Articles: mechanical-ventilation.
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Protective lung ventilation requires calculating predicted body weight (BW) from height. Thus, inaccuracy of height data in the electronic health record (EHR) is a risk factor for ventilator-induced lung injury. Charted height data often have uncertain accuracy. Study purposes were (1) to evaluate the difference between patient height charted in the EHR and predicted height (PH) from ulnar length and (2) to determine how the height data source affects predicted BW and the resulting values for protective tidal volume (V(T)). ⋯ For overall populations, mean height calculated from values charted in the EHR is similar to that estimated from ulnar length. However, for individuals, differences in height between the 2 sources can be large, leading to large differences in predicted BW and resultant V(T) set in terms of mL/kg.
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Editorial Randomized Controlled Trial Multicenter Study
THE ASSOCIATION BETWEEN PHYSIOLOGIC DEAD-SPACE FRACTION AND MORTALITY IN PATIENTS WITH THE ACUTE RESPIRATORY DISTRESS SYNDROME ENROLLED INTO A PROSPECTIVE MULTI-CENTERED CLINICAL TRIAL.
We tested the association between pulmonary dead-space fraction (ratio of dead space to tidal volume [V(D)/V(T)]) and mortality in subjects with ARDS (Berlin definition, P(aO2)/F(IO2) ≤ 300 mm Hg; PEEP ≥ 5 cm H2O) enrolled into a clinical trial incorporating lung-protective ventilation. ⋯ Markedly elevated V(D)/V(T) (≥ 0.60) in early ARDS is associated with higher mortality. Measuring V(D)/V(T) may be useful in identifying ARDS patients at increased risk of death who are enrolled into a therapeutic trial.
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Expert Rev Neurother · Jun 2014
EditorialNewly identified precipitating factors in mechanical ventilation-induced brain damage: implications for treating ICU delirium.
Delirium is 1.5 to 4.1 times as likely in intensive care unit patients when they are mechanically ventilated. While progress in treatment has occurred, delirium is still a major problem in mechanically ventilated patients. ⋯ This argues for minimizing the duration and tidal volumes of mechanical ventilation and for more effectively reducing sustained D2R signaling than achieved with haloperidol alone. The latter might be accomplished by reducing D2R cell surface expression and D2R-mediated Akt inhibition by elevating protein expression of dysbindin-1C.