000			03444nam a22003737a 4500
008			180818s20182018 xxu||||| |||| 00| 0 eng d
022			_a1069-6563
024			_a10.1111/acem.13546 [doi]
040			_aOvid MEDLINE(R)
099			_a30084149
245			_aBedside End Tidal Carbon Dioxide in Evaluation for Pulmonary Embolism.
251			_aAcademic Emergency Medicine. 2018 Aug 06
252			_aAcad Emerg Med. 2018 Aug 06
253			_aAcademic emergency medicine : official journal of the Society for Academic Emergency Medicine
260			_c2018
260			_fFY2019
266			_d2018-08-16
501			_aAvailable online from MWHC library: 1997 - present, Available in print through MWHC library:2005-2007
520			_aCopyright This article is protected by copyright. All rights reserved.
520			_aPulmonary 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.
546			_aEnglish
650			_aIN PROCESS -- NOT YET INDEXED
651			_aMedStar Health Research Institute
651			_aMedStar Washington Hospital Center
656			_aEmergency Medicine
657			_aJournal Article
700			_aGoyal, Munish
700			_aMete, Mihriye
700			_aWallis, Marianne C
700			_aWilson, Matthew
790			_aGoyal M, Koroshetz L, Mete M, Soares R, Wallis MC, Wilson MD
856			_uhttps://dx.doi.org/10.1111/acem.13546 _zhttps://dx.doi.org/10.1111/acem.13546
942			_cART _dArticle
999			_c3661 _d3661