Articles: respiratory-distress-syndrome.
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Monaldi Arch Chest Dis · Oct 1995
ReviewRole of surfactant in the pathophysiology of the acute respiratory distress syndrome (ARDS).
Acute respiratory distress syndrome (ARDS) has become a well-recognized condition that can result from a number of different causes that lead to injury of the alveolar-capillary membrane. This results in high-permeability pulmonary oedema that disturbs the pulmonary surfactant system. In ARDS, the treatments available are still inadequate and morbidity, mortality, and costs remain unacceptably high. ⋯ It has been suggested that the increased permeability changes, along with the inflammatory response, lead to accumulation of plasma components in the alveolar space, causing inhibition of the instilled surfactant in a dose-dependent way. Thus, for treatment of ARDS, a high concentration of surfactant is required to overcome the inhibitory effect of plasma components. However, a few questions remain unanswered, including: When should surfactant treatment start? Which dosage? Of which type of surfactant? Which method of administration should be used, in combination with which type of ventilatory support, etc.?
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To review the pathophysiology, epidemiology, and therapy of patients with acute respiratory distress syndrome (ARDS). ⋯ The mortality of ARDS continues to be 70%. Pharmacists can play an active role in the supportive therapy of patients with ARDS, which is currently the only way to impact mortality.
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Clinical Trial Controlled Clinical Trial
Interleukin 8-related neutrophil elastase and the severity of the adult respiratory distress syndrome.
The interaction between activated neutrophils and pulmonary endothelium is thought to contribute to the pathogenesis of the adult respiratory distress syndrome (ARDS), but its relation to ARDS severity, which may support a pathogenetic role, is unclear. Therefore, circulating inflammatory mediators, including the neutrophil chemoattractant and activator interleukin 8 (IL-8), the acute phase cytokine IL-6, and the neutrophil product elastase complexed to alpha 1-antitrypsin (alpha 1-AT), were measured prospectively, together with gas exchange, ventilatory and radiographic variables, in 13 mechanically ventilated patients with ARDS, mostly owing to sepsis, at admission into the intensive care unit. Measurements were repeated in the eight improving patients at the time that positive end-expiratory pressure could be reduced to 0 cm H2O. ⋯ For pooled data, the LIS and the arterial PO2/inspiratory O2 fraction, the oxygenation ratio, correlated with plasma levels of IL-8 (rs = 0.60, P < 0.01 and rs = -0.65, P < 0.005, respectively), with levels of IL-6 (rs = 0.60, P < 0.01, and rs = -0.68, P < 0.005, respectively), and the oxygenation ratio related to elastase-alpha 1-AT (rs = -0.70, P < 0.005). Levels of IL-8 and IL-6 interrelated (rs = 0.61, P < 0.01) and related to the elastase complexes (rs = 0.45, P < 0.05). Hence, our data support a role of cytokine-induced activation of neutrophils in the clinical severity of ARDS.
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Revista médica de Chile · Oct 1995
Review Case Reports[Extracorporeal membrane oxygenation in adult respiratory distress syndrome. Experience in 2 patients].
We report two female patients with adult respiratory distress syndrome and severe respiratory failure in whom extracorporeal membrane oxygenation was used. Its indication was due to a bad response to conventional treatment with mechanical ventilation and high levels of positive end expiratory pressure. A 2.0 or 2.2 m2 membrane oxygenator in a veno-venous circuit with systemic anticoagulation was used, maintaining mechanical ventilation. ⋯ The second patient was connected to the procedure after three weeks of respiratory distress syndrome and no increase in arterial oxygenation was achieved. The patient died due to an intracranial hemorrhage, probably hastened by systemic anticoagulation. The real benefits of extracorporeal membrane oxygenation are not defined yet.
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Comparative Study
Cardiopulmonary effects of positive pressure ventilation during acute lung injury.
To assess the gas exchange and hemodynamic effects of pressure-limited ventilation (PLV) strategies in acute lung injury (ALI). We hypothesized that in ALI, the reduction of plateau airway pressure (Paw) would be associated with less alveolar overdistention and thus have better hemodynamic and gas exchange characteristics than larger tidal volume (Vr) ventilation. ⋯ Changes in lung volume determine Ppc and Ppl. PLV strategies do not alter hemodynamics but result in less of an increase in VD/VT than would be predicted from the obligatory decrease in VT.