Critical care medicine
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To describe the physiologic mechanisms of ventilator-induced lung injury and to define the major ventilator and host-dependent risk factors that contribute to such injury. ⋯ Ventilation with high tidal volumes can increase vascular filtration pressures; produce stress fractures of capillary endothelium, epithelium, and basement membrane; and cause lung rupture. Mechanical damage leads to leakage of fluid, protein, and blood into tissue and air spaces or leakage of air into tissue spaces. This process is followed by an inflammatory response and possibly a reduced defense against infection. Predisposing factors for lung injury are high peak inspiratory volumes and pressures, a high mean airway pressure, structural immaturity of lung and chest wall, surfactant insufficiency or inactivation, and preexisting lung disease. Damage can be minimized by preventing overdistention of functional lung units during therapeutic ventilation.
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To identify the neurologic complications of critical medical illnesses, and to assess their effect on mortality rates and on medical ICU and hospital lengths of stay. ⋯ Neurologic complications are associated with increased mortality rates and longer medical ICU and hospital lengths of stay. These conditions are probably underrecognized at present. ICUs have the potential to serve as environments for neurologic teaching and research.
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Critical care medicine · Jan 1993
Randomized Controlled Trial Comparative Study Clinical TrialAlterations in feline tracheal permeability after mechanical ventilation.
Previous investigations of ventilator-induced airway injury focused on histopathologic changes associated with various ventilators and strategies for their use. We hypothesized that mechanical ventilation is associated with alterations in tracheal epithelial permeability, and designed a study using an animal model to evaluate changes in tracheal epithelial permeability after administering different types of mechanical ventilation to test this hypothesis. ⋯ Mechanical ventilation was associated with increases in tracheal permeability to large and small nonionic molecules. These changes occurred with all studied ventilators, used as they are clinically. Permeability changes paralleled ventilatory rate changes.
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Critical care medicine · Jan 1993
Epinephrine as an inotropic agent in septic shock: a dose-profile analysis.
To characterize the acute actions and physiologic dose profile of epinephrine, as a single inotrope, in patients with septic shock. ⋯ Epinephrine increases DO2 in septic shock by increasing cardiac index without an effect on systemic vascular resistance index or PAOP.
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Critical care medicine · Jan 1993
Randomized Controlled Trial Multicenter Study Comparative Study Clinical TrialContinuous intravenous cimetidine decreases stress-related upper gastrointestinal hemorrhage without promoting pneumonia.
To determine whether a continuous i.v. infusion of cimetidine, a histamine-2 (H2) receptor antagonist, is needed to prevent upper gastrointestinal (GI) hemorrhage when compared with placebo and if that usage is associated with an increased risk of nosocomial pneumonia. Due to the importance of this latter issue, data were collected to examine the occurrence rate of nosocomial pneumonia under the conditions of this study. ⋯ The continuous i.v. infusion of cimetidine was highly effective in controlling intragastric pH and in preventing stress-related upper GI hemorrhage in critically ill patients without increasing their risk of developing nosocomial pneumonia. While the number of risk factors and intragastric pH may have pathogenic importance in the development of upper GI hemorrhage, neither the risk factors nor the intragastric pH was predictive. Therefore, short-term administration of continuously infused cimetidine offers benefits in patients who have sustained major surgery, trauma, burns, hypotension, sepsis, or single organ failure.