1999
DOI: 10.1001/jama.282.1.54
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Effect of Mechanical Ventilation on Inflammatory Mediators in Patients With Acute Respiratory Distress Syndrome

Abstract: Mechanical ventilation can induce a cytokine response that may be attenuated by a strategy to minimize overdistention and recruitment/derecruitment of the lung. Whether these physiological improvements are associated with improvements in clinical end points should be determined in future studies.

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Cited by 1,621 publications
(356 citation statements)
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References 44 publications
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“…99 Confirming that these strategies may target an important source of continued inflammation in the injured lung, both the pulmonary and systemic cytokine responses were reduced in a recent study of a protective ventilatory strategy. 100 Coagulation Pathway Dysregulation of the coagulation and fibrinolytic cascades has been well described in ALI/ARDS. [101][102][103] A variety of markers of activation of coagulation have been measured in the plasma, bronchoalveolar lavage fluid, or pulmonary edema fluid of patients at risk for 104 or with established ARDS 105,106 including tissue factor, a highly thrombogenic mediator in the extrinsic coagulation pathway.…”
Section: Oxidant-mediated Injurymentioning
confidence: 99%
“…99 Confirming that these strategies may target an important source of continued inflammation in the injured lung, both the pulmonary and systemic cytokine responses were reduced in a recent study of a protective ventilatory strategy. 100 Coagulation Pathway Dysregulation of the coagulation and fibrinolytic cascades has been well described in ALI/ARDS. [101][102][103] A variety of markers of activation of coagulation have been measured in the plasma, bronchoalveolar lavage fluid, or pulmonary edema fluid of patients at risk for 104 or with established ARDS 105,106 including tissue factor, a highly thrombogenic mediator in the extrinsic coagulation pathway.…”
Section: Oxidant-mediated Injurymentioning
confidence: 99%
“…Excessive volumes lead to high transpulmonary pressures with consequent stretch of the pulmonary tissues [29]. Recently, greater attention has been focused on intratidal collapse and reinflation, which can generate shear forces that increase capillary permeability and induce activation of inflammatory factors, leading to local and systemic inflammatory response ("biotrauma") [30].…”
Section: Ventilator-associated Lung Injury and The Prone Positionmentioning
confidence: 99%
“…The clinical implications of these changes suggest that patients with IAH may develop a secondary ARDS pattern with a cytokine profile and bacterial translocation propensity which creates a ventilatorinduced lung change resembling primary ARDS. 78,79 The ventilator strategy in these patients is specific and distinct from that of an ARDS case where the reduction in FRC and the trend towards pulmonary oedema suggests a role for a greater utilization of muscle relaxation and higher PEEP values despite its risk for barotrauma, 80 keeping alveoli recruited and open with permissive hypercapnia, a restricted tidal volume and peak inspiratory pressure that more readily permits weaning. 81,82 In summary the pulmonary effects of IAH are complex with diaphragmatic elevation increasing intra-thoracic and pleural pressure causing a reduction in FRC and all lung volumes commensurate with a restrictive lung deficit combined with basal compression atelectasis, with increases in mean, plateau and peak airway pressures and pulmonary vascular resistance.…”
Section: Respiratory System Dynamicsmentioning
confidence: 99%