Articles: respiratory-distress-syndrome.
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We describe two cases of pulmonary edema, bradycardia, and hypotension associated with massive verapamil overdose. A noncardiogenic etiology of the pulmonary edema was indicated in one patient by normal thermodilution cardiac output and pulmonary artery occlusion pressure, and in the other patient by a normal echocardiogram. We hypothesize that calcium channel blocker overdose predisposes patients to develop pulmonary edema.
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Am. J. Respir. Crit. Care Med. · Sep 1996
Comparative StudyEfficacy of tracheal gas insufflation in acute respiratory distress syndrome with permissive hypercapnia.
This study was conducted to assess the CO2-elimination efficiency of tracheal gas insufflation (TGI) in 20 patients with acute respiratory distress syndrome and to compare its efficacy during volume-controlled (VCV) and pressure-controlled ventilation (PCV). TGI was initially applied as an adjunct to VCV, with continuous flows (Vcath) of 4 and 6 L/min delivered through a catheter positioned 2 cm above the carina. Total effective tidal volume (VTeff) was held constant. ⋯ Twelve patients were subsequently switched to PCV combined with Vcath 6 L/min, which provided a % delta PaCO2 of 16.1 +/- 3.0% (p = NS versus 17.1 +/- 2.6% during VCV). These data suggest that in patients with ARDS the change in PETCO2 may be helpful in predicting the decrement in PaCO2 during TGI, and the existence of a high VDalv tends to limit its effectiveness. Further, the efficacy of TGI with VCV is equivalent to that with PCV.
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Critical care medicine · Sep 1996
Increased interleukin-8 concentrations in the pulmonary edema fluid of patients with acute respiratory distress syndrome from sepsis.
To test the hypothesis that significantly higher concentrations of interleukin-8 (IL-8) are found in the pulmonary edema fluid and plasma of patients with a septic vs. a nonseptic etiology of acute respiratory distress syndrome (ARDS). ⋯ The high concentrations of IL-8 in pulmonary edema fluid, coupled with the relatively low concentrations of IL-8 in the plasma, suggest that the lung was the primary source of IL-8 in the patients with ARDS. The markedly increased concentrations of IL-8 in the pulmonary edema fluid of patients with ARDS from sepsis suggests that this group of patients may be particularly suitable for potential trials directed at inhibiting the activity of this important chemokine.
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Adjunctive ventilatory strategies have been developed to improve oxygenation and carbon dioxide (CO2) removal during mechanical ventilation of critically ill patients. These techniques allow clinicians to attain their clinical goals at lower levels of ventilatory support. In this article, the authors discuss extracorporeal CO2 removal, venovenous intravena caval oxygenator, and tracheal gas insufflation as adjuncts to CO2 removal and nitric oxide, surfactant replacement therapy, perfluorocarbon-associated gas exchange, and prone positioning as adjuncts to oxygenation.
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Comparative Study
Bronchoalveolar and systemic cytokine profiles in patients with ARDS, severe pneumonia and cardiogenic pulmonary oedema.
The aim of this study was to investigate whether bronchoalveolar lavage (BAL) and serum levels of proinflammatory cytokines discriminate between different entities of patients with acute respiratory failure. BAL and circulating concentrations of interleukin-6 (IL-6), interleukin-8 (IL-8) and tumour necrosis factor-alpha (TNF-alpha) were measured in 74 mechanically-ventilated patients and 17 healthy controls. Patients were classified as cardiogenic pulmonary oedema (CPO), acute respiratory distress syndrome (ARDS), primary severe pneumonia (PN) and a combined group (PN+ARDS). ⋯ TNF-alpha was rarely detected in BAL samples, but increased serum concentrations were measured in ARDS and/or PN patients. Bronchoalveolar lavage levels of interleukin-6 and interleukin-8, but not tumour necrosis factor-alpha, and serum concentrations of interleukin-6 are consistently elevated in acute respiratory distress syndrome and/or severe pneumonia, discriminating these entities from cardiogenic pulmonary oedema. Alveolar and systemic cytokine profiles do not differentiate between acute respiratory distress syndrome in the absence of lung infection and states of severe primary or secondary pneumonia, which evidently present with comparable local and systemic inflammatory sequelae.