neonatal intensive care.
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On the basis of currently available data, it can be suggested that maintained spontaneous breathing during mechanical ventilation should not be suppressed even in patients with severe pulmonary dysfunction if no contraindications, such as increased intracranial pressure, are present. Improvements in pulmonary gas exchange, systemic blood flow, and oxygen supply to tissues, which have been observed when spontaneous breathing was allowed during ventilatory support, are reflected in the clinical improvement in the patient's condition, as indicated by significantly fewer days with ventilation, earlier extubation, and shorter stays in the intensive care unit. ⋯ If ventilatory modalities are limited to those whose positive effects have been documented, then partial ventilatory support can be used as a primary modality even in patients with severe pulmonary dysfunction. Whereas controlled mechanical ventilation followed by weaning with partial ventilatory support modalities has been the earlier standard in ventilation therapy, this approach should be reconsidered in view of the available data.