Citation: Academic Emergency Medicine. 2018 Aug 06.Journal: Academic emergency medicine : official journal of the Society for Academic Emergency Medicine.Published: 2018ISSN: 1069-6563.Full author list: Wallis MC; Wilson MD; Mete M; Koroshetz L; Soares R; Goyal M.UI/PMID: 30084149.Subject(s): IN PROCESS -- NOT YET INDEXEDInstitution(s): MedStar Health Research Institute | MedStar Washington Hospital CenterDepartment(s): Emergency MedicineActivity type: Journal Article.Medline article type(s): Journal ArticleOnline resources: Click here to access onlineDigital Object Identifier: https://dx.doi.org/10.1111/acem.13546 (Click here)Abbreviated citation: Acad Emerg Med. 2018 Aug 06.Local Holdings: Available online from MWHC library: 1997 - present, Available in print through MWHC library:2005-2007.Abstract: Pulmonary embolism (PE) is associated with approximately 100,000 deaths per year in the United States and the incidence of deep vein thrombosis/pulmonary embolism in the US is estimated at more than 350,000 cases annually (1). The diagnosis of pulmonary embolism poses a diagnostic challenge in the Emergency Department (ED), despite, validated decision rules, lab tests, and radiographic imaging (2, 3). While a simple lab test would be ideal for diagnosis, the well-known D-dimer test is, at its best, only about 54% specific (4). The gold standard pulmonary artery Computed Tomography Angiography (CTA) has numerous downsides including a requirement of clinical stability for transport to radiology, administration of potentially nephrotoxic contrast agents, and radiation exposure to patients, some of whom may be pregnant. Hemodynamically significant PE increases pulmonary dead space and therefore increases the alveolar dead space fraction, however calculating this involves invasive testing with ABG and a slightly cumbersome calculation (5, 6). Studies suggest that it is possible to use ETCO2 alone to screen for PE with the resultant increase in dead space causing the amount of exhaled ETCO2 to be lower in patients with clinically significant PE as opposed to invasive ABG testing (7, 8). However, these studies have typically included patients admitted to the hospital, which represent a fraction of those seen in the ED, and likely have a higher prevalence of PE. No study has prospectively evaluated real-time ETCO2 in ED patients suspected of having PE. We sought to determine if ETCO2 can rule out hemodynamically significant PE, hypothesizing that no patients with hemodynamically significant PE would have an ETCO2 greater than 35 mm Hg. Our secondary hypothesis was that the mean ETCO2 would be significantly lower in patients with PE versus those without PE. Full IRB approval was obtained through MedStar Washington Hospital Center's IRB prior to initiation of this study. This article is protected by copyright. All rights reserved.Abstract: Copyright This article is protected by copyright. All rights reserved.