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Wet-to-dry weight ratios rose from four.82 ?0.16 in control animals to six.34 ?0.83 in the HTVMV group (P < 0.05, n = 4). Light microscopic examination of histologic sections showed mononuclear white cell infiltrates around small arteries and within the alveolar walls of mice in the HTVMV group but not in control mice. Elastance rose nonsignificantly during the HTVMV protocol. Conclusions In this in vivo mouse model, high tidal volume mechanical ventilation caused pulmonary edema and lung tissue infiltration with white blood cells. However, measurements of lung mechanics showed minimal changes during the course of the experiment, indicating that they are less useful in detecting early edema.Figure 1 (abstract P190)Figure 2 (abstract P190)P190 Pressure dependency of respiratory resistance in patients with acute lung injury and acute respiratory distress syndromeC Stahl1, H Knorpp1, S Schumann1, D Steinmann1, K M ler1, J Guttmann1 1An thesiologische Universit sklinik, Freiburg, Germany; 2Biomedical Engineering, HFU, Villingen-Schwenningen, Germany Critical Care 2007, 11(Suppl 2):P190 (doi: 10.1186/cc5350) Introduction The analysis of the nonlinearity of respiratory compliance to guide ventilator settings in ALI and ARDS is wellestablished. The pressure dependency (or volume dependency respectively) of respiratory resistance of these patients is mostly ignored. This study was performed to investigate the pressure dependency of resistance in ALI and ARDS over a wide range of pressures. Methods Twenty-one patients with ALI or ARDS were analyzed. Ventilation was interrupted by a respiratory manoeuvre: the volume was increased from ZEEP in steps of 100 ml with constant inspiratory flow until the plateau pressure reached 45 cmH2O. Each step was followed by a hold of 3 seconds. Inspiratory resistance during each step was determined by a least-squares fitting procedure. Results Resistance decreased from 10.7 ?5.1 cmH2O /l at 5 cmH2O to 8.1 ?4.0 cmH2O /l at 40 cmH2O (P < 0.05). Figure 1 shows individual absolute values and means ?SD of all patients. Most of the decrease was found up to 20 cmH2O; at higher pressures, changes were not uniform. The average relative changes in inspiratory resistance ( D) of all patients are shown in Figure 2. Conclusion Inspiratory resistance in ALI and ARDS is not constant. Especially at higher pressures, individual resistance may change unpredictably. The assumption of a constant resistance should therefore be avoided.SCritical CareMarch 2007 Vol 11 Suppl27th International Symposium on Intensive Care and Emergency MedicineP191 Alveolar microscopy: on the automatic determination of alveolar size during ventilationD Schwenninger1, K Moeller1, C Stahl2, S Schumann2, J Guttmann2 1Furtwangen University, Villingen-Schwenningen, Germany; 2University of Freiburg, Germany Critical Care 2007, 11(Suppl 2):P191 (doi: 10.1186/cc5351) PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/20740215 Introduction Alveolar microscopy appears to provide critical insight into alveolar dynamics for the duration of mechanical ventilation [1,2]. The utility of this strategy is restricted as a result of higher efforts necessary to evaluate sequences of images with respect to alveolar geometry. The evaluation ?performed by hand ?is time consuming, places a high cognitive load on the examiner and is error prone. Reproducibility of outcomes is low. This project aims to establish a GPR39-C3 manufacturer computer-assisted tool that supplies semi-automatic evaluation of video sequences acquired with alveolar endoscopy. Approaches We developed a computer program primarily based on Matl.

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Author: heme -oxygenase