[Noninvasive determination of tracheal pressure in ventilated children--a model study].
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Biomedical subjects
Publications and source records attributed to K Geiger.
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PURPOSE: Acute Lung Injury (ALI) is a clinical condition which is associated with a high lethality. It is characterized by an increased pulmonary capillary permeability and non-cardiogenic pulmonary edema. This study was designed to answer the question whether double isotope albumin-flux measurement is a useful tool both for diagnosis of increased pulmonary capillary permeability and for monitoring therapeutic interventions (nitric oxide (NO) inhalation). METHOD: In 12 patients with clinical signs of ALI, transvascular albumin-flux was measured by a double radioisotope technique before, during and after NO inhalation. 99mTc labeled albumin and 51Cr labeled autologous erythrocytes were used as tracer. The radioactivity of both radiopharmaceuticals was measured externally over the right lung by a radiation probe and simultaneously in arterial blood. For quantification of transvascular albumin-flux Normalized Index (NI) and Normalized Slope Index (NSI) were calculated. Furthermore, pulmonal vascular pressures and other physiological parameters were recorded. RESULTS: All 12 patients showed markedly increased NSI before inhalation of NO. NSI decreased from 0.0074 +/- 0.0046 min-1 without nitric oxide to -0.0051 +/- 0.0041 min-1 during nitric oxide and increased to 0.0046 +/- 0.0111 min-1 after nitric oxide. The decrease of the NSI correlated well with decrease of venous pulmonary resistance during inhalation of NO. CONCLUSION: Inhalation of NO reduces transvascular albumin-flux in patients with ALI. Double isotope albumin-flux measurement enables diagnosis of increased capillary permeability as well as monitoring therapeutic interventions.
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OBJECTIVE: To develop a scoring system for stratifying patients in intensive care units (ICUs) by risk of developing nosocomial pneumonia (NP), based on variables generally available in an ICU, and to determine the probability of a patient developing NO in the ICU. DESIGN AND SETTING: a 2-year prospective cohort study conducted in a medical and surgical ICU. PATIENTS: 756 patients admitted to the ICU for 48 h or more were followed up until the development of NP or death or discharge from the ICU. MEASUREMENTS AND RESULTS: 129 (17.1%) patients developed NP, 106 (14%) in the first 2 weeks. The following independent risk factors were identified by multivariate analysis: no infection on admission [relative risk (RR) = 3.1, 95% confidence intervals (CI) = 2.0 to 4.81; thorax drainage (RR = 2.1, 95% CI = 1.2 to 3.5); administration of antacids (RR = 2.1, 95% CI = 1.4 to 3.1); partial pressure of oxygen (PO2) > 110 mmHg (RR = 1.6, 95% CI = 1.0 to 2.6); administration of coagulation factors (RR = 1.8 95% CI = 1.0 to 3.2); male gender (RR = 2.7, 95% CI = 1.2 to 6.3); urgent surgery (RR = 2.4, 95% CI = 0.9 to 6.4); and neurological diseases (RR = 4.2, 95% CI = 1.9 to 9.4). To obtain a predictive risk index for NP, a scoring system was developed using a multivariate model. The probability of developing NP varied between 11.0% in the lowest risk group and 42.3% in the highest risk group. The patients' risk of acquiring NP was seven times higher in the highest score category (i.v.) than in the lowest one (I). CONCLUSIONS: ICU patients can be stratified into high- and low-risk groups for NP. No infection on admission, thorax drainage, administration of antacids, and PO2 > 110 mmHg were associated with a higher risk of NP during the entire 2-week period.
OBJECTIVE: Study on simultaneous O2 supply/uptake relationships in liver and gut during endotoxaemia, to determine whether signs of dysoxia develop uniformly in the splanchnic region. DESIGN: Animal study to assess the early effects of endotoxaemia on oxygenation of both liver and small intestine. INTERVENTIONS: Eight anaesthetized pigs received a continuous portal venous infusion of lipopolysaccharide (0.5 microgram.kg-1.h-1) for 6 h. Systemic, pulmonary and splanchnic haemodynamics as well as systemic and splanchnic O2 supply/uptake relationships were determined. RESULTS: There was a multiphasic haemodynamic response pattern characterized by an early (within the 1st h) and a subsequent more prolonged phase (between the 2nd and 6th h) of decreases and recovery of hepatic arterial, portal venous and superior mesenteric arterial blood flows (electromagnetic flow probes) and splanchnic O2 deliveries. Unrelated to perfusion pressure and O2 delivery, there were early and sustained decreases in ileal mucosal surface partial pressure of oxygen (PO2) (multiwire PO2 electrode) and pH (tonometry). This was not reflected by ileal serosal surface PO2, O2 uptake and arteriomesenteric venous pH and partial pressure of carbon dioxide (PCO2) gradients. There was little evidence of concomitant hepatic dysoxia as evaluated by surface PO2. CONCLUSIONS: The study demonstrates early and sustained regional (mucosa) intestinal hypoxia with little evidence of simultaneous hepatic dysoxia during initial endotoxaemia.
BACKGROUND: It has been shown that inhaled nitric oxide (NO) reduces intrapulmonary venous admixture (QVA/QT) and improves oxygenation in patients suffering from acute respiratory distress syndrome (ARDS). The change in QVA/QT during NO inhalation varies individually. Factors known to influence the respiratory response to NO are the NO concentration and the level of shunt before NO administration. Other factors that may modify the effect on gas-exchange during NO breathing are unknown. METHODS: We studied the effect of 40 ppm inhaled NO on pulmonary gas-exchange and haemodynamics in 37 patients with acute lung injury (ALI) and ARDS, respectively, and factors that may influence the respiratory response to NO. RESULTS: Inhalation of 40 ppm NO produced a decrease in mean pulmonary artery pressure (MPAP) from 33.1 +/- 7.2 to 30.2 +/- 6.8 (mean +/- SD) mmHg (P < 0.0001) while pulmonary artery wedge pressure (PAWP), cardiac output and mean arterial pressure remained constant. Change in QVA/QT during NO inhalation depended on the preinhalation cardiac output and had no association with mixed venous oxygen tension, MPAP-PAWP, and QVA/QT before NO delivery. QVA/QT decreased in 26 patients (group 1) and increased in 11 patients (group 2) during NO inhalation. In group 1, cardiac output was lower than in group 2 (8.6 vs 12.2 l.min-1; P < 0.0005). CONCLUSION: We conclude that the change in venous admixture during inhalation of 40 ppm NO depends on cardiac output. If preinhalation cardiac output is high, 40 ppm NO can adversely affect gas exchange in patients with ALI and ARDS.
Navigation in honeybees is discussed against the background of the types of memories employed in the navigational task. Two questions are addressed. Do bees have goal-specific expectations, and when are novel routes travelled? Expectations are deduced from (1) context stimuli as determinants for local cue memories, (2) landmark-dependent path integration, (3) sequential learning of landmarks, and (4) motivation- and context-dependent memory retrieval. Novel routes are travelled under two conditions: (1) goal-cue-based piloting and (2) integration of simultaneously activated vector memories. Our data do not support the conclusion that memory integration in bees is organised by a cognitive map. The assumption of purely separate memories that are only retrieved according to the chain of events during navigational performance also appears to be inadequate. We favour the view that multiple memories are integrated using external and internal sources of information. Such configural memories lead to both specific expectations and novel routes.
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