Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về ngành y học đề tài: Respiratory pulse pressure variation fails to predict fluid responsiveness in acute respiratory distress syndrome. | Lakhal et al. Critical Care 2011 15 R85 http content 15 2 R85 KS CRITICAL CARE RESEARCH Open Access Respiratory pulse pressure variation fails to predict fluid responsiveness in acute respiratory distress syndrome Karim Lakhal1 Stephan Ehrmann2 Dalila Benzekri-Lefevre3 Isabelle Runge3 Annick Legras2 2 2 11 3 Pierre-Frangois Dequin Emmanuelle Mercier Michel Wolff Bernard Régnier Thierry Boulain Abstract Introduction Fluid responsiveness prediction is of utmost interest during acute respiratory distress syndrome ARDS but the performance of respiratory pulse pressure variation ArespPP has scarcely been reported. In patients with ARDS the pathophysiology of ArespPP may differ from that of healthy lungs because of low tidal volume Vt high respiratory rate decreased lung and sometimes chest wall compliance which increase alveolar and or pleural pressure. We aimed to assess ArespPP in a large ARDS population. Methods Our study population of nonarrhythmic ARDS patients without inspiratory effort were considered responders if their cardiac output increased by 10 after 500-ml volume expansion. Results Among the 65 included patients 26 responders the area under the receiver-operating curve AUC for ArespPP was 95 confidence interval CI95 to and a best cutoff of 5 yielded positive and negative likelihood ratios of CI95 to and CI95 to respectively. Adjusting ArespPP for Vt airway driving pressure or respiratory variations in pulmonary artery occlusion pressure APAOP a surrogate for pleural pressure variations in 33 Swan-Ganz catheter carriers did not markedly improve its predictive performance. In patients with APAOP above its median value 4 mmHg AUC for ArespPP was 1 CI95 to 1 as compared with CI95 to otherwise P . A 300-ml volume expansion induced a 2 mmHg increase of central venous pressure suggesting a change in cardiac preload in 40 patients but none of the 28 of 40 nonresponders responded to an .
