American journal of respiratory and critical care medicine
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Am. J. Respir. Crit. Care Med. · Aug 1995
Etiology of extubation failure and the predictive value of the rapid shallow breathing index.
Failure of weaning from mechanical ventilation is thought to result from an imbalance between respiratory muscle capacity and respiratory demand. The ratio of respiratory rate to tidal volume (f/VT, rapid shallow breathing index) during spontaneous unsupported respiration increases when this imbalance exists, and may predict the success or failure of weaning from mechanical ventilation. Using f/VT, Yang and Tobin demonstrated a positive predictive value (PPV) of 0.78 (f/VT < or = 105 and weaning success) (1). ⋯ This study confirms the high PPV for an f/VT < 100. The FPR of approximately 0.20 is best explained by extubation failure caused by processes for which f/VT is physiologically or temporally unlikely to predict success or failure. The negative predictive value (f/VT > or = 100 but extubation success) for f/VT may be lower than previously reported.
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Am. J. Respir. Crit. Care Med. · Aug 1995
Comparative StudyShould mechanical ventilation be optimized to blood gases, lung mechanics, or thoracic CT scan?
This study was aimed at providing data for optimization of mechanical ventilation in patients with acute respiratory distress syndrome (ARDS). The effects of ventilation with positive end-expiratory pressure (PEEP) titrated to blood gases were studied by thoracic computed tomographic (CT) scans and lung mechanics measurements in eight patients. CT density histograms at end-expiration were used to investigate the effects of PEEP on three differently aerated zones. ⋯ With regard to plateau pressures, only one patient was ventilated above the deflection point. However, monitoring of volumes showed that these four patients had an end-inspiratory volume above this point. We conclude that mechanical ventilation may be initially adjusted on the basis of blood gas values and then optimized on the basis of lung mechanics to limit the risk of baro-volotrauma.
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Am. J. Respir. Crit. Care Med. · Aug 1995
Effects of an antibody to interleukin-5 in a monkey model of asthma.
To investigate the role of interleukin-5 (IL-5) on airway hyperreactivity and pulmonary inflammation in nonhuman primate airways, the effect of a neutralizing monoclonal antibody to murine IL-5 (TRFK-5) was investigated in a cynomolgus monkey model of allergic asthma. Anesthetized Ascaris-sensitive monkeys underwent bronchoalveolar lavage (BAL) to assess the granulocyte content of this fluid before and 24 h after aerosolized Ascaris suum extract inhalation. Airway reactivity was assessed by the concentration of inhaled histamine required to produce a 40% reduction in dynamic lung compliance (Cdyn40). ⋯ In contrast, only small nonsignificant changes in airway reactivity and granulocyte influx into the BAL occurred after aerosolized saline as a sham challenge. When the monkeys were treated 1 h before Ascaris challenge with the TRFK-5 antibody (0.3 mg/kg, intravenously), there was no increase in airway reactivity after Ascaris challenge (Cdyn40 = 0.032 +/- 0.016% before Ascaris; Cdyn40 = 0.217 +/- 0.196% after Ascaris) and there were only small increases in the number of eosinophils and neutrophils in the BAL after Ascaris challenge. The inhibition of this pulmonary eosinophilia and bronchial hyperresponsiveness by TRFK-5 was seen for up to 3 mo after treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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Total venous return decreases with positive end-expiratory pressure (PEEP). It is likely that the liver plays an important role in this response, either through the development of an increase in venous resistance or through an increase in the venous backpressure at the outflow end of the liver. In addition, hepatic arterial flow is reported to be selectively decreased by the application of PEEP. ⋯ Ppvback and right atrial pressure (Pra) increased equally (from 5.1 +/- 0.3 to 9.9 +/- 0.4 mm Hg, p < 0.05, and from 4.0 +/- 0.2 to 8.6 +/- 0.5 mm Hg, p < 0.05, respectively, at PEEP 15). The reduction in portal venous flow was related to an increase in the backpressure to flow (as a result of an increase in Pra) and to an increase in liver venous resistances that may cause blood pooling in the splanchnic compartment and decrease venous return through the liver. PEEP increased Phaback (from 11.2 +/- 0.9 to 14.5 +/- 0.7 mm Hg at PEEP 15, p < 0.05) but did not change hepatic arterial resistance.(ABSTRACT TRUNCATED AT 250 WORDS)
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The aim of the study was to determine whether closing pressures or vascular distensibility can be used to describe liver venous hemodynamics when right atrial pressure is raised. The study was performed using a vascularly isolated pig liver preparation that allowed the independent control of portal vein and hepatic artery inflows and of outflow pressure (Pout). Pressure-flow (P-Q) relationships of both liver vessels were generated at multiple levels of Pout. ⋯ The behavior of the liver vein system is characterized by a zero flow pressure mimicking a classic vascular waterfall and by distensibility, once the waterfall is exceeded. Both factors act to minimize the reduction in venous return with an increased central venous pressure. Flow through the hepatic artery is affected by an increase in backpressure occurring upstream from the sinusoids, reducing arterial inflow for a constant perfusion pressure.