Articles: respiratory-distress-syndrome.
-
Journal of critical care · Mar 1996
Diagnosis and therapy of acute respiratory distress syndrome in adults: an international survey.
In an attempt to identify the range of opinions influencing the diagnosis and therapy of patients with the adult respiratory distress syndrome (ARDS), a postal survey was mailed to 3,164 physician members of the American Thoracic Society Critical Care Assembly. The questionnaire asked opinions regarding the factors important in the diagnosis of ARDS and its treatment. Thirty-one percent of physicians surveyed responded within 4 weeks, the vast majority of which were board certified or eligible in Internal Medicine, Pulmonary Disease, and/or Critical Care Medicine. ⋯ It was reported that modest levels of positive end-expiratory pressure (PEEP) were used in incremental fashion as FiO2 requirements increased. Perceived indications for insertion of pulmonary artery catheters and compensation of the effects of PEEP on the pulmonary artery occlusion pressure varied widely among the responders. We conclude that reported practice patterns regarding the care of ARDS patients vary widely even within a relatively homogenous group of critical care practitioners.
-
Journal of critical care · Mar 1996
Pulmonary lactate release in patients with sepsis and the adult respiratory distress syndrome.
Elevated arterial lactate concentrations in patients with sepsis have been interpreted as evidence of peripheral, nonpulmonary tissue hypoxia. These patients often develop pulmonary failure manifested by the acute respiratory distress syndrome (ARDS). As the result of tissue hypoxia or inflammation, the lungs of patients with sepsis and ARDS may become a source of lactate release into the circulation. ⋯ The lungs of patients with sepsis and ARDS may produce lactate. Pulmonary lactate release correlates with the severity of lung injury. The contribution of pulmonary lactate release should be considered when interpreting arterial lactate concentration as an index of systemic hypoxia.
-
Intensive care medicine · Mar 1996
Clinical Trial Controlled Clinical TrialPhysiological effects of reduced tidal volume at constant minute ventilation and inspiratory flow rate in acute respiratory distress syndrome.
To assess the effect of changes in tidal volume (VT) with a constant inspiratory flow and minute ventilation (VE) on gas exchange and oxygen transport in acute respiratory distress syndrome (ARDS). ⋯ Tidal volumes can be reduced to 6-8 ml/kg in ARDS patients without compromising oxygen transport, while adequate CO2 elimination can be maintained.
-
Critical care medicine · Mar 1996
ReviewPerfluorocarbon-associated gas exchange improves oxygenation, lung mechanics, and survival in a model of adult respiratory distress syndrome.
To compare the effectiveness of perfluorocarbon-associated gas exchange to volume controlled positive pressure breathing in supporting gas exchange, lung mechanics, and survival in an acute lung injury model. ⋯ Perflurocarbon-associated gas exchange enhanced gas exchange, pulmonary mechanics, and survival in this model of acute lung injury.
-
Am. J. Respir. Crit. Care Med. · Mar 1996
Randomized Controlled Trial Comparative Study Clinical TrialDirect comparison of inhaled nitric oxide and aerosolized prostacyclin in acute respiratory distress syndrome.
Inhalation of NO and aerosolization of PGI2 have been suggested to achieve selective pulmonary vasodilation and improvement of arterial oxygenation in patients with ARDS. We directly compared these two modes of transbronchial vasodilator therapy in 16 ARDS patients mechanically ventilated (mean lung injury score [1] 2.75 +/- 0.05). Patients were randomized to receive either first NO and then PGI2, or vice versa. ⋯ Two further patients displayed an improvement of arterial oxygenation in response to either NO or PGI2. NO decreased mean pulmonary artery pressure from 34.8 +/- 2.2 to 33.0 +/- 1.8 mm Hg, and PGI2 from 35.0 +/- 2.2 to 31.9 +/- 1.7 mm Hg (p<0.05). We conclude that individually titrated doses of inhaled NO and aerosolized PGI2 effect selective pulmonary vasodilation and redistribute blood-flow from shunt-areas to well-ventilated regions with nearly identical efficacy profiles.