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Acute Pulmonary Oedema (acute + pulmonary_oedema)
Selected AbstractsOpiates and acute pulmonary oedema: Addicted to the wrong therapyEMERGENCY MEDICINE AUSTRALASIA, Issue 5 2008Luke Hermann No abstract is available for this article. [source] Validation of a tool to safely triage selected patients with chest pain to unmonitored bedsEMERGENCY MEDICINE AUSTRALASIA, Issue 4 2002Ronald V Sultana Abstract Objective: To externally validate a chest pain protocol that triages low risk patients with chest pain to an unmonitored bed. Methods: Retrospective study of all patients admitted from the emergency department of a tertiary referral public teaching hospital with an admission diagnosis of ,unstable angina' or suspected ischemic chest pain. Data was collected on adverse outcomes and analysed on the basis of intention-to-treat according to the chest pain protocol. Results: There were no life-threatening arrhythmias, cardiac arrests or deaths within the first 72 h of admission in the group assigned to an unmonitored bed by the chest pain protocol ([0/244]; 0.0%: 95% confidence interval 0.0,1.5%). Four patients had an uncomplicated myocardial infarction, two patients had recurrent ischemic chest pain and one patient developed acute pulmonary oedema ([7/244]; 2.9%: 95% confidence interval 1.2,5.8%). Conclusion: This retrospective study externally validated the chest pain protocol. Care in a monitored bed would not have altered outcomes for patients triaged to an unmonitored bed by the chest pain protocol. Compared to current guidelines, application of the chest pain protocol could increase the availability of monitored beds. [source] Role of proteinuria in defining pre-eclampsia: Clinical outcomes for women and babiesCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 4 2010Charlene E Thornton Summary 1.,The presence of proteinuria is not essential to the diagnosis of pre-eclampsia under many diagnostic consensus statements. The aim of the present study was to assess maternal and perinatal outcomes after proteinuric pre-eclampsia compared with other non-proteinuric disease presentations. 2.,An individual patient data review (n = 670) was undertaken for 2003,2006 at a tertiary referral centre in Sydney (NSW, Australia). Women were diagnosed in accordance with the Australasian Society for the Study of Hypertension in Pregnancy Consensus Statement. Data were analysed with the Chi-squared test, t -tests and non-parametric tests. Statistical significance was set at P < 0.05. 3.,The proteinuric cohort had higher systolic and diastolic blood pressure recordings than the non-proteinuric cohort (160/102 and 149/94 mmHg, respectively; P < 0.001), and were also administered magnesium sulphate more frequently (44 vs 22%, respectively; P < 0.001), delivered at earlier gestation (37 vs 38 weeks, respectively; P < 0.001), required operative delivery more frequently (63 vs 48%, respectively; P < 0.001) and received more antihypertensive medications during the antenatal period (72 vs 57%, respectively; P < 0.001). Acute renal failure and acute pulmonary oedema were rare. Four cases of eclampsia all occurred in non-proteinuric women. The perinatal mortality rate was lower for the offspring of women with proteinuric pre-eclampsia compared with offspring of non-proteinuric women (13/1000 and 31/1000, respectively; P = 0.006). 4.,The results of the present study indicate that the presence of proteinuria denotes a group of women who have higher antenatal blood pressure, who deliver at earlier gestation and require operative delivery more commonly, although it is not an indicator of other markers of maternal morbidity or perinatal mortality. [source] The Lung Is The Major Site That Produces Nitric Oxide To Induce Acute Pulmonary Oedema In Endotoxin ShockCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 4 2001Ru Ping Lee SUMMARY 1. The present study was undertaken to determine the locus of nitric oxide (NO) production that is toxic to the lung and produces acute pulmonary oedema in endotoxin shock, to examine and compare the effects of changes in lung perfusate on endotoxin-induced pulmonary oedema (EPE) and to evaluate the involvement of constitutive and inducible NO synthase (cNOS and iNOS, respectively). 2. Experiments were designed to induce septic shock in anaesthetized rats with the administration of Escherichia coli lipopolysaccharide (LPS). Exhaled NO, lung weight (LW)/bodyweight (BW) ratio, LW gain (LWG) and lung histology were measured and observed to determine the degree of EPE 4 h following LPS. The EPE was compared between groups in which LPS had been injected either into the systemic circulation or into the isolated perfused lung. The lung perfusate was altered from whole blood to physiological saline solution (PSS) with 6% albumin to test whether different lung perfusions affected EPE. Pretreatment with various NOS inhibitors was undertaken 10 min before LPS to investigate the contribution of cNOS and iNOS to the observed effects. 3. Endotoxin caused profound systemic hypotension, but little change in pulmonary arterial pressure. The extent of EPE was not different between that induced by systemic injection and that following administration to isolated lungs preparations. Replacement of whole blood with PSS greatly attenuated (P < 0.05) EPE. In blood-perfused lungs, pretreatment with NOS inhibitors, such as N, -nitro- L -arginine methyl ester, aminoguanidine and dexamethasone, significantly prevented EPE (P < 0.05). 4. The major site of NO production through the whole blood is in the lung. The NO production mediated by the iNOS system is toxic to the endothelium in the pulmonary microvasculature. Inhalation of NO for patients with sepsis may be used with clinical caution. Therapeutic consideration of lung extracorporeal perfusion with PSS and pharmacological pretreatment with iNOS inhibitors may be warranted. [source] | ||||||||||